CERVICAL CONDITIONS Pathophysiology:
- Acceleration-Deceleration Injuries
Cervical Axial Pain
Cervical Strain and Sprains
Cervical Radiculopathy and Radicular
Pain
Cervical Joint Pain
Cervical Internal Disk Disruption
Cervical Myelopathy
Cervicogenic Headaches
Torticollis
GENERAL MEDICAL BACKGROUND
Definition
- Cervical Axial Pain: Pain occurring in all
or part of the area extending from the
inferior occiput to the superior
interscapular region, localizing to the
midline or paramidline
Epidemiology
- Occupational cervical complaints
increases with age
• 10% at age of 25
• 35% at age of 40
• 95% at age of 65
- Cervical radiculopathy occurs less
commonly
Etiology
- Degenerative changes
- Trauma
- Affectations of the IV disc, facet joints,
cervical ligaments and muscles
COMMON CLINICAL DISORDERS
A. Cervical Strain and Sprains
Definition:
- Cervical strain: Musculotendinous injury
produced by an overload injury due to
excessive forces imposed on the cervical
spine.
- Cervical sprain: Overstretching or
tearing injuries of spinal ligaments
Epidemiology:
- 85% of neck pain results from acute,
repetitive, or chronic neck injuries
- Increase risk in women and individuals
30-50 years old
- Automobile-related cervical sprain and
strain injuries are more common in
western societies and in metropolitan
areas having higher densities of motor
vehicles
Etiology:
- Non-catastrophic sports injury
- Motor vehicle accident
- Trauma or abnormal stress applied to
cervical spine
• After a rear-end impact, head
initiates forward flexion followed by
rapid eccentric extension, increasing
the risk of injury
- Physiological forces acting on normal
cervical spine results to typical soft
tissue strain in non-athletes
- In individuals with thoracic kyphosis and
consequential cervical lordosis and
extension, strain occurs in the Levator
Scapulae, Superior Trapezius,
Sternocleidomastoid, scalene and
Suboccipital muscles
- Repetitive motions (recreational
activities) can shorten and decondition
Cervical Rotators, Extensors and lateral
Flexors that are present in those with
cervical spondylosis
Clinical Manifestations
- Sharp or dull headache localize to the
cervical or shoulder girdle musculature
- Sharp or dull neck pain often localized
- Neck fatigue or stiffness that lessens
with gradual activity
- Decreased cervical Range of Motion
Diagnosis
- Imaging and electro-diagnostic
evaluations are not indicated unless
neurologic or motor abnormalities are
detected
- Plain radiography to evaluate bony
misalignment or fractures
- X-rays to evaluate for instability prior to
prescribing rehabilitation
Points of Emphasis in Examination
- History of the mechanism of injury: an
acute event of MVA, sports injury, fall,
or industrial accident
- Exact onset of pain
- Location of symptoms, any referral
pattern, or associated symptoms
- Range of Motion
- Manual Muscle Testing
- Palpation of involved region which is
usually uncomfortable or moderately
painful
Medical, Surgical, and Pharmacologic
Management
- Pharmacologic approach:
• NSAIDs and Acetaminophen to
control pain and nurture restorative
sleep patterns
• Muscle Relaxants: To improve sleep
• Tizanidine or Tricyclic Anti-
Depressants for spasms not
improved by analgesics or proper
positioning
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PT Management • Computed tomographic
- Light massage: For sedation, reduction myelography: Gold standard against
of adhesions, muscular relaxation and which other imaging modalities
vascular changes ought to be judged in evaluating
- Superficial and Deep Heat with degenerative cervical spine
Ultrasound: For analgesia and muscle conditions
relaxation, resolve inflammation, • MRI: Modality of choice for cervical
increase connective tissue elasticity radiculopathy because it details
- TENS: Modulating musculoskeletal pain disk, ligamentous, osseous, and
- Soft Cervical Collar: To ease painful neural tissue very well.
sleep disturbance and reduce further - Electro-diagnostic evaluation
neck strain • Nerve conduction studies and
electromyography: Used to assess
B. Cervical Radiculopathy and Radicular Pain neurophysiologic function of nerve
roots, plexus, and peripheral nerves
Definition
- A pathologic process involving Points of Emphasis in Examination
neurophysiologic dysfunction of the - History and Physical Examination
nerve root. • CIDH-Related Radiculopathy: History
of cervical pain followed by an
Epidemiology explosive onset of upper limb pain
- Peak incidence ages 50-54 years old • Spondylitic Radicular Pain: Presents
- 15% of patients has history of trauma or more gradually
physical exertion preceding the onset of • Pain increases with activities that
symptoms raise subarachnoid pressure
- Order of decreasing frequency of • If stenosis is present  cervical
involved levels is C7, C6, C8 and C5. extension amplify symptoms
- Before 55 years old due to disc • MMT
herniation • Sensory Examination
- After 55 years old due to degenerative
changes Medical, Surgical, and Pharmacologic
Management
Etiology - Pharmacological Approach
- MC is Cervical Intervertebral Disk
• NSAIDS – 1st line of pharmacologic
Herniation (CIDH)
intervention prescribed
- Degenerative changes
• Muscle Relaxants for sedation and
- Spondylitic spinal changes
relaxation of muscles and aids in
- Stenosis
sleep
• Tricyclic Anti-Depressants
Pathophysiology
(Amitriptyline, Nortriptyline) to
Cervical Degenerative
decrease radicular pain and aids in
Intervertebral Changes
sleep
Disc Herniation ↓
• Antiepileptic (Gabapentin) to
↓ Ligamentous
modulate neuropathic pain
Inflammatory hypertrophy,
• Opiate Analgesics for severe pain
Response and Hyperstosis, Disc
- Nerve Root Injection
Pressure Degeneration,
- Percutaneous Discectomy
Gradient Facet Joint
- Surgery
↓ Arthropathy,
Radicular Pain Osteophytes,
PT Management
Cysts
- Thermotherapy: Which thermal agent to
↓
use is driven by patients perception of
Stenosis and
which provides best pain relief. Deep
Impingement
heating modalities (ex: US) is avoided
Radiculopathy
because increase metabolic response
and subsequent inflammation can
Clinical Manifestations
aggravate nerve root injury
- Myotomal weakness
- TENS
- Paresthesia
- Cervical Orthoses
- Sensory disturbances
- Cervical Traction: For decompression of
- Hyporeflexia
cervical soft tissue and IV disks,
contraindicated in patients with
Diagnosis
myelopathy, (+) L’hermitte’s sign,
- Imaging studies

2|Page
 Rheumatoid Arthritis, and Atlanto-
occipital subluxation
- Cervical Strengthening: Start with
isometric exercise first in supine to
sitting then in standing. Progress to
concentric isotonic exercise
C. Cervical Joint Pain
Definition
- Cervical zygapophyseal joint are a
common source of chronic post
traumatic neck pain
- Occurs in association with symptomatic
IV disk at the same level
Epidemiology
- 58-88% complain of headaches
- 50-53% C2-C3 zygapophyseal joint pain
and complains of posterior headache
after whiplash injury
Etiology
- Spondylosis
- Trauma
- Improper biomechanics
Pathophysiology
- Zygapophyseal Joint Fractures
- Intra-Articular Hemorrhage
- Capsular Tears
distribution of a particular
zygapophyseal joint
• Focal tenderness to palpation
posteriolaterally over joint
• Mechanism of Injury
Medical, Surgical, and Pharmacologic
Management
- Pharmacologic Approach
• NSAIDS: Control pain and
inflammation
• Opiates: Facilitate restorative sleep
pattern
- Facet Joint Injections: Appropriate for
those who have not improved from
pharmacologic and physical modalities
- Percutaneous Radiofrequency
Neurotomy: For chronic cases and if
injections fail to relieve the pain
PT Management
- Patient Education
- Superficial Cryotherapy: Ice application
preferred than heat due to analgesic
and anti-inflammatory effect
- Soft tissue Mobilization and Massage
- Soft Cervical Collars: Worn for a short
period of time up to 72 hours after the
initial injury
- Cervicothoracic Stabilization
- Strengthening Exercises

Clinical Manifestation D. Cervical Internal Disk Disruption

- Trauma to zygapophyseal joint at C2-C3
is likely to cause unilateral occipital Definition:
headaches - Indicates that an IV disk has lost its
- Unilateral paramidline neck pain tends normal internal structure but maintains
to be more painful a preserved external contour in the
- Site of pain (unilateral or bilateral) absence of nerve root compression
according to involved zygapophyseal
joint site: Epidemiology:
• C1-C2 and C2-C3 Occiput - 20% caused from traumatically induced
• C3-C4 and C4-C5 chronic neck pain
Posterior Neck - 41% caused from concomitant
• C5-C6 Supraspinatus zygapophyseal joint injury
Fossa
• C6-C7 Scapula Etiology
• C1-C5 Face - Trauma: The end plate of the IV disk
• C3-C6 Head fractures due to excessive load

Diagnosis Clinical Manifestations

- Imaging Studies - Posterior neck pain
• Plain Radiography: Detect cervical - Occipital and Sub-occipital pain
zygapophyseal joint subluxation - Upper trapezius pain
• CT Scan: For joint fractures - Inter and Periscapular pain
- Non-radicular arm pain
Points of Emphasis in Examination - Vertigo
- History and Physical Examination - Tinnitus
• Assess neurologic function - Ocular Dysfunction
• Assess cervical ROM - Dysphagia
• Patient should be able to pin point - Facial pain
the spot of maximal pain or define - Anterior chest wall pain
the pain typical for the referral
Diagnosis

3|Page
 - Imaging studies
• Plain Films: Reveal hyperostosis
and disc space collapse but
frequently do not correlate with
pain symptoms
• MRI: Detects symptomatic
cervical discs
• Provocative Discography:
Diagnose painful disk level
Points of Emphasis in Examination
- History and Physical Examination
• History preceding trauma: In
absence of event leading to
injury, symptoms can start
spontaneously or gradually
• Exacerbating Factors: prolonged
sitting, coughing, sneezing or
lifting
• Alleviating Factors: Lying supine
with head support
• Neuromuscular examination: To
exclude myelopathy or
radiculopathy
• Palpation: Over the cervical
spinous process of the involved
level can elicit pain in that
region
Medical, Surgical, and Pharmacologic
Management
- Transforaminal Epidural Steroid
Injections: Can address biochemically
stimulated nociception
- Surgery
• If the diskogram reveals one or
two contiguous levels producing
concordant pain  patient
might be a surgical candidate
• Fusion – only surgical treatment
for CIDD: Accomplished by
anterior cervical discectomy and
fusion or by posterior fusion, by
fusing the bony vertebral
element, motion is eliminated
thereby reducing diskogenic
pain.
E. Cervical Myelopathy
Definition
- Injury to the spinal cord located in the
cervical area
Epidemiology
- Most common cervical cord lesion
- Onset: After 50 years old
- Men > Female
Etiology
- Disc herniation
- Stenosis
- Osteophytes
- Swelling with trauma as well as
spondylosis
Pathophysiology
Degeneration (Spondylosis)
↓
Osteophyte formation, Ossification of the PLL
and Hypertrophied posterior elements
↓
Compression, Instability, Vascular insufficiency
↓
Myelopathy, Vascular Myelopathy
Clinical Manifestations
- Cervical Axial Pain: Primary complaint in
70% of patients
- Numbness and Paresthesia in the distal
limbs and extremities
- Weakness more often in the LE than UE
- Bladder Function disturbances
- Pain and Temperature disturbances
- Proprioception and Vibratory deficits
- (+) Upper motor neuron signs
Diagnosis
- Imaging Studies
• Radiographic evaluations:
Demonstrate cervical cord
compression
• Plain radiography: Information
regarding the osseous diameter
of the central canal and
decreased height of the IV disk
spaces and presence of
posterior hyperostosis,
foraminal encroachment and
subluxation
• MRI: Detects Myelomalacia 
progressive cord compression,
signal alteration, atrophy, and
amount of CSF volume
surrounding the spinal cord
Points of Emphasis in Examination
- History
• Onset is typically insidious
- Physical Examination
• MMT
• Sensation
• Reflexes
Medical, Surgical, and Pharmacologic
Management
- Surgery: Indicated for patients with
severe or progressive symptoms or
when conservative measures fail
• Cervical discectomy and Fusion
if CIDH alone is causing cord
compression
• Anterior decompression with
corpectomy: Vertebral body is
removed in addition to IV disks
and the segment is then fused
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 with a fibula auto graft or
allograft of a bone cage
• Posterior decompression
involves laminectomy with or
without fusion or laminoplasty
F. Cervicogenic Headaches
Definition
- A constellation of symptoms that
represent the common referral patterns
of cervical spinal structures.
Epidemiology
- From 2.5% to 36.2% of the general
population complain of headaches
- Female > Male
Etiology
- Degenerative Changes
- Trauma
- Idiopathic
Clinical Manifestations
- Unilateral and stemming from the
posterior occipital region
- Referral of Pain: Vertex of Scalp,
Ipsilateral Anterolateral Temple,
Forehead, Midface, and Ipsilateral
Shoulder Girdle
- Type: From deep aching to sharp and
stabbing
- Duration: Fluctuates from initial episodic
bouts of pain, progressing to more
chronic and constant pain, ranges from
few hours to few weeks but last longer
than migraine
- Intensity: Less excruciating than cluster
headaches, non-throbbing
- Dizziness, Vertigo
- Decreased ROM due to muscle guarding
- Soft tissue inflexibility
Diagnosis
- Physical Examination
• Cervical IV Disks-Induced
Headache: Begins as midline
pain that spreads across the
spine and into the head or face
• Zygapophyseal Joint Pain:
Unilateral occipital headache
symptoms greater than neck
pain
- Imaging studies
• CT Scan: To delineate osseous
injury
• MRI: Evaluate IV disk for
desiccation, decreased disk
height, and herniation
G. Torticollis
Definition
- Also called Wry neck or Cervical Scoliosis
- Deformity of the neck that includes
elements of both rotation and flexion
• Usually involves SCM: Tilting of the
head toward the affected side and
rotation of the chin towards the
opposite side
Epidemiology
- 4/1000 live births
- 75% involves the Right side
Classification
- Congenital Torticollis: Deformity is
present at birth
• Etiology
 Faulty Fetal position
 Nerve injury
 Direct trauma to muscle
• Epidemiology
 Female > Male
• Clinical Manifestation
 Not noticed until child is
able to sit and stand
 Ipsilateral shoulder
elevated
 Restricted rotation and
lateral bending of neck
 Palpable mass on
muscle
 Severe flattening and
shortening of the face
on the side of which the
head is tilted
- Acquired Torticollis
• Acute Traumatic or
Inflammatory: Caused by
Cervical Injuries, Atlantoaxial
Rotary Subluxation, or
Inflammations of the muscles or
of the Cervical Lymph Nodes
• Chronic Infectious or Neoplastic:
Caused by Osteomyelitis,
Tuberculosis, or Tumors of the
Spine or Spinal Cord
• Arthritic: Caused by RA,
Ankylosing Spondylitis or OA
• Cicatricial: Caused by the
contracture of scar tissue after
burn
• Paralytic: Caused by asymmetric
flaccid or spastic paralysis of
neck muscles
• Hysterical: Caused by
psychogenic inability of the
patient to control the neck
muscles
• Spasmodic: Caused by a CNS or
cervical root lesion and
manifested by involuntary
rhythmic contractions of the
neck muscles
5|Page
 PLAN OF CARE Clinical Manifestations
PROBLEM LIST POC INTERVENTION - May or may not be painful
S - If (+) pain, pain felt over side of
Muscle Increase Strengthening involvement with possible reference
weakness muscle exercises into areas innervated by CN 5
strength
- Pain increases with movement
Developing Prevent Stretching,
contractures contractures ROM, cross - (+) Complete capsular shortening leads
friction to opening is less than functional
massage - Decreased lateral movement of
Limitation of Increase Range Stretching and mandible to opposite side
motion of Motion Traction - Bilateral Restriction: Lateral movements
↓ ↑ Aerobic most restricted, mouth opening and
Cardiovascular Cardiovascular exercises and
protrusion limited, closing is free.
endurance endurance Conditioning
exercises
PT Management
Fatigue Decrease Relaxation
- Therapeutic Modalities
fatigue techniques
Pain Decrease pain TENS, US, IFC • Ice or heat to decrease pain and
Recurrence of Prevent Pt education on muscle guarding
injury reoccurrence protection and • Ultrasound with active motion
proper body or prolonged static stretch
mechanics - Joint Mobilization Techniques
• Enhance Capsular Extensibility
TMJ DYSFUNCTION
• Distraction, Medial Glide and
Mobility Impairment Translation
Hypomobility - Self-Treatment Techniques
Hypermobility • Maintain normal rest position of
Capsulitis and Retrodiskitis tongue: TUTALC
Degenerative Joint Disease
• Active Stretch (Active opening
Derangement of the Disk
and closing of mandible)
A. Mobility Impairment - Passive Stretch
Hypomobility • Place a number of stacked
tongue blades horizontally
Definition between teeth to increase
- Limitation of the functional movements
mandibular opening x 5-10
of the TMJ
minutes
• Normal translation begin after
Etiology
- Disorders of the mandible or cranial 11 mm or 6 tongue blades
bone: - Self-Stretch: Use the thumb crossed
• Aplasia over the index finger, index is placed on
the lower teeth as posteriorly as
• Dysplasia
possible and thumb is on the upper
• Hypoplasia, hyperplasia
teeth.
• Fractures and Neoplasms
- Post-Isometric Relation Techniques (PIR)
- Temporomandibular Dysfunctions: • Use Active muscle contractions
• Ankylosis (Fibrous or Bony) at various intensities from a
controlled position in a specific
• Arthritis
direction against a counter force
• Structural Bony changes
to facilitate motion
• Disk Displacement
• Inflammation or Joint effusion
Hypermobility
- Masticatory Muscle Disorders:
• Myofascial Pain Definition
• Muscle Splinting - Most common mechanical disorder of
• Myositis, Spasms the TMJ
• Contracture and Neoplasia

6|Page
Etiology - Occurs with encroachment of the
- Unknown condyle on the articular disk and causes
- Predisposing Factors: inflammation or exacerbation of an
• Joint laxity existing inflammatory condition
• Psychiatric disorders
• Skeletal disorders Etiology
- Para functional Habits that contribute to - Chronic repetitive microtrauma when
hypermobility: condyles are displaced posteriorly
• Prolonged bottle feeding, because of anterior disk displacement
thumb sucking, and pacifier use - Acute external trauma to the chin
in children forcing the condyles posteriorly into the
tissues
Clinical Manifestations
- Early or excessive anterior translation of Clinical Manifestations
mandible - Constant pain and palpable tenderness
- Translation occurs within first 11mm of posterior and lateral to the joint
opening rather than last 15-25mm - Pain increases with clenching or moving
- Excessive anterior translation results in the mandible to affected side which
laxity of surrounding capsule and permits the condyle to press against
ligaments inflamed tissue
- Chewing on contralateral side increases
PT Management pressure on inflamed joint and increases
- Therapeutic Modalities pain (Advise patient to chew on side of
• Ice or heat if condition is painful involved joint)
- Temporomandibular Joint Rotation and
Translation Control PT Management (Capsulitis and Rektrodiskitis)
- Strengthening and Stabilization Exercise - If caused by a single traumatic event
- Isotonic or Dynamic Exercises • Limit mandibular function
• Mild Analgesics
B. Capsulitis and Retrodiskitis • Ice and Moist heat
Capsulitis  Cryotherapy: Most
common used modality
Definition after trauma or surgical
- Inflammation of the fibrous capsule,
intervention
synovial membrane, and retrodiskal
 Ultrasound:
tissues
Phonophoresis,
Ionophoresis to
Etiology
- Overloading of joint from bruxism decrease pain and
- Excessively hard chewing muscle guarding
- Trauma  Laser Therapy
- Strain  Massage
- Infection  Biofeedback
- Habits such as bruxing, tongue  Relaxation Techniques
thrusting, gum chewing and pencil - If caused by chronic micro trauma or
chewing disk displacement
• Joint Stabilization Splint: May
Clinical Manifestations reduce bruxism and decrease
- Pain at rest pressure in the joint
- Pain on side of involvement with • (+) Anterior Disk Displacement
possible reference of pain into areas → Anterior repositioning
innervated by CN 5 therapy
- Minor joint restriction to total - After inflammation, pain, and muscle
immobilization guarding
• Stretching
Retrodiskitis • Muscular Re-education

Definition

7|Page
C. Degenerative Joint Disease
Definition
- Also known as “Osteoarthritis”
- Primary disease of middle or old age
- Alters the force-bearing surface of the
TMJ leading to secondary inflammation
of capsular tissue
- Joint space narrows with spur formation
and marginal lipping of the joint
Clinical Manifestations
- Similar to those other forms of joint
dysfunction
- Pain and Crepitation
PT Management
- Physical Therapy
• Active ROM Exercises
• Mobilization Techniques
• Stretching during Chronic phase
• Joint protection techniques:
Avoid excessive opening and
parafunctional habits, proper
resting position of the tongue
and mandible
D. Derangement of the Disk
Definition
- Displacement of the articular disk above
the condyles
Classification
- Anteriorly displaced disk that reduces
during joint translation
- Anteriorly displaced disk that does not
reduce during joint translation
Etiology
- Malocclusion: Over closure of the
mouth with backward displacement of
the condyle
- Excessive pressure on the joint from
clenching or trauma
- Deterioration of the disk and
cartilaginous surfaces
- Stretching of the joint ligaments by
frequent subluxation
Clinical Manifestations
- Pain of the TMJ on the involved side
- Pain increases during functional and
parafunctional movements of the
mandible
- Anterior dislocation with reduction
• Loud click or pop on opening
accompanied by palpable jarring
of joints (crepitus)
• Opening click followed by
subtler click during closing
• Mandibular ROM is normal and
amount of vertical opening may
be greater than normal
- Anterior Dislocation without reduction
• Absence of joint noises with
reproducible restrictions during
mandibular movements
• Most obvious sign: Restricted
maximum opening of 20-25mm
• Mandible sharply deflected to
affected side at the end of
opening
• Lateral excursion to
contralateral side is limited
Diagnosis
- Hallmark: Joint sounds such as clicking
- Clicking may occur as one or more clicks
in one or both joints
- Opening Click: Caused by anterior
displacement of disk with condyle
displaced posteriorly and superiorly
- Click early in Jaw Opening: Small degree
of anterior disk displacement
- Clicking near Maximal Opening: Further
anterior displacement
- Closing Click: Condyle slips behind the
posterior edge of the band of the disk;
disk displaced anterior and medially
- Closing Click results in disk displacement
and Opening Click occurs as disk snaps
back to its normal position.
Medical, Surgical, and Pharmacologic
Management
- Arthroscopic Surgery: Indicated for
diagnosis and treatment of intracapsular
derangement and joint adhesions
- Arthrotomy Surgery: Indicated for a
derangement of disk that has not
responded to non-surgical management
Points of Emphasis in Examination
- ROM
- MMT
- Palpation
- Sensory Testing
- Postural Assessment
- Functional Assessment
Problem List
- Pain
8|Page
 - LOM
- Muscle Weakness
- Muscle Guarding

PT Management
- Anterior Dislocation with Reduction
• Heat and Ice to decrease pain
and muscle guarding
• Relaxation exercises of muscles
of the jaw and cervical area
• Patient Education: Avoid
parafunctional habits, proper
positioning of the tongue and
mandible
- Anterior Dislocation without Reduction
• Joint mobilization techniques of
distraction (caudal) and
translation (protrusion) to
involved side
• Therapeutic modalities, soft
tissue mobilization, myofascial
release, and massage to
decrease pain

SOURCE:
- Therapeutic Exercise: Moving Toward
Function by Carrie M. Hall
- Physical Medicine and Rehabilitation by
Braddom
- Handbook of Orthopaedic Surgery 10th
Ed by Brashear

9|Page
 LOW BACK PAIN Metabolic LBP Low back pain due to
a problem in the
GENERAL MEDICAL BACKGROUND biochemical process
that happens within
Definition us (i.e. osteoporotic
- Is a symptom, not a disease fracture)
- Pain between the costal margin and Pregnancy Related Low Back Pain due to
gluteal folds LBP structural or
metabolic changes
happening in
Classification
pregnancy
Classification Definition
Psychosomatic LBP Low back pain due to
1. Static vs Kinetic
mental problems (i.e.
Static Pain at rest depression)
Kinetic Pain on motion Referred LBP Low Back Pain due to
2. Acute vs Chronic an impingement of a
Acute Lasts a short time nerve
(less than 3 months)
May be mild, Epidemiology
moderate, or severe - 40% claim having LBP within the past 6
and is most often
months
caused by injury. This
may be serious, such - 84% of lifetime prevalence
as a fall or an auto - Onset usually begins in teens to early 40s
accident, or less - Most episodes resolve with or without
serious, such as treatment
sprains, muscle
strain, or overuse Pathophysiology
Chronic -over 3 months and - Degenerative Disc Disease Pathology
often returns (this
• In the 3rd decade of life, the
usually involves
nucleus pulposus becomes
either disk or facet).
Chronic pain: May be replaced with fibrocartilage
mild, moderate, or • Decrease in proteoglycans,
severe and have the water, and non-collagenous
same causes as acute protein concentration
low back pain, with • Increase in collagen
symptoms being
concentration being more
more constant or
persistent. pronounced in the nucleus and
- May be related to posterior quadrants of the disk
other medical - Herniated Nucleus Pulposus
illnesses, such as • Water-retaining ability of the
severe arthritis, or nucleus pulposus declines
emotional factors
progressively with age. This is
such as stress,
depression, or associated with the degree of
substance abuse. proteoglycan deterioration and
3. According to Etiology the decrease in hydration
Mechanical LBP Low back pain due to • Hyaluronan long chains shorten
problems associated and swelling pressure decreases
with the structures or due to deterioration
the structures
• Decrease in mechanical stiffness
themselves found at
the low back (i.e. OA) of the IV Disc
Inflammatory LBP Low back pain due to • Anulus Fibrosus bulges,
an inflammation (i.e. corresponds to loss of disc and
RA) foramina height
Neoplastic LBP Low back pain due to
any new or abnormal Pathomechanics
growth due to cell
- Normal stress on an unprepared normal
multiplication being
uncontrolled (i.e. back
osteosarcoma)

10 | P a g e
 - Normal stress on a deconditioned has a kyphotic
normal back posture that cannot
- Normal back used improperly when be corrected.
lifting Lumbar Spondylolysis Usually provoked by
& Spondylolisthesis back extension and
- Abnormal stress on a normal back
neurogenic
- Normal stress on an abnormal back claudication may be
present.
Clinical Manifestations Osteoporosis Systemic skeletal
- May appear suddenly (primary) disease
- May appear for no reason characterized by low
- May appear insidiously bone mass.
Psoriatic Arthritis Involves skin and nail
- May be fixed or may move from one
lesions; has distal
side to another joint involvement.
- Pain: mild, moderate, severe, periodic,
constant, deep, aching, stabbing, Prognosis
throbbing - 90% of cases of acute LBP will recover
within 6 weeks (limited to some cases)
Complications - With the usual lumbar muscle strain or
- Disability sprain as the cause, over 90% of pts. Are
• LBP is the number one leading completely recovered within one month
cause of disability in the world - Risk of a recurrence within a year was
and the most common are between 66 and 84%
work-related such as heavy - About 20% of the pop w/ LBP are
lifting temporarily or chronically disabled by
- Nerve Damage their form of LBP
• The Sciatic nerve is the most
common affected nerve in Low General Healthcare Management
Back Pain
Diagnosis Medical, Surgical, and Pharmacologic
- CT scanning is an effective diagnostic Management
study when the spinal and neurological 1. Medical & Pharmacologic
levels are clear and bony pathology is Medicine Definition
suspected. NSAIDS short-term
- MRI is most useful when the exact spinal symptomatic relief;
and neurologic levels are unclear, when Acetaminophen,
a pathological condition of the spinal Aspirin
cord or soft tissues is suspected, when Opioids short-term treatment
postoperative disk herniation is possible, for severe pain;
or when an underlying infectious or Transdermal opioids
neoplastic cause is suspected. (fentanyl), Oxycodone
- Myelography is useful in elucidating Codeine for mild to
nerve root pathology. moderately severe
pain; frequently
Differential Diagnosis combined with
Pathology Definition acetaminophen
Achilles Tendon It is the rupture of Benzodiazepines usually for chronic
Injuries & Tendinitis the Achilles tendon low back pain; Valium
which is a complaint Oxycodone
of a sudden snap in Tricyclic used when LBP is
the lower calf region Antidepressants accompanied with
accompanied by depression
acute, severe pain. 2. Surgical
Coccyx Pain Referred to as the Surgical Procedure Definition
‘lowest form’ of LBP; Percutaneous removal of herniated
pain area is found Discektomy disc material
lower. Laminectomy removal of the
Lumbar Compression Pain corresponds to lamina; usually for
Fracture location of fracture spinal stenosis
site; Patient typically

11 | P a g e
 Vertebroplasty & used to treat • Bowstring Sign: (+)
Kyphoplasty compression Reproduction of pain: Sciatica
fractures; the Pathology
surgeon inserts a
• Slump Test: (+) Radicular Pain:
small balloon into the
vertebra and inflates Sciatica Nerve Tension
it, returning the bone • Femoral Nerve Stretch Test: (+)
to the normal Reproduction of pain in the
position, then injects anterior thigh: L2,L3 or L4 nerve
a bone cement into root compression
the fractured
• Patrick’s Test/FABER Test: (+) SI
vertebrae
Surgeries for Tumors Removal for the Pathology
tumor • Stork Test: (+) Reproduction of
Spinal Fusion or use of a bone graft to pain: Spondylolysis pain
Arthrodesis hold or fuse bones
together permanently Problem List
- Herniated Nucleus Pulposus
Physical Therapy Examination, Evaluation &
• Acute back discomfort radiating
Diagnosis
down the lower limbs
• Weakness, numbness,
Points of Emphasis in Examination
paresthesias or pain 2° to
- Observation & Palpation
chemical or mechanical stimuli
• Skin
to the disc or nerve root
• Overall posture and deformity
• Lateral lumbar shift.
• LLD : true or apparent
• Exacerbation during:
• Posture
 Lumbar motion
• Gait
(Forward flexion –
• Muscle spasm central and posterior-
• Tenderness lateral HNP; Extension –
• Trigger points/ tender points lateral HNP)
- AROM (Forward flexion, extension, side  Sitting, Sneezing,
bending and rotation) Coughing or Valsalva
- Neurologic maneuvers; neural
• MMT tension tests
• Muscle bulk - Cauda Equina Syndrome
• Reflexes • Lumbar, buttock, perianal
• Sensory discomfort and LE weakness
• Balance and coordination • Bowel, bladder abnormalities
testing (Retention, frequency
- Special Tests incontinence) and sexual
• Straight Leg Raise/Laségue Test: dysfunction
(+) SLR suggests pathology of • Saddle anesthesia including the
Sciatic involvement/L5 or S1 back of the legs, buttocks and
nerve root soles of feet
 SLR 1 (basic): Sciatic - Spinal Stenosis
Nerve and Tibial Nerve • Gradual back discomfort with LE
 SLR 2: Tibial Nerve involvement
 SLR 3: Sural Nerve • Neurogenic pseudo
 SLR 4: Common claudication: Pain in the
Peroneal Nerve buttock, thigh or leg with
 SLR5/Well-Leg/Cross standing or walking; relieved
SLR Test: Sensitive and with sitting or leaning forward
specific for a herniated - Spondylolysis
L5-S1 or L4-L5 lumber • Localized back pain exacerbated
disc by: hyperextension, standing,

12 | P a g e
 lying prone and relieved by
flexion
- Spondylolisthesis
• Pain exacerbated with motion.
• Hamstring tightness
• Radicular symptoms may occur
with marked slippage
- Compression Fracture
• Sudden onset of constant
thoracolumbar pain
• Exacerbated with Valsalva
maneuver, turning in bed,
coughing or incidental trauma
- Facet Syndrome
• Back pain exacerbated with
rotation and extension.
• Referred pain pattern in non-
dermatomal presentation
• No neurological abnormalities
- Sacroiliac Joint Dysfunction
• Tenderness upon palpation
• (+) Patrick test
• Lumbosacral pain with radiation
to buttocks, groin or thigh area
- Sprain/Strain
• Muscle aches with associates
spasm and guarding in the
region of injury
• DOMS can occur within 24-48
hours after an eccentric
overload injury
• Normal neurologic exam
- Malingering
• Exaggerated complaints with
non-anatomical basis and
without an organic pathology.
Diagnosis
- Weber-Barstow Maneuver
• Femoral length asymmetry ; (+)
LLD
- Supine “True” LLD and Supine
“Apparent” LLD
• Femoral/Tibial length
asymmetry; (+) LLD
- Craig test
• Femoral ante-version or
forward torsion of the femoral
neck
- Gaenslen’s test
• (+) Ipsilateral SI dysfunction, hip
pathology or an L4 nerve root
lesion.
- Fulcrum’s test
• (+) Possible stress fracture on
the femoral shaft
- Nelaton’s Line Test
• (+) dislocated hip or coxa vara.
- Gillet’s Test
• (+) SI joint pathology
- Piriformis Tightness Test
• (+) piriformis tightness;
piriformis syndrome
- 90-90 SLR
• (+) Hamstring contracture
- Tripod Sign
• (+) Hamstring contracture
- Ely’s Tightness Test
• (+) Rectus Femoris tightness
- Thomas Test
• (+) hip flexion Contracture
- Patrick’s Test
• (+) iliopsoas spasm; SI pathology
- Trendelenburg’s Test
• Unstable hip on the affected/
stance side; (+) Weak gluteus
medius
- Valsalva Test
• Increase spinal pressure; (+) disc
lesion
- Straight Leg Raise/Laségue Test: (+) SLR
suggests pathology of Sciatic
involvement/L5 or S1 nerve root
• SLR 1 (basic): Sciatic Nerve and
Tibial Nerve
• SLR 2: Tibial Nerve
• SLR 3: Sural Nerve
• SLR 4: Common Peroneal Nerve
- SLR5/Well-Leg/Cross SLR Test: Sensitive
and specific for a herniated L5-S1 or L4-
L5 lumber disc
• Very sensitive for a herniated
L5-S1 or L4-L5 lumbar disc; (+)
space occupying lesion
- Bilateral SLR
• Pain BEFORE 70° hip flexion; (+)
SI joint lesion
• Pain AFTER 70° hip flexion; (+)
lesion in the lumbar spine area
- Unilateral SLR
• 80°-90° hip flexion is normal, if
one leg is lifted
- Bowstring Sign
• reproduction of pain; (+) sciatica
pathology
- Slump Test
• radicular pain ; (+) sciatica nerve
tension
- Femoral Nerve Stretch Test
13 | P a g e
 • reproduction of pain in the Orthosis Definition
anterior thigh; (+) L2,L3 or L4 1. Flexible Spinal Orthosis
nerve root compression Lumbar Binder Offers trunk support
- Stork Test via elevation of
intraabdominal
• reproduction of pain :
pressure and
spondylolysis pain
reminds the patient
- Kernig Test of proper posture
• (+) meningeal irritation; nerve Lumbosacral Corset Deload the
root involvement; dural vertebrae and discs
irritation Thoracolumbosacral Trunk stabilization,
- Babinski Test Corset deload the
vertebrae and discs,
• Pathologic reflex; possible upper
restricts spinal
motor lesion; (+) - Babinski sign motions/ reminder
- Oppenheim Test to restrict motion
• Pathologic reflex; possible 2. Rigid Spinal Orthosis
upper motor lesion; (+) Babinski Plastic Body Jacket For maximum
sign orthotic
immobilization and
Physical Therapy Diagnosis control of spine
Plan of Care
- Relieve pain - Use of an assistive device: To decrease
- Reduce swelling load on affected part
- Prevent onset of joint and/or soft tissue Orthosis Definition
contractures 1. Rigid Spinal Orthosis
- Reduce edema Chair back Brace Flexion & extension
- Retard atrophy control
Knight Brace Flexion, extension &
- Maintain muscle strength
lateral flexion control
Williams Brace Extension & lateral
Interventions (Modality)
flexion control
- Thermal Agents
Taylor Brace Thoracolumbosacral
• To relive pain flexion & extension
• Ice- best used initially control
• Deep heating: Delayed until Knight-Taylor Brace Thoracolumbosacral
signs of inflammation are flexion, extension &
reduced to minimal lateral flexion control
Cowhom Brace Thoracolumbosacral
• Superficial moist heat: To
flexion, lateral flexion &
decrease pain & spasms rotation control
secondary to an acute Jewett Brace Thoracolumbar flexion
inflammation. However, if control
applied, check with patient if
this is effective - Alteration of body mechanics of daily
- Electrical Stimulation habits: To prevent contributing factors
• To relieve pain in chronic cases to further or repeated injuries
• To retard atrophy if used during - Limb elevation to relieve pain
immobilization - Manual Therapy techniques
• When coupled with pressure • Soft tissue immobilization: Post
bandages, may be effective in inflammatory stage only
reducing edema • Centripetal Massage: To reduce
- Pressure Bandaging edema
• To reduce Edema - Exercises: To prevent contractures or
limitation of motion
Intervention (Non-Modality) • ROM exercises: In acute stage,
- Temporary Mobilization: To rest the should be limited only in pain
affected part and promote healing, free range
preferably in ideal resting position • Muscle strengthening exercises:
Usually through isometric

14 | P a g e
contractions during
immobilization stage &
progressed afterwards

15 | P a g e
 SCOLIOSIS
Definition
- Comes from the Greek word “scolio”,
which means “twisted”
- Lateral curvature of the spine
- Either structural or nonstructural
- Characterized by
• Asymmetrical side bending
• Fixed areas of the spine
- Identified by the convexity of the curve
- Usually occurs in the Thoracic Region
between T4 and T12
Definition of Terms
- Compensatory Curve
• Curve to compensate and
preserve body alignment
• Less severe curve
• May develop in the opposite
direction of major curve
• Structural or Nonstructural
- Decompensated Curve
• Curve that does not equal the
deformity of the major curve
• Shoulders are not leveled
• Lateral shift of the trunk to one
side
• Amount is measured by the
horizontal distance between the
gluteal cleft and occipital
protuberance
- Double Major Curve
• Two curves of equal severity or
significance
• Usually structural
- Transitional Vertebra
• Neutral vertebra at each curve
end
• Transitions from one curve to
another
- Apical Vertebra
• Vertebra farthest from the
midline
• Found in the middle / apex of
the curve
Curve Shapes
- Long C Curve
• Usually extends the length of
thoracic and lumbar spine
• Often uncompensated
• May be caused by long-term
asymmetric positioning,
weakness, or inadequate
control of sitting balance
- S Curve
• Most common type of
idiopathic scoliosis
• Usually (R) thoracic and (L)
lumbar curve
• Involves a major and
compensatory curve
• Associated with structural
changes in the vertebrae
Classification of Curve Severity
- Normal
• <10°
- Mild
• <20°
- Moderate
• 20° - 40°
- Severe
• >40°
- Significant rotational deformity
- Adults with severe curves are associated
with pain and DJD of the spine
- 60° - 70° are associated with significant
cardiopulmonary changes and ↓ life
expectancy
Epidemiology
- >1M Americans have significant degree
of scoliosis
- 8x more common in adolescent ♀
• ↑ joint laxity has been
associated with idiopathic
scoliosis
• Accounts for 80% of scoliosis in
the US, which is 2 – 8% of the
whole population
• Most common type of scoliosis
• Appears in ♀ beginning at age
10
- Other 20% caused by other etiologies
- Family history is positive in 30% of all
cases
Structural Scoliosis
- Irreversible lateral curvature č fixed
vertebral rotation
- Vertebral bodies rotate to the convex
side
- Greatest rotation is found at the apex of
the curve / apical vertebra
- As the curve ↑, rotation also ↑
Etiology
- Idiopathic
• 75 – 85% of all cases
• Theories involve:
 Bone malformation
 Asymmetric muscle control
 Abnormal postural control
 Abnormal distribution of muscle
spindle in paraspinal
musculature
- Chronologically divided into:
• Infantile
 Birth to 3 years old
 More common in ♂
• Juvenile
 4 - 9 years old
• Adolescent
- Congenital
• Abnormal vertebral formation or
hemiverterba or vertebral absence
16 | P a g e
 • Partial formation or lack of
separation can cause asymmetrical
growth and resultant deformity
• Caused by disturbance in vertebral
development during the 3rd and 5th
week of gestation
• Child may have other neurological
spine anomalies
- Neuromuscular
• 15 – 20% of structural scoliosis
• From congenital, acquired
neuropathic or myopathic diseases
• Associated with paralytic disorders
that cause asymmetrical paralysis
• Spinal deformity is common and
often severe
 Patients do not walk because of the
underlying neurological disease
Etiology of Neuromuscular Scoliosis
- Neuropathic Causes
• Often Long C Curve
• Congenital
 Cerebral Palsy
 Neurofibromatosis
• Acquired
 Anterior Horn Cell Diseases
 Traumatic Paraplegia
- Myopathic Causes
• Usually not severe
• Congenital
 Amyotonia Congenita
 Muscular Dystrophy –
Progressive
- Osteopathic Causes
• Congenital
 Secondary Hemivertebra
• Acquired
 Osteomalacia
 Fracture
 Spine dislocation
Nonstructural Scoliosis
- Postural scoliosis
- Reversible curvature that tends to be
positional / dynamic in nature
- No structural or rotational changes
Etiology
- Leg Length Discrepancy
• True
• Apparent
• Congenital
 Causes asymmetric variations
that lead to pelvic obliquity and
a compensatory curve
- Spasm in Back Muscles
• Splinting in response to injury
• Posterolateral disc protrusion in
lumbar spine
 Causes Sciatic Scoliosis
- Habitual Asymmetric Posture
Pathophysiology
- Lateral flexion causes the trunk to shift
away from midline
• Alters COG
• Shortens spine
- Spine rotates on its longitudinal axis
• Contributes to clinical
manifestations
- Vertebra becomes permanently wedge-
shaped
- Increased by additional factors
• Weight of the trunk
• Contracted muscles on concave side
• Disturbed forces on active growing
vertebra
- Changes in rib cage shape
• Thoracic cavity narrows
• Ribs don’t move in a plan that
allows normal lung expansion
- Left untreated, may cause the ff. in later
life:
• Back pain
• Degenerative arthritis
• Disturbances in cardiopulmonary
function
- Psychogenic and social problems
relating to body image
Clinical Manifestations
- Complaints of:
• Poor posture
• Shoulder hump
• Uneven waistline
• Prominent hip on one side
• Crooked neck
• Rib hump
• ↓ height
• Prominent scapula on convex side
- Visualization of deformity
- Back pain
- Cardiopulmonary failure
- Misalignment of spinous processes
- Asymmetry of flanks
- Asymmetry of thoracic cage
Complications
- ↓ Vital Capacity č an angle >60°
- Pulmonary Hypertension č an angle >80°
- Back Pain
- Chronic Fatigue
- Spinal Nerve Impingement
- SOB due to ↓ chest expansion
- GIT disturbances from crowded
abdominal organs
- Progressive spinal curvature č ↓ height
- Cardiopulmonary failure
- Cosmetic deformity
Diagnosis
- History and Family Medical History
- Physical Examination
- Radiographic Findings for confirmation
- Forward Bending Test
17 | P a g e
 - Lateral Bending Test
• Whether curve corrects or reverses
- Assessment of neurological stats of Les
- Inclusion of clinical photographs for
future references
- X-Rays of spine to identify and measure
curves
- Intravenous pyelography for children
with congenital scoliosis due to
associated renal anomalies
- Moire Topography
• Photography that detects
asymmetry of opaque surfaces
Measurement Techniques
- Measurement of lateral curvature
• Cobb Method
 More reliable
 Line is drawn perpendicular to
margin of vertebra that inclines
most toward concavity
 Line is drawn on the inferior
border of lower vertebra with
greatest angulation toward
concavity
 Angle of intersecting lines is
recorded
• Risser-Ferguson Method
 Find the apex
 Draw a line from the vertebra
that inclines most toward the
concavity to the apex
 Draw a line from the vertebra
with greatest angulation
towards the concavity to the
apex
 Angle of intersecting lines is
recorded
- Measurement of rotational deformity
• Position of pedicles is noted on a
posteroanterior X-Ray
• The degree of rotation is graded 0
to +4
Prognosis
- Best when curve is mild during initial
diagnosis and effective treatment is
initiated early
- If curve is >20° and child has several
more years to grow when deformity is
detected, changes of progression ↑
- Thoracic and double major curves are
more likely to progress than lower
curves
- Idiopathic scoliosis has significant
progression spontaneously after end of
vertebral growth
- Curves > 40° at maturity may progress
during adult life, but at a slower rate
- Curves > 100° are likely to lead to
cardiopulmonary disability
- Fusion of vertebral ring apophyses is a
more reliable indication of spinal
growth, and structural curves may ↑
because of degeneration
- During childhood, deformities of
structural scoliosis progress rapidly
- In adults with lumbar curves, pain is
common in the 4th decade of life
- Without treatment, idiopathic scoliosis
in children can cause severe deformity
and disability
- The younger the patient and the earlier
the onset, the more guarded the
prognosis
- Curves in thoracic and cervicothoracic
have poorer prognosis
Medical, Surgical Management
- Usually the treatment of choice for
correction of scoliosis with:
• Curves greater than 40°
• Curves resistant to correction with
non-operative measures
• Decompensated curves
• Cosmetically unacceptable curves
• Deformity causing significant back
pain
- Preoperative Correction
• To elongate the spine and ↓
severity of deformity prior to
surgery, especially in curves >60°
• Traction or cast may be used
 Halo-Femoral Traction
 Maximum correction is attained
for several weeks
 Halo-Pelvic /Dewald Traction
• Upright bars can be lengthened
to elongate spine
• Patient is ambulatory before
surgery
- Exercise
- Surgical Interventions with
Instrumentation and Spinal Fusion
• Done for severe cases where
 Curve has progress >40°
 Curves with lesser degree
are compounded with
imbalance or rotation of
vertebrae
• Goal of surgery is stabilization
Methods include:
• Harrington Rod and Posterior Spinal
Fusion
 Longer period of post-operative
bed rest
• Dwyer/Zelke Instrumentation and
Anterior Spinal Fusion
 Difficult doe to anterior fusion
• Segmental/Luque Spinal
Instrumentation and Posterior
Spinal Fusion
 Rigid internal fixation at the
level of each vertebra
• Cotrel-Dubousett Bilateral
Segmental Fixation
18 | P a g e
  Provide three-dimensional
correction
 Shorter period of immobilization
- Postoperative Management
• For surgery involving posterior
spinal fusion
 Body cast or brace must be
worn for 6 – 9 months, or as
long as 12 months
 Ambulation usually permitted
• For Luque and Cotrel-Dubousett
procedures
 No bracing or cast is necessary
 Immobilization is not required
after procedure
 Physical exertion during 1st year
should be no more strenuous
than walking
Points of Emphasis in Examination
- Postural Assessment
• Asymmetric shoulder level
• Prominence of scapula
• Protrusion of hip to one side
• Pelvic Obliquity
- Flexibility of the Curve
- Evaluation of Muscle Strength
• Convex side muscles weakens
• Trunk flexors and extensors
weakens
• Hip muscles weakens due to faulty
posture
PT Management
- Casts
• Č pressure pads over curve apices
• Passive correction
• Spine is elongated and rubs are
rotated back to normal position as
much as possible cast is applied
• Either preoperative or postoperative
- Traction
• May be used prior to surgery
 Passive traction
 Cotrel Traction: Applied nightly
with the use of a head halter
and a pelvic girdle attached to a
weight and pulley system;
Rigorous elongation, derotation
and lateral flexion is performed
when not in traction; After
several weeks of traction and
exercise, a cast is applied and
worn for several more weeks;
Consists of a cycle of traction-
exercise and casting
• Skeletal Traction
• Used preoperatively with severe
or persistent curves to elongate
the spine as much as possible
- Spinal Bracing
• Major goal is to prevent progression
of curve or give permanent
correction and stabilization to curve
• Types of Braces:
 Milwaukee Brace: Used to
immobilize spine after a
Harrington Rod or Dwyer
procedure; Most common form
of treatment for mild and
moderate idiopathic scoliosis in
patients with 2+ years of
skeletal growth; Also used for
children with severe curves who
are not candidates for spinal
fusion
 Boston Brace: Not
recommended for curves with
apices above T8
- Electrical Stimulation
• For mild and moderate scoliosis
- Exercises
• Cannot halt progression or
correction if used alone
• Exercises with Milwaukee Brace
 Patient must actively participate
in the correction of the
deformity with a daily exercise
routine
 Effectiveness of the brace
depends on the patient wearing
the brace for 23 hours a day and
carrying out a specific set of
exercises
 Strengthen muscles to provide
stability and ↓ and corrects
spinal curves
• Preoperative Exercise Prior to
Surgery
 ↑ flexibility of trunk for best
possible correction
 Goals include:
• ↑ mobility of tight
structures of spine due to
curvature
• Improve pulmonary
function as much as
possible before surgery
• Improve postural control
with general strengthening
of trunk musculature
• Preoperative Stretching Prior to
Surgery. Stretch the following:
 Tight structures on the concave
side of the curve
 Tight hip flexors
 Tight erector spinae
 Tight hamstrings
• Deep Breathing Exercises
 ↓ postoperative pulmonary
complications
 ↑ chest mobility on concave
side of curve
19 | P a g e
 • Exercises for Mild Idiopathic
Scoliosis
 Improve strength and postural
control of trunk musculature
 Increase mobility of any tight
structures of the trunk
 Improve overall posture
- Patient Education
• Teach proper body mechanics
• Give postural training
- Physical Activities
• Child should be encouraged to
participate in all kinds of physical
activities and sports
• Only contact sports are
contraindicated

20 | P a g e
 MUSCULOSKELETAL DISORDERS OF THE
EXTREMITIES (UPPER EXTREMITY)
Shoulder Region
Sternoclavicular Joint Sprain
Clavicle Fractures
Acromioclavicular Joint Sprains
Osteolysis of the Distal Clavicle
Rotator Cuff Tendonitis and
Impingement
Glenohumeral Joint Instability
Adhesive Capsulitis / frozen shoulder
Suprior Labral anterior to Posterior
lesions (SLAP lesion)
Elbow Region
Lateral Epicondylitis / Tennis elbow
Medial Epicondylitis / Golfer’s elbow
Olecranon Bursitis
Osteochondrosis (Panner’s disease) and
Osteochondritis Desiccans of the
Capitellum
Elbow Dislocations
Wrist and Forearm Region
De’Quervain’s Syndrome (Stenosing
Tenosynovitis)
Scapholunate Instability
Scaphoid Fracture
Distal Radial Fractures
Kienbock’s Disease
Hand and Finger Region
Extensor Tendon Central Slip Disruption
(Boutonniere Injury)
Terminal Extensor Tendon Disruption
(Mallet Finger)
Flexor Digitorum Profundus Rupture
(Jersey Finger)
Proximal IP joint dislocations
1st MCP Joint Ulnar Collateral Ligament
Sprain (Gamekeeper’s Thumb)
GENERAL MEDICAL BACKGROUND
Classification
Shoulder Region
1. Sternoclavicular Joint Sprain
Epidemiology:
- Accounts for <1% of all joint
dislocations.
- 2/3 occurs anteriorly, whereas 1/3
occurs posteriorly.
Etiology:
- Usually traumatic
Clinical Manifestation:
- Anterior SC joint injuries can cause
the medial end of the clavicle to
become more prominent
- Posterior SC joint injuries have more
pain with a less prominent medial
clavicular end
Complications:
- Posterior dislocations can be
associated with vascular
compromise to the ipsilateral upper
limb, and neck, upper limb venous
congestion, difficulty in breathing,
and difficulty in swallowing
Diagnosis:
- Accurate history and physical
examination
- Radiologic evaluation
 Antero-posterior radiograph
of the chest or SC joint
 CT scan
- Ligamentous Injury Grading Scale
1 – Tenderness to palpation without
subluxation or dislocation
2 – Tenderness to palpation with
subluxation but a good end point
3 – Tenderness to palpation with
associated dislocation and no end
point
Treatment:
- Grade 1 and 2 – sling immobilization
for comfort and protection during
the acute phase of rehabilitation;
activity can progress as tolerated
with an anticipated return to activity
after 1-2 weeks for grade 1 injury
and 4-6 weeks for grade 2 injury
- Grade 3 – can be treated non-
operatively as described for grade 1
and 2; those that remain unstable
post-reduction might require
surgical intervention
2. Clavicle Fractures
Epidemiology:
- Majority can occur in childhood and
adults <25 years of age
- 80% occur in the middle third of the
clavicle
- 15% occur in the lateral 1/3
- 5% occur in the medial 1/3
Etiology:
- Mostly results from a direct blow to
the point of the shoulder
- Small percentage occurs from
FOOSH injury
Diagnosis:
- History and physical examination
- Radiologic evaluation
 Antero-posterior
radiographs of the clavicle
for visualization of clavicular
middle third fractures
 Serendipity view for
proximal third fractures
 15° cephalic tilt antero-
posterior view centered on
the AC joint using a soft
tissue technique (Zanca
view) and an axillary lateral
view for lateral third
fracture
- CT scan
21 | P a g e
 Treatment:
- If fracture has good alignment,
immobilization is done (use of sling
or figure of eight bandage)
- If 15-20mm of shortening occurs as
a result of displacement, surgical
intervention should be considered
- Other indications for surgical
intervention includes displaced
fractures with tissue interposition
between the fracture ends, open
fractures, neurovascular
compromise, tenting of the skin
over the fracture site that might
lead to tissue necrosis, and displace
fractures located at the lateral third
of the clavicle
3. Acromioclavicular Joint Sprains
Epidemiology:
- Accounts for 9% of all shoulder
injuries
- Most frequent in males in their 3rd
decade of life and are usually partial
rather than complete sprains
Etiology:
- Mostly occurs from direct trauma
from a fall or blow to the acromion
Clinical Manifestation:
- (+) point tenderness
- (+) horizontal adduction test
- (+) O’Brien test
Diagnosis:
- History and physical examination
- Radiographic evaluation
 Antero-posterior and lateral
views of the AC joint
 Zanca view
- Rockwood classification of AC joint
sprain
 Type 1 – mild injury to the
AC ligaments and radiologic
evaluation is normal
 Type 2 – complete
disruption of the AC
ligament but with intact
coracoclavicular ligaments;
radiographs might
demonstrate clavicular
elevation relative to the
acromion but <25%
displacement
 Type 3 – complete
disruption of the AC and
coracoclavicular ligaments
but the deltotrapezial fascia
remains intact; radiographs
reveal a 25-100% increase
in the coracoclavicular
interspace relative to the
normal shoulder
 Type 4 – complete
disruption of the
coracoclavicular and AC
ligaments with posterior
displacement of the distal
clavicle into the trapezius
muscle
 Type 5 – coracoclavicular
and AC ligaments are fully
disrupted along with
rupture of the
deltotrapezial fascia; results
in increase in the
coracoclavicular interspace
to greater than 100% of the
normal shoulder
 Type 6 – involves complete
disruption of the
coracoclavicular and AC
ligaments as well as the
deltotrapezial muscular
attachments, with
displacement of the distal
clavicle below acromion or
coracoid process
Treatment:
- Type 1, 2, and 3 are usually treated
non-operatively (brief period of sling
immobilization for pain control)
- Indications for surgical intervention
for type 3 includes persistent pain
or unsatisfactory cosmetic results
- Surgical treatment required for type
4, 5, and 6 sprains
4. Osteolysis of the Distal Clavicle
Epidemiology:
- Occurs mostly in young weight
lifters who perform a significant
amount of bench press and military
press lifts
- Frequently occurs bilaterally
Etiology:
- Can result from repetitive overload
of the distal clavicle
Clinical Manifestation:
- Distal clavicular subchondral bone
loss and cystic changes
- Widening of the AC joint (can occur
in late stages)
Diagnosis:
- Radiographic evaluation
 Same as for AC joint injuries
- Bone scan
 (+) during active disease
and can be used to confirm
the diagnosis
Treatment:
22 | P a g e
 - Non-operative treatment involves
avoidance of the aggravating
activities and application of the
previously discussed rehabilitation
principles
- Occasionally, AC joint intraarticular
corticosteroid injections can assist
pain control
- For athletes who fail to improve
with non-operative measures or are
unable to modify their activities,
distal clavicular resection is the
surgical procedure of choice
5. Rotator Cuff Tendonitis and
Impingement
Etiology:
- Causative factors leading to primary
impingement includes:
 Hooked acromion or a thick
coracoacromial ligament
- Causes of secondary impingement:
 GH joint instability
 Weak scapular stabilizers
 Scapulothoracic dyskinesis
 Instability
Clinical Manifestation:
- Anterior or lateral shoulder pain
that occurs with overhead activities
and also at night when trying to
sleep
- Stiffness
- Weakness
- Catching
Diagnosis:
- Physical examination
 Evaluation of cervical spine
 Assess proper scapula-
thoracic mechanics
 MMT of rotator cuff
 Special test – Neer-Walsh
and Hawkins-Kennedy
impingement tests; should
also include tests to detect
GH joint instability
- Radiographic evaluation
 Anteroposterior
- should be performed in
the neutral, external,
and internal rotation
positions to adequately
visualize the GH joint
and lesser tuberosities
 Supraspinatus outlet
- for categorization of the
acromion type and will
reveal AC joint
osteophytes
 Axillary radiographs
 Double-contrast
anthrograms
- identify full-thickness
rotator cuff tears,
partial thickness
articular surface tears,
and biceps tendon
pathology
- Ultrasound and MRI have high levels
of sensitivity and specificity for
rotator cuff pathology
- Neer classification of Rotator cuff
injury
 Stage 1 – inflammation and
edema in the rotator cuff
 Stage 2 – progressed to
fibrosis and tendonitis
 Stage 3 – partial or
complete rotator cuff tear
- Elimination of pain provoked by
impingement testing after injection
of 10mL of 1% lidocaine into the
subacromial space confirms
diagnosis of impingement
Treatment:
- Non-operative treatment should
include application of previously
described rehabilitation principles
- Strengthening exercises for scapular
stabilizing muscles (muscles that
retract and depress the scapula)
should be emphasized in the acute
rehab stage
- Stretching muscles that protract and
elevate the scapula reduce
impingement
- Neuromuscular retraining to re-
establish normal scapulothoracic
kinematics
- Rotator cuff muscle strengthening
should begin with close chain
exercises to promote stability and
proprioception; open chain
exercises can be used to correct
strength imbalances
- Surgical intervention is done to
patients who fail to respond to any
intervention or to those who have
sustained an acute full-thickness
rotator cuff tear
6. Glenohumeral Joint Instability
Classification according to:
- Degree
 Dislocation – humeral head
is dissociated from the
glenoid fossa and often
requires manual reduction
 Subluxation – humeral head
translates to the edge of the
glenoid, beyond normal
physiological limits,
followed by self-reduction
 Microinstability – due to
excessive capsular laxity, is
multi directional, and is
frequently associated with
internal impingement of the
rotator cuff
- Frequency
23 | P a g e
  Acute – new injury resulting
in subluxation or dislocation
of the GH joint
 Chronic – repetitive
instability episodes
- Etiology
 Traumatic – frequently
causes unidirectional
instability resulting in
disruption of the GH joint
 Atraumatic – GH joint
instability resulting from
congenital capsular laxity or
repetitive microtrauma
• Voluntary – an
individual who
volitionally subluxes
or dislocates his or
her GH joint
• Involuntary – does
not volitionally
subluxes or
dislocates his or her
GH joint
- Direction of Instability
 Unidirectional – instability
in one direction; most
frequent type is traumatic
anterior instability
 Multidirectional – instability
in two or more direction
and is usually due to
congenital capsular laxity or
chronic repetitive
microtrauma
Etiology:
- Anterior GH joint Instability
 Traumatic anterior GH
dislocation frequently tears
ant-inf GH joint capsule and
avulses the ant-inf glenoid
labrum with or without
some underlying bone from
the glenoid rim (Bankart
lesion)
 Humeral avulsion of the
glenohumeral ligament
 Superior labral anterior-
posterior lesion (SLAP)
 Injury to rotator interval or
rotator cuff tears
(particularly subscapularis)
- Inferior GH joint Instability
 Capsuloligamentous laxity
 Absence of glenoid fossa
upward tilt
 Lesions to rotator interval,
IGHL, superior GH ligament,
coracohumeral ligament,
and inferior glenoid labrum
- Posterior GH joint Instability
 Congenital glenoid
hypoplasia or excessive
glenoid or humeral
retroversion
 Excessive
capsuloligamentous laxity or
tear to injury to rotator
interval, post. band of IGHL,
superior GH ligament,
coracohumeral ligament, or
subscapularis muscle
 Tear of posterior inferior
glenoid rim causing
separation from the glenoid
fossa rim (reverse bankart
lesion)
 Fracture of posterior
inferior glenoid fossa rim
 Reverse Hill-Sachs defect
representing an impaction
fracture of anterior humeral
head
- Mutildirectional Instability
 Primary or secondary
capsuloligamentous laxity
 Seen bilaterally and can be
accompanied by generalize
ligamentous laxity
 Recurrent unilateral joint
instability occasionally
stretches the GH
capsuloligamentous
structures to the point that
multidirectional instability
develops secondarily
 Underlying connective
tissue disorder: Marfan or
Ehlers-Danlos Syndromes
Clinical Manifestation:
- Pain
- Popping
- Catching
- Locking
- Unstable sensation
- Stiffness
- Swelling
Diagnosis:
- Patient History
 History of acute, chronic or
repetitive microtrauma
 History of GH joint
dislocation
 History of generalized
ligamentous laxity or
connective tissue disorders
- Physical examination
 Inspection
 Palpation
 GH joint ROM
 Analysis of scapulothoracic
kinesis
 Upper limb strength
 Sensation (including
proprioception)
 Reflex evaluations
 Special tests
24 | P a g e
 - Radiographic evaluation
 Anteroposterior shoulder
view – allows visualization
of the osseous structures of
the shoulder including
scapula, clavicle, upper ribs,
humeral head, and glenoid
rim; allow visualization of
Hill-Sachs defect
 Axillary lateral view – can
assess anterior or posterior
subluxation or dislocation
as well as fractures of the
anterior or posterior glenoid
rim
 Scapular “Y” view – help in
assessment of GH joint
alignment after acute
dislocations
 Garth view and West point
view – detection of Bankart
fractures
 Stryker Notch view –
evaluation of Hill-Sachs
defect
 Stress view –
documentation of degree of
GH joint instability
- Magnetic resonance arthrography –
provides optimal visualization of
labrum, cartilage, and joint capsule
Treatment:
- Strengthening program – should
begin with close chain exercises that
promote co-contraction of GH joint-
stabilizing musculature
- Progress to functional open chain
exercises as stability is achieved
- Proprioceptive close and open chain
exercises to recoordinate the
stabilizing shoulder girdle
musculature
- Close reduction in all pts. who
sustained an acute GH joint
dislocation that does not
spontaneously reduced
- Standard sling immobilization for
comfort
7. Adhesive Capsulitis / frozen shoulder
- Characterized by painful, restricted
ROM in patients with normal
radiographs
Epidemiology:
- Occurs 2-5% of the general
population
- 2-4x more common in women
- Frequently seen in individual aging
40-60 years old
Etiology:
- Idiopathic
- Associated with diabetes mellitus,
inflammatory arthritis, trauma,
prolonged immobilization, thyroid
disease, CVA, myocardial infarction,
or autoimmune disease
Clinical Manifestation:
- Painful and restricted shoulder ROM
- Stages
 Stage 1 (1-3mos) – painful
shoulder movement ,
minimal restriction in
motion
 Stage 2 (3-9mos) – "freezing
stage”; painful shoulder
movement, progressive loss
of GH joint motion
 Stage 3 (9-15mos) – “frozen
stage”; reduced pain with
shoulder movement,
severely restricted GH joint
motion
 Stage 4 (15-24mos) –
“thawing stage”; minimal
pain, progressive
normalization of GH joint
motion
Diagnosis:
- GH joint arthrography – shows
significant reduction in the capsular
volume
Treatment:
- Stage 1 and 2
 Physical modalities,
analgesics, and activity
modification to reduce pain
and inflammation
 Up to 3 intraarticular
corticosteroid injections to
reduce inflammation and
pain, facilitate
rehabilitation, and shorten
the duration of the
condition
- Postural retraining to reduce
kyphotic posture and forward
humeral positioning
- Passive joint glides and non-painful
passive ROM exercises early in the
rehabilitation process
- Early scapular stability exercises and
close chain rotator cuff exercises
- AAROM and AROM along with open
chain and proprioceptive exercises
as the patient’s condition improve
- Capsular hydrodilatation,
manipulation under anesthesia, and
arthroscopic lysis of adhesions can
be considered for patients who does
not improve after 6 months of non-
operative treatment
8. Suprior Labral anterior to Posterior
lesions (SLAP lesion)
- Injuries to superior labrum and
biceps tendon complex
Etiology:
- FOOSH
- Traction injuries
25 | P a g e
 - Torsional peeling back of the labrum
during late cocking phase of
overhead throwing
- Traction forces from long head of
the biceps tendon during
deceleration phase of overhead
throwing
Clinical Manifestation:
- Pain with overhead throwing
- Mechanical symptoms such as
clicking, catching, or grinding
Diagnosis:
- Physical examination
 (+) underlying GH joint
instability
 (+) O’Brien test
- Gadolinium-enhanced MRI
- Arthroscopy – gold standard for
diagnosing SLAP lesion
- Classification System
 Type 1 – involves fraying
injury to the superior
labrum without detachment
of the biceps tendon
 Type 2 – biceps tendon is
detached from the
supraglenoid tubercle
 Type 3 – bucket handle
tearing of the superior
labrum without detachment
of the biceps tendon
 Type 4 – tear of the superior
labrum that extends into
the biceps tendon
Differential Diagnosis:
- Impingement
- AC joint pain
- Bicipital tendonitis
- GH joint instability
Treatment:
- Surgery – standard treatment
- Correction of strength and flexibility
deficits, and normalization of
scapulothoracic mechanics should
help with post-surgical recovery
Elbow Region
1. Lateral Epicondylitis / Tennis elbow
Epidemiology:
- Common tendinopathy in the lateral
elbow
- Occurs up to 50% of tennis players
(M>F)
- Common in patients aging 35<
- Peaks: between 40-50 years old
Etiology:
- Excessive repetitive stress on the
lateral forearm
Diagnosis:
- Physical examination
 (+) point tenderness over
lateral epicondyle
 (+) Cozen’s test
- Radiographs
 Oblique view might reveal
punctuate calcifications in
the extensor tendon origin
Differential Diagnosis:
- Posterior interosseous branch of
radial nerve entrapment
Treatment:
- Discontinuation of provocative
activities
- Oral analgesics
- Physical modalities
- Bracing
- Eccentric strengthening of wrist
extensors
2. Medial Epicondylitis / Golfer’s elbow
Epidemiology:
- 3-7x less frequent than lateral
epicondylitis
Etiology:
- Traumatic - from acute rupture of
the ulnar collateral ligament
- Risk factors:
 Training errors
 Faulty equipment
 Repetitive activities
requiring wrist flexion and
forearm pronation and
supination
 Biomechanical
abnormalities
Clinical Manifestation:
- Gradual onset of pain over medial
epicondyle exacerbated by activities
that require repetitive gripping,
wrist flexion, and forearm pronation
and supination
- Feeling of grip strength weakness
- Concomitant ulnar neuropathy
Diagnosis:
- Physical examination
 Tenderness to palpation
over medial epicondyle
 Weakness in grip strength
 Pain when a tight fist is
made
 Pain with resisted wrist
flexion and forearm
pronation
- Radiographs
Differential Diagnosis:
- Degenerative changes in the
posterior medial aspect of the
olecranon
Treatment:
- Non-operative
 Discontinuation of
aggravating activities
 Analgesics
 Physical modalities
 Bracing
 Extra corporeal shockwave
therapy
26 | P a g e
 - Operative treatment for those who
fail to improve with conservative
measures
3. Olecranon Bursitis
- Inflammation of the olecranon
bursa
Classification:
- Aseptic – acute hemorrhagic bursitis
- Septic
Epidemiology:
- Aseptic bursitis – frequently seen in
football or hockey players
Etiology:
- Aseptic bursitis – microtrauma insult
to the bursa or chronic bursitis
caused by repetitive microtrauma
- Septic bursitis – result of localized or
systemic infection
Clinical Manifestation:
Aseptic Bursitis
- Initial period of swelling that feels
like a liquid pouch if the injury is
chronic and recurrent
Septic Bursitis
- Significant edema, erythema, and
hyperthermia in the infected bursa
and is frequently accompanied with
systemic symptoms of infection
Diagnosis:
- Physical examination
 Edematous area over the
olecranon which is tender
to palpation
 LOM on elbow 2° to tissue
tightness and pain
 If the bursa is infected, the
area can feel warm, and pt.
can have increase white
blood cell count
- Radiographic evaluation – to
determine whether pt. has an
osteophyte over the tip of
olecranon or calcification within the
bursal sac
- Laboratory analysis (septic bursitis)
 Gram stain, culture, and
sensitivity
 Crystal analysis
Treatment:
Aseptic Bursitis
- Sterile aspiration of the bursa
followed by application of a
compressive dressing
- NSAID medication and frequently
apply ice to the area
- Olecranon should be protected from
further insult using elbow pad
- Sclerotherapy using a tetracycline
injection into the bursa (if bursitis is
recalcitrant to standard treatment)
- Surgical excision of pt. does not
improve using the above measure
Chronic Bursitis
- Ice
- Intermittent NSAIDs
- Application of elbow pads
- Compressive dressing (for edema)
- Intrabursal injection or
corticosteroid
- Surgical excision of pt. does not
improve using the above measure
Septic Bursitis
- Aspiration for symptomatic relief
and to obtain fluid sample for
laboratory analysis
- Compressive dressing
- Pt. should be instructed to elevate
the arm
- Intravenous antibiotics (systemic
symptoms
- Oral antibiotic (localized symptoms)
- Incision and drainage if pt. does not
improve using the above measures
4. Osteochondrosis (Panner’s disease) and
Osteochondritis Desiccans of the
Capitellum
- Panner’s disease – osteochondrosis
of the capitellum
- Osteochondritis Desiccans –
involves focal lesion of the
capitellum
Epidemiology:
Osteochondrosis (Panner’s disease)
- Usually occurs in children between
7-10 years old
Osteochondritis Desiccans
- Occurs in throwing athletes
between 9-15 years old
Etiology:
Osteochondrosis (Panner’s disease)
- Idiopathic
- Appears to be related to disordered
endochondral ossification in
association with trauma or vascular
impairment
Pathophysiology:
Osteochondrosis (Panner’s disease)
- Begins with degeneration of
necrosis of the capitellum
- Followed by regeneration and
calcification of this area
Clinical Manifestation:
Osteochondrosis (Panner’s disease)
- Dull, aching lateral elbow pain
aggravated with throwing activities
- (+) effusion of the elbow, but ROM
is usually not restricted
Complications:
Osteochondrosis (Panner’s disease)
- Late articular collapse of the
capitellum (uncommon)
Osteochondritis Desiccans
- Insidious onset of lateral elbow pain
accompanied by an elbow flexion
contracture of 15° or more
- (+) catching and locking of elbow
- (+) elbow effusion
27 | P a g e
 Diagnosis:
Osteochondritis Desiccans
- Radiologic evaluation –
anteroposterior, lateral, and oblique
view of the elbow
- MRI – study of choice
Differential Diagnosis:
- Ostechondrosis VS Osteochondritis
7-10 yeard old 9-15 years old
Involves entire Focal lesions to
capitellum the capitellum
Usually self- Frequently
limited and leads to loose
resolves with body formation
rest and time
Treatment:
Osteochondrosis (Panner’s disease)
- Non-operative and initially involves
discontinuation of throwing
activities
- Posterior long arm splint
occasionally use for pain control
Osteochondritis Desiccans
- Rest, ice, and analgesics
- Elbow immobilization using
posterior long arm splint
- Gentle progressive ROM and
strengthening exercises once pain
has resolved
- Protection from forceful activities
(minimum of 6 weeks to allow
healing)
- Gradual return to functional
activities
- Surgical intervention
5. Elbow Dislocations
Epidemiology:
- Most frequently occur in the
posterolateral direction
- Anterior, lateral, and posteromedial
dislocation less frequent to occur
Etiology:
- FOOSH injury with elbow in
hyperextension
Complications:
- Disruption of the ulnar and radial
collateral ligaments of the elbow
(posterlateral elbow dislocation)
- Occasionally disruption of the flexor
pronator forearm musculature, or
periarticular, and intraarticular
fractures (posterlateral elbow
dislocation)
- Acute anterior forearm
compartment syndrome
- Flexion contractures
Diagnosis:
- Complete neurovascular
examination of the injured limb
- Standard anterior-posterior, lateral,
and oblique radiographs to correctly
classify the direction of dislocation
to identify any associated fractures
- Pre-reduction and post-reduction
films should be obtained to ensure
proper reduction
Treatment:
- Should begin with reduction of
dislocation
- Open reduction (if elbow cannot be
reduced)
- Early surgical intervention (if flexor-
pronator musculature has been
disrupted along with the UCL)
- Conservative treatment includes
sling or posterior arm splint for 2-3
days followed by progressive ROM
exercises
- Prolonged immobilization should be
avoided because flexion
contractures are a frequent
complication of this injury
- Hinged elbow brace that allows
flexion and extension of the elbow
can be used to facilitate early ROM
activities
- Ice and analgesics can assist pt.
comfort
- Progressive strengthening exercises
and full return to activities can begin
in approximately 8 weeks
- Surgical intervention for those with
chronic recurrent elbow instability
Forearm and Wrist Region
1. De’Quervain’s Syndrome (Stenosing
Tenosynovitis)
Epidemiology:
- Most common tendonitis of the
wrist
- Frequently seen in pts. who perform
activities requiring forceful gripping
with ulnar deviation of the wrist or
repetitive use of the thumb
Etiology:
- Shear and repetitive micro trauma
Clinical Manifestation:
- Insidious onset of pain over dorsal
radial aspect of the wrist aggravated
with activities such as racquet
sports, golf, or fly fishing
- Wrist crepitus
Diagnosis:
- Physical examination
 Mild edema localized to the
dorsal radial wrist and
tenderness to palpation
over the first dorsal
compartment
- Finkelstein test (pathognomonic for
the diagnosis)
Treatment:
- Rest, modalities, analgesics, and a
thumb spica splint
- First dorsal compartment
peritendinous corticosteroid
injection reduces symptoms in 62%-
100% of cases
28 | P a g e
2. Scapholunate Instability
Epidemiology:
- Most common type of wrist
ligament injury
Etiology:
- Falling on a pronated outstretched
hand with the wrist in extension and
ulnar deviation
Clinical Manifestation:
- Wrist edema
- Ecchymosis
- Restricted ROM
- DISI pattern (dorsal intercalated
segmental instability) – after
scapholunate ligament disruption,
the scaphoid moves into flexed
position, whereas the lunate and
triquetrum become extended
Complications:
- Progressive wrist arthrosis and
scapholunate advanced collapse
when not diagnosed early and
treated properly
Diagnosis:
- Physical examination
 Tenderness over the
scapholunate joint
particularly on the dorsum
of the wrist
 (+) Watson test
- Radiographic evaluation
 Anteroposterior – gap more
than 3mm between
scaphoid and lunate
 Anteroposterior with a
clenched fist
 Lateral – reveal presence of
DISI pattern injury
(scapholunate angle is >60°)
 Oblique views
 Assess for presence of
associated fractures
- Arthrography or MRI
- Wrist arthroscopy – gold standard in
diagnosing
Treatment:
- Acute and chronic injuries should be
treated surgically
- Partial wrist arthrodesis can
improve chronic scapholunate
instability
- Proximal row carpectomy is
frequently used to treat advance
scapholunate collapse
3. Scaphoid Fracture
Epidemiology:
- 6% of all fractures involve carpal
bones
- 70% of carpal fractures involve the
scaphoid
- 80% occurs in the middle third
- 15% in the proximal third
- 4% in the distal third
- 1% occurs through the distal
tubercle
Etiology:
- Falling on extended wrist
Clinical Manifestation:
- Dorsal radial wrist pain
- Mild anatomic snuffbox edema
- Ecchymosis
Complications:
- Avascular necrosis and non-union as
a result of disruption in the blood
supply
Diagnosis:
- Physical examination
 Tenderness in palpation of
anatomical snuffbox
- Neurovascular function
- Radiologic evaluation
 Anteroposterior, lateral,
right, and left oblique
clenched fist views
 Scaphoid fractures can be
very subtle and not readily
apparent on radiographs
 Assess associated carpal
instability pattern
- MRI or bone scan
Treatment:
- Early cast immobilization for edema
- For non-displaced middle third or
proximal third fractures, the first 6
weeks should use long arm – thumb
spica cast with the elbow in 90° of
flexion, wrist in neutral, and thumb
in slight extension and abduction;
long arm – thumb spica cast can be
switched to short arm – thumb spica
cast after 6 weeks, with total
duration of immobilization being 12-
20 weeks depending on radiographic
union
- For distal third fractures or high
index suspicion for scaphoid
fracture not seen in radiographs,
short arm – thumb spica cast with
the wrist and thumb positioned
same as above can be used;
immobilization is required between
10-12 weeks. Radiographs should be
repeated every 2-3 weeks until
radiographic union is documented
- ROM and strengthening exercises of
the non-immobilized parts should
be performed during period of
immobilization
- After immobilization, restoration of
pain-free full ROM and
strengthening of imm0billized
musculature should be performed
4. Distal Radial Fractures
Epidemiology:
29 | P a g e
- Most frequently fractured area of
the body
- Post-meopausal women and
children are particularly susceptible
- Most common distal radius fracture:
Frykman type 1 called “Colles
Fracture”
Etiology:
- Falling on an extended wrist
Clinical Manifestation:
- Colles fracture is characterized by a
fracture line 2 cm proximal to the
distal radius with dorsal angulation
of the distal fragment and radial
shortening
Diagnosis:
- Physical examination
 Localized edema,
ecchymosis, and deformity
at the fracture site
 Fracture site tender to
palpation
- Document normal neurovascular
function during the examination
- Radiographic evaluation
 Anteroposterior – allows
measurement of radial
inclination and length
 Lateral – evaluation of volar
tilt
 Oblique
- Frykman’s Classification
 Type 1 and 2 –
extraarticular fractures
 Type 3 and 4 – intraarticular
fractures involving
radiocarpal joint
 Type 5 and 6 – intraarticular
fractures involving
radioulnar joint
 Type 7 and 8 – intraarticular
fractures involving both
radioulnar and radiocarpal
joints
Treatment:
- Minimally displaced Frykman type 1
or 2 – close reduction and
immobilization with a double sugar-
tong splint with the wrist in slight
flexion and ulnar deviation, forearm
in neutral, and elbow flexed in 90°
- Frykman type 3 or higher,
comminuted fractures, or fractures
with significant displacement and
instability – referred to orthopedist
- Patients with minimally displaced
fractures who are s/p reduction
should be placed in long arm cast
with the wrist in slight flexion and
ulnar deviation, forearm in neutral,
and elbow flexed in 90° for 3-4
weeks; switched to short arm cast
with the wrist in neutral for 3-4
more weeks until healing has
occurred; repeat radiographs
weekly for the first 3 weeks and
then every 2 weeks until healing is
complete
- Non displaced fractures can be
placed in a short arm cast
approximately 3 days post injury;
wrist should be in neutral position
for approximately 6 weeks, with
repeat radiographs every 2 weeks
for the first 6 weeks
- ROM exercises for the joints that are
not immobilized, and after
discontinuation of cast, a
rehabilitation program should be
instituted to ensure restoration of
full joint ROM and upper limb
strength
5. Kienbock’s Disease
- Characterized by progressive
collapse or micro fractures in the
lunate
Epidemiology:
- Occurs more frequently in pts. who
have ulnar-minus variant wrists
Etiology:
- Repetitive compressive forces to the
wrist
Pathophysiology:
- Repetitive compressive forces to the
wrist
- Causes micro fractures in the lunate
- Leads to vascular compromise,
avascular necrosis, and eventual
collapse of lunate
Clinical Manifestation:
- Pain and stiffness in the wrist
Diagnosis:
- Physical examination
 LOM on the wrist
 Tenderness to palpation
over lunate on the dorsum
of the wrist
- Radiographic evaluation
 Ulnar-minus variant in the
wrist
 Lunate can appear normal
in early cases but frequently
becomes sclerotic with
cystic changes followed by
fragmentation and collapse
 Bone scan – might
demonstrate increase
uptake even when
radiographs are negative
- MRI
Treatment:
- Immobilization to attempt to allow
revascularization
- If pt. has ulnar-minus wrist variant,
ulnar lengthening procedure or
radial shortening procedure can be
performed to relieve lunate trauma
30 | P a g e
 - Partial wrist arthrodesis or lunate
excision with soft tissue or silicone
replacement for more advanced
cases
Hand and Fingers Region
1. Extensor Tendon Central Slip Disruption
(Boutonniere Injury)
- Rupture of the central slip of the
extensor tendon at the base of the
middle phalanx resulting in
boutonniere deformity
Etiology:
- Rupture of the central slip tendon
- Avulsion fracture at the central slip’s
insertion on the dorsal proximal
aspect of the middle phalanx
- Mechanism of injury includes: Crush
injury, forced flexion of IP joints, or
lateral volar PIP joint dislocation
Clinical Manifestation:
- Inability to actively extend PIP joint
but able to maintain full PIP
extension if they are passively
placed in this position
Diagnosis:
- Physical examination
 Boutonniere deformity
 Tenderness to palpation
over the dorsum of PIP joint
- Radiographic evaluation –
performed to check for associated
avulsion fracture of the dorsal
proximal aspect of the middle
phalanx
Treatment:
- Pt. education to compliance of
treatment because even a single
episode of PIP flexion can prevent
successful treatment
- If the injury is evaluated within
approximately 6 weeks and pt. has
full passive extension of the PIP joint
– continuous extension splinting of
the PIP joint for 5-6 weeks
- DIP joint can be left unsplinted and
flexion exercises of the DIP joint
should be initiated early
- Serial casting or splinting to restore
full passive ROM – for those with
chronic boutonniere or if the PIP
joint cannot be passively extended
- Early surgical intervention – if pt. is
not able to regain significant PIP
joint extension ROM or if a large
displaced avulsion fracture from the
dorsal proximal aspect of the middle
phalanx accompanies the
boutonniere deformity
2. Terminal Extensor Tendon Disruption
(Mallet Finger)
- Disruption of the distal extensor
tendon at its insertion on the dorsal
proximal aspect of the distal phalanx
resulting to and injury called “Mallet
finger”
Etiology:
- Tendon rupture or an avulsion
fracture of the dorsal proximal distal
phalanx
- Hyper flexion force to an extended
DIP joint
Clinical Manifestation:
- DIP joint pain
- Inability to extend DIP joint
Diagnosis:
- Physical examination
 DIP joint is in flexed position
and the pt. is unable to
extend actively
 Tenderness to palpation
over the dorsal aspect of
the DIP joint
 Accompanying erythema,
ecchymosis, and edema (for
recent injuries)
- Radiologic studies – to check for
avulsion fracture of the dorsal
proximal aspect of the distal phalanx
Treatment:
- DIP splinting in extension 24 hrs. for
6-8 weeks
- Pt. education on the importance of
not allowing DIP flexion because in
can prevent adequate healing and
predispose to permanent extension
lag
- ROM, strength, flexibility, and
endurance exercises in the forearm
and hand musculature
- Surgical intervention for those with
accompanying large avulsion
fractures
3. Flexor Digitorum Profundus Rupture
(Jersey Finger)
Etiology:
- Vigorous gripping activities
Clinical Manifestation:
- Sudden severe pain associated with
a “pop”
- Inability to actively flex the affected
DIP joint
Diagnosis:
- Physical examination
 Inability to actively flex the
affected DIP joint apparent
when pt. is asked to make a
fist
 Retracted tendon mass
palpable in the palm of the
hand
- Radiographic evaluation –
performed to rule out associated
avulsion fracture of the proximal
volar aspect of the distal phalanx
Treatment:
- Surgical repair – primary treatment
31 | P a g e
 - If tendon has retracted to the palm,
repair should be performed within
7-10 days to prevent adhesion
formation
- If tendon does not retract, delayed
repair can be performed within 6-8
weeks
4. Proximal IP joint dislocations
Epidemiology:
- Most frequently dislocated joint of
the hand
- Can occur in dorsal, volar, and
lateral directions; dorsal direction is
the most frequent
Etiology:
- Dorsal dislocations – occur as a
result of an axial load to the joint
combined with hyperextension
- Volar dislocations – due to varus or
valgus force across the joint
combined with volar force to the
middle phalanx
Clinical Manifestation:
- Deformity
- Pain
- Ecchymosis
- Edema
Complications:
- Dorsal dislocations – various levels
of injuries to the volar plate of the
PIP joint, radial, ulnar collateral
ligament (UCL), and can also be
accompanied by a fracture
- Volar dislocations – radial and UCL
sprain, slip injuries, partial volar
plate injuries, and fractures
Diagnosis:
- Physical examination
 Tenderness to palpation
over the injured structures
- Varus and valgus stress test – assess
radial and UCL injuries after
reduction
- Having the pt. passively extend a
flexed PIP joint – assess disruption
of central slip
- Digital block for anesthesia followed
by stabilizing the proximal phalanx
and exerting a translational volar
and dorsal force to the phalanx –
determines dorsal and volar
instability
- Radiologic evaluation – radiographs
of PIP joint to assess associated
fractures
Treatment:
- 45° extension block splint of the PIP
to allow for healing of the volar
plate injury and associated collateral
ligament injuries; angle can be
reduced by 10° each week, with a
return to full extension in the 5th
week
- If splinting is discontinues, buddy
taping the injured finger to the
adjacent finger for a few weeks to
will some stability for the joint as
healing continues and ROM
exercises are instituted
- If stable close reduction of a volar
PIP joint dislocation can be attained,
treatment can proceed with
splinting of the PIP joint in full
extension for 4-5 weeks; followed by
buddy taping for approximately 2
weeks and resumption of normal
activities as tolerated
- Surgical indications
 Radiologic or gross
instability after reduction
 Fractures involving >50% of
the articular surface
 Inability to reduce
dislocation
 Pilon fractures
 Recurrent instability
5. 1st MCP Joint Ulnar Collateral Ligament
Sprain (Gamekeeper’s Thumb)
- Radially directed forces across the
1st MCP joint can result in UCL injury
referred to as “Gamekeeper’s
thumb)
Epidemiology:
- Frequently seen in skiers and
athletes who participate in sports
such as basketball and football
Etiology:
- Radially directed forces across 1st
MCP joint
Clinical Manifestation:
- “Pop” and a feeling of instability
Complications:
- Stener lesion (possibility of
interposition of the adductor pollicis
aponeurosis between 1st proximal
phalanx and ruptured end of UCL) –
can prevent adequate healing and
can lead to chronic joint pain and
instability
Diagnosis:
- Physical examination
 Tenderness to palpation
over the UCL
 If Stener Lesion is present,
there is palpable mass on
the ulnar side of the 1st MCP
joint representing an
avulsed UCL
 UCL stress examination –
performed with the joint
both in full extension and
30° of flexion; complete
tear is indicated by an
angular difference of >15-
30° between the injured
and uninjured 1st MCP joint
and lack of endpoint
32 | P a g e
 - Radiologic evaluation
 Anteroposterior
 Lateral
 Oblique radiographs
To detect presence of fractures
or joint subluxation
- MRI – better visualization of soft
tissue injuries
- Ligamentous Injury Grading Scale
1 – Tenderness to palpation without
subluxation or dislocation
2 – Tenderness to palpation with
subluxation but a good end point
3 – Tenderness to palpation with
associated dislocation and no end
point
Treatment:
- Partial tears – modalities, analgesics,
and immobilization in a thumb spica
cast for 10-14 days followed by a
wrist-hand-thumb spica orthosis for
2-4 weeks
- For pts. who participate in contact
sports, they should continue
wearing thumb spica splint during
competition
- Local taping for stability after period
of splinting is completed
- Gentle progressive ROM exercises
should begin after cast
immobilization by removing the
splint twice daily, and activity should
be progressed as tolerated
- Early surgical repair – for complete
UCL ruptures and if Stener lesion is
present, also for individuals with
avulsion fracture of the base of the
proximal phalanx with angulation
and displacement >3mm or with
chronic recurrent instability
GENERAL HEALTHCARE MANAGEMENT
Pharmacological
- Opioid and non-opioid analgesics for
pain control during acute phase of
rehabilitation
- NSAIDs for their analgesic and anti-
inflammatory properties; NSAIDs
however are not entirely benign and can
cause significant gastrointestinal, renal,
cardiovascular, hematologic,
dermatologic, and neurologic side
effects; should be used only when local
physical modalities and less toxic
medications (eg. acetaminophen) are
not effective
- Oral and injected corticosteroids for pain
control and reduction of inflammation
during acute phase of rehabilitation;
side effects include suppression of
hypothalamic-pituitary-adrenal axis,
osteoporosis, avascular necrosis,
infection, and tendon or ligament
rupture; their use should only be limited
to vary select cases
PHYSICAL THERAPY EXAMINATION, EVALUATION,
AND DIAGNOSIS
Points of Emphasis on Examination
1. History
- Identify whether injury is acute,
chronic, or acute exacerbation of a
chronic injury
- Mechanism of injury
- Identifying tissues overloaded by
injury as well as those directly
injured
2. Physical Examination
- Palpation for presence of
tenderness and inflammation
- ROM for presence of limitation of
motion and flexibility imbalances
- MMT for presence of strength
imbalances
- LGM for presence of inflammation
- Special tests
SPECIAL TESTS FOR UPPER EXTREMITY
Shoulder
1. Anterior apprehension and relocation
tests
- Rationale: For anterior GH stability
- Position: Supine; pt.’s shoulder
abducted to 90° and elbow flexed
to 90°
- Procedure: One hand is used to
slowly externally rotate the
humerus with the forearm as the
lever. Other hand is placed posterior
to the proximal humerus and an
anteriorly directed force is exerted
on the humeral head.
- Result: (+) if the pt. indicates a
feeling of impending anterior
dislocation; (+) for relocation test if
the pt. reports a reduction in
apprehension when the examiner
places the hand over the anterior
proximal humerus and applies a
posteriorly directed force.
2. Posterior Apprehension Test
- Rationale: For posterior GH stability
- Position: Affected shoulder forward
flexed to 90° and maximally
internally rotated. A posteriorly
directed force is the placed on the
pt.’s elbow.
- Result: (+) result cases 50% or
greater posterior translation on the
humeral head or a feeling of
apprehension in the pt.
3. Sulcus sign
- Rationale: Evaluates inferior GH
stability
- Position: Pt. is seated or standing
with arm relaxed in shoulder
adduction. Pt.’s forearm is grasped
33 | P a g e
 and a distal traction force is applied
through the pt.’s arm.
- Result: (+) sulcus present in
between the humeral head and
acromion.
4. O’Brien Test
- Rationale: Evaluates AC joint and
labral abnormalities
- Position and Procedure: Shoulder is
flexed to 90° with the elbow fully
extended. Arm is then adducted to
15° and the shoulder is internally
rotated so that the pt.’s thumb is
pointing downward. A downward
force is applied which the pt. will
resist. Shoulder is then externally
rotated so that the palm is facing up
and the examiner applies a
downward force which is resisted by
the pt.
- Result: (+) if there is pain during the
first part of the maneuver with the
pt.’s thumb pointing downward
which is lessened or eliminated
when the pt. resists a downward
force with the palm facing up. Pain
in the region of AC joint indicates AC
pathology, whereas pain or painful
clicking deep inside the shoulder
suggests labral pathology.
5. Horizontal adduction test
- Rationale: Evaluation of AC joint
pathology and posterior capsular
tightness
- Position and Procedure: Shoulder is
passively flexed to 90° and then
horizontally adducted across the
chest.
- Result: (+) pain on region of the AC
joint suggests AC joint pathology. (+)
pain on posterior shoulder suggests
posterior capsular tightness.
6. Speed’s test
- Rationale: For biceps tendonitis
- Position and Procedure: Shoulder is
forward flexed to 90° with the
elbow fully extended and the palm
facing up. A downward force is
applied against pt.’s active
resistance.
- Result: (+) pain in region of bicipital
groove suggests bicipital tendonitis.
7. Yergason’s test
- Rationale: For bicipital tendonitis
and bicipital tendon instability
- Position and Procedure: With the
arm at the side, the elbow is flexed
to 90° and the forearm is pronated.
The pt. then tries to simultaneously
supinate the forearm and externally
rotate the shoulder against the
examiner’s resistance.
- Result: (+) pain in pt.’s with bicipital
tendonitis. (+) painful pop in pt.’s
with bicipital tendon instability.
8. Neer-Walsh Impingement Test
- Rationale: For rotator cuff tendonitis
- Position and Procedure: The
shoulder is internally rotated while
at the side. The examiner passively
forward flexes the pt.’s shoulder to
180° while maintaining internal
rotation.
- Result: (+) pain in the subarcomial
area suggests rotator cuff
tendonitis.
9. Hawkins-Kennedy Impingement test
- Rationale: For subacromial
pathology
- Position and Procedure: Shoulder
and elbow are each passively flexed
to 90°. Examiner then grasps the
pt.’s forearm, stabilizes the pt.’s
scapulothoracic joint, and uses the
forearm as a lever arm to internally
rotate the GH joint.
- Result: (+) pain in subacromial
region occurring with internal
rotation.
10. Drop arm test
- Rationale: For rotator cuff tear
- Position and Procedure: Pt.’s
shoulder is passively abducted to
90°. Pt. is then asked to slowly lower
the arm back to the side.
- Result: (+) pain and inability to
slowly lower the arm to side
suggests a rotator cuff tear.
Elbow
1. Cozen’s test
- Rationale: For lateral epicondylitis
- Position and Procedure: Pt. is asked
to fully extend the elbow, pronate
the forearm, and make a fist. The
examiner then resists the pt.’s
attempt to extend and radially
deviate the wrist.
- Result: (+) pain in the lateral
epicondyle suggests presence of
lateral epicondylitis.
2. Ligamentous instability test
- Rationale: To test the stability of the
radial and ulnar collateral ligament.
- Position and Procedure: Elbow is
flexed to 20-30° and the arm is
stabilized by placing a hand at the
elbow and a hand on the distal
forearm. Varus and valgus forces are
placed across the elbow to test
stability of radial and ulnar collateral
ligament.
Wrist and Hand
1. Finkelstein test
- Rationale: Use to detect
tenosynovitis of the extensor pollicis
brevis and abductor pollicis longus
34 | P a g e
 tendons (de Quervain’s Recovery -Restore - Open kinetic
tenosynovitis). flexibility, chain exercises to
- Position and Procedure: Pt. makes a strength, and correct strength
fist with the thumb inside the
proprioceptio imbalances
fingers, and the examiner passively
deviates the wrist in ulnar direction. n of the - Close chain
- Result: (+) pain in the affected injured limb exercises to
tendons -Correct provide joint
2. Watson test strength and stabilization
- Rationale: Asses scapholunate flexibility through muscle
stability. imbalances contraction
- Position and Procedure: Pt.’s wrist
and - Progress to
begins in an ulnarly deviated
position. The examiner places a maladaptive functional
dorsally directed force against the movement activities toward
proximal volar pole of the scaphoid. patterns and the end of this
The examiner then radially deviates muscle phase.
the wrist while continuing to place substitutions
the same force against the
- Maintain
scaphoid.
cardiovascula
- Result: (+) pop or subluxation of the
scaphoid r and general
fitness
PHYSICAL THERAPY PROGNOSIS AND PLAN OF Functional - Continue to -Functional
CARE address activities
maladaptive incorporated to
Plan of Care and Intervention
movement rehabilitation
Stage Plan of Care Intervention patterns and program with a
Acute -Reduce pt.’s - Immobilization muscle vocational or
symptoms through splinting substitutions avocational-
-Facilitate or casting specific
tissue healing - RICE (rest, ice, progression that
-Maintain compression, eventually leads to
cardiovascula elevation) –rest return to normal
r fitness, should not be activities
strength, and absolute; pt
flexibility should maintain
SOURCE:
cardiovascular
fitness, strength, Physical Medicine and Rehabilitation 4th edition
and flexibility by Randall L. Braddom
- Cryotherapy to
decrease pain,
inflammation,
muscle guarding,
edema, and local
blood flow
- High frequency
electrical
stimulation to
reduce muscle
guarding and
increase local
circulation
- Core
strengthening
- Aerobic
conditioning
MUSCULOSKELETAL DISORDERS OF THE
EXTREMITIES (LOWER EXTREMITY)

35 | P a g e

General approach to Osteoarthritis
Stress Reactions and Stress Fractures
Hip Region
Femoral Neck Stress Fractures
Avascular Necrosis (Osteonecrosis)
Legg-Calve-Perthes Disease
Hip Dislocations
Labral Injuries
Thigh Region
Conditions of the ITB, Including
Trochanteric Bursitis
Disorders of the Hamstring Muscle
Group (Hamstring Strain, Ischial Avulsion
Injury, and Hamstring Tendinopathy)
Disorders of the Adductor Muscle Group
(Adductor Strain)
Quadriceps Contusions and Myositis
Ossificans
Knee Region
Patellofemoral Arthralgia
Osteochondritis Dissecans
Meniscal Injuries
Knee Ligament Injuries (ACL, PCL, MCL,
LCL Tear)
Prepatellar Bursitis (Housemaid’s knee)
Patellar Tendinopathy (Jumper’s Knee)
Osgood-Schlatter Disease and Sinding-
Larsen-Johansson Disease
Leg Region
Achilles Tendinopathy and Rupture
Tibialis Posterior Overload or Medial
Tibial Stress Syndrome (Shin Splints)
Compartment Syndrome
Ankle and Foot Region
Osteochondral Lesions of the Ankle
Sprains
Flexor Hallucis Longus Overload
Injury to the Plantar Foot muscles and
Plantar Fascia; Plantar Fascitis
Morton’s Interdigital Neuroma,
Metatarsalgia, and Sesamoiditis
GENERAL MEDICAL BACKGROUND
Classification
General approach to Osteoarthritis in the Lower
Limb
Etiology:
- Joint trauma, malalignment, and
obesity predispose an individual to
develop osteoarthritis in weight-
bearing joint
- Genetic predisposition
Clinical Manifestation:
- Joint pain that is worse with weight-
bearing and improved with rest
- Pain and stiffness in the morning
that lasts <1 hr
- For Hip OA
 Pain in the groin region and
can be referred in the
anterior thigh
- For Knee OA
 Can affect the medial and
lateral tibiofemoral
compartment,
patellofemoral joint, or all
three compartments;
medial compartment is
often involved first
 Varus alignment
 Joint line tenderness
 Crepitus
 Palpable osteophytosis
- For Ankle and Foot OA
 Frequent locations include
the 1st MTP joint, subtalar
joint, and tibiotalar joint
 OA of the 1st MTP (hallux
rigidus) results in loss of
dorsiflexion, joint swelling,
and pain
 OA in the subtalar joint will
manifest as pain when
walking in even and uneven
surfaces
 OA in the tibiotalar is
characterized by pain,
swelling, and stiffness in the
anterior ankle
Diagnosis:
- Physical examination
 For Hip OA
- Antalgic gait on the
affected side
- Reproduction of groin
pain with passive hip
internal rotation
 For Knee OA
- Varus alignment
- Tenderness upon
palpation of joint
- Palpable osteophytosis
 For Ankle and Foot OA
- Pain, swelling, and
stiffness in the affected
area
- Loss of dorsiflexion
(hallux rigidus)
- Plain films - study of choice to
assess osteoarthritis
 Radiologic hallmarks:
- Decrease joint space
- Marginal osteophytosis
- Subchondral cyst
formation
- Subchondral sclerosis
Differential Diagnosis:
- Inflammatory arthropathies
(morning pain usually lasts >1 hr.)
- Referred pain from the lumbar spine
(for Hip OA)
Treatment:
36 | P a g e
 - Modifying activities – switching
from higher impact activities to
lower impact activities can decrease
or eliminate joint pain
- Ice, acitaminophen, and NSAIDs can
all reduce joint pain
- Strength training and aerobic
exercise can improve joint control
and decrease pain
- Strategies to reduce load on joints
includes:
 Weight loss
 Cushioned shoes
 Walking aids such as cane
- Intraarticular injection of anesthetic
and steroids
- Arthroplasty for improvement in
pain and function for those pts. with
recalcitrant pain or severe
functional limitations
Stress Reactions and Stress Fractures in the
Lower Limb
Epidemiology:
- Common in physically active
individuals esp. those who
participate in endurance activities
(distance running)
Etiology:
- Repetitive overload injuries to the
bones of the LE
- Risk Factors
 Intrinsic Risk Factors
- Poor dietary habits
- Altered menstrual
status
- Biomechanical
abnormalities that do
not allow for proper
distribution of forces
along the kinetic chain
 Extrinsic Risk Factors
- Hard training surfaces
- Training errors
- Improper footwear and
foot soles
Clinical Manifestation:
- Insidious onset of focal pain, that is
exacerbated with weight-bearing
activities
Diagnosis:
- History taking
 Pt. usually provides a history
of a recent acceleration in
the intensity or duration of
training before the onset of
symptoms
- Imaging studies – for individuals
who remain symptomatic and are
unable to return to full activities
 Radiographs – initial
imaging study of choice but
are relatively insensitive and
detects <50% of stress
fractures
 Bone scans – sensitive for
detecting stress fractures
but lack anatomic
definition; can also remain
positive long after
symptoms have resolved
 MRI – provides excellent
anatomic information and
can be more useful in
grading lesions and
assessing soft tissue
structures
 Computed tomography (CT)
– provides optimal
definition of bone
architecture
Treatment:
- Activity modification – most stress
fractures can heal without any
complications and can allow return
to sport in 4-8 weeks
- Initial treatment includes:
 Pain management
- Use crutches to
minimize weight-
bearing for the first 7-
10 days
- Modalities (ice)
- Analgesics
(acetaminophen)
 Activity modification
- Eliminating impact
activities for a period of
time until daily
ambulation is pain free
- Continue to perform
strengthening and
cross training during
this time to keep the
cardiopulmonary
system fit
 Strengthening
- Should begin
immediately after
diagnosis of stress
fracture has been made
- Exercises prescribed
should not cause pain
on the fracture site
 Fitness maintenance
- Fitness must be
maintained in ways that
avoid overloading the
bone
- Common cross training
activities include:
cycling, swimming,
water running, rowing,
and stair master
 Risk factor modification
- Progress activities as pain subsides,
and progress must be monitored
clinically by the presence and
37 | P a g e
 absence of symptoms and local
signs
- Some stress fractures tend to
develop complications and require
specific treatment. These includes
stress fractures of the femoral neck,
anterior cortex of the middle third
of the tibia, navicular, and proximal
fifth metatarsal fractures; they will
be discussed separately in their
respective anatomic regions
Hip Region
1. Femoral Neck Stress Fractures
Clinical Manifestation:
- Inflammation
- Pain
Complications:
- Displacement
- Avascular necrosis
Diagnosis:
- MRI – should be obtained when
suspicion is present
Prognosis:
- Fractures on the tension side
(lateral) are less common and
require immediate surgical referral;
fractures on the compression side
(medial) are more common
- If the fracture line extends more
than 50% of the width of the
femoral neck, percutaneous fixation
should be considered because the
likelihood of displacement is higher
Treatment:
- Strict non–weight-bearing status is
necessary for about 4 to 6 weeks
until the patient is pain free.
- Followed by functional
rehabilitation with progressive
weight-bearing over the next 4 to 8
weeks according to symptoms
2. Avascular Necrosis (Osteonecrosis)
- Death of bone resulting from a lack
of blood supply
Etiology:
- Trauma
- High doses of corticosteroids
- Alcohol abuse
- Systemic illnesses (such as diabetes,
lupus, and sickle cell anemia)
Pathophysiology:
- There is death of bone resulting
from a lack of blood supply. This can
lead to micro fractures and
eventually collapse of the bone.
Clinical Manifestation:
- Inflammation
- Groin Pain
- Limited motion and pain with
internal rotation, flexion, and
adduction of the hip.
Complications:
- Bone collapse
Diagnosis:
- Radiographs – can reveal sclerosis of
the femoral head or in severe cases,
collapse of the femoral head
- MRI and CT can detect the condition
in its earlier stages
Treatment:
- Conservative treatment might
include minimizing weight-bearing
of the affected joint and use of pain
medications. Once collapse occurs,
joint replacement surgery is
indicated.
3. Legg-Calve-Perthes Disease
- Idiopathic osteonecrosis of the
femoral head in children
Epidemiology:
- Children are most affected
- More common in boys between the
ages 4 and 8 years old
Etiology:
- Idiopathic
Clinical Manifestation:
- Limping
- Limited hip motion
- Groin or thigh pain
Diagnosis:
- MRI
- CT scan
Differential Diagnosis:
- Avascular necrosis
Prognosis:
- Prognosis is significantly better
compared with adults with avascular
necrosis
Treatment:
- Use of an abduction brace to
maintain the femoral head in a
spherical state is reasonable.
- Osteotomy is sometimes performed
in older children.
4. Hip Dislocations
Epidemiology:
- Hip dislocation is more common
than hip fractures
- Most common: the head of the
femur dislocates posteriorly relative
to the acetabulum.
Clinical Manifestation:
- Acute posterior hip dislocation
presents with severe hip pain and
the pt. tends to hold the hip in
flexion, internal rotation, and
adduction
- Less common anterior dislocations
presents with the hip held in an
extended, abducted, and externally
rotated position
Complications:
- Lumbosacral plexopathy
- Sciatic neuropathy
- Femoral neuropathy
- Post-traumatic osteoarthritis
- Avascular necrosis
Diagnosis:
38 | P a g e
 - Physical examination
 Obvious deformity
 Pt. will not tolerate ROM
and MMT testing
- Neurologic examination – assess for
lumbosacral plexopathy, sciatic
neuropathy, and femoral
neuropathy
- Radiographs are indicated to
confirm the clinical diagnosis and
look for associated injuries
- CT or MRI is obtained if further
characterization of associated
injuries is needed
Treatment:
- Closed reduction under anesthesia –
should be performed as soon as
possible
- Surgery if attempts at close
reduction are unsuccessful
- Non–weight-bearing for 3 to 4
weeks, followed by protected
weight-bearing for an additional 3
weeks
- Gradually progressive rehabilitation
can start a few days to a couple of
weeks after reduction, depending
on the patient’s comfort level and
whether surgery was performed
5. Labral Injuries
Etiology:
- Acute or repetitive trauma
Clinical Manifestation:
- Painful catching of the hip,
especially when the hip is at a
particular angle
Diagnosis:
- Femoral – acetabular grind
maneuvers – might reproduce
symptoms
- MRI with gadolinium contrast –
imaging study of choice
- Arthroscopy or open surgery –
definitive diagnosis
Treatment:
- Acetaminophen or NSAIDs
- Relative rest
- Intraarticular steroid injections
- Surgical debridement or repair
- Arthroscopic and open surgical
approaches
Thigh Region
1. Conditions of the ITB, Including
Trochanteric Bursitis
Etiology:
- Direct trauma
- Improper training techniques
- Abnormal biomechanics
Pathophysiology:
Clinical Manifestation:
- Localize pain on the lateral hip
- Pain sometimes felt along the path
of the ITB in the lateral thigh
- Lateral snapping hip syndrome –
audible snap heard as ITB rubs over
the greater trochanter
Diagnosis:
- Physical examination
 Tenderness to palpation
directly over the greater
trochanter or immediately
posterior to it
 MMT – weakness of the
gluteus medius and hip
external rotators
 Muscle imbalance – TFL
tightness and g.max
weakness
 Special test – Modified
Thomas Test
Treatment:
- Exercise prescription should be
based on the patient’s relevant
biomechanical defecits
- Eliminate or reduce exacerbating
activities
- Icing – to reduce pain and
inflammation
- ITB massage, myofascial release,
ultrasound, and local injection of
corticosteroid can facilitate pt.’s
rehabilitation program
- Off-the-shelf and Custom-made-
orthoses can be helpful in reducing
impact and improving subtalar
positioning and tibial rotation
2. Disorders of the Hamstring Muscle
Group (Hamstring Strain, Ischial Avulsion
Injury, and Hamstring Tendinopathy)
Epidemiology:
Hamstring Strain
- Common in individual participating
in ballistic activities
- Most common strained muscle
group – Hamstring group
Ischial Avulsion Injury
- Most common in ages 15-25 years
old
Etiology:
Hamstring Strain
- Forceful eccentric contraction of the
hamstring muscles especially when
the muscle is at a mechanical
disadvantage near full flexion or
extension
Ischial Avulsion Injury
- Gymnastics, Hurdling, Dancing
- In skeletally mature individuals, the
weakest link might be the tendon
rather than the bone, causing the
proximal hamstring tendon to
avulse
Pathophysiology:
Ischial Avulsion Injury
- In proximal hamstring injuries, bone
fails before the muscle or tendons
39 | P a g e
 fails, resulting in an ischial avulsion
injury
Clinical Manifestation:
Hamstring Strain
- Pain over the hamstring muscles
- Strain can occur near the hamstring
origin
- Severe hamstring strains will
produce visible ecchymosis at and
distal to the site of injury
Ischial Avulsion Injury
- Sudden onset of pain at the ischial
tuberosity
Hamstring Tendinopathy
- Pain with activities
- Change in pt.’s activity level such as
a recent rapid increase in running
Diagnosis:
Hamstring Strain
- Physical examination
 Pain is produced by passive
stretching of the muscle,
resistance testing, and by
direct palpation of the
injured area
- MRI – imaging modality of choice
Ischial Avulsion Injury
- Physical examination
 Point tenderness at the
ischial tuberosity
 Pain with passive hamstring
stretch
 Pain with knee flexion or hip
extension with resistance
- Plain films
Hamstring Tendinopathy
- Physical examination findings are
similar with hamstring strain but are
usually less dramatic
Treatment:
Hamstring Strain
- Relative rest
- Ice
- Early gentle ROM exercises
- Gentle progressive strengthening
exercises as tolerated
- Exercises progress to higher weight
and include more ballistic and sport-
specific movements when tolerated
Ischial Avulsion Injury
- Treated similarly to other hamstring
injuries although period of relative
rest might be longer to allow for
bone healing
- Crutches – if symptoms are severe
and prevents comfortable
ambulation
- Icing – applied first few days, to
decrease pain and swelling
- Orthopedic consultation – needed if
the avulsion fragment is displaced
>2 cm, or if resolution of symptoms
does not occur in the expected
period
- Slowly progressive hamstring
stretching and strengthening as pain
decreases over the first 1-2 weeks
Hamstring Tendinopathy
- Relative rest
- Ice
- Hamstring stretching and
strengthening
- Identifying and correcting errors in
training technique, running gait,
cycling, or jumping mechanics, and
relevant biomechanical deficits
3. Disorders of the Adductor Muscle Group
(Adductor Strain)
Epidemiology:
- Common in individual involved in
soccer, hockey, and skiing
- Most commonly involved muscle –
Adductor longus
Etiology:
- Forceful activation of the muscle,
especially when in lengthened
position
- Acute or repetitive overload
Diagnosis:
- Physical examination
 Pain reproduced with
passive stretching and
active resistance testing of
the adductor group
- Radiographs – useful when looking
for bone injuries such as avulsion
fractures
- MRI
Treatment:
- Early gradually progressive ROM
exercises
- Strengthening exercises with return
to sport specific exercises when
tolerated
- Core exercise program to stabilize
pelvis
4. Quadriceps Contusions and Myositis
Ossificans
Epidemiology:
- Quadriceps contusion – common
- Myositis ossificans – occurs 10-20%
of all thigh contusions; most
common location is the quadriceps
Etiology:
- Quadriceps contusion – direct and
forceful blow to the quadriceps
- Myositis ossificans – occurs after a
severe quadriceps contusion when
the intramuscular hematoma can
undergo calcific transformation
Clinical Manifestation:
Quadriceps Contusion
- Pain at the site of injury
- Stiffness
- Difficulty with weight bearing
- Antalgic gait
Myositis Ossificans
- Pain and stiffness
40 | P a g e
 Diagnosis:
Quadriceps Contusion
- Physical examination
 Antalgic gait
 Tenderness to palpation
 Presence of echymosis, and
swelling in the anterior
thigh
 Restricted knee flexion ROM
- Radiographs – obtained to look for
underlying femur fracture
Myositis Ossificans
- Radiographs
- Bone scan or MRI to look for
calcification in the muscle; more
sensitive in the early stages
Treatment:
Quadriceps Contusion
- Ice – to decrease swelling and pain
- Early ROM exercises
Myositis Ossificans
- Progressive ROM exercises
- Medication
- Surgical intervention – for
unresponsive cases
Knee Region
1. Patellofemoral Arthralgia
- Pain in the joint between the patella
and femur
Epidemiology:
- Most common cause of knee pain in
the younger population
Etiology:
- Acute traumatic event such as fall
onto the knee
Pathophysiology:
- Acute traumatic event
- Leads into injury to the bone and
subchondral cartilage
Clinical Manifestation:
- Pain to the anterior knee
- Pt. can even say that pain is "under
the knee cap"
Complications:
- Patellar tendonitis – can coexist with
patellofemoral arthralgia
Diagnosis:
- Physical examination
 Tenderness with palpation
under the medial and lateral
aspects of the patella
 Pain or apprehension with
medial/lateral glide and tilt
maneuvers of the patella
- Functional examination
 Look for all the
biomechanical deficits
 Single-leg and double-leg
squats, and lunges – useful
in functional examination of
a pt. with patellofemoral
symptoms
Differential Diagnosis:
- Infrapatellar or suprapatellar
bursitis
- Synovial plica
- Quadriceps tendonitis
- Patellar tendonitis
- Sinding-Larsen-Johansson disease
- Intraarticular pathology such as
meniscal tear
Treatment:
- Ice
- Acetaminophen or NSAIDs
- Strengthening weak or imbalance
muscle groups in the core and lower
limbs
- Stretching tight structures such as
the ITB
- Activity modification
- Patellofemoral taping techniques to
improve patellofemoral tracking and
decrease pain
- Specific patellofemoral control
braces to decrease pain and
improve muscle activation in up to
50% of all pts.
- Surgical release of the lateral
retinaculum and tightening or
reconstruction of the medial
patellofemoral ligament can
improve patellar positioning within
the groove and improve symptoms
2. Osteochondritis Dissecans
- lesion of subchondral bone with or
without involvement of the
overlying articular cartilage
Classification
- Grade 1 – involves compression of
subchondral trabeculae with
preservation of the cartilage
- Grade 2 – involves incomplete
detachment of an osteochondral
fragment
- Grade 3 – involves complete
avulsion of an osteochondral
fragment without dislocation
- Grade 4 – involves complete
avulsion of an osteochondral
fragment with dislocation
Epidemiology:
- Most common site is the inferior
portion of the medial femoral
condyle
Clinical Manifestation:
- Focal pain and swelling with activity
and is lessened with rest
- Mechanical symptoms (locking,
catching, crepitus, grinding) can
occur as a result of irregularities of
the articular surface
Diagnosis:
- Imaging studies or direct
arthroscopic visualization
Treatment:
- Depends on the grading of the
lesion and severity of symptoms
41 | P a g e
 - Surgical techniques can be: - LCL tear – rarely injured in isolation
 Palliative – arthroscopic Etiology:
debridement - ACL tear
 Reparative – microfracture  Contact or noncontact
 Restorative – autologous injuries
chondrocyte implantation,  Rotating on a planted foot
osteochondral graft with the knee in flexion and
3. Meniscal Injuries with the quadriceps
Epidemiology: activating strongly
- Injuries to the menisci are common - PCL tear
Etiology:  Blow to the proximal,
- Acute trauma or gradual anterior legs
degeneration  Examples:
- Most common mechanism of injury: - Soccer goalkeepers who
sudden or forceful twisting motion get kicked in the shin
on planted foot when sliding to make a
Clinical Manifestation: save
- Slow onset of swelling after the - Individuals who fall onto
injury their shins
- Pain with weight bearing and - Motor vehicle accidents
twisting maneuvers when a front-seat
- Clicking within the knee passenger has the shin
- Locking of knee – suggests the driven into the
presence of bucket handle meniscus dashboard: “dashboard
tear injury”
Diagnosis: - MCL tear
- Physical examination  Sustaining a sudden valgus
 Hallmark: medial or lateral force with the foot planted
joint line tenderness, - LCL tear (“fibular collateral
effusion, (+) McMurray test ligament”)
- MRI – study of choice to look for  Can be torn in multi-
meniscus tears ligament injuries and knee
Prognosis: dislocations
- Simple tears have greater chance of Clinical Manifestation:
healing than complex tears - ACL tear
- Tears in the outer portion of the  Hearing or feeling a “pop”
meniscus, referred as Vascularized followed by effusion
“Red Zone” have greater healing  Sensing of knee instability
potential than tears located especially with twisting
centrally in the Avascular “White activities such as changing
Zone” direction when walking
Treatment: - MCL tear
- Ice  Localize pain at the medial
- Elevation side of the knee
- NSAIDs Diagnosis:
- Bracing - ACL tear
- 3-6 weeks of relative rest and  MRI
rehabilitation for older athletes with  Plain films
no mechanical symptoms present  (+) Anterior drawer’s and
- Arthroscopic intervention (includes Lachman’s tests
repair of the meniscus tear or - PCL tear
debridement of the meniscus with  MRI
partial meniscectomy) is considered  Plain films
if pt. remains limited in function, has  (+) Posterior drawer test
persistent mechanical symptoms, or - MCL tear
has recurrent episodes of pain and  Tenderness along the
swelling course of MCL
4. Knee Ligament Injuries (ACL, PCL, MCL,  (+) Valgus Stress test
LCL Tear)  MRI or plain films such as
Epidemiology: X-ray
- ACL tear – most common Treatment:
devastating injury - ACL tear
- PCL tear – less common than ACL  Ice, elevation and
tear compression

42 | P a g e
  Knee immobilizer or hinged
knee brace
 Crutches if needed
 Early, gentle knee flexion
and extension exercises
 Straight leg raises in the
knee immobilizer
- PCL tear
 Ice, elevation, and pain
control
 Early gentle range of motion
exercises
 Knee immobilizers and
crutches for 1 to 2 weeks;
return to full activities after
functional rehabilitation
 Surgical reconstruction
- MCL tear
 Ice and elevation
 Knee immobilizer for 1 to 2
weeks
 Gentle knee flexion and
extension exercises in the
first 1 to 2 weeks
 Gradual return to full
activities as tolerated is
progressed over 1 to 4
weeks
5. Prepatellar Bursitis (Housemaid’s knee)
- Inflammation of the prepatellar
bursa
Epidemiology:
- Common in activities such as carpet
laying and gardening
- Also seen in wrestlers 2° to irritation
or friction from the wrestling mat
Clinical Manifestation:
- Pain and swelling in the anterior
part of the patella within the bursa
- Knee ROM can be mildly limited
Treatment:
- Avoiding aggravating activities
- Ice, compression, NSAIDs to
decrease pain and swelling
- Aspiration followed by instillation of
corticosteroid can be helpful, but
septic bursitis should be ruled out
first
- Drainage or excision of the bursa
indicated for some individuals
6. Patellar Tendinopathy (Jumper’s Knee)
- Overload of the patellar tendon
Epidemiology:
- At risk for patellar tendon overload:
those who participate in repetitive
knee flexion and extension activities
(basketball players, volleyball
players, bicyclists, rowers, and
mogul skiers)
Etiology:
- Overload at the patellar tendon
Clinical Manifestation:
- Pain – usually at the inferior pole of
the patella, but can occur anywhere
along the course of the tendon
Diagnosis:
- History and Physical examination
 Tenderness along the
course of the tendon
 Assess for biomechanical
deficits that can lead to
unequal distribution of
forces along the links in the
kinetic chain that are most
involved with jumping
- MRI and Ultrasound – provide
adequate visualization of the tendon
Treatment:
- Ice
- NSAIDs
- Cross-friction massage
- Modalities
- Quadriceps stretching
- Strengthening exercises
- Addressing relevant biomechanical
deficit
- Surgical debridement of the tendon
for long standing refractory cases
that will not respond to
rehabilitation
7. Osgood-Schlatter Disease and Sinding-
Larsen-Johansson Disease
- Osgood-Schlatter – pain at the tibial
tuberosity that is exacerbated with
activities and direct contact
- Sinding-Larsen Johansson – similar
manifestations with Osgood-
Schlatter but can be seen at the
origin of the patellar tendon at the
inferior pole of the patella
Epidemiology:
- Common in active adolescents
Etiology:
- No clear cause but repetitive
overload of the patellar tendon
insertion can cause inflammation,
irregularity and/or partial avulsions
of the secondary ossification center
of the tibial tuberosity
Clinical Manifestation:
- Pain at the tibial tuberosity –
symptoms might be
intermittent or persistent until
the growth plate close, at which
point symptoms resolve
spontaneously Complications
Diagnosis:
- Physical examination
 Significant pain and
tenderness at the tibial
tubercle
- Radiographic hallmark: Irregularity
and fragmentation of the tibial
tuberosity (Osgood-Schlatter)
Treatment:
43 | P a g e
 - Ice
- Gentle progressive quadriceps
stretching
- Careful pain-free quadriceps
strengthening
- Activity modification
Leg Region
1. Achilles Tendinopathy and Rupture
- Acute or insidious overload of deep
or superficial muscles in the
posterior leg
- Two types: Acute and Chronic
Epidemiology:
- Achilles tendon overload is common
Etiology:
- Sudden or repetitive eccentric
overload
- Sudden powerful eccentric force can
cause acute rupture of Achilles
tendon
Clinical Manifestation:
Chronic Achilles tendon Overload
- Swollen, nodular, tender Achilles
tendon
Acute Achilles tendon Overload
- Audible “pop” with inability to
continue the activity
- Pts. commonly relate as if they were
“kicked in the calf”
Diagnosis:
Chronic Achilles tendon Overload
- Ultrasound and MRI – show typical
changes
Acute Achilles tendon Overload
- Physical examination
 Swelling in the region of
Achilles tendon
 Palpable defect in the
tendon
 Difficulty with plantar
flexion
Treatment:
Chronic Achilles tendon Overload
- Ice
- NSAIDs
- Activity modification
- Stretching
- Eccentric strength training
Acute Achilles tendon Overload
- Surgical reconstruction
- Immobilization as long as 3 months
- Aggressive rehabilitation
2. Tibialis Posterior Overload or Medial
Tibial Stress Syndrome (Shin Splints)
- Medial Tibial Stress Syndrome or
Shin Splints is a spectrum of
overload pathology in the medial leg
Epidemiology:
- Dysfunction of tibialis posterior is
common
Clinical Manifestation:
- Pain and tenderness along the
medial and/or posteromedial border
of the tibia
Complications:
- Persistent stress can cause
progression of pathology to involve
the periosteum of the tibia, a
condition called Periostitis
- Stress fracture occurs when further
stress is placed on the bone
Treatment:
- Ice
- Activity modification
- Tibialis posterior strengthening
- Kinetic chain functional exercises
- Off-the-shelf or custom made foot
orthoses – can be helpful to provide
shock absorption and accommodate
for pes planus foot
- Gradual return to higher level
activities
- If pt. fails to improve with
rehabilitation program, imaging
should be made to look for
presence or periostitis, stress
reaction, or stress fracture
3. Compartment Syndrome
- Refers to the condition in which the
pressure within a given muscle
compartment is abnormally
elevated
- Two types: Acute and Chronic
Epidemiology:
- Chronic exertional compartment
syndrome (CECS) – most common in
high volume runners
Etiology:
- Acute compartment syndrome –
significant trauma such as a fracture
or crush injury
Clinical Manifestation:
CECS
- Recurrent leg cramping –
occasionally, pt. can localize the
cramping to a particular
compartment of the leg; but more
often, it is difficult to localize
- Pain with activities
- Neurologic symptoms such as
temporary foot weakness – can
occur when high compartment
pressure cause ischemia to the tibial
or peroneal nerves
Diagnosis:
CECS
- Intramuscular compartment testing
- History and physical examination
 One or more of the ff.
criteria must be met:
 Pre-exercise
pressure > or = to
15 mmHg
44 | P a g e
  1 min post exercise
pressure > or equal
to 30 mmHg
 5 min post exercise
pressure > or = to
20 mmHg
Treatment:
- Avoiding inciting activities
- Massage therapy – can sometimes
be helpful
- Activity modification
- Fasciotomy or Fascietomy –
considered when prolonged activity
modification and rehabilitation are
unsuccessful
Ankle and Foot Region
1. Osteochondral Lesions of the Ankle
- Can affect medial or lateral talus
Epidemiology:
- Talus ranks 3rd in location for
osteochondral lesions
- Occurs in 6.5% of all ankle sprains
- 80% of cases has history of trauma
Etiology:
- Medial lesions occur after a
compressive force with an
inversion-flexion movement
- Lateral lesions occur after forced
eversion and dorsiflexion
Clinical Manifestation:
- Deep ankle pain that is worse with
weight-bearing and improved with
rest
Diagnosis:
- Physical examination
 Tenderness with palpation
in the region of the subtalar
joint and with subtalar joint
maneuvers
- MRI – more sensitive than plain
films in visualizing lesion and
assessing soft tissue structures
Prognosis:
- Medial lesions are less severe and
are more likely to undergo
spontaneous healing
- Lateral lesions have more
pronounced symptoms and self-
healing occurs less frequently
- Non-operative treatment of
symptomatic osteochondral lesions
fails in 30%-40% of pts.
Treatment:
- Stage 1 is treated non-operatively
- Stage 2 and 3 – treated
conservatively on the medial side
and surgically on the lateral side
- Stage 4 – treated operatively
2. Sprains
Epidemiology:
- Most common musculoskeletal
injury in the lower limb
- Account for up to 25% of all sports
injuries
- Most commonly injured ligament is
the anterior talofibular ligament
- Sprains of deltoid ligament on the
medial aspect of ankle are far less
common than lateral ankle sprains
Etiology:
- Forceful and sudden inversion
usually combined with plantar
flexion
- Forceful and sudden ankle eversion
Clinical Manifestation:
- Pain and swelling
Diagnosis:
- MRI
- (+) Anterior Drawer test
- Grading:
 Stage 1 – simple distortion
or partial tear in the
ligament with no instability
 Stage 2 and 3 – partial or
complete tear of the
ligament with instability
Treatment:
- Ice, elevation and compressive
wrapping of the ankle
- Brace
- Crutches if needed
- Use of orthopedic shoes for first 1-2
weeks until pain subsides
- Surgical – screw or pin fixation
- Walking boot can be used for the 1-
4 weeks on the injuries
- Balance and proprioceptive training
3. Flexor Hallucis Longus Overload
Epidemiology:
- Seen in dancers, gymnasts, and
other active individuals who
perform repetitive and forceful toe
flexion
Etiology:
- Repetitive and forceful toe flexion
Clinical Manifestation:
- Pain anywhere along the course of
the flexor hallucis longus muscle
tendon unit
Diagnosis:
- Physical examination
 Symptoms reproduced with
flexion of the great toe
against resistance
 Pain upon palpation of the
tendon
 Passive stretch of the
muscle-tendon does not
reproduce symptoms as
reliably as other injuries
- Imaging studies – not initially
indicated but when necessary, MRI
is the study of choice
Treatment:
- Ice
- Acetaminophen or NSAIDs
- Activity modification
- Strengthening exercises
45 | P a g e
 - Local injection of anesthetic and
corticosteroid around the tendon to
decrease pain and inflammation
4. Injury to the Plantar Foot muscles and
Plantar Fascia; Plantar Fasciitis
- Plantar fasciitis – inflammation and
pain in the plantar fascia
Etiology:
- Overload of the four plantar foot
muscles that originate from the
volar calcaneus
Pathophysiology:
- There is overload of the adductor
hallucis, quadratus plantae, flexor
digitorum brevis, and abductor digiti
minimi
- Causes inflammation and pain in the
plantar fascia
Clinical Manifestation:
- Volar heel pain that is often but not
always worse with their first few
steps in the morning
Diagnosis:
- Physical examination
 Tenderness upon palpation
at the volar aspect of the
heel, usually slightly medial
to the midline
 Assess dynamic function of
the hip external rotators
 Assess for other
biomechanical deficits
- Imaging studies – indicated if there
is a history of acute trauma or
symptoms become recalcitrant
Treatment:
- Rehab should be focused on
restoring ROM, strength,
endurance, and motor control of
the heel cord and foot intrinsic
muscles
- Resting night splint – helpful in
preventing overnight tightening of
the heel cord and plantar structures
- Local injection of corticosteroid can
assist in decreasing local
inflammation and pain
 Precaution: can increase
risk of rupture of plantar
fascia
5. Morton’s Interdigital Neuroma,
Metatarsalgia, and Sesamoiditis
- Neuroma – pain in the region of the
metatarsal heads (esp. between 3rd
and 4th metatarsal heads)
- Metatarsalgia – pain in the
metatarsal heads
- Sesamoiditis – pain coming from an
injured bone
Epidemiology:
- Common location for interdigital
neuroma is between the 3rd and
4th metatarsal heads
- 2nd metatarsal head is commonly
involved in metatarsalgia
Etiology:
- Morton's neuroma – caused by
irritation of one of the interdigital
nerves of the foot as it passes below
the transverse ligament of the
metatarsal heads
- Metatarsalgia – can be caused by
jumping, toe running, and high heels
(overload to the metatarsal heads)
Clinical Manifestation:
- Morton's Neuroma
 Pain in the region of the
metatarsal heads (esp.
between 3rd and 4th
metatarsal heads)
exacerbated with forefoot
weight-bearing, narrow toe
boxes, and high heels
 Referral of pain or
paresthesia in the two toes
innervated by interdigital
nerve
 Pt. sometimes describes a
feeling of having a pebble in
their shoe or a wrinkle in
their sock
- Metatarsalgia
 Pain coming from the
metatarsal heads
themselves
Diagnosis:
- Physical examination
 Assess for neurologic
symptoms
 If no neurologic symptoms,
distinguish between pain
coming from between two
metatarsal heads and pain
coming from the metatarsal
heads themselves
 There's a click when
palpating a large or firm
neuroma especially when
palpation is combined with
squeezing the metatarsal
heads together from the
medial and lateral sides
- MRI or bone scan
Differential Diagnosis:
- Injury to the sesamoid bones in the
flexor hallucis tendon, such as stress
response or stress fracture
Treatment:
- Avoiding high heels is
recommended – shoes that have
larger toe boxes can be helpful
- Gel inserts – effective at distributing
force more evenly
- Custom-made foot orthoses with
pre-metatarsal pads or pre-
metatarsal pads alone to help
unload painful area
46 | P a g e
 - Local injection with anesthetic and
steroid to decrease pain for
interdigital neuroma
- Surgical excision to be considered if
there is recalcitrant neuroma
symptoms that are unresponsive to
conservative treatment
GENERAL HEALTHCARE MANAGEMENT
Pharmacological
- NSAIDs – controls pain and reduce
inflammation
 Precaution: Evidence shows that
NSAIDs can impair muscle
healing by inhibiting the fusion
of myogenic precursor cells, and
this knowledge should be
considered before prescribing
this medication
PHYSICAL THERAPY EXAMINATION AND
PROGNOSIS
Points of Emphasis on Examination
 Physical examination
- Ocular inspection
 Soft tissue or bony contour
abnormalities
 Atrophy
 Edema
 Skin discoloration
 Scars
 Alignment and symmetry of the
pelvis, hips, knees, ankles, and
feet
- Palpatory examination
 Areas of tenderness, warmth,
swelling
- Musculoskeletal examination
 ROM and MMT – might reveal
gross deficits or subtle side to
side differences that can be
important
 Gait – should be evaluated in
the sagittal and frontal plane
 Special tests
SPECIAL TESTS FOR LOWER EXTREMITY
Hip
1. Thomas Test
- Rationale: Asses hip flexors tightness
- Position: Supine with the pelvis near
the end of the examination table
- Procedure: The hips and knees are
flexed and the pt. is asked to hold
the knees to the chest to flatten
lumbar lordosis. The pt. is asked to
continue holding one knee to the
chest and let the limb tested fall
toward the table
- Result: (+) the limb being tested will
not fall into the table; indicates tight
hip flexors
2. Modified Thomas Test
- Rationale: Assess for tight iliotibial
band and rectus femoris; assess the
flexibility of multiple muscle groups
of the hip
- Position: Same with Thomas Test
- Procedure: Knee is pulled to the
ipsilateral side (Iliotibial band)
- Result: (+) knee does not fall easily
into flexion; indicates tight ITB and
rectus femoris
3. Ely Test
- Rationale: Assess tightness of the
rectus femoris
- Position: Prone
- Procedure: PT passively flexes the
pt.'s knee
- Result: (+) hip on the same side
spontaneously flexes upon flexion of
the knee; indicates tight rectus
femoris on that side
4. Ober Test
- Rationale: Assess tightness of ITB
- Position: Pt. lies on the side with the
thigh next to the table flexed to
reduce lumbar lordosis
- Procedure: The upper leg being
tested is positioned with the knee
flexed to 90°. The PT holds the ankle
with one hand and steadies the pt.'s
hip with the other. The upper leg is
abducted and extended
- Result: (+) leg will remain passively
abducted; indicates tight ITB
5. Faber or Patrick Test
- Rationale: Assess SI joint pathology
and hip pathology
- Position: Supine with the hip flexed,
abducted, and externally rotated,
with the ankle resting on
contralateral knee
- Procedure: PT applies pressure to
contralateral ilium and ipsilateral
knee to further externally rotate the
hip
- Result:
(+) pain in the buttocks; indicates SI
joint pathology
(+) pain in the groin; indicates hip
pathology
6. Scour Test
- Rationale: Assess hip joint pathology
- Position: Supine
- Procedure: PT flexes and adducts
the hip to end range where
resistance is felt. Hip is then moved
into abduction while maintaining
the flexed position. The motion
from adduction to abduction should
be in a circular arc while applying an
axial load down the shaft of the
femur
- Result: (+) pain, locking, crepitus, or
clicking; indicates hip joint
pathology
47 | P a g e
Knee
1. Lachman Test
- Rationale: Assess for ACL instability
- Position: Supine
- Procedure: PT holds the knee in 15°
of flexion. The femur is stabilized
with one hand while pressure is
applied to the posterior aspect of
the proximal tibia in an attempt to
translate it anteriorly
- Result: (+) excessive anterior
translation of the tibia with a soft
endpoint; indicates ACL instability
2. Posterior Drawer Test
- Rationale: Assess torned PCL
- Position: Supine with the hip flexed
to 45°, knee flexed to 90°, and foot
in neutral position on the table
- Procedure: PT stabilizes the foot by
sitting on it while placing both hands
behind the proximal tibia and
thumbs on the tibial plateau. A
posterior force is applied to the tibia
- Result: (+) increase posterior tibial
displacement; indicates torn PCL
3. Valgus and Varus Stress Test
- Rationale: Assess medial or lateral
collateral ligament tear
- Position: Supine
- Procedure:
 Valgus Testing – PT takes
the leg, placing one hand
over the lateral aspect of
the knee and holding the
ankle with the other hand. A
valgus stress is applied to
the knee with 30° of knee
flexion
 Varus Testing – one hand is
placed over the medial knee
with the ankle being held by
the other. Varus stress is
applied to the knee with 30°
of knee flexion
- Result: (+) excess motion and lack of
firm endpoint; indicates MCL or LCL
tear
4. Patellofemoral Grind Test
- Rationale: Assess patellofemoral
dysfunction
- Position: Supine with the knees
extended
- Procedure: PT places the web space
of the thumb on the superior aspect
of the patella. Pt. is asked to
contract the quadriceps muscle
while the PT applies downward and
inferior pressure on the patella
- Result: (+) anterior knee pain;
indicates patellofemoral dysfunction
5. McMurray Test
- Rationale: Assess meniscal injury
- Position: Supine
- Procedure: Knee is flexed and
steadied by the PT's hand which is
placed along the medial and lateral
joint lines. With the other hand, the
PT holds the foot by the heel and
rotates the leg on the thigh with the
knee remaining in flexion. By
externally rotating the leg, the
medial cartilage is tested. By
internally rotating the leg, the
lateral cartilage is tested. By altering
the degree of flexion of the knee,
various aspects of the cartilage can
be assessed
- Result: (+) click reproducing the pt.'s
pain; indicates torn meniscus
Ankle
1. Anterior Drawer Test
- Rationale: Assess integrity of lateral
ankle ligaments , particularly the
anterior talofibular ligament
- Position: Sitting at the edge of the
examination table
- Procedure: Ankle is positioned at
90°, and the ankle is held on the
tibial side with one hand. The index
finger of this hand is placed over the
talus with the middle finger over the
medial malleolus. The heel of this
hand braces the anterior leg while
the heel is pulled anteriorly with the
other hand
- Result: (+) relative anteroposterior
motion between the talus and the
tibia that can be palpated or
visualized
2. Talar Tilt Test
- Rationale: Assess lateral ligament
rupture
- Position: Same with anterior drawer
test
- Procedure: Ankle is held on the tibial
side with one hand while the other
hand grasps the heel and applies a
supination force to the hind foot
- Result: (+) relative anteroposterior
motion between the talus and the
tibia that can be palpated or
visualized
3. Syndesmosis Squeeze Test
- Rationale: Assess syndesmotic injury
- Procedure: Fibula is compressed to
the tibia above
- Result: (+) pain over the tibiofibular
ligament; indicates syndesmotic
injury
4. Thompson's Test
- Rationale: Assess integrity of
Achilles tendon
- Position: Prone with the feet
hanging loosely over the edge of
examination table
48 | P a g e
 - Procedure: Calf muscles are
squeezed. Passive plantar
movement is seen normally
- Result: (+) no plantar movement of
the foot; indicates Achilles tendon
rupture

PHYSICAL THERAPY PROGNOSIS AND

INTERVENTION

Plan of Care and Intervention

- Physical rehabilitation of each condition is
presented in the classification. Several terms
are used which might not be familiar,
including:
 Kinetic chain – model of human
motion that analyzes and treats
dysfunction along connected
anatomic region rather than
focusing only on the location of
pain. Treatment plans that address
only the painful site and ignore
underlying pathologic conditions at
other sites along the motion chain,
have less chance of success than at
treatment plan that restores proper
function along the entire chain.
Kinetic chain considerations are
most relevant when treating muscle
and tendon pathologic conditions
but should not be ignored when
addressing bone and joint
pathologic findings
 Biomechanical deficit – refers to
deficiencies in ROM, flexibility,
strength, endurance, or motor
control
 Muscle imbalance – divergence
from normal function of different
muscle groups that work as agonists
or antagonists to stabilize a body
part or create motion. They often
occur on muscles at the anterior
versus posterior side of the joint, or
on the medial versus lateral side of
the joint.
 Functional exercise – exercise
movement that stimulates muscle
groups to work in a way that they
normally work during functional or
athletic activities. "Sports specific"
exercises are functional exercises
that use motion patterns that
athletes must perform in their
athletic events

SOURCE:

Physical Medicine and Rehabilitation 4th edition

by Randall L. Braddom

CHRONIC PAIN

GENERAL MEDICAL BACKGROUND

49 | P a g e

Definition
- Pain is an unpleasant sensory and
emotional experience associated with
actual or potential tissue damage, or
described in terms of damage
(according to the International
Association for the Study of Pain).
- Chronic pain is designated 3 to 6 months
after the initiating event and in many
cases may not be associated with any
obvious ongoing noxious event or
pathologic process.
Classification
- According to Acuity
1. Acute – an unpleasant sensory,
perceptual, emotional, and
mental experience provoked by
acute disease or injury with
autonomic, psychological, and
behavioral responses.
2. Sub-acute – does not have a
structured definition but exists
as a useful category for patients
who have pain somewhat longer
than healing time would
account for, but whose pain is
not so long standing that it
caused significant behavioral
and / or physiological
alterations.
3. Chronic – persistent pain that
lasts beyond the expected time
frame for tissue healing.
- According to Tissue of Origin
1. Neuropathic – pain from injury
or irritation of the nervous
system; described as “burning”
and “aching” pain
2. Musculoskeletal – pain from
injury or irritation of fascia,
muscle, bone, and / or joint
structures; easily localized and
understood by patient
3. Visceral – pain arising from
injury or irritation of internal
organs; often felt quite distant
from the site of tissue irritation
(referred pain); often least
understood by patients
- According to Mind – Body Dualism
Epidemiology
- Represents an accelerating public health
concern and a fiscal “black hole” in the
U.S. economy
- Varies widely from 2% - 55% in general
population studies
Pathophysiology
PHYSIOLOGY
• Transduction – one form of energy is
converted into electrochemically into
nerve impulses in primary afferents
• Transmission – coded information is
transferred from primary afferent fibers
to spinal cord dorsal horn and onto
brain stem, thalamus, and higher
cortical areas
• Modulation – involves activity-and signal
– induced dorsal horn neural plasticity,
which includes altered receptor and
channel function, gene expression, and
changes in brain – mediated descending
inhibition and facilitation
• Perception – begins with activation of
sensory cortex. The cortex in intimate
communication with motor and
prefrontal cortices, which initiate
efferent responses, as well as more
primitive structures involves in the
emotive aspects of pain
-With chronic pain there is a shift of focus to the
process of modulation and perception, these
processes are the following:
1. Neuroplasticity
- Is the concept that our CNS
reorganizes in response to
peripheral input. As these
changes occur, some of them
predispose individuals to
experience chronic pain.
- A complex set of activation –
dependent posttranslational
changes occurring at the dorsal
horn, brainstem, and higher
cerebral sites which results in an
increase calcium influx
contributing to potentiation of
the cell by activation of calcium
– dependent enzyme protein
kinase.
2. Wind – up
- The receptive fields of the CNS
neurons expand, sensitizing the
individual’s nervous system and
effectively lowering the
threshold to transmission of
nociceptive impulses.
- There is prolonged
depolarization of the post
synaptic cell causing voltage -
dependent magnesium
removal, opening the channel
and allowing additional sodium
and calcium to enter the cell.
Complications
Deconditioning
- Overall decrease in muscle strength,
endurance, and cardiovascular fitness
Depression
50 | P a g e
 - Major depressive disorder is common in
pts. with chronic pain (change in
appetite, change in weight, loss of
energy, sleep disturbance)
Pain-related Anxiety
- Most disabling aspect of ongoing
chronic pain
- Closely related to avoidance of activities
which serve to promote ongoing pain,
physical deconditioning and social
isolation
Anger
- Due to failure in achieving pain relief
and repeated unsuccessful attempts to
escape pain
- Will serve as an additional target for
pharmacologic and behavioral
treatments
Diagnosis
- Visual Analog Scale
- Body Diagrams
- Pain Questionnaires
- Functional Impairment / Health –
Related Quality of Life Measures
Prognosis
- Poor prognosis for central pain because
changes in the CNS are difficult or
impossible to reverse.
- Yellow flags are associated with poorer
prognosis in chronic LBP (Alert flags for
chronic pain: Sullivan pp.1134, table
25.5)
- Medical co-morbidities, anxiety, or
history of sexual abuse may compromise
prognosis.
- Regular exercise, adequate stress
management strategies, and good
emotional function lead to improved
prognosis.
GENERAL HEALTHCARE MANAGEMENT
Medical Management
Laboratory tests
- Thyroid hormone levels, sedimentation
rates, lime titers, or general blood
screening to rule out conditions that are
treatable.
Electromyogram (EMG)
- Not indicated unless there is suggestion
of specific myopathy.
Diagnostic nerve blocks, Joint blocks,
provocative discography
- Can help determine whether a given
structure is involved.
Interventional/Surgical Management
Joint block
- for facet or SI pain
- anesthesia is injected with or without
steroids in facets or SI joint
Trigger point injection
- for myofascial pain syndrome
- BOTOX A injected to trigger points
Nerve block
- for low back pain and complex regional
pain syndrome (CRPS)
- anesthesia injected with or without
steroids to peripheral nerve, celiac
plexus, paravertebral sympathectomy,
medial branch block, stellate ganglion
block, cervical paravertebral
sympathectomy
Epidural and intrathecal injection
- for neck pain, LBP, radiculopathy,
postherpetic neuralgia
- steroid injected with or without local
anesthesia; opioid injected into
intrathecal space
Ablative techniques
- for neuropathic, facet, musculoskeletal
pain
- chemical denervation, cryoneurolysis,
cryoablation, thermal intradiscal
procedures, radiofrequency radiation
Implanted electrical stimulator
- for PNI, neuropathic pain, CRPS, failed
low back surgery, phantom limb pain,
cauda equina injury, radiculopathy, PVD,
visceral pain, MS
- subcutaneous peripheral nerve
stimulation and spinal cord stimulation
Implantable drug delivery
- for cancer, refractory spasticity,
infractable pain
- Infusion of medication into spinal cord or
specific arteries serving involved
structures.
Minimally invasive spinal procedures
- for osteoporotic compression fracture ,
radiculopathy
- vertebroplasty, kyphoplasty,
percutaneous disc decompression,
nucleopathy.
Pharmacological Management
- Summarized table for medications –
Sullivan pp.1142, table 25.7.
Acetaminophen
- taken at the start of treatment
NSAIDS and topical medications
- NSAIDS are beneficial for arthritic pain
and LBP, but ineffective for neuropathic
pain.
- Topical medications:
Cooling sensation – menthol based;
works as counter irritant via gate control
mechanism.
Warmth sensation – capsaicin based;
counter irritant effect begins
immediately after application but the
neurogenic effect requires daily use for
6-8 weeks.
51 | P a g e
 Lidocaine cream or patch – beneficial P – provoking or precipitating factors
for peripheral neurogenic pain. Q – quality of pain
Adjuvant medications R – region and radiation
Includes: S – severity or associated symptoms
- Anti depressants: used at much lower T – temporal factors or timing
dosages; Tricyclic anti depressants have SOCRATES
demonstrated benefit for neurogenic S – site of pain
pain, fibromyalgia, LBP, headaches, and O – onset of pain
irritable bowel. C – characteristic of pain
- Anti seizures: strong evidence in treating R – radiation
neuropathic pain including fibromyalgia A – associations (other symptoms such
and lumbar radiculopathy. as numbness, paresthesia, etc)
- Muscle relaxants: muscle relaxants and T – time course
benzodiazepines are generally not E – exacerbation or relieving factors
recommended for prolonged use S – severity of pain
because risks are relatively high and Psychosocial issues
there is little evidence of benefit; - abuse history, anxiety, depression, etc.
Cyclobenzaprine however has been Lifestyle
shown to be effective in fibromyalgia, - use or abuse of medications, alcohol, or
and conditions involving chronic muscle other drugs.
spasm. Cardiovascular/Pulmonary Assessment
- Sleep medications - vital signs, respiratory rate (breathing
pattern)
Consequence of using multiple drugs in Integumentary Assessment
treating same condition: Serotonin - examine old injuries or surgeries that
Syndrome (serotonin toxicity); medications could compromise fascial mobility or
involved are anti-depressants (TCA, SSRI, lymphatic flow
SNRI), some opiates, tiptans, and anti Neuromuscular Assessment
biotics; Symptoms: agitation, anxiety, - balance, locomotion, transfers
confusion, hypomania, hyperthermia, - testing for clonus, hyperreflexia,
tachycardia, diaphoresis, flushing, mydriasis, hypertonicity (if there is suspicion of
hyperreflexia, clonus, myoclonus, shivering, serotonin syndrome)
tremor, and hypertonia. Musculoskeletal Assessment
- Brighton Criteria (Sullivan pp.1147, box
Other Healthcare Management 25.7) for hypermobility syndrome or
Social Support Ehlers-Danlos syndrome
- General or global social support and Communication, Affect, Cognition, and Learning
social reinforcers for wellness and
behavior. Problem List
Therapeutic recreation - Pain
- Specialists evaluate and plan leisure - Fatigue
activities for the promotion of mental - Deconditioning
and physical health - Risk for falls
- - Sleep disturbance

PHYSICAL THERAPY EXAMINATION, EVALUATION PHYSICAL THERAPY PROGNOSIS AND

AND DIAGNOSIS INTERVENTION

Points of Emphasis on Examination PROBLEM LIST POC INTERVENTION

- Summarized table – Sullivan pp. 1146, Pain -Improve -Pt. and family
box 25.6 ability to education about
cope with chronic pain
Pain Assessment pain -HMP, paraffin
- Pain should be examined both at rest -Teach non wax, ice
and with movement. pharmacologi massage, topical
- Standard tools for quantifying pain: cal pain rubs, and TENS
VAS (visual analog scale) management to decrease pain
NRS (numeric rating scale) – MC used techniques -Lumbar and
VRS (verbal rating scale) – not accurate -Decrease cervical traction
- Other pain assessment tools appropriate pain to decompress
for chronic pain: Sullivan page 1138- spinal structures
1139, table 25.6 and decrease
- Mnemonics for Pain Assessment: pain
PQRST

52 | P a g e
 Fatigue -Decrease Relaxation Physical Rehabilitation 5th edition by O’Sullivan
fatigue techniques and Schmitz
(diaphragmatic Physical Medicine and Rehabilitation 4th edition
breathing, by Randall L. Braddom
biofeedback,
progressive
relaxation,
stretching,
aerobic exercise,
imagery,
autogenic
training) to relax
overactive
muscles
Deconditioning -Increase -Aerobic
physical conditioning to
strength, improve overall
endurance, function
and -Graded
cardiovasvula exercise(starting
r fitness from a level that
-Improve the pt can
mobility, perform and
independenc gradually
e, and increased) to
functional increase
ability strength and
-Return to endurance
previous -Postural
levels of exercises to
activity at improve posture
home, and decrease
workplace muscular
and leisure imbalances
pursuits
Risk for falls -Decrease -Balance and
risk for falls proprioceptive
training to
decrease risk for
falls
-Assistive
devices for pts
with persistent
activity
limitations
Sleep -Improve -Proper sleep
disturbance sleep hygiene
(avoidance of
caffeine,
nicotine,
alcohol, and
medications
with stimulants)
-Simple
exercises and
stretching may
also improve
sleep quality

SOURCES: MYOFASCIAL SYNDROMES

53 | P a g e
Myofascial Pain Syndrome
Fibromyalgia Syndrome
GENERAL MEDICAL BACKGROUND
Definition
Myofascial Pain Syndrome
- A regional pain syndrome characterized
by muscle pain caused by myofascial
trigger points
Fibromyalgia Syndrome
- A generalized chronic pain syndrome
characterized by widespread pain and
tenderness to palpation at multiple
anatomically defined soft tissue body
sites
Etiologic Classification
Myofascial Pain Syndrome
1. Peripheral irritation or sensitization on
the nociceptors in the muscle
- Muscle trauma (strain)
o Actively induced: acute strain,
chronic strain, chronic repetitive
micro trauma
o Passively induced: mechanical
(contusion, laceration,
compression, penetration, and
traction), chemical (strong acid),
thermal (burns, hypothermia),
electrical (burns), radiation, etc.
- Inappropriate muscle activity
(DOMS)
- Muscle diseases: polymyositis,
myotonia, muscular dystrophy,
etc.
2. Peripheral irritation to the peripheral
Nerve (mechanical or chemical)
- Nerve traumas (compression,
traction, laceration, etc.)
- Nerve entrapments (CTS,
piriformis syndrome, etc.)
- Other nerve lesions
3. Central irritation to the central pathway
in the CNS
- CNS traumas
- CNS diseases
- Other CNS lesions
4. Central sensitization in the spinal cord
or a higher CNS center
- Referred pain
- Hyperalgesia
- Allodynia
- Activation of myofascial trigger
points
- Other
5. Systemic decrease of pain threshold
- Fibromyalgia
- Other
Fibromyalgia Syndrome
1. Primary FMS – defined as "pure" FMS
having no association with other
medical conditions
2. Secondary FMS – FMS associated with
other medical conditions: RA, SLE, and
hypothyroidism
Pathophysiology
Myofascial Pain Syndrome
- Muscle pain can be elicited by
any irritation of the pain
pathway from the muscle to the
cerebral cortex. The location of
pain is determined by the
traditional physiologic concept
of the law of projection.
Fibromyalgia Syndrome
- Neurosensory dysfunction
o Neurochemicals such as serotonin and
substance P are involved
o Serotonin is a neurotransmitter for the
descending ant nociceptive system; it
inhibits the release of substance P in the
spinal cord; a dysfunction of the
descending ant nociceptive system is
the most likely mechanism for the pain
of fibromyalgia
Clinical Manifestation
Myofascial Pain Syndrome
1. Taut band
2. Painful or Tender spot - a circumscribed
spot in the muscle with pain or
tenderness
3. Referred tenderness - occurs when a
distant muscle has pain in response to
compression of a trigger point
4. Local twitch response - sudden brisk
contraction in response to a snapping
palpation
5. Motor dysfunction (pain induce muscle
weakness)
6. Autonomic phenomena (abnormal
sweating, tearing, salivation)
Fibromyalgia Syndrome
- Chronic widespread severe pain
involving bilateral body sites including
posterior neck, anterior chest, upper
and lower back, shoulders, buttocks,
and extremities
- Pain longer than 3 months
Diagnosis
Myofascial Pain Syndrome
1. Basic diagnostic criteria
- Exquisite spot tenderness
- Pain recognition
- Taut band
2. Confirmatory signs
- Referred pain
- Local twitch response
3. History and physical examination
- Pain distribution pattern
- Pointed out by the patient
54 | P a g e
 - Palpation
- Provocative tests PHYSICAL THERAPY EXAMINATION, EVALUATION
4. Laboratory findings AND DIAGNOSIS
- Bio chemicals associated with
pain and inflammation Points of Emphasis on Examination
- Thermography Myofascial Pain Syndrome
- Sonography Pain Assessment
- Magnetic resonance - Visual analog pain scale or numerical
electrography rating scale
Fibromyalgia Syndrome History and Physical Examination
- No gold standard - Pain distribution pattern
- American College of Rheumatology  MTrPs in muscles innervated by
Criteria for the Classification of FMS - the same nerve root –
applied to community care radiculopathy
 MTrPs surrounding joints –
Differential diagnosis arthropathy of that joint or
Criteria MPS FMS ligament lesions around that
Affectation Regional Generalized joint
muscle pain chronic pain at  MTrPs in agonists – lesion of the
in any soft multiple soft common tendon
tissue tissue body  MTrPs in certain muscles
sites related to facet joints – facet
Pathogenesis Soft tissue Lower pain joint lesion
injury threshold - Pointed out by the patient
induced by related to - Palpation – considered to be unreliable
activation of dysfunction of thus special training is usually required
trigger descending anti to obtain reliability
points nociceptive
system Criteria for Diagnosis:
Pain intensity Symmetrical Asymmetrical Spot tenderness
Characteristic Trigger point Tender point Taut band
Pain recognition
Prognosis
Confirmatory signs:
GENERAL HEALTHCARE MANAGEMENT Referred pain
Local twitch response
Medical/Pharmacological Management
Myofascial Pain Syndrome - Provocative tests
- Myofascial Trigger point (MTrP)  MTrP pain during compression
injection with 0.5 to 1mL solution of of a spot with a soft tissue
0.5% lidocaine without epinephrine lesion – soft tissue lesion at that
when local twitch response is elicited spot
- Local steroid injection if the injured  MTrP pain during active
lesion responds poorly to conservative contraction – tendinopathy of
treatment the contracting muscle
- Spinal facet joint injection can inactivate  MTrP pain during stretching of a
MTrPs simultaneously (for MTrPs ligament – lesion of that
triggered by spinal facet joint irritation) ligament
- Injection of botulinum toxin A can pre-  MTrP pain during compression
synaptically block Ach release and of a bursa – lesion of that bursa
relieve the taut band in the MTrP region  MTrP pain during facet joint
compression or stretch – facet
Fibromyalgia Syndrome lesion
- Low dose tricyclic, sedative, hypnotic
medication (for sleep disorder) and Fibromyalgia Syndrome
analgesic-level dosage of NSAIDs (for History and Physical Examination
pain) - Pain experienced in four quadrants of
- Amitriptyline, cyclobenzaprine, the body for the last 3 months (both
alprazolam, trazodone, and fluoxetine sides of the body, above and below the
can increase serotonin availability waist, and in the trunk)
- Pain induced by palpation of tender
Other Healthcare Management points (pain must be inducible at 11 or
Fibromyalgia Syndrome more of the following 18 tender point
- Cognitive Behavior Therapy sites) :

55 | P a g e
  1-2: Occipitus (at the sub - Laser
occipital muscle insertion) - Shockwave
 3-4: Low cervical (anterior - Dry needling (move in and out to
aspects of the intertransverse multiple direction)
spaces at c5-c7)
 5-6: Trapezius (at the midpoint Rationale for all intervention: Relieve or
of the upper muscle border) decrease pain.
 7-8: Supraspinatus (near the
origins above the spine of the Fibromyalgia Syndrome
scapula) - Pt. education on Fibromyalgia Syndrome
 9-10: Second rib (upper surface - Conditioning exercise can activate
just lateral to the second endogenous opioid system
costochondral junction)
 11-12: Lateral epicondyle SOURCE:
(extensor muscle, 2cm distal to
the epicondyle) Physical Medicine and Rehabilitation 4th edition
 13-14: Gluteal (in the upper by Randall L. Braddom
outer quadrants of buttocks in
anterior fold of muscle)
 15-16: Greater trochanter
(posterior to the trochanteric
prominence)
 17-18: Knees (at the medial fat
pad proximal to the joint line
and condyle)

Problem List
- Pain

PHYSICAL THERAPY PROGNOSIS AND

INTERVENTION

Intervention
Myofascial Pain Syndrome
Note: Treating underlying etiologic lesions that
cause activation of MTrPs is the most important
strategy in treating Myofascial Pain Syndrome; if
an acute lesion is not well controlled, it can
become a chronic lesion with progressive scar
tissue formation (this scar tissue is the major
cause of degenerative lesions, which can be a
source of MTrP activation later in life)

- Pt. education on Myofascial Pain

Syndrome
- Icing for acute lesion to facilitate healing
process and immobilization to avoid re-
injury during the healing period
- Thermotherapy and manual therapy can
begin after the active bleeding or local
heat has subsided
Manual Therapy:
- Stretching (intermittent cold and
stretch)
- Deep pressure soft tissue massage
- Trigger point pressure release
- Voluntary contraction and release
method:
 muscle energy technique
 reciprocal inhibition
 post-isometric relaxation
Modalities:
- HMP, US
- IFC, TENS

56 | P a g e
 ARTHROPATHIES
Seropositive
Rheumatoid Arthritis
Juvenile Arthritis (JRA) or Still's Disease
Systemic Lupus Erythematosus
Progressive System Sclerosis/Scleroderma
Dermatomyositis (DM)
Polymyositis (PM)
Sjogren's Syndrome
Seronegative
Osteoarthritis
Ankylosing Spondylitis
Psoriatic Arthritis
GENERAL MEDICAL BACKGROUND
1. RHEUMATOID ARTHRITIS
DEFINITION:
- A connective tissue disease
characterized by chronic inflammatory
changes in the synovial membrane and
other structures, by migratory swelling
and stiffness of the joints in its early
stage, and by a variable degree of
deformity, ankylosis and invalidism in its
late stage.
CLASSIFICATION:
- Stage I, Early
• No destructive changes on
radiographic examination.
• Radiographic evidence of
osteoporosis may be present.
- Stage II, Moderate
• Radiographic evidence of
osteoporosis, with or without
slight subchondral bone
destruction; slight cartilage
destruction may be present.
• No joint deformities, although
limitation of joint mobility may
be present.
- Stage III, Severe
• Radiographic evidence of
cartilage and bone destruction
in addition to osteoporosis.
• Joint deformity, such as
subluxation, ulnar deviation, or
hyperextension, without fibrosis
or bony ankylosis.
• Extensive muscle atrophy.
• Extra-articular soft tissue
lesions, such as nodule and
tenosynovitis may be present.
- Stage IV, Terminal
• Fibrous or bony ankyloses
Criteria of stage III
EPIDEMIOLOGY:
- Affect 3.6 million persons in the United
States
- Varies little with differences in climate
- Women > men
- 25-50 yrs old = 80% of cases
- 35-40 yrs old = highest incidence rate
ETIOLOGY:
- Cause of RA has not been determined
- -Slight familial tendency has been
demonstrated:
- The main histocompatibility complexes
HLA-DW4 and DR4 are present in
increased frequency in populations with
seropositive rheumatoid arthritis.
- Hypotheses of the etiologic factor have
included:
• Infection
• Abnormality of the peripheral
circulation
• Endocrine imbalance
• Metabolic disturbance
• Allergic phenomenon
• Faulty adaptation to physical or
psychic stress
• And many other concepts
PATHOPHYSIOLOGY/PATHOMECHANICS:
The fundamental pathologic lesion is an
inflammatory process beginning in the synovial
membrane.
The inflammation results from or is closely
associated with an immune response, the origin
of which in unknown.
↓
Antibodies (rheumatoid factor, IGm and others)
are produced in response to an antigen on the
Fc fragment of IgG
(whether this protein, IgG has been previously
altered by viral infection or by other agents in
such a way as to make the body react to it as
foreign is unknown.
↓
Joint disease associated with increase serum
levels of rheumatoid factor is referred to as
seropositive arthritis.
CLINICAL MANIFESTATIONS:
- Onset is insidious, with joint pain and
stiffness developing gradually over
several months.
- Articular (inflammation of jt. and
synovitis, more common) and extra-
articular involvement.
- Jt. involvement is polyarticular and
symmetrical.
- Includes MCP, PIP, CMC.
- Inflammation of structures around the
joints (e.g. tendinitis).
57 | P a g e
 - Rotator cuff tendinitis, atlanto-axial jt. • Episcleritis (a condition that
involvement ---has danger of could lead to blindness) may be
neurological involvement. present.
- Articular pain.
- Stiffness especially at AM. DIAGNOSIS:
- Rheumatoid nodules. DIAGNOSTIC CRITERIA:
- Flexor contractures. - Morning stiffness (in and around the
- Finger deformities: joints, lasting at least 1 hr)
• Swan neck deformity – MCP - RA of 3 or more jts. (14 possible areas:
flexion, PIP hyperextension, DIP right or left PIP, MCP, wrist, elbow,
flexion; more common ankle and MTP joints)
• Boutonniere deformity - PIP - RA of hand joints (at least 1 area swollen
flexion, DIP hyperextension in a wrist, MCP or PIP joint)
- Constitutional systems – e.g. weakness - Symmetrical arthritis
and fatigue. - Rheumatoid nodules
- Malaise and low grade fever – common - Serum RF (+)
during periods of acute jt. inflammation. - Radiographic changes
- Influence by emotional and *you must have 4 of 7 criteria to satisfy;
psychological factor. criteria 1 to 4
- Deconditioning *must be there for 6 weeks
• Results from both direct and
indirect impairments DIFFERENTIAL DIAGNOSIS:
- Direct impairments - Rheumatic fever
• Loss of type II muscle fibers • In its acute phase, may initially
• Systemic fatigue appear as migratory
• Cachexia (wasting of lean body polyarthritis simulating early
mass) rheumatoid arthritis.
• Shortening of contractile tissues • Pt. with acute rheumatic fever is
- Indirect impairments more likely to have a
• Inactivity streptococcic throat infection
- Elevated resting energy expenditure and high fever.
(calories required by the body during a • After the acute phase of
24-hour period under resting rheumatic fever the joints
recover completely.
conditions)
- Osteoarthritis or degenerative joint
COMPLICATIONS: disease
- Vascular and Neurologic Complications
• Most forms of vascular lesions RA OA
associated with RA are difficult Systemic; pts. Pts. are not
to diagnose. are sick sick
 Skin Vasculitis -> the easiest Acute Weight-
to observe and can present inflammatory bearing joints
as discoloration of the nail signs and
beds, purpura (red or purple cutaneous
discoloration), and changes
petechiae (red or purple In the fingers, DIP are more
spots). the PIP are affected
- Cardiopulmonary Complications more affected (Heberden’s
• Due to a greater prevalence of nodes)
ischemic heart disease (-) (+)
2˚accelerated atherosclerosis. subcutaneous subcutaneous
(etiology for accelerated nodules nodules
atherosclerosis is unclear-> It is Osteoporosis Osteoporosis
hypothesized that metabolic and bony and bony
and vascular effects of chronic ankylosis ankylosis are
inflammation may be the uncommon
causive factor.) ↑ Erythrocyte Erythrocyte
• Pleuritis and Pulmonary nodules sedimentation sedimentation
may be present; nodules may and serologic and serologic
be .40 to 3 in. in size and could testing testing are
affect gas exchange. normal
- Ocular Complications - Pyogenic Arthritis
• A single large joint is involved

58 | P a g e
 • High fever and leukocytosis
- Gonococcal Arthritis
• Frequently, the gonococcus
(bacteria) can be demonstrated
in the joint fluid.
- Joint tuberculosis
• Tuberculosis is more often
monarticular, more insidious in
its onset and is likely to show
more bone destruction.
- Gout
• High blood uric acid level
• Joint quickly loses its tenderness
between attacks.
• Great toe is often the first part
of the body to be affected.
- Systemic Lupus Erythematosus
• The patient usually shows
minimal joint changes, severe
systemic symptoms and the
characteristic lupus
erythematosis cell
phenomenon.
PROGNOSIS:
- -Factors associated with a poor
prognosis:
• Early age of onset, high levels of
rheumatoid factor in serum
• The presence of rheumatoid
nodules
• Persistent sustained disease of
more that a year's duration.
Although no cure is yet available, rational use of
drugs and physical measures can delay the
progression and lessen the consequence of the
disease
GENERAL HEALTHCARE MANAGEMENT
MEDICAL, SURGICAL, PHARMACOLOGICAL
SURGICAL:
- Synovectomy - when synovial
inflammation persists for months
despite thorough nonsurgical treatment.
- Tenosynovectomy (excision of tendon
sheath lining) - in RA, tendon sheath
lining may be inflamed and thickened.
- Arthrodesis
- Tendon reconstruction
PHARMACOLOGICAL:
- NSAIDs
• Salicylates- to alleviate pain and
suppressing inflammation;
mainstay in the treatment of RA
• Phenylbutazone- often relieves
arthritic symptoms but not
curative. (discontinue use when
symptoms are suggesting a
peptic ulcer)
• Indomethacin- anti-
inflammatory drug sometimes
helpful in rheumatoid arthritis
(contraindicated to children)
- Gold salts or chrysotherapy – may
suppress or even arrest the active
rheumatoid process.
- D-Penicillamine- may be helpful in
refractory cases of RA; used in place of
gold when toxic reactions develop to
gold therapy.
- Steroids- should be reserved for
temporary use in small doses as
supplementary treatment to patients in
whose joints rheumatoid inflammation
is not adequately suppressed by other
forms of treatment.
OTHER HEALTHCARE
(REHABILITATIVE/SUPPORTIVE):
- Casts and Splints- for immobilization to
provide rest for the affected joint when
pain in acute stage is severe.
- Appropriate footwear or insoles
PHYSICAL THERAPY EXAMINATION, EVALUATION
AND DIAGNOSIS
POINTS OF EMPHASIS IN EXAMINATION (FOCUS):
- Patient History
- ROM
- Muscle strength
- Joint Stability
- Cardiovascular status
- Functional examination
- Mobility
- Gait
- Balance
- Sensory integrity
- Psychological status
PHYSICAL THERAPY DIAGNOSIS:
- MS4: impaired joint mobility, motor
function, muscle performance, and
range of motion associated with
connective tissue dysfunction.
PROBLEM LIST:
- Pain
- LOM
- Weakness
- ↓ Cardiovascular endurance
- ↓ Functional activities
- ↓ Balance
- ↓ Gait
PHYSICAL THERAPY PROGNOSIS (PLAN OF CARE):
- ↓ Pain
- ↑ ROM
- ↑ Muscle strength
- ↑ Cardiovascular endurance
- ↑ Functional activities
- ↑ Balance
- ↑ Gait
INTERVENTION (INCLUDING RATIONALE):
59 | P a g e
 - Modalities for pain relief:
• (Superficial heat) Paraffin wax
bath, hot packs, IRR,
hydrotherapy.
• Cryotherapy
• TENS
- Range of motion and flexibility exercise
• AROME (to maintain motion)
• PNF techniques
• Stretching exercises
- Strengthening exercises:
• Isometric exercises
- Cardiovascular training
• Aerobic exercises
• Walking
• Stationary bike
• Pool-based aerobics
- Functional training
• Use of adaptive equipment
- Balance training
- Gait training
2. JUVENILE ARTHRITIS (JRA) OR STILL’S DISEASE
DEFINITION:
- Most common chronic rheumatologic
disease in children
- One of the most common chronic
diseases of childhood
EPIDEMIOLOGY:
- Approximately 300,000 children in the
United States are estimated to have
some type of arthritis.
- The prevalence has ranged from 1.6 to
86.1 cases per 100,000.
ETIOLOGY:
- Autoimmune
- Certain gene mutations may make a
person more susceptible to
environmental factors — such as viruses
— that may trigger the disease.
PATHOPHYSIOLOGY/PATHOMECHANICS:
- Current literature suggests that T-cells
are activated and cause development of
antigen-antibody complexes that
release cytokines into specific organs
such as the joints and the skin.
CLINICAL MANIFESTATIONS:
- The systemic form of which is
accompanied with fever and
enlargement of lymph nodes and the
spleen.
- Development of morbilliform rash
- History findings in children with JRA may
include the following:
- Arthritis present for at least 6 weeks
before diagnosis (mandatory for
diagnosis of JIA)
- Either insidious or abrupt disease onset,
often with morning stiffness or gelling
phenomenon and arthralgia during the
day
- Complaints of joint pain or abnormal
joint use
- History of school absences or limited
ability to participate in physical
education classes
- Spiking fevers occurring once or twice
each day at about the same time of day
- Evanescent rash on the trunk and
extremities
- Psoriasis or more subtle dermatologic
manifestations
COMPLICATIONS:
- Iridocyclitis
• Frequent complication
May lead to blindness
DIAGNOSIS:
Diagnosis of JRA is based on the history and
physical examination findings. When physical
findings do not document definite arthritis,
further evaluation is warranted. Laboratory
studies that may be considered include the
following:
- Inflammatory markers:
- Erythrocyte sedimentation rate (ESR) or
CRP level
- Complete blood count (CBC) and
metabolic panel
- Liver function tests and assessment of
renal function with serum creatinine
levels
- Antinuclear antibody (ANA) testing
- Rheumatoid factor (RF) and anti–cyclic
citrullinated peptide (CCP) antibody
- Additional studies: Total protein,
albumin, fibrinogen, ferritin, D-dimer,
angiotensin-converting enzyme (ACE),
antistreptolysin 0 (AS0), anti-DNAse B,
urinalysis
- When only a single joint is affected,
radiography is important to exclude
other diseases. Basic radiographic
changes in JIA include the following:
- Soft tissue swelling
- Osteopenia or osteoporosis
- Joint-space narrowing
- Bony erosions
60 | P a g e
 - Intra-articular bony ankylosis
- Periosteitis
- Growth disturbances
- Epiphyseal compression fracture
- Joint subluxation
- Synovial cysts
Other imaging modalities that may be helpful
include the following:
- Computed tomography
- Magnetic resonance imaging
- Ultrasonography and echocardiography
- Nuclear imaging
- Other studies and procedures that may
be considered include the following:
- Dual-energy radiographic
absorptiometry (DRA)
- Arthrocentesis and synovial biopsy
- Pericardiocentesis
PROGNOSIS:
- Prognosis is favorable with 3/4s of the
patients regaining satisfactory joint
function, crippling arthritis sometimes
continues into adult life.
GENERAL HEALTHCARE MANAGEMENT:
MEDICAL, SURGICAL, PHARMACOLOGICAL:
PHARMACOLOGICAL:
- Non-steroidal anti-inflammatory drugs
(NSAIDs). These medications, such as
ibuprofen (Advil, Motrin IB, others) and
naproxen sodium (Aleve), reduce pain
and swelling. Side effects include
stomach upset and liver problems.
- Disease-modifying antirheumatic drugs
(DMARDs). Doctors use these
medications when NSAIDs alone fail to
relieve symptoms of joint pain and
swelling. Commonly used DMARDs for
children include methotrexate (Trexall)
and leflunomide (Arava)Side effects may
include nausea and liver problems.-
Biologic agents. Also known as biologic
response modifiers, this newer class of
drugs includes tumor necrosis factor
(TNF) blockers, such as etanercept
(Enbrel) and adalimumab (Humira).
These medications can help reduce pain,
morning stiffness and swollen joints.
- Corticosteroids. Medications such as
prednisone may be used to control
symptoms until a DMARD takes effect or
to prevent complications, such as
inflammation of the sac around the
heart (pericarditis).
PHYSICAL THERAPY EXAMINATION, EVALUATION
AND DIAGNOSIS
POINTS OF EMPHASIS IN EXAMINATION:
PHYSICAL THERAPY DIAGNOSIS:
- MS4: impaired joint mobility, motor
function, muscle performance, and
range of motion associated with
connective tissue dysfunction.
3.SYSTEMIC LUPUS ERYTHEMATOSUS
DEFINITION:
- A chronic inflammatory disease that has
protean manifestations and follows a
relapsing and remitting course. It is
characterized by an autoantibody
response to nuclear and cytoplasmic
antigens. SLE can affect any organ
system, but it mainly involves the skin,
joints, kidneys, blood cells, and nervous
system
EPIDEMIOLOGY:
- The annual incidence of SLE averages 5
cases per 100,000 population.
- Higher rates reported in blacks and
Hispanics.
- The prevalence of SLE is highest in
women aged 14 to 64 years.More than
90% of cases of SLE occur in women,
frequently starting at childbearing
age.The female-to-male ratio peaks at
11:1 during the childbearing years.
ETIOLOGY:
- An autoimmune disorder characterized
by multisystem inflammation with the
generation of autoantibodies.
- (Although the specific cause of SLE is
unknown, multiple genetic
predispositions and gene-environment
interactions have been identified)
• Heredity - There is a high prevalence
of SLE in first-degree relatives. The
immune abnormalities associated
with SLE can be triggered by both
internal and external factors.
• Stress - It has been determined that
stress can provoke changes in the
neuroendocrine system causing
changes in the function of immune
system cells.
• Bacterial or viral infection- The
Epstein-Barr virus has been found to
be a risk factor for the development
of SLE.
61 | P a g e
 • Sunlight or UV exposure
• Immunizations
• Pregnancy- The evidence about
whether or not pregnancy can cause
exacerbations of SLE is very
inconclusive because some studies
state that pregnancy does affect the
course of SLE, while others state
that it has no affect on the course of
the disease.
• Abnormal levels of estrogen
• Certain drugs- Drugs such as
hydralazin, anticonvulsants,
penicillin, sulfa drugs, and oral
contraceptives can change the
cellular responsiveness and
immunogenicity of self-antigens and
therefore make a person more
susceptible to SLE
PATHOPHYSIOLOGY/PATHOMECHANICS:
The anti-bodies to nuclear (ANA) alone are
harmless. Their presence does not harm living
cells since antibodies do not penetrate the
membrane of a living cell.
↓
However, ANA participates in the pathogenesis
of SLE by forming antigen-antibody complexes
with specific antigens.
↓
Therefore classifies as an IMMUNE-COMPLEX
disease that affects the different parts of the
bodylike the joints, pleura, pericardium and etc.
CLINICAL MANIFESTATIONS:
- Skin and mucous membrane findings
• Malar rash (a fixed erythema that
typically spares the nasolabial folds. It is
a butterfly-shaped rash that can be flat
or raised over the cheeks and bridge of
the nose)
• Photosensitive rash (often macular or
diffusely erythematous in sun-exposed
areas of the face, arms, or hands and
generally persists for more than 1 day)
• Discoid rash (occurs in 20% of patients
with SLE and can result in disfiguring
scars. The discoid rash can present as
erythematous patches with keratotic
scaling over sun-exposed areas of the
skin.)
• Palatal ulcers are most specific for SLE.
• Panniculitis, bullous lesions, vasculitic
purpura, and urticaria are other skin
lesions that are sometimes seen in SLE.
• Sensitivity to the sun or light
(photosensitivity)
• Hair loss
• Raynaud’s phenomenon
- Musculoskeletal
• Arthritis of the proximal interphalangeal
(PIP) and metacarpophalangeal (MCP)
joints of the hands, as well as the wrists,
is the most common musculoskeletal
finding in SLE.
• Tenderness, edema, and effusions
accompany a polyarthritis that is
symmetric, nonerosive, and usually
nondeforming. Jaccoud arthropathy is
the term used to describe the
nonerosive hand deformities due to
chronic arthritis and tendonitis that
develop in 10% of patients with SLE.
• Myositis may manifest as weakness in
SLE but is more commonly related to
overlap syndromes or corticosteroid-
induced myopathy.
• Fibromyalgia, distinguished as
myofascial tenderness without
weakness, is commonly concomitant
with SLE, causing generalized
widespread pain, arthralgia, and
myalgia.
• Avascular necrosis involving large joints
such as the hip and the knee.
- Cardiopulmonary
• Pleuropericardial friction rubs and signs
of effusions may be found. Tachypnea,
cough, and fever are common
manifestations of lupus pneumonitis.
- Kidney involvement (lupus nephritis)
COMPLICATIONS:
- Renal disease and CNS involvement
decreases survival
- Most frequent causing death:
• Uremia
• Heart failure
• Hemorrhage
• CNS disease
• Intercurrent bacterial infections
DIAGNOSIS:
Criterion Definition
SLE can be diagnosed if any 4 or more of the
following 11 criteria are present, serially or
simultaneously, during any interval of
observation.
Fixed, flat or raised
erythema over the malar
1. Malar rash
eminences, tending to
spare the nasolabial folds
Erythematous raised
patches with adherent
keratotic scaling and
2. Discoid rash
follicular plugging (older
lesions may demonstrate
atrophic scarring)
Skin rash as a result of
3. unusual reaction to
Photosensitivity sunlight, by patient history
or physician observation
62 | P a g e
 Oral or nasopharyngeal
4. Oral ulcers ulceration, usually painless,
observed by a physician
Nonerosive arthritis
involving =2 peripheral
5. Arthritis joints, characterized by
tenderness, swelling, or
effusion
(A) Pleuritis: Convincing
history of pleuritic pain or
rub heard by a physician or
evidence of pleural effusion
6. Serositis
or
(B) Pericarditis:
Documented by ECG or rub
or evidence of pericardial
effusion
(A) Persistent proteinuria
>0.5 g/day or >3+ if
quantitation not performed
7. Renal or
disorder
(B) Cellular casts: May be
red blood cell, hemoglobin,
granular, tubular, or mixed
(A) Seizures: In the absence
of offending drugs or
known metabolic
derangements (eg, uremia,
ketoacidosis, electrolyte
imbalance)
8. Neurologic
disorder or
(B) Psychosis: In the
absence of offending drugs
or known metabolic
derangements (eg, uremia,
ketoacidosis, electrolyte
imbalance)
(A) Hemolytic anemia: With
reticulocytosis
or
(B) Leukopenia: <
4000/mm3 total on =2
occasions
9. Hematologic
disorder or
(C) Lymphopenia: <
1500/mm3 on =2 occasions
or
(D) Thrombocytopenia: <
100,000/mm3 in the
absence of offending drugs
(A) Anti-DNA: Antibody to
native DNA in abnormal
titer
or
(B) Anti-Sm: Presence of
antibody to Smith (Sm)
nuclear antigen
or
(C) Positive finding of
10.
antiphospholipid antibodies
Immunologic
based on (1) an abnormal
disorder
serum level of IgG or IgM
anticardiolipin antibodies,
(2) a positive test result for
lupus anticoagulant using a
standard method, or (3) a
false-positive serologic test
for syphilis known to be
positive for =6 months and
confirmed by Treponema
pallidum immobilization or
fluorescent treponemal
antibody absorption tests
An abnormal titer of
antinuclear antibody by
immunofluorescence or an
11. Antinuclear equivalent assay at any
antibody (ANA) point in time and in the
absence of drugs known to
be associated with drug-
induced lupus syndrome
- Laboratory tests:
• Complete Blood Count: Low white blood
cell or platelet counts can be indicative
of SLE, whereas low red blood cell
counts can be indicate of anemia which
commonly occurs in conjunction with
SLE.
• Erythrocyte Sedimentation Rate: An
elevated erythrocyte sedimentation rate
can reveal a systemic problem. This test
is not specific to SLE, but a postitive test
could reveal that the patient could
potentially have SLE.
• Kidney and Liver Tests: These tests are
completed to determine if a patient's
kidneys and liver are functioning
properly since SLE can affect these
systemic organs.
• Urinalysis: This test is performed to
determine if there are proteins or red
blood cells present in a patient's urine.
If so, this could indicate that the kidneys
are damaged, potentially from SLE.
• ANA test: A positive test reveals that a
patient could potentially have SLE, but
other infections and diseases can cause
this test to be positive as well. If
63 | P a g e
 positive, further testing is necessary to
determine if the positive results
occurred due to SLE.
• Chest X-ray: This test is performed to
determine if there is inflammation
present in the patient's lungs or
excessive fluid surrounding his/her
heart.
• Syphilis Test: A false-positive syphilis
test can reveal that a patient has anti-
phospholipids present, and this false-
positive test result is indicative that the
patient could have SLE.
DIFFERENTIAL DIAGNOSIS:
- Rheumatoid arthritis (RA) –Important
distinguishing features are that the joint
deformities in SLE are often reducible,
and infrequently erosive on plain
radiographs.
Antinuclear antibodies (ANA) may be
positive in up to one-half of patients with
RA. Conversely, rheumatoid factor (RF)
may be present in approximately one-
third of SLE patients.
- Sjögren’s syndrome – Patients with
Sjögren’s syndrome may have
extraglandular manifestations that can
be observed in SLE, such as neurologic
and pulmonary abnormalities. However,
patients with Sjögren’s syndrome should
have objective signs of
keratoconjunctivitis sicca and
xerostomia, and characteristic findings
on salivary gland biopsy which are not
typical of SLE.
- Vasculitis – Patients with medium and
small vessel vasculitides such as
polyarteritis nodosa (PAN),
granulomatosis with polyangiitis (GPA)
(Wegener’s), or microscopic polyangiitis
(MPA) may present with overlapping
features of SLE including constitutional
symptoms, skin lesions, neuropathy and
renal dysfunction. However, patients
with these types of vasculitides are
usually ANA-negative.
- Dermatomyositis (DM) and polymyositis
(PM) – Patients with SLE can present with
a low-grade myositis, whereas patients
with DM and PM generally demonstrate
more overt proximal muscle weakness. A
positive ANA is observed in
approximately 30 percent of patients
with DM and PM, compared with almost
all patients in SLE. Patients with DM may
have characteristic skin findings
including Gottron’s papules, a heliotrope
eruption and photodistributed
poikiloderma (including the shawl and V
signs). Clinical findings characteristic of
SLE such as oral ulcers, arthritis,
nephritis, and hematologic abnormalities
are absent in DM and PM.
- Adult Still’s disease (ASD) – Some of the
clinical manifestations observed in ASD
such as fever, arthritis or arthralgias, and
lymphadenopathy, are not unusual for
patients with SLE. However, patients
with ASD often present with a
leukocytosis rather than the leukopenia
observed in SLE, and they typically are
negative for ANA.
- Fibromyalgia – Patients with SLE may
present with generalized arthralgias,
myalgias, and fatigue, much like patients
with fibromyalgia. However, other
characteristic features of SLE such as a
photosensitive rash, arthritis, and
multisystem organ involvement are
absent.
- Multiple sclerosis (MS) – Although rare,
patients with SLE can present with
cranial neuropathies that must be
distinguished from MS. Unilateral optic
neuritis and pyramidal syndrome, with
lesions detected by magnetic resonance
imaging (MRI) suggesting dissemination
in space and time are characteristic of
MS.
PROGNOSIS:
- Prognostic factors from the 2007
European League Against Rheumatism
(EULAR) recommendations included the
following :Clinical findings: Skin lesions,
arthritis, serositis, neurologic
manifestations such as seizures and
psychosis, and renal involvemen
- Diagnostic study results: Anemia,
thrombocytopenia, leukopenia,
increased serum creatinine levels
- Immunologic test results: Serum C3 and
C4 concentration (which may be low), as
well as the presence of anti–double-
stranded DNA (anti-dsDNA), anti-Ro/
Sjögren syndrome A (SSA), anti-
La/Sjögren syndrome B (SSB), and
antiphospholipid (aPL), and anti-
ribonucleoprotein (anti-RNP)
GENERAL HEALTHCARE MANAGEMENT:
MEDICAL, SURGICAL, PHARMACOLOGICAL:
PHARMACOLOGICAL:
- NSAIDs (provide symptomatic relief for
arthralgias, fever, headache, and mild
serositis)
• Ibuprofen- is the drug of choice
for patients with mild to
64 | P a g e
 moderate pain. It inhibits
inflammatory reactions and pain
by decreasing prostaglandin
synthesis.
• Naproxen- is used for relief of
mild to moderate pain. It
inhibits inflammatory reactions
and pain by decreasing activity
of the enzyme cyclooxygenase,
resulting in prostaglandin
synthesis.
• Diclofenac - inhibits
prostaglandin synthesis by
decreasing activity of enzyme
cyclo-oxygenase, which in turn
decreases formation of
prostaglandin precursors.
- Anti-malarial drugs (useful in preventing
and treating lupus skin rashes,
constitutional symptoms, arthralgias,
and arthritis; antimalarials also help to
prevent lupus flares and have been
associated with reduced morbidity and
mortality in SLE patients followed in
observational trials)
• Hydroxychloroquine (Plaquenil)-
commonly used for suppression
and treatment of malaria.
- Disease-modifying antirheumatic drugs
(DMARDS)(immunomodulatory agents
that act as immunosuppressives and
cytotoxic and anti-inflammatory
medications)
• Cyclophosphamide - is used for
immunosuppression in cases of
serious SLE organ involvement,
especially severe CNS
involvement, vasculitis, and
lupus nephritis.
• Methotrexate- is used for
managing arthritis, serositis,
cutaneous, and constitutional
symptoms.
• Azathioprine- is an
immunosuppressant and a less
toxic alternative to
cyclophosphamide.
- Low-dose corticosteroids
• Methylprednisolone -is used for
acute organ-threatening
exacerbations.
• Prednisone -is an
immunosuppressant for
treatment of autoimmune
disorders.
OTHER HEALTHCARE:
(REHABILITATIVE/SUPPORTIVE)
- Occupational therapy
- Speech therapy
- Recreational therapy
PHYSICAL THERAPY EXAMINATION, EVALUATION
AND DIAGNOSIS
POINTS OF EMPHASIS IN EXAMINATION:
- Cardiopulmonary assessment
PHYSICAL THERAPY DIAGNOSIS:
- MS4: impaired joint mobility, motor
function, muscle performance, and
range of motion associated with
connective tissue dysfunction.
PROBLEM LIST:
- Generalized fatigue
PHYSICAL THERAPY PROGNOSIS:
PLAN OF CARE:
- ↑ Cardiovascular endurance
INTERVENTION (INCLUDING RATIONALE):
- Cardiovascular endurance:
• Ergobike
• Swimming
• Aerobics Exercise ( warm-up,
exercise proper & cool down)
• Pt. Education on energy
conservation techniques (also to
protect joints that are
susceptible to damage)
4. PROGRESSIVE SYSTEMIC SCLEROSIS/
SCLERODERMA
DEFINITION:
- Is a multisystem disorder of unknown
cause characterized by fibrosis of the
skin, blood, vessels and visceral organs,
including GIT, lungs, heart and kidneys.
EPIDEMIOLOGY:
- -4-9 times higher in women than in
men.
- -The peak onset occurs in individuals
aged 30-50 years.
- -higher general and age-specific
incidence rate in blacks than in whites
ETIOLOGY:
- Unknown
- Genetic factors (different genes) appear
be important in the disease. Although
exposure to certain chemicals may play
a role in some people having
scleroderma
• Silica exposure
65 | P a g e
 • Solvent exposure (vinyl chloride,
trichloroethylene, epoxy resins,
benzene, carbon tetrachloride
• Radiation exposure or radiotherapy
PATHOPHYSIOLOGY/PATHOMECHANICS:
- Marked deposition of collagen and
- Vascular changes involving capillaries,
arteries and arterioles.
- Wound infections
DIAGNOSIS:
- Blood tests to check for elevated blood
levels of certain antibodies produced by the
immune system.
- Biopsy of your affected skin for examination
for abnormalities.
- You may also need breathing tests
(pulmonary function tests), a CT scan of your
lungs and an echocardiogram of your heart.

PROGNOSIS:
- Factors associated with a more severe
prognosis are as follows:
• Younger age
• African descent
• Rapid progression of skin symptom
• Greater extent of skin involvement
• Anemia
• Elevated erythrocyte sedimentation
rate (ESR)
• Pulmonary, renal, and cardiac
involvement

GENERAL HEALTHCARE MANAGEMENT

MEDICAL, SURGICAL, PHARMACOLOGICAL
PHARMACOLOGICAL:
- Pharmacologic therapy consists
principally of treatment directed toward
complications of the disease and
CLINICAL MANIFESTATIONS: providing symptomatic relief
- Raynaud’s phenomenon
- Skin thickening, swelling and tightening PHYSICAL THERAPY EXAMINATION, EVALUATION
- Telangiectasia (refers to a visibly dilated AND DIAGNOSIS
blood vessel on the skin or mucosal POINTS OF EMPHASIS IN EXAMINATION:
surface)
PHYSICAL THERAPY DIAGNOSIS:
- Calcium deposits in the skin or other
- MS4: impaired joint mobility, motor
areas function, muscle performance, and
- Heartburn range of motion associated with
- Shortness of breath
connective tissue dysfunction.
- Joint pain
5. DERMATOMYOSITIS (DM) / POLYMYOSITIS
COMPLICATIONS: (PM)
- Pleuritis
- Interstitial fibrosis DEFINITION:
- Pulmonary HTN - It is an inflammatory disease of muscle
- Weight loss and skin often associated with profound
- Constipation weakness of skeletal muscle, including
- Dysphagia the heart, with or without the presence
- “crest syndrome” of a rash.
• Calcinosis - Are principal subtypes of diseases in
• Raynaud phenomenon which muscle appears to be injured by
• Esophageal dysmotility the immune system
• Sclerodactyly - Myositis means inflammation of the
• Telangiectasia muscles (myo = muscle, itis =
- Digital infarction inflammation). Polymyositis affects
- Myositis many areas (poly = many), mainly the
- Renal failure larger muscles like those around your

66 | P a g e
 shoulders, hips and thighs. When
polymyositis develops alongside a skin
rash, the condition is called
dermatomyositis (derm = skin)
EPIDEMIOLOGY:
- Rare diseases, affecting only 6–8 people
out of 100,000.
- They mostly affects adults, although
children can be affected by a type of
dermatomyositis called juvenile
dermatomyositis.
ETIOLOGY:
- Autoimmune
PATHOPHYSIOLOGY/PATHOMECHANICS:
- DM has immune complex deposition
injury and PM has T-cell mediated
injury.
CLINICAL MANIFESTATIONS:
Most people will only have mild and short-lived
symptoms. These can include:
- Weak and tired muscles – making
normally easy tasks very tiring inflamed
muscles – causing pain (known as
myalgia) and feeling tender to the touch
- Generally feeling unwell (malaise)
- Weight loss
- Night sweats
If you have dermatomyositis, you may get some
of the above symptoms as well as:
- A red/pink rash on your upper eyelid,
face and neck, and on the backs of your
hands and fingers
- Swelling of the affected skin, causing a
characteristic puffiness and colouring
around your eyes.
COMPLICATIONS:
- Osteoporosis (due to long term use of
steroids)
- Occasionally polymyositis can also affect
breathing and swallowing. This may
happen at the start of severe cases,
when the muscles used become very
weak. It may also cause weakening of
your heart, and inflammation of your
lungs may cause scarring.
- Children with dermatomyositis may
develop painful calcium deposits in
damaged muscles. These deposits,
combined with immobility, can
occasionally result in the joints
becoming permanently bent (flexion
contracture).
DIAGNOSIS:
Diagnostic criteria for
polymyositis/dermatomyositis
1. Symmetrical proximal muscle weakness of
the limb girdle muscles and anterior neck
flexors,
with or without dysphagia or respiratory
muscle involvement; progressing weeks to
months
2. Elevation of serum levels of skeletal-
muscle enzymes
3. Evidence of an inflammatory myopathy on
muscle biopsy
4. Electromyographic features of a myopathy
5. Characteristic cutaneous eruption present
in DM, but not in PM
PROGNOSIS:
- Dermatomyositis:
• People who have an associated
malignancy; those with cardiac,
pulmonary, or esophageal
involvement; and those who are
elderly (ie, > 60 years) have a poorer
prognosis. Dermatomyositis may
cause death because of muscle
weakness or cardiopulmonary
involvement. Patients with an
associated cancer may die of the
malignancy.
- Polymyositis:
• Poor prognostic factors include the
following:
 Advanced age
 Female sex
 African American race
 Interstitial lung disease
 Presence of anti-Jo-1 (lung
disease) and anti-SRP antibodies
(severe muscle disease, cardiac
involvement)
 Associated malignancy
 Delayed or inadequate
treatment
 Dysphagia, dysphonia
 Cardiac and pulmonary
involvement
GENERAL HEALTHCARE MANAGEMENT
MEDICAL, SURGICAL, PHARMACOLOGICAL
PHARMACOLOGICAL:
- Steroids
Usually given in high doses to begin with. This
should reduce the inflammation very quickly and
settle muscle pain and the feeling of being
unwell. High doses of steroids can have side-
effects so your doctor will reduce the dosage as
quickly as possible. You may be given
bisphosphonates, calcium tablets and vitamin D
tablets to guard against osteoporosis.
PHYSICAL THERAPY EXAMINATION, EVALUATION
AND DIAGNOSIS
67 | P a g e
POINTS OF EMPHASIS IN EXAMINATION (FOCUS):
- Patient History
- ROM
- Muscle strength
- Joint Stability
- Cardiovascular status
- Functional examination
- Mobility
PHYSICAL THERAPY DIAGNOSIS:
- MS4: impaired joint mobility, motor
function, muscle performance, and
range of motion associated with
connective tissue dysfunction.
PROBLEM LIST
- Decreased cardiovascular endurance
- Muscle weakness
- Possible flexion contracture
- Decreased ROM
PHYSICAL THERAPY PROGNOSIS:
PLAN OF CARE:
- Improve cardiovascular endurance
- Improve muscle strength
- Prevent / decrease flexion contracture
- Improve ROM
INTERVENTION (INCLUDING RATIONALE):
- Cardiovascular endurance
• Aerobic exercise to help restore
muscle strength and improve
stamina.
• Patient education on energy
conservation techniques
- Muscle strength
• PREs using dumbbells, theraband or
ankle weights
• Isometric exercises
- Flexion contracture and ROM
• (Prevention) Splint to maintain in
extended position
• (To decrease)
• Heating modalities- PWB, HMP,
ultrasound, IRR (to increase tissue
extensibility)
• Prolonged stretching
• Contract- Relax
• Hold-relax
6. SJOGREN’S SYNDROME
DEFINITION:
- Is a systemic chronic inflammatory
disorder characterized by lymphocytic
infiltrates in exocrine organs.
EPIDEMIOLOGY:
- Estimated to be the second most
common rheumatologic disorder (in the
United States)
- Sjögren syndrome affects 0.1-4% of the
population.
- 9:1 (female:male)
- Sjögren syndrome can affect individuals
of any age but is most common in elderly
people.
- Onset typically occurs in the fourth to
fifth decade of life.
ETIOLOGY:
- The decrease in tears and saliva seen in
Sjögren's syndrome occurs when the
glands that produce these fluids are
damaged by inflammation.
PATHOPHYSIOLOGY/PATHOMECHANICS:
- Autoimmunity with lymphoma, and of
autoimmunity with neuroendocrine
disorders.
CLINICAL MANIFESTATIONS:
- The onset is insidious.
- Main clinical presentations in adults.
• Xerophthalmia (dry eyes)
• Your eyes may burn, itch or feel gritty
— as if there's sand in them.
• Xerostomia (dry mouth) Your mouth
may feel like it's full of cotton,
making it difficult to swallow or
speak.
Some people with Sjogren's syndrome also
experience one or more of the following
- Joint pain, swelling and stiffness
- Swollen salivary glands — particularly
the set located behind your jaw and in
front of your ears
- Skin rashes or dry skin
- Vaginal dryness
- Persistent dry cough
- Prolonged fatigue
COMPLICATIONS:
The most common complications of Sjogren's
syndrome involve your eyes and mouth
- Dental cavities. Because saliva helps
protect the teeth from the bacteria that
cause cavities, you're more prone to
developing cavities if your mouth is dry.
- Yeast infections. People with Sjogren's
syndrome are much more likely to
develop oral thrush, a yeast infection in
the mouth.
- Vision problems. Dry eyes can lead to
light sensitivity, blurred vision and
corneal ulcers.
68 | P a g e
 - Less common complications may affect
your:
- Lungs, kidneys or liver. Inflammation
may cause pneumonia, bronchitis or
other problems in your lungs; may lead
to problems with kidney function; and
may cause hepatitis or cirrhosis in your
liver.
- Lymph nodes. A small percentage of
people with Sjogren's syndrome develop
cancer of the lymph nodes (lymphoma).
- Nerves. You may develop numbness,
tingling and burning in your hands and
feet (peripheral neuropathy).
DIAGNOSIS:
American-European Consensus Sjögren’s
Classification Criteria
I. Ocular Symptoms (at least one)
- Dry eyes >3 months?
- Foreign body sensation in the eyes?
- Use of artificial tears >3x per day?
II. Oral Symptoms (at least one)
- Dry mouth >3 months?
- Recurrent or persistently swollen salivary glands?
- Need liquids to swallow dry foods?
III. Ocular Signs (at least one)
- Schirmer's test, (without anesthesia) ≤5 mm/5
minutes
- Positive vital dye staining (van Bijsterveld ≥4)
IV. Histopathology Lip biopsy showing focal
lymphocytic sialoadenitis
- (focus score ≥1 per 4 mm2)2
V. Oral Signs (at least one)
- Unstimulated whole salivary flow (≤1.5 mL in 15
minutes)
- Abnormal parotid sialography3
- Abnormal salivary scintigraphy4
VI. Autoantibodies (at least one)
- Anti-SSA (Ro) or Anti-SSB (La)
- Blood tests
Your doctor may order blood tests to check for:
• Levels of different types of blood
cells
• Presence of antibodies common in
Sjogren's syndrome
• Evidence of inflammatory conditions
• Indications of problems with your
liver and kidneys
- Eye tests
• Your doctor can measure the
dryness of your eyes with a test
called a Schirmer tear test. In this
test, a small piece of filter paper is
placed under your lower eyelid to
measure your tear production
- Imaging
Certain imaging tests can check the function of
your salivary glands.
• Sialogram. A special X-ray called a
sialogram can detect dye that's
injected into the salivary glands
located in front of your ears. This
procedure shows how much saliva
flows into your mouth.
• Salivary scintigraphy. This nuclear
medicine test involves the
intravenous injection of a
radioactive isotope, which is tracked
over the course of an hour to see
how quickly it arrives in all your
salivary glands.
• Biopsy. Your doctor may also want
to do a lip biopsy to detect the
presence of clusters of
inflammatory cells, which can
indicate Sjogren's syndrome. For
this test, a small sliver of tissue is
removed from salivary glands
located in your lip and examined
under a microscope.
DIFFERENTIAL DIAGNOSIS:
PROGNOSIS:
- Generally good prognosis, prognosis is
more closely related to the associated
disorder (eg, SLE, lymphoma)
GENERAL HEALTHCARE MANAGEMENT
MEDICAL, SURGICAL, PHARMACOLOGICAL
PHARMACOLOGICAL:
- Pilocarpine (Salagen) and cevimeline
(Evoxac) can increase the production of
saliva, and sometimes tears. Side effects
may include sweating, abdominal pain,
flushing and increased urination.
- Nonsteroidal anti-inflammatory drugs
(NSAIDs) or other arthritis medications- for
arthritic symptoms.
- Yeast infections in the mouth should be
treated with antifungal medications.
- Treat systemwide symptoms.
Hydroxychloroquine (Plaquenil), a drug
designed to treat malaria, is often helpful in
treating Sjogren's syndrome. Drugs that
suppress the immune system, such as
methotrexate, also may be prescribed.
PHYSICAL THERAPY DIAGNOSIS:
- MS4: impaired joint mobility, motor
function, muscle performance, and
range of motion associated with
connective tissue dysfunction.
69 | P a g e
 GENERAL MEDICAL OA
BACKGROUND
(Seronegative Arthritis)
Definition -is marked by 2 localized features: progressive
destruction of articular cartilage & bone formation @
margins of joint
-the disease process confines itself to the affected joint
-impairment, functional limitation, and disability related
to OA can reach far beyond the perimeters of the
affected articular cartilage & subchondral bone
Classification Criteria of Kellgren & Lawrence:
Grade 0: normal radiograph
Grade 1: Doubtful narrowing of the joint space &
possible osteophytes
Grade 2: Definite osteophytes & absent or questionable
narrowing of the joint space
Grade 3: moderate osteophytes & joint space
narrowing; some sclerosis; possible deformity
Grade 4: LARGE osteophytes; marked narrowing of joint
space, severe sclerosis & definite deformity
Epidemiology • MC condition @ 40 y.o
• Men > women (before 50 y.o)
• Men < women (after age 5 y.o)
Ankylosing Spondylitis
-is the stiffening/ restriction of the normal ROM of a Jt.
by tissue changes within/ without the cavity
-may occur when Jt. is in a position favorable to fx
European Spondyloarthropathy Study Group (ESSG)
criteria (classification of spondyloarthropathy)
Inflammatory spinal pain or synovitis, which is:
• Asymmetrical or
• Predominantly in the lower limbs
and ≥1 of the following:
• Alternate buttock pain
• Sacroiliitis
• Enthesitis (inflammation of the tendon or
ligament attachments to bone)
• Positive FHx spondyloarthropathy
• Psoriasis
• Inflammatory bowel disease
• Urethritis or cervicitis or acute diarrhoea
occurring within 1 month before arthritis.
• More common in white people
• Onset: late teens – 40 y.o.
• Male > Female (3:1)
Psoriatic Arthritis
-a polyarthritis associated ć psoriasis
-distinguishing feature: frequent involvement of DIP
joint
Criteria of Fournie & co-workers:
(cut-off for PA is 11 points)
1. Psoriasis antedating/concomitant ć jt.
symptom onset (6 pts.)
2. Family Hx of psoriasis (if criterion 1 is negative)
or psoriasis postdating jt. symptom onset (3
pts.)
3. Arthistis of DIP jt. (3 pts.)
4. Inflammatory involvement of cervical &
thoracic spine (3 pts.)
5. Asymmetric monoarthritis or oligoarthritis (1
pt.)
6. Buttock, heel pain, spontaneous ant. chest wall
pain, diffuse inflammatory pain in the enthuse
(2 pts.)
7. Radiologic criterion (5 pts. for any present):
erosion of DIP, osteolysis, ankyloses,
juxtaarticular periostitis, phalangeal tuft
resorption
8. HLA B16 (38,39) or B17 (6 pts.)
9. Negative RF (4 pts.)
• Young adults
• Middle aged adults
• Not specific with gender
• affects 2.5% of the white population of North
America but is less prevalent in the African
American and Native American populations.
• Men=women
Etiology UNKNOWN DIRECT CAUSE TO OA
Indirect causes that may lead to OA:
1. Trauma that may initiate the remodeling of
bone that alters joint mechanics
2. Microtrauma
3. obesity
Pathophysiology Early Stages:
• ↑ water content (this suggests that
proteoglycans have been allowed to swell far
beyond normal)
• Change in the newly synthesized proteoglycan
Late stages:
• Proteoglycans are lost → diminishes water
content of cartilage → articular cartilage starts
to lose its compressive stiffness & elasticity →
to compensate for loss of stiffness & elasticity,
stress is now transmitted to underlying bone
-first noticeable changes in cartilages: mild fraying or
“flaking” of superficial collagen fibers
-in areas of greater weight bearing: deeper fraying or
fibrillation
Clinical Manifestation >Early Stage
• Pt. complains of stiffness of 1 or more jts.
• aching pain (involvement is more on
monarticular)
• Slight enlargement of affected jts. (may be
tender; noticeable in the fingers and knees)
*Symptoms are worse in cold weather
*Heberden’s nodes
1. Fibrous/partial/false • infection
o when CT adhesions between articular • trauma
surfaces are not accompanied by actual • environmental factors
bony union
o may follow: Jt. inflammation, intraarticular
fractures, repeated intraarticular
hemorrhages OR extraarticular changes
from infection or prolonged
immobilization
2. bony/complete/true
o when solid new bone has been formed
between articular surfaces
o is often the end result of a more severe
infection/ more advanced RA
Enthesitis, in both the axial and the appendicular Unknown pathophysiology
skeleton, is the primary pathologic feature of the
spondyloarthritides. The enthesis is where the tendon or
ligament attaches to bone. The progression is typically
edema of bone followed by erosion, then ossification,
then finally ankylosis. The sacroiliac joints exhibit
inflammation followed by ankylosis. In the spine, one
can see inflammation at the junction of the annulus
fibrosis of the disk cartilage with the margin of vertebral
bone. Ultimately, this leads to formation of
syndesmophytes, with bridging that leads to the
radiographic appearance of a bamboo spine. The spinal
facet joint can exhibit synovitis followed by ankylosis. In
the peripheral skeleton, one sees synovitis and
enthesitis.
1. fibrous ankylosis The Classification Criteria for Psoriatic Arthritis
o small amt. of motion may be present (CASPAR)consist of established inflammatory articular
o pain may be experienced disease with at least 3 points from the following
2. bony ankylosis features:
o no Jt. motion is possible
3. presence of fine trabeculae Current psoriasis (assigned a score of 2)
o most reliable roentgenographic criterion of A history of psoriasis (in the absence of current
bony ankylosis psoriasis; assigned a score of 1)
71 | P a g e
 -bony enlargement of the DIP jts.
*Bouchard’s nodes
-enlargement of the PIP jts.
>Late Stage
• Limited Jt. motion & disability; especially in
larger weight-bearing jts.
• Malalignment of jt. 2⁰ to irreg. degeneration &
loss of articular cartilage
• crepitation (crackling/rattling sound) may be
noticed
• transient locking due to loose intra-articular
fragments (knee)
• tendency of early fatigue
• many Pt’s are obese
• abnormal weight-bearing lines on the feet,
knees, & hips; resulting in Jt. strains
Complications
Diagnosis Radiographic Findings
1. ABCDES
• No Ankylosis: alignment may be abnormal
• Bone mineralization: bony spurs/osteophytes
• No Calcification on cartilage
• Deformities of Herberden’s/Bouchard’s nodes
• No Erosions
• Slow progression over the years
Laboratory Findings
1. ESR is normal
2. RF negative
3. ANA not present
4. Synovial fluid
• High viscosity ć good string sign
• Color is yellow & clear
• WBC count is typically < 1000-2000/mmᶟ
• No crystals & negative cultures
A family history of psoriasis (in the absence of current
psoriasis and history of psoriasis; assigned a score of 1)
Dactylitis (assigned a score of 1)
Juxta-articular new-bone formation (assigned a score of
1)
RF negativity (assigned a score of 1)
Nail dystrophy (assigned a score of 1)
↓ ability for locomotion
Heterotropic ossification
Lab tests Laboratory findings
MRI imaging No specific diagnostic tests are available for psoriatic
arthritis. The most characteristic laboratory
abnormalities in patients with the condition are as
follows:
• Elevations of the erythrocyte sedimentation
rate (ESR) and C-reactive protein level
• Negative rheumatoid factor in 91-95% of
patients
• In 10-20% of patients with generalized skin
disease, the serum uric acid concentration may
be increased
• Low levels of circulating immune complexes
have been detected in 56% of patients
• Serum immunoglobulin A levels are increased
in two thirds of patients
• Synovial fluid is inflammatory, with cell counts
ranging from 5000-15,000/µL and with more
than 50% of cells being polymorphonuclear
leukocytes; complement levels are either
72 | P a g e
 within reference ranges or increased, and
glucose levels are within reference ranges
Radiographic studies
Radiologic features have helped to distinguish psoriatic
arthritis from other causes of polyarthritis. In general,
the common subtypes of psoriatic arthritis, such as
asymmetrical oligoarthritis and symmetrical
polyarthritis, tend to result in only mild erosive disease.
Early bony erosions occur at the cartilaginous edge, and
cartilage is initially preserved, with maintenance of a
normal joint space.
The following radiographic abnormalities are suggestive
of psoriatic arthritis:
• Pencil-in-cup deformity
• Joint-space narrowing in the interphalangeal
joints, possibly with ankylosis
• Increased joint space in the interphalangeal
joints as a result of destruction
• Fluffy periostitis
• Bilateral, asymmetrical, fusiform soft-tissue
swelling
• Unilateral or symmetrical sacroiliitis
• Large, nonmarginal, unilateral, asymmetrical
syndesmophytes (intervertebral bony bridges,
seen in the image below) in the cervical,
thoracic, and lumbar spine, often sparing some
of the segments

Magnetic resonance imaging studies

• Particularly sensitive for detecting sacroiliitic
synovitis, enthesitis, and erosions; can also be
used with gadolinium to increase sensitivity
• May show inflammation in the small joints of
the hands, involving the collateral ligaments
and soft tissues around the joint capsule, a
finding not seen in persons with RA

Differential Diagnosis *Refer to the Differential Diagnosis table of RA • Congenital Spinal Deformity • Gout and Pseudogout
• Degenerative Disk Disease • Osteoarthritis

73 | P a g e
 • Diabetic Ulcers • Reactive Arthritis
• Herniated Nucleus Pulposus • Rheumatoid Arthritis
• Heterotopic Ossification Imaging • Septic Arthritis
• Imaging in Diffuse Idiopathic Skeletal
Hyperostosis
• Kyphosis
• Lower Cervical Spine Fractures and Dislocations
• Lumbar Disc Disease
• Lumbar Spine Fractures and Dislocations
• Lumbar Spondylosis
• Osteoarthritis
• Osteofibrous Dysplasia
• Psoriatic Arthritis
• Reactive Arthritis
• Spinal Stenosis
• Spondylolisthesis, Spondylolysis, and
Spondylosis
• Thoracic Spine Fractures and Dislocations
Prognosis 1. Worse prognosis • Pt.’s having this disease have a better outcome • 40% of patients may develop erosive and
• Obese than RA deforming arthritis
• Condition is in its later stages • Poor outcome: peripheral joint involvement,
2. Better prognosis young age of onset, elevated erythrocyte
• Patient has a normal weight sedimentation rate (ESR), and poor response to
• Condition is addressed earlier nonsteroidal anti-inflammatory drugs (NSAIDs).
GENERAL HEATLHCARE Medical Surgical Pharmacological
MANAGEMENT 1. Reassurance 1. THR • Methotrexate
Medical, Surgical, and 2. Rest Pharmacological • Sulfasalazine
Pharmacologic 3. Modification of activity 1. NSAIDS • Cyclosporine
Pharmacologic 2. injectable steroids • Leflunomide
1. Oral analgesics 3. DMARDS • Biologic agents, such as the anti–TNF-alpha
• Acetaminophen medications
o Drug of 1st choice Surgical
o No inflammatory effect • Arthroscopic synovectomy has been effective
o Does not cause GI bleeding but can cause in treating severe, chronic, monoarticular
liver & kidney bleeding synovitis
2. NSAIDS • Joint replacement and forms of reconstructive
3. Corticosteroid injections therapy are occasionally necessary
• Intra-articular corticosteroid injections

74 | P a g e
 o Used for acute episodes ć modest • Patients in severe pain or with significant
response contractures may be referred for possible
o MC site: knee surgical intervention; however, high rates of
Surgery recurrence of joint contractures have been
1. Synovectomy noted after surgical release, especially in the
o Soft tissue release & tendon transfers hand
2. Osteotomy • Hip and knee joint replacements have been
3. Prosthetic arthroplasty successful
4. Arthrodesis • Arthrodesis and arthroplasty have also been
5. Total Joint Athroplasty used on joints, such as the proximal
interphalangeal joint of the thumb
• The wrist often spontaneously fuses, and this
may relieve the patient's pain without surgical
intervention
• For arthritis mutilans, surgical intervention is
usually directed toward salvage of the hand;
combinations of arthrodesis, arthroplasty, and
bone grafts to lengthen the digits may be used

PHYSICAL THERAPY 1. Musculoskeletal assessment

EXAMINATION, 2. postural assessment
EVALUATION AND 3. Gait analysis
DIAGNOSIS 4. palpation
Points of Emphasis in
Examination (Focus)
Physical Therapy MS4: Impaired Joint Mobility, motor function, muscle performance and range of motion associated with connective
Diagnosis tissue dysfunction
Problem List 1. pain
SAME AS RHEUMATOID ARTHRITIS 2. ↓ ROM, joint play, MMT
3.(+) postural deviations
4. pt. may be dependent in some ADLs
PHYSICAL THERAPY
PROGNOSIS
Plan of Care
Intervention 1. Early Stages of Jt. involvement 1. Rest: Local and systemic
o proper tx of the 1⁰ ds. Or injury 2. Exercise: Passive, active, stretching,
o Early protected mov’t of diseased Jts. strengthening, and endurance
(immobilization inhibit repair processes) 3. Modalities: Heat, cold
2. IF KNEE/HIP IS INVOLVED: 4. Orthotics: Upper and lower extremities, spinal

75 | P a g e
o Traction applied below the Jt. and designed to 5. Assistive devices for gait and adaptive devices
lessen the pressure of the apposed articular for self-care tasks: Including possible
surfaces modifications to homes and automobiles
3. DURING FIBROUS ANKYLOSIS 6. Education about the disease, energy
o Physical therapy (to preserve or ↑a useful conservation techniques, and joint protection
ROM in Jt. 7. Possible vocational readjustments
o Vigorous active exercise is essential
o preliminary heat and massage may help
o passive motion shouldn’t be forced if mov’t
causes pain
o electrical stimulation of muscles around Jt.,
active contraction of muscles may help
4. IF FORCIBLE MOTION OF PARTIALLY
ANKULOSED JT. IS NECESSARY
o manipulation should be done gently under
anesthesia

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 BURNS AND PRESSURE ULCERS
- The skin is the largest organ in the body
compromising approximately 15% of a
person’s total body weight.
- Has 3 distinct layers:
• Epidermis
 The outermost layer which
is exposed to the
environment
 Is avascular but has its vital
functions with its
corresponding layers:
i. S. Corneum: Gives the skin
its waterproof characteristic
and protects the skin from
infection.
ii. S. Granulosum: Responsible
for water retention and
heat regulation
iii. S. Spinosum: Adds a layer of
protection to the stratum
basale layer.
iv. S. Basale: Enables the
epidermis to regenerate
and contains melanocytes.
• Dermis
 Considered as the “true
skin” and contains blood
vessels, lymphatics, nerves,
collagen and elastic fibers.
 Encloses the sweat,
sebaceous glands and hair
follicles and is 20-30 times
thicker than the epidermis.
 Has 2 layers:
i. Superficial Papillary Layer:
Integrates with the
epidermis and contains the
vascular plexuses that
nourish the epidermis
through osmosis.
ii. Deep Reticular Layer:
Attaches to the
subcutaneous tissue by an
irregular network of fibrous
connective tissue.
• Subcutaneous fat layer
- Skin Functions:
• Temperature regulation
• Secretion of oils for skin
lubrication
• Vitamin D synthesis
• Sensation
• Cosmetic appearance &
identity
Burns
GENERAL MEDICAL BACKGROUND
Definition
- Injury and destruction of tissue
Etiology
- May be caused by:
• Minor Burns:
 Electrical Contact
 Chemical
 Tar
 Radiation
 Grease Injuries
• Major Burns:
 Flame
 Fire
 Scald Injuries
- Amount of skin destruction is based
on the temperature & length of
time the tissue is exposed:
• Below 111°F (44°C): Local
damage will not occur
unless there is prolonged
exposure
• Between 111°F- 124°F
(44°C- 51°C): Cellular death
doubles with each degree in
rise in temperature, short
exposure leads to cell death
• Excess 124°F (>51°C):
Exposure time needed to
determine tissue damage.
Epidemiology
- Affects 1-1.25 million people
annually in the United States
- 45,000 are hospitalized while
500,000 received medical treatment
- Affects the population between the
ages of 20-40, which presents 70%
of the total burn population
- 65% of most injuries are from non-
work related accidents while minor
 injuries which occur at work are
only 17%

Classification
- According to Depth:
• Superficial Burn/1st Degree
Burn
• Superficial Partial Thickness
Burn/2nd Degree Burn
• Deep Partial Thickness
Burn/2nd Degree Burn
• Full Thickness Burn/3rd
Degree Burn
• Subdermal Burn/4th Degree
Burn

- According to Size:
• Lund & Browder Diagram
1st 2 nd
2nd 3rd 4th
Degree Degree Degree Degree Degree
Burn Burn Burn Burn Burn

(+)cell (+) (+) Complete

damage damage damage damage Deep
to the thru to the to injuries
- According to Burn Wound Zones:
epiderm epiderm epiderm epidermi affectin
is is & is thru s and g • Zone Of Coagulation
papillary the dermis muscle,  Cells are irreversibly
skin is layer reticular tendon damaged & skin
red/ layer Covered & bone death occurs
erythem Intact by hard-  Increase risk of
atous blister Nerve parchme May infection & is in
and endings nt-like require need for careful
sunburn moderat & eschar amputat monitoring, use of
a classic e edema epiderm ion or antibiotics &
example al (+) extensiv treatment in a
Healing appenda Edema e specialized burn
spontan after 7- ges are which debride center
eous 10/20 injured may ment • Zone Of Stasis
healing days cause  Injured cells that
with (-) with Marked compress may die within 24
scar minimal edema ion hours without
formatio scarring diligent treatment
n Heals on Skin  Infection may result
3-5 grafting in conversion of
weeks & is potentially
with necessar salvageable tissue
hypertro y to completely
phic and necrotic tissue
keloid • Zone Of Hyperemia
scars  Site of minimal cell
• Provides a systemic method of damage
TBSA for both child and adult.  Tissue recovery
within several days
• A more accurate way.
without lasting
effects
• Rule of Nines
 Used clinically as a quick
Pathophysiology
estimate of TBSA
- Burn Mechanism
 A more practical use for
• For burn injury, the extent of
assessment
tissue damage depends on the
 Less accurate but more
location, duration, temperature
rapid and practical
and age

78 | P a g e
 Vasoconstriction at site of injury ↓
↓ Wound contraction
Vasodilation, ↑capillary
permeability & plasma leakage MATURATION PHASE
↓ Reduction of fibroblasts, ↓ vascularity
Release of histamine and cell ↓
swelling Remodeling of collagen is more parallel
↓ ↓
↑ Extravascular edema & Collagen breakdown
intravascular hypovolemia ↓
↓ Scar formation
Inflammatory mediators are
released Diagnosis
↓ - Major concerns at to severity:
↓ Intravascular volume, ↑ systemic • Percentage of Total Body
vascular resistance ↓ CO2, end-organ Surface Area
ischemia & metabolic acidosis • Depth of Injury
Clinical Manifestations
- Mechanism Of Healing - Loss of ability to regulate evaporative
• Epidermal water loss
• Occurs if there are viable - Increase susceptibility to infection
epithelial cells lining the - Loss of massive amounts of body fluids
wound especially in open wounds
- Local burn wound sepsis 2o to bacterial
Stimulation for epithelial growth contamination
↓ - Presence of hypertrophic scarring
Intact epithelium attempts to cover an exposed Presence of keloid scar
wound
↓ Complications
Epithelial cell migration stops once they contact - Infection
other epithelial cells - Pulmonary
↓ • Inhalation injury
Formation of various layers of epithelium • Pneumonia
↓ • CO2 poisoning
Cells maintain a connection with the normal - Neurologic
epithelial cells at wound margin • Localized neuropathies
• Peripheral neuropathy
• Dermal • Mononeuritis
- Scar formation occurs • Pruritis
- Bones & Joints
INFLAMMATORY PHASE • Septic Arthritis
Vasoconstriction • Subluxation & dislocation
↓ • Contractures
Platelets aggregate, fibrin is deposited
• Osteophytes
to form a clot
• Heterotrophic Ossification
↓
• Bony changes
Vessel vasodilation, ↑ blood flow to
• Scoliosis & Kyphosis
area
- Pain
↓
- Skin
↑ Permeability of blood vessels, with
leaking of plasma • Hypertrophic Scarring
↓ • Blisters
Leukocyte infiltration • UV Sensitivity & Skin
Pigmentation
PROLIFERATIVE PHASE - Metabolic
Fibroblasts are migrating & proliferating • Temperature Regulation
↓ • Catabolic State
Collagen is deposited in random alignment - Psychosocial
↓ • Depression
Granulation tissue is formed • Sleep Disturbance
↓
Newly formed blood vessels

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Methods of determining TBSA
• Rule of Nines
• Lund and Browder
 Was developed due to the relative inaccuracy of the Rule of Nines method
 More accurate but seldom used in general acute care setting
 Most often used within a specialized burn unit setting
REGION Birth-1 yr. 1-4 yrs. 5-9 yrs. 10-14 yrs. 15 yrs. ADULT
Head 19% 17% 13% 11% 9% 7%
Neck 2% 2% 2% 2% 2% 2%
Ant.
13% 13% 13% 13% 13% 13%
Trunk
Post.
13% 13% 13% 13% 13% 13%
Trunk
Each
2½% 2½% 2½% 2½ 2½% 2½%
Buttock
Genitalia 1% 1% 1% 1% 1% 1%
Each
Upper 4% 4% 4% 4% 4% 4%
Arm
Each
3% 3% 3% 3% 3% 3%
Forearm
Each
2½% 2½% 2½% 2½% 2½% 2½%
Hand
Each
5½% 6½% 8% 8½ 9% 9%
Thigh
Each Leg 5% 5% 5½% 6% 6½% 7%
Each Foot 3½% 3½% 3½% 3½% 3½% 3½%

- The ABA has also identified criteria for
admission to a designated burn center:
• Partial and full thickness burns >
10% TBSA in patients under 10 or
over 50 years old
• Partial and full thickness burns >
20% TBSA in other age groups
• Full thickness burns > 5% TBSA in
any age group
• Partial and full thickness burns
involving the hands, feet, face,
perineum, or skin overlying major
joints
• Electrical burns, including lightning
injury
• Chemical burns
• Patients with inhalation injury
• Burn injury in patients with pre-
existing illness that could complicate
management
• Any patient with a burn in whom
concomitant trauma poses an
increased risk of morbidity or
mortality may be treated initially in
a trauma center until stable before
transfer to a burn center
• Burn injury in patients who will
require special social and emotional
or long term rehabilitative support,
including cases involving suspected
child abuse
- In major burns, additional diagnostic
examination may be required, such as:
• Bronchoscopy
• Wound biopsy with quantitative
microbiology culture
Differential Diagnosis
- See Pressure Ulcers
Prognosis
- Mortality rate is increased with age and
inhalation injuries & more severe/larger
injuries
- Medical advances have significantly
reduced the number of deaths from
burned injuries
- Factors affecting the severity of a burn
injury and it’s prognosis are:
• Depth
• Extent
• Age of patient
• General condition
• Position/location of burn
• Delay of treatment
• Type of first aid given prior to
treatment
• Other complications present
• Etiological agent
General Healthcare Management
- Initial Management and Wound Care
• Goals
 Establish and maintain airway
 Prevent cyanosis, shock and
hemorrhage
 Establish baseline data
 Prevent/ reduce fluid loss

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  Clean the patient and wound • Silver Nitrate: Effective against most
 Examine injuries gram-positive organisms and most
 Prevent pulmonary and cardiac strains of pseudomonas. Penetrates
complications only 1-2mm of eschar
• Debridement • Silver Sulfadiazine: Most commonly
 Removal of eschar and necrotic used topical antibacterial agent
tissue • Mafenide Acetate: Effective against
 Prepares a viable base for gram-negative or gram-positive
wound healing and grafting organisms
Two types: • Mafenide Acetate Solution: Topical
 Mechanical: solution with antimicrobial function
Hydrotherapy with against gram-positive and gram-
water temp. negative organisms
between 98.6 °F & • Bacitracin/Polysporin: Bland
104° F (37-40°C) ointment that is effective against
 Surgical gram-positive organisms
• Topical cream application • Collagenase, Accuzyme: Enzymic
Two techniques: debriding agent selectively debrides
 Open: Application without necrotic tissue; no antibacterial
dressing. Allows for ongoing action
inspection of the wound and
monitoring of the healing Physical Therapy Examination, Evaluation and
process. Diagnosis
 Closed: Application with
dressing Points of Emphasis on Examination
- Patient History
- Surgical Management  Age
• Escharotomy  Sex
 Is done of compartment  Lifestyle
syndrome occurs  Occupation
 Surgical decompression of the  HPI
compartment to avoid necrosis  PMH
of the underlying tissue  Medications/Laboratory tests
• Grafting  C/C
 Homograft/Allograft: Tissue is - Systems Review
taken from one’s own species  Neurologic
including cadaveric tissue and  Musculoskeletal
human fetal membranes  Integumentary
 Heterograft/Xenograft: Tissue  Cardiopulmonary
taken from non-human species - Tests & Measures
used as human graft  ROM
 Autograft: Taken from patient’s  MMT
own skin from an unburned  Pain
area  Aerobic Capacity & endurance
• Mesh Grafts: Help enlarge the  Posture
available skin to cover a larger area.  Functional Assessment
A surgical instrument puts tiny holes  TBSA
into the skin after it has been - Problem List
harvested  Pain
• Sheet Grafts: Cover an area equal to  Scar formation
that of the donor site from which  LOM
the skin was removed. Sheets grafts  Contractures
are used for faces, hands, and over  Muscle weakness
joint surfaces when possible. The  Impaired gait and posture
use of the sheet graft gives a better  Decreased aerobic capacity
cosmetic and functional result.  Decrease functional independence
• Skin substitutes: Consists of - Plan Of Care
autologous skin which is grown in a  Increase wound healing
laboratory from a biopsy of a  Decrease complications, infection
patient’s own tissue. and edema
 Decrease scar formation
Pharmacologic Management  Increase ROM
- Topical Antibacterial Agents  Increase muscle strength
 Increase aerobic capacity

81 | P a g e
  Restore pre-injury level
cardiovascular endurance
 Achieve independent ambulation
 Patient & family education
- Intervention
1. Elevation of extremity with active
exercise
2. Positioning and splinting
 Anterior Neck: position with
firm cervical orthosis
 Shoulder: position with an
axillary splint (airplane
splint)
 Elbow: position with a
posterior splint
 Hand: Position in intrinsic
plus position with resting
hand splint
 Hip: position in extension
abduction and neutral
rotation
 Knee: Position in extension
with posterior knee splint
 Ankle: Position with foot-
ankle in neutral with splint
and ankle foot orthosis
3. Pressure garments & dressings;
Deep friction massage
4. AROM & PROM on all extremities
and trunk; heating modalities
5. Strengthening exercises/ PREs
(isokinetic, isotonic)
6. Ambulation training after skin graft
with figure-8 bandage with assistive
device to no assistive device
7. Walking, cycling/rowing ergometry,
treadmill walking, stair climbing
8. HEP/HIP on:
 ROM, massage
 Practice on ADLs
 Splinting and positioning
schedules
 Proper skin care
 Avoid the sun if possible
 Pressure program should be
continued
 Wash areas 2x daily with
antibiotic cram and non-
adherence dressing
 Patting than scratching
 Monitor vital signs

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 PRESSURE ULCERS -Noxious application of pressure on and
shear stress on skin
GENERAL MEDICAL BACKGROUND - Prolonged pressure leads to ulcers if it
exceeds the tissue capillary pressure of 32
Definition
- Localized injury to the skin/underlying mmHg
tissue, usually over a bony prominence as - Unrelieved pressure 4-6 times the systolic
a result of pressure/ pressure combined blood pressure causes necrosis in less
with shear & friction than 1 hour
- Deep muscle layers that cover bony
Etiology prominences are often exposed to high
- Associated with: stresses which leads to increase muscle
• Immobility stiffness, making the muscle more prone
• Impaired mental status/sensation to ischemia and infarction
• Poor hygiene/nutrition - Shear stress exacerbate the tendency for
ulceration
• Dark skin color
Common Sites of Affectation
• Multiple comorbidity factors
- Ischium 28%
- Shear & friction
- Sacrum 17-27%
- Muscle atrophy
- Trochanter 12-19%
- Impaired vascular status
- Heel 9-18%
- Anemia
- Pressure
Clinical Manifestations
- Earliest clinical evidence of impending skin
Epidemiology breakdown is skin inflammation (for 30
- Incidence of 7% and a prevalence of 15%
minutes) that blanches with digital
- 90% of the ulcers were at stage I or II and
pressure.
73% occurred in patients over 65 years old
- According to Depth:
- Patients in critical care have higher risk of
• STAGE I
developing pressure ulcer with an
 Non-blanchable erythema
incidence range from 38%- 124%
not resolved in 30
minutes
Classification
 Epidermis is intact and is
- Chronic venous/Edematous ulcers of the
reversible with
leg
intervention
• Affects lower third of the leg due
• STAGE II
to impaired venous return,
 Partial thickness of loss of
incompetence of venous
skin involving epidermis
perforators /loss of integrity of
possibly into the dermis
the leg fascia in patients with
 May appear as blisters
normal arterial flow.
with erythema
- Neuropathic ulcer
• STAGE III
• Due to repetitive trauma to distal
 Full thickness destruction
extremities, usually on weight-
through dermis into
bearing on bony prominences
subcutaneous tissue
- Ischemic Ulcers
• STAGE IV
• Occurs on limbs with impaired
 Deep tissue destruction
arterial inflow caused by
through subcutaneous
arteriosclerotic disease and in the
tissue to fascia, muscle,
setting of diabetes, microvascular
bone or joint
disease
• UNSTAGEABLE
Pathophysiology

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  Wound is covered with - Ankle-Brachial Index
dead cells, eschar and • Is the ratio of the systolic BP of
exudate so the depth the ankle to that of the arm
cannot be determined • Normal ABI is 0.8-1.3 and can be
Complications determined by a portable Doppler
- Autonomic Dysreflexia instrument and a BP cuff
- Bladder distension - Pulse Volume Recording
- Osteomyelitis • Continuous monitoring of
- Pyarthroses pressure within cuffs applied to
- Sepsis the thigh, calf and ankle
- Amyloidosis - Angiography
- Anemia - Pressure and Shear Assessment
- Urethral fistula - Skin Biopsy
- Gangrene
- Malignant transformation (rarely) Differential Diagnosis
- see Burns
Risk factors
- SCI patients Prognosis
- Elderly population with ages 85 years and - With higher stages, healing time is
older prolonged
- Diabetic patients - Pressure ulcers do not regress in stage as
- Malnutrition they heal
- Anemia - A pressure ulcer is becoming shallower
- Arteriosclerosis with healing is described in terms of its
- End-stage renal disease original deepest depth
- Smoking - 75% of stage II ulcers heal within 8 weeks;
- Parkinson’s disease 62% of stage IV pressure ulcers ever heal;
- UMND 52% heal within 1 year
- Dementia
- Osteoporosis General Healthcare Management
- Noncompliance, abuse and neglect Medical management:
- Wound Bed Preparation
Diagnosis • Maintain a moist environment
- Wound Area and Volume Assessment • Optimizes the rate of healing
• Wound Area - Wound Care
 Documentation of the • Provide the wound with the most
wound’s perpendicular optimal healing environment
linear dimensions; the • Factors:
maximum distance length  Level of moisture
and perpendicular  Debridement
distance width  Wound Cleansing
• Wound Volume  Protection Of Wound
 The area is multiplied by - Provision of Appropriate Seating Systems
depth to find the volume and Mattresses
• Wound Appearance - Pulsatile Lavage with Suction (PLWS)
 Red-yellow-black term is • Method of wound irrigation
used combined with suction. It removes
• Computerized Assessment of irrigation fluid, wound exudates
Wound geometry and loose debris and collects
- Perfusion Assessment wound exudates and debris
• Macrocirculation efficiently and delivers topical

84 | P a g e
 antibiotics, antiseptics and - Neurologic
antibacterial solutions efficiently - Musculoskeletal
- Integumentary
Surgical management - Cardiopulmonary
- Direct Closure Tests and Measures
- Skin Grafting - Pain Analog Scale
- Skin and Musculocutaneous flaps - Wound Assessment
- Free flaps - ROM
- Bio surgery - MMT
• a.k.a maggot debridement therapy or - Gait Assessment
maggot larval therapy. - Postural Assessment
• Sterile, newly hatched larvae are - Aerobic capacity & endurance
placed on chronic wounds and held in - Functional Assessment
place with dressings or a bio bag for 2
-5 days before removal, Problem List
• Removes devitalized tissue, decrease - Pain
risk of infection, improve wound - Soft tissue damage
healing without side effects. - ↓ ROM
- ↓ muscle strength and bulk
Pharmacological management - ↓ Aerobic capacity and endurance
- Topical Agents - impaired gait
• Povidone-Iodine - impaired posture
• Hypochlorite Solutions - ↓ functional independence
• Acetic Acid Solution
• Hydrogen Peroxide Solution Plan of Care
- Analgesics - Patient and family education
- Creams and Ointments - ↑ wound healing
- ↓ pain
Nutritional Management - ↑ ROM
- Nutrition - ↑ muscle strength
• Focus on protein and vitamins - ↑ aerobic capacity and endurance
and amino acids - correct gait pattern
- Protein intake - correct posture
• With pressure ulcers: 1.25-1.5 - ↑ functional independence
g/kg per day
• Stage II: 1.2-1.5 g/kg per day Intervention
• Stage III or IV: 1.5-2 g/kg per day - Use of effective cushions to ↓ risk of
- Micronutrients pressure ulcers
• Vitamins A, C, E, zinc and Arginine - static and dynamic mattresses
- Teaching of family members proper
Physical Therapy Evaluation, Examination and positioning of the patient
Diagnosis - Turning of patient every 2 hours
- Proper wound care and dressing
Points of Emphasis on Examination - Hydrotherapy (Whirlpool) for wound
- HPI debridement
- PMH - Electrical Stimulation for chronic wounds
- HFD - Negative Pressure Wound Therapy to ↓
- Age bacterial load and edema
- Sex - Therapeutic Ultrasound to ↑ vascularity
- Comorbidities of the wound tissue
- Occupation - Electromagnetic Therapy
Systems Review

85 | P a g e
- PROME → AAROM → AROM
- PREs
- Walking exercises
- Teach patient to assume proper posture
- Visual, Verbal and Manual cueing for
proper posture
- integrate ADLs into exercises

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 CARDIAC CONDITIONS - smooth muscle of a coronary artery
undergoes a sudden contraction that
Coronary Artery Disease (CAD) narrow the lumen of a blood vessel
Heart Failure
Cardiovascular Disease (CVD) Pathophysiology
Hypertension - Initial injury causes changes within the
Valvular Heart Disease intima of the blood vessel and progresses
Electrical Conduction Abnormalities to luminal narrowing.
Conduction Delays and Blocks - Luminal narrowing is usually due to a fixed
atherosclerotic lesion.
GENERAL MEDICAL BACKGROUND - Luminal narrowing leads to the primary
impairment of CAD: imbalance of
CORONARY ARTERY DISEASE myocardial oxygen supply to meet the
Definition myocardial oxygen demand (MVO2)
- Pathologic process of atherosclerosis
affecting the coronary arteries Clinical Manifestation
- results in coronary heart disease (CHD) - sx of CAD are not experienced until the
- CHD – a condition in which the heart lumen is at least 70% occluded
muscle is damaged because of an - 3 common clinical presentations of CAD:
inadequate amount of blood due to 1. Angina
obstruction of its blood supply 2. Injury
- Acute Coronary Syndrome (ACS) – the new 3. Infarction
terminology for ischemic heart disease or
CAD 1. Angina
- AKA Cardiac-related chest pain
Epidemiology - due to ischemia (reduced blood flow to the
Coronary Risk Factors myocardium)
Non-modifiable Modifiable - Characteristics:
a. Age: risk ↑ with age a. Cholesterol > 200 1. Described as tight or squeezing sensation
-CAD usually occurs mg/dl over the chest wall.
after 40 y.o. 2. sx begin at low intensity, increases over
b. Sex : b. Hypertension 2-3 mins, and last a total of less than 15
male > female - alcohol consumption mins
before menopause -dietary sodium intake 3. pain radiates to left arm, or to the jaw,
male=female after teeth or throat
menopause - 3 major types:
c. Family hx of c. smoking
atherosclerosis Unstable Stable Angina Variant Angina
Angina
d. Race d. diabetes mellitus Onset of -preinfarction - occurs during -Prinzmetal
Caucasians > Blacks > pain angina or exercise or angina
Asians crescendo activity -occurs at rest
e. sedentary lifestyle angina -pain is instead of during
- occurs at experienced at exercise and
rest w/o a certain most frequently
Etiology obvious intensity of early morning
A. Atherosclerosis precipitating exercise when and most often at
- Arteriosclerosis – thickening of the walls of factors or the myocardial night
arteries and loss of elasticity minimal oxygen - caused by
exertion demand vasospasm of
- disease in which lipid-laden plaque is exceeds blood coronary artery
formed within the intimal layer of the supply to the in the absence of
blood vessel wall of moderate and large myocardium occlusive disease.
size arteries; over time the plaque may - pt. describes
sensation <
extend into the lumen causing a decreased
5/10 which
luminal diameter improves to
- Atherosclerotic plaques - accumulated 0/10
cholesterol, triglyceride cells

B. Coronary Artery Spasm

87 | P a g e
Method -Less terminating -respond to NTG myocardium; an abnormal Q wave
of relief responsive to exercise and for short term mx appears
rest and use of of chest pain
nitrates nitroglycerin -long term
2. Zone of injury – ST elevation occurs at
- immediate (NTG) pharmacological area of injury
medical choice: calcium 3. Zone of Ischemia – ST depression and/or
intervention channel blocker T-wave inversion occurs in area of
due to (reduce calcium
decreased perfusion (ischemia)
impending influx into
risk for smooth ms of
further arteries and B. Cardiac Enzyme Level
complication reduce -Increase in Creatine Kinase MB sub unit
vasospasm. (CK-MB) in blood with myocardial damage
Intensity -increases in Intensity and -Pain is more
and severity, duration of intense of longer
duration frequency, pain does not duration than Differential Diagnosis
and duration change stable angina - Ischemic pain
Angina Scale • Accompanied by signs and symptoms
1+ Light, barely noticeable of compromised cardiac output:
2+ moderate, bothersome 1. Dizziness
3+ severe, very uncomfortable 2. Lightheadedness
4+ most severe pain ever experienced 3. Weakness
4. Diaphoresis
2. Injury 5. Fatigue
- represents the presence of new
myocardial infarction (MI) - Non-ischemic pain
- used because myocardial tissue is being • Chest pain from other etiologies like
acutely injured sudden heart attack pulmonary chest pain, pleural pain, or
musculoskeletal pain
3. Infarction • No accompanying signs of
- depicts an old heart attack with dead compromised CO.
tissue that cannot be reversed
- Irreversible changes start to appear 20 General Healthcare Management
mins-2 hrs from onset of myocardial A. Medical, Surgical, and Pharmacologic
ischemia 1. Revascularization Procedures
- preceded by angina
- acute MI Pain Intensity : 10/10 a. Percutaneous Transluminal Coronary
- results from complete occlusion of vessel angioplasty (PTCA)
by stationary blood clot (thrombus) or - A catheter with a balloon and collapsed
embolus stents is inserted to the radial or femoral
- s/sx: to the aorta to the opening of coronary
1. Chest pain and heaviness arteries. The balloon is then inflated and
2. Radiating pain the stent expands compressing the plaque
3. Weakness against the interior artery walls thus
4. Nausea increasing luminal area.
5. Vomiting
b. Coronary Artery Bypass Graft (CABG)
6. Syncope - uses donor vessel to bypass the lesion and
7. Diaphoresis establish an alternate blood supply
8. Shortness of breath - donor vessel could be:
1. Radial artery of non-dominant UE
Complication 2. Saphenous vein
- Major complication of MI 3. Internal mammary artery
1. Recurrence of Ischemia
2. LV failure 2. Pharmacologic Management
3. Ventricular arrhythmias - Beta Blockers – decrease beta-sympathetic
activity on heart resulting in ↓HR and
Diagnosis contractility
A. ECG - Calcium Channel blockers- prevents
ECG following an MI coronary smooth ms spasm  ↑
1. Zone of Infarction – infarction occurs myocardial blood supply
through the full thickness of the

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 - Nitrates – vasodilators that ↓ preload and
afterload and therefore ↓myocardial work
- Angiotensin –converting enzyme (ACE)
inhibitors and Angiotensin receptor Blocker
(ARB’s)
• Afterload reducers
• Normalize BP and reduce workload
on the heart.
Heart Failure
Definition
- A syndrome characterized by impaired
cardiac pump unction resulting in
inadequate systemic perfusion and an
inability to meet the body’s metabolic
demands
- AKA: Congestive heart failure (CHF)
Epidemiology
- US ~ 5.7 M individuals w/ approx. 670,000
of heart failure diagnosed annually
- European population ~ 0.4-2%
- North America and Europe ~ lifetime risk in
both sexes age 40 is approx. 1 in 5
- >65 y.o. 6%-10% have heart failure
- ↑ men ↓women but women constitute
half of all cases because of their longer life
expectancy
- Most frequent cardiac diagnosis for
hospital admissions and readmissions.
Etiology
- MC is cardiac ms dysfunction
- Cardiac Muscle Dysfunction (CMD) –
general term describing altered systolic
and/or diastolic activity of the myocardium
that usually develops as a result of an
underlying abnormality w/in the cardiac
structure or function.
- Precursors for CMD
• Hypertension
• CAD
• Cardiac dysrhytmias
• Valve abnormalities
• Pericardial pathology
• Cardiomyopathies
Classification
Class I > (-) limitation to physical activities;
ordinary activities does not cause
symptoms
> 6.5 METS
Class II > slight limitation; comfortable at
rest & ordinary activities leads to
symptoms: Fatigue, Palpitations,
dyspnea, angina (FPDA)
> 4.5 METS
Class III > marked limitation; comfortable at
rest & less than ordinary activities
leads to FPDA
> 3.0 METS
Class IV > inability to carry physical activities
without discomfort
Pathophysiology
1. Left Ventrcular Failure
↑ workload & end diastolic volume  lack of O2
 diminished LV function  blood pools into the
ventricle and atrium  enlarge LV with stretched
tissue blood eventually back up to the pulmonary
capillaries  ↑capillary pressure  pulmonary
edema
2. Right Ventricular Failure
↑Pulmonary pressure  hypertrophy of RV 
blood congestion in vena cava and systemic
circulation  ↑central venous pressure & jugular
vein distention  peripheral edema (MC in LE)
Types of Heart Failure
A. Structural
1. Left-sided Heart failure
- Occurs with LV insult
- If LV fails first, it can’t pump out all the
blood it receives thus resulting to backing
up of the blood in the lungs causing
Pulmonary edema
- 2 hallmark pulmonary sign:
• shortness of breath (SOB)
• cough
2. Right-sided heart failure
- Occurs from direct insult to RV caused by
conditions that increase Pulmonary Artery
(PA) pressure.
- ↑PA pressure = ↑afterload  greater
demands to RV leading to failure
- Blood backs up in the systemic vessels
resulting to 2 hallmark:
• jugular venous distention
• peripheral edema
3. Biventricular failure
- Severe LV pathology, fluid from LV backs
up to the lungs  ↑PA pressure  fluid
backs up to right side of heart and the
systemic venous vasculature
- Presents w/ both pulmonary and systemic
signs of heart failure
B. Functional
1. Systolic dysfunction
- Characterized by compromised
contractile function of the
ventricles causing ↓stroke vol
(SV), CO, ejection fraction (EF)
- EF < 40%
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 2. Diastolic dysfunction
- Compromised diastolic function of
the ventricles
- Ventricles can’t relax and fill
appropriately during diastolic phase
- ↓ CO, ↓SV, EF is unaltered with
normal value 55-75%
Clinical Manifestations
- Compensated heart failure – pt.’s
congestive symptoms can be relieved by
medical intervention
- Non-compensated – showing s/sx of
congestion and requires medical and
pharmacologic readjustments
Common s/sx:
- Fatigue
- Dyspnea
• Paroxysmal nocturnal dyspnea (PND)
– sudden episodes of SOB occurring
at night
- Orthopnea – increased SOB in recumbent
position
- Edema
• Pulmonary edema – evident w/ chest
x-ray, auscultation of adventitious
sounds
• Peripheral edema – evident in gravity
dependent LE’s by presence of
indentations when pressure is applied
(Pitting edema)
- Fluid weight gain
- Presence of S3 heart sound
• Due to poor ventricular compliance
and turbulence of blood within the
ventricle
- Heart murmurs, crackles and rales
- Renal dysfunction
- Early onset of fatigue
- ↓ exercise tolerance
Dyspnea Scale
+1 mild, noticeable to pt but not to observer
+2 mild, some difficulty, noticeable to
observer
+3 moderate difficulty but can continue
+4 severe difficulty, pt cannot continue
Diagnosis
1. Radiographic Findings
- 3 hallmark chest x-ray
characteristics
• Enlarged cardiac silhouette
• Opacities in lung field with
interstitial and parenchymal
edema
• Blunting of the costophrenic
angle
2. Laboratory Findings
- ↑ B-type or brain natriuretic
peptide (BNP)  released due to
volume overload in chambers
- Normal BNP = 100 pg/ml
- >500 pg/ml BNP  (+)Heart
Failure
3. Echocardiogram and Nuclear imaging
General Healthcare Management
A. Medical, Surgical, and Pharmacologic
Pharmacologic Management
1. Positive inotropes – drugs that increase
contractility
- e.g.: digoxin
2. Diuretics – decrease preload
3. Afterload reducers – blocks the effect of
rennin-angiotensin system
- e.g.: ACE inhibitors, ARB’s
Mechanical and Surgical Support
1. Heart transplantation
- Replacing the pt’s heart with a donor
heart.
2. Left ventricular assist device (LVAD)
- temporary pump inserted into the
patient to perform work of the LV
3. Myoplasty
- Enlarged LV undergoes size reduction
by removing dilated, scarred
myocardium that is ineffective in
contributing to contractility.
4. Pacemaker
- A device that is placed subdermally
near the heart and consist of an
implantable pulse generator and lead
wires that connect the pacemaker to
the myocardium.
- Indications:
1. HR that is too slow (symptomatic
bradycardia)
2. HR that fails to increase
appropriately with exercise
(chronotropic incompetence)
3. Electricity pathway that is blocked
resulting atrioventricular delays or
bundle branch blocks
Cardiovascular Disease (CVD)
- Refers to the pathologic process of
atherosclerosis affecting the entire arterial
circulation.
- Conditions that underlie CVD are
atherosclerosis, altered myocardial muscle
mechanics, valvular dysfunction,
arrhythmias, and hypertension.
Hypertension (HTN)
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 - Persistent elevation of the systolic arterial
blood pressure above 140 mmhg or
diastolic BP above 90 mm Hg
- Labile HTN – BP in not consistently
elevated and fluctuates between
hypertensive and normal values
Stages of Hypertension
Stages Systolic BP Diastolic BP
(mmhg) (mmhg)
Prehypertension 120-130 80-89
Stage 1 130-140 90-100
Stage 2 140-160 100-110
Stage 3 >160 110
Types of Hypertension
1. Primary (essential) HTN
- Diagnosed when there is no known
cause for the elevation in BP values
- 90-95% of all pt’s w/ HTN
- Factors that predispose a person to
this type are: genetic factors,
environmental influences (dietary
sodium intake), stress, obesity,
alcohol consumption, age, lack of
exercise, and glucose intolerance
2. Secondary (nonessential) HTN
- 5-10% of hypertensive population
- Caused by identifiable medical
problem such as renal, endocrine,
vascular, or neurological
complications.
Medical Management of Hypertension
Pharmacological – primary treatment
1. Beta-adrenergic blockers
2. Alpha-adrenergic blockers
3. Angiotensin-converting enzyme (ACE)
inhibitors
4. Diuretics
5. Vasodilators
6. Calcium channel blockers
Valvular Heart Disease
1. Stenosis
- Narrowing of the heart valve limiting
the flow of blood through the valve
- Results to hypertrophy of chamber
behind valve to pump against the
obstruction
Mitral stenosis – narrowing of mitral valve
by scar formation or congenital defects
Aortic Stenosis – narrowing of aortic
semilunar valve
2. Proplase
- Enlarge valve cusps that become
floppy and bulge backward.
Mitral Valve Prolapse – an inherited d/o in
which a portion of the mitral valve is
pushed back too far during ventricular
contraction
3. Regurgitation
- Forward and backward movement of
blood resulting from incomplete valve
closure
Mitral Valve insufficiency – backflow of
blood from LV into the LA due to damaged
mitral valve or ruptured chordate
tendinae
Aortic Insufficiency – backflow of blood
from aorta into the LV
Electrical Conduction Abnormalities
Arrhythmias – Any alteration in the electric
conduction of the heart from the normal beat.
1. Ectopic beats
- Beat that originates from a site other
than the sinus node
- Common Ectopic beats
A. Atrial (premature atrial
contraction [PAC])
B. Ventricular (premature ventricular
contraction [PVC])
2. Supraventricular Ectopy
- Beat that originates from a site other
than the sinus node
- Rapid firing of an ectopic focus that
originates in any location above the
ventricles (atrial or junctional area)
3. Ventricular Ectopy
- Ectopic beats that originate in the
ventricle and may present as irregular
rhythms
4. Ventricular Tachycardia
- A run of four or more PVC in a row
5. Ventricular Fibrillation
- Quivering of the ventricles resulting
from inadequate electrical stimulation
6. Atrial fibrillation
- Quivering of the atria resulting from
inadequate electrical stimulation
Conduction Delays and Blocks
- Changes in length of the PR interval, the
width of QRS complex and the length of QT
interval
Conduction Delays through the A-V node
1. First-degree heart block
- Conduction time through the A-V
node is prolonged, increased length of
PR interval
2. Second-degree heart block
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 - Mobitz type 1 (Wenckeback) –
gradual increase in PR interval length
in preceding beats and then an
eventual dropped beat.
- Mobitz II – normal PR intervals in all
beats preceding the dropped beat.
3. Third-degree heart block
- a mismatch of atrial and ventricular
conduction exists
Bundle branch block
- Conduction delays through the bundle of
His
- Not true arrhythmias because there is no
change in actual rhythm, just in the timing
of conduction in the bundle of his
EVALUATION AND DIAGNOSIS
A. Points of Emphasis in Examination
- Medical Record Review
• Medical problems, PMH,
physician’s examination
• Medications including type, dosage,
and schedule
• Laboratory tests
• Results of any diagnostic studies:
 Chest x-rays, ECG’s etc.
• Nursing and other Health care
providers
- Patient Interview
• Cognition: orientation, memory,
learning needs, comprehension
• Lifestyle
• Patient’s response to health and
status, support system and
knowledge of the disease
- Physical Examination
• Observation and Inspection
 Skin color (cyanosis, pallor)
 Diaphoresis
 Skin temperature
 Edema
• Heart Auscultation
 Normal heart sound: S1 (lub);
S2 (dub)
 Murmurs – abnormal heart
sounds as a result of valvular
d/o due to changes in blood
flow around the altered
blood.
 S3 – Ventricular gallop
o occurs after s2
o associated w/ LV failure
 S4 – atrial gallop
o occurs before s1
o associated with MI or
chronic HTN
 Pericardial friction rub – high
pitched with leathery and
scratchy quality
o Results from
inflammation of
pericardial sac, either
with or without excessive
fluid
• Lung Auscultation
 Normal:
o Vesicular sounds (soft-
low pitched);longer and
louder w/ inspiration
o bronchial (loud- high
pitched); longer and
louder w/ expiration
 Crackles – pt with LV failure
o Jugular Venous Distention
o Pitting edema
o Exercise tolerance
o Assessment of Aerobic
Capacity and Endurance
B. Problem List
- Decreased aerobic capacity
- Muscle weakness
- Decreased strength, power and endurance
- Decreased ability to perform ADL’s
C. Physical Therapy Diagnosis
CP4: Impaired aerobic capacity/ endurance
associated with cardiovascular pump dysfunction
or failure.
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PHYSICAL THERAPY PROGNOSIS
1. Interventions for Patients with CAD
- Exercise Prescription
• Intensity
 MC: based on HR which is 70-85% of HRmax
 More deconditioned pt: 50-60% of HRmax
- Frequency
• 3-5x per week
- Duration
• Goal: 30-40 mins aerobic exercise with an additional 5-10 mins warm-up and cool down
• Deconditioned pt: require interval work, brief rest every 5 mins
- Mode of exercise (type)
• Treadmill, stair climbers, bicycles, rowers, cross country ski stimulators, reclining bicycles,
steppers, arm ergometers

2. Cardiac Rehabilitation
- Candidates for cardiac rehab
• Post MI
• Post-CABG
• Post transplant
• Postvalvular surgery
- 2 primary goals for cardiac rehab
1. Increase functional capacity
2. Alter natural history of cardiac disease to reduce morbidity and mortality

Three Phases of Cardiac Rehabilitation (From De Lisa 2nd ed)

PHASE I PHASE II PHASE III
Name In-Hospital Phase Early Post-Hospitalization Phase Maintenance Phase
Timing Admission to hospital - 2 wk. post-discharge or
- 6-8 wks post-MI
-3-4 wks post-coronary bypass
Duration Up to discharge from hospital 8-12 wks lifetime

Candidate - Acute MI pt - Phase I graduate - Phase II graduate

- post-coronary bypass pt
- post-percutaneous coronary
angioplasty pt
- pt with angina pectoris
Major Goals - prevent deconditioning
- patient and family education
- functional mobilization/training
- early hospital discharge
Supervision Highly supervised
Major Program of progressive activity
Activity
Initial 2-3 METS increasing by 1 Met
Intensity
Monitoring HR & BP response
Others - Pre-discharge stress test
recommended; not> 5 METS
- low fat (</= 30% of total calories)
& low cholesterol (</=300 mg/day)
diet prescribed
- any coronary artery disease pt with or
without associated risk factors
- develop cardiovascular endurance - maintain a lifetime exercise
through exercise conditioning program for CVS endurance
- complete return to work
Highly supervised Home program
Aerobic exercise of 15-20 min Aerobic exercise
70-85% 70-75% only
HR HR
- most intensive & rigorous
- always with 5-10 min, warm up &
cool down
- decreased intensity/ high frequency
training discouraged  orthopedic
complications common; compliance
poor

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Guideline for the Graduation to the maintenance - Gradually increase exercise endurance at the
Phase same intensity as acute phase
Age Total Physical work Capacity Pre-requisite: previous in-patient rehab
Male Female Intensity: same as target HR used at the end
49 y.o or less 10 METS 8 METS of the Acute phase
50-59 9 7 3. Training Phase (6-8 wks, 3xweek)
60-69 8 6.5 Pre-requisite:
70 y.o or older 7 6.5 - symptom limited Exercise Tolerance Test
(ETT)
Exercise Precautions Activity:
- No heavy meals before exercising - Stretching & aerobic exercise (treadmills,
- Exercise in cool environment UE or LE ergometer, airdynes, rowing
- Drink water before exercising; allow sips of machines, walking, running, calisthenics)
water during exercise Contraindications:
- Clothing should be loose and comfortable - Dangerous arrhythmia on ETT
- Best time to exercise is early morning or late - Decreasing HR with increasing exercise
evening intensity
Intensity: Target HR is computed from the
Goals In cardiac rehabilitation (Braddom) max HR on ETT
Phase I – prevent secondary complication of - If w/ benign end point on ETT, can use 85%
inactivity and resume functional activities in of max HR as target HR
stepwise manner - If w/ serious arrhythmia or ECG changes but
Phase II – achieve strong scar in area of ischemia no chest pain on ETT  use lower intensity
Phase III – improve cardiovascular endurance; return - Target HR as low as 60% can still result in
to work and previous activities if possible effective cardiac training
Phase IV – maintain increased cardiovascular Monitoring
endurance - Carotid pulse HR, ECG telemetry if
progressing the exercise, Borg scale
4 Phases of cardiac rehabilitation (Braddom) 4. Maintenance Phase
1. In-Hospital Phase (first 2 wks post MI) - Exercise program is continued by patient at
Goal: home; same as last phase of the three
- Prevent complications of bedrest phased cardiac rehabilitation program
- Resume functional activities
Activities:
1. Step-ladder program of functional Cardiac Rehab (Sullivan)
activities 1. Phase 1 (inpatient)
2. Patient education - Role of PT
Discharge Requirements: • Monitor activity tolerance
- Does self-monitoring of exercise response/ • Prepare for discharge
response to activity • Educate pt to recognize symptoms
- Knowledgeable on energy conservation & with activity
pacing of activities • Give emotional support
- Simple Convalescent phase exercise program - Intensity: Low level intensity (fairly light)
has prescribed - For an ↑ 1-2 METS; HR ↑ of 10-20 is
- Advise on recommended lifestyle changes appropriate if (-) Beta-blockers
reinforced - (+) Beta-blockers = no standardization
2. Convalescent Phase (remainder of 6 wk post- • If HR ↑ by 20 bpm = pt is
infarction period) inadequately medicated
Purpose:
• If HR ↓ = check for arrhythmia
- Allow for strong scar formation in
myocardium Level 1
- Reduce risk for ventricular aneurysm or - Pt is in ICU and stable
rupture
- PT intervention only begins after 1st 24
Treatment goal:
- Maintain early mobilization hours from admission or stable

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 - Moving comfortably within bed 15 – hard 7 – very strong
- Ankle pumps 16 8
17 – very hard 9
• DBE 18 10 – very very strong
- Limited personal care 19 – very very hard (almost maximum)
maximal
Level 2 –
- Progress to out of bed (OOB) exercises
- PT should be alert for OH 3. Intervention for Patients with CHF
- Pt walks to bedside chair; allow pt to sit for Goals:
30 mins a few times a day 1. Physiologic response to increased O2
demand is improved
- LE ex: ankle pumps, knee extension, march
2. Improvement in self-management
in place 3. Increased ability to perform physical tasks
4. Reduced disability associated w/ acute or
Level 3 –
chronic illness
- Pt gradually ↑ ambulation
5. Reduced risk to secondary impairment
- Use of Borg Scale 6. Improved awareness and use of community
resources
Level 4-6 –
7. Increased performance and independence
- pt. Gradually ↑ frequency time of walks at
in ADL
comfortable leisurely place
- Goal: 2 mins -> 5 -> 10 mins - Exercise prescription
- Stair climbing (step-to pattern)  Aerobic exercise
- Educate pt in energy conservation  Low intensity and gradually increase
as pt tolerates
2. Phase 2 (Outpatient)  Should be kept at a rating of fairly
- ETT: 4-6 wks post- MI light
• strengthening  Strength training
 begin with elastic bands &  Light resistance work (e.g. elastic
light weight (1-3 lbs) band for mild UE and LE resistance
 progress to load that allows work)
12-15 reps comfortably  Ventilatory Muscle Training
 DBE – reduce excessive accessory ms
3. Phase 3 (Maintenance) use and reduce work of breathing
Same with the maintenance from Braddom.  Pursed-lip breathing – slow down
respiratory rate in pt with heart
Borg’s Rate of Perceived Exertion Scale and the failure
revised 10-Grade Scale  Activity Pacing and Energy conservation
RPE 10 grade rating scale technique
6 0 – nothing at all
7 – very very light 0.5 – very very weak (just SOURCES:
8 noticeable) - Physical Rehabilitation 6th Ed by O’Sullivan
9 – very light 1 – very weak - Physical Medicine and Rehabilitation by
10 2 – weak (light) Braddom
11 – fairly light 3 – moderate
- Physical Medicine and Rehabilitation:
12 4 – somewhat strong
13 – somewhat hard 5 – strong (heavy) Principles and Practice by DeLisa
14 6

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 PERIPHERAL VASCULAR DISORDERS - Nicotine
- Diet
Arterial Insuffeciencies - Hypertension
Acute - Diabetes
Chronic - Stress
Arteriosclerosis Obliterans - Sedentary lifestyle
Buerger's Disease (Thromboangitis
Obliterans)  Non-modifiable
Vasospastic Disorder (Raynauds Disease) - Age
Venous Disorders - Gender
Thrombophlebitis - Genetic predisposition
Deep Vein Thrombosis - HFD
Venous Insufficiency/Stasis
Chronic Venous Insufficiency III. PATHOPHYSIOLOGY
Varicose Veins - Most common theory reaction to injury
Lymphatic Disorder
Lymphedema Two types of atherosclerosis lesions:
A. Fatty streaks
GENERAL MEDICAL BACKGROUND - Are yellow and smooth protrude slightly
into the lumen of the artery and are
DEFINITION composed of lipids and elongated
- Are conditions that may affect the circulatory smooth muscle cells
system external to the heart that involves arterial, B. Fibrous plaque
venous, lymphatic circulatory system. - Composed of smooth muscle cells,
A. Arteries collagen fibers, plasma components and
- These are vessels through which the lipids
blood passes away from the heart to - Can develop at any point in the body,
various parts of the body but certain sites are more vulnerable,
B. Capillaries typically bifurcation or branch areas
- Thin- walled vessels through which
nutrients and waste products pass IV. CLINICAL MANIFESTATIONS
- Allow the exchange of fluid and -intermittent claudication
nutrients between the blood and the -rest pain
interstitial spaces -tissue loss
C. Veins -embolic events
- Transport deoxygenated blood tissues -decreased or absent pulses; bruits
back to the heart and lungs for
oxygenation V. Diagnostic Exams
D. Lymphatic System - Specific to the body system affected
- Transport fluids that have escaped from 1. Arteriography of the involved area
the blood vascular system to the blood 2. CT scan
3. MRI
ARTERIOSCLEROSIS 4. Non-invasive testing of the vascular system
- thickening, hardening, and loss of a. Duplex studies
elasticity of arterial walls. b. Sequential Doppler studies
ATHEROSCLEROSIS c. Ankle-brachial index
I. DEFINITION Interpretation:
-is the most common form of  Above 0.90 = normal
arteriosclerosis, associated with damage to the  0.71-0.90 = mild obstruction
endothelial lining of the vessels and the formation of  0.41-0.70 = moderate obstruction
lipid deposits, eventually leading to plaque  0.00-0.40 = severe obstruction
formation.
VI. MEDICAL AND PHARMACOLOGICAL
II. ETIOLOGY/RISK FACTORS MANAGEMENT
 Modifiable -modifiable of risk factors

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 -prescriptive management - Once dislodged, an embolus may
A. anticoagulants travel and lodge in an arterial branch
B. antiplatelet therapy - Formation of a soft coagulum near
C. lipid- lowering agents the area of stagnant blood flow –
D. antihypertensives secondary thrombus
E. vascular rehabilitation and exercise - No adequate circulation, the distal
tissues are deprived of oxygen –
VII. SURGICAL MANAGEMENT ischemia, pain and paresthesia in the
Endovascular procedures: affected area – muscle necrosis
1. A. Percutaneous transluminal angioplasty
-done to relieve arterial stenosis when V. CLINICAL MANIFESTATIONS
lesions are accessible through the use of - Acute pain
special inflatable balloon catheters and - Paralysis
metal stems. - Paresthesia of the part
2. Endovascular grafting - Pallor
- Placement of prosthetic graft via - Coldness
transluminal approach - Pulselessness
- Edema
ARTERIAL INSUFFECIENCIES - Rigidity of extremity
ACUTE
I. DEFINITION VI. DIAGNOSTIC EXAMS
- Is a sudden decrease in the arterial 1. Neurovascular assessment of
supply to an extremity affected area
2. Doppler ultrasonography,
II. EPIDEMIOLOGY segmental limb pressure and
- MC location: femoral-popliteal pulse volume recordings
bifurcation - may indicate decreased blood flow
♥ Acute embolic occlusion 3. Radionuclide scan
– common in those who have had - May identify clot
recent MI, atrial fibrillation or other 4. Arteriography
source of possible embolus - Determines location of obstruction
♥ Acute thrombotic occlusion and character of arterial circulation
- common in those who have had proximal and distal to obstruction
experienced previous symptoms of
claudication w/o cardiac dysfunction VII. MEDICAL MANAGEMENT
A. Medications
- Anticoagulants: Heparin
III. ETIOLOGY / RISK FACTORS - Thrombolytics: Streptokinase,
- Most common cause: embolization Urokinase
- Consist of thrombus, atheromatous B. Surgery
debris and tumor - Embolectomy must be performed
- Originate in the heart, occur after with 6-10 hrs
invasive procedures - Amputation of limb
- Arteriosclerosis may cause - Exercise, prolonged ps’ning
roughening or ulceration of the (pressure skin breakdown), tight
atheromatous plaques clothing (compromise bloodflow),
- May also be associated with support hose, heat over painful area
immobility, anemia, and dehydration are C/I
- Emboli tend to lodge at bifurcations
and atherosclerotic narrowings CHRONIC
- Other causes include: trauma, I. DEFINITION
thrombus, venous outflow - Condition where there is inadequate
obstruction blood flow in arteries

IV. PATHOPHYSIOLOGY II. ETIOLOGY / RISK FACTORS

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 - 1O cause: atherosclerosis obliterans - Avoid procedures or bed positions
- Thromboangiitis obliterans that interfere with gravitational
- Cystic degeneration of the popliteal blood flow
artery - Protect the affected extremity
- Some connective tissue disorders - Instruct patient to avoid nicotine
2. Pain related to peripheral ischemia
III. PATHOPHYSIOLOGY - Assess quality and degree of pain
- Progressive narrowing caused by - Provide comfortable position
atherosclerosis - Bed mobility
- Progressive occlusion that leads to - Begin PRE’s
hypoperfusion and ischemia 3. Impaired skin integrity related to
- Arms and legs – most vulnerable impaired circulation
- Assess skin, temperature and
IV. CLINICAL MANIFESTATIONS integrity
- Intermittent claudication - Provide daily skin care
- Ischemic rest pain - Ensure that skin is thoroughly dry
- Edema - Treat ulcers if there is
- Sensory changes: numbness of foot - Medications and dressings- avoid
or toes, paresthesia adhesive tapes directly on skin
- Avoid use of tight constricting socks /
V. DIAGNOSTIC EXAMS hose
- Doppler Ultrasonography
ARTERIOSCLEROSIS OBLITERANS
VI. MEDICAL MANAGEMENT I. DEFINITON
A. Medications - Aka Chronic Occlusive Arterial dse.,
- Anticoagulants, vasodilators and Peripheral Arterial Occlusive dse.,
antiplatelets Atherosclerotic Occlusive dse
- Pentoxitylline ( Trental ) – decreases
- MC Chronic, progressive occlusion of
blood viscosity
B. Surgery peripheral circulation, most often in large &
- Percutaneous transluminal medium arteries of LE
angioplasty - Slowly developing, degenerative process
- Arterial revascularization, and manifestations occur insidiously.
reconstruction
II. EPIDEMIOLOGY
VII. EVALUATION - M>F aging 50-70 years old
 Arterial pulses - MC sites: Superior femoral artery,
- Palpation: slightly reduced or absent aortoiliac segment, popliteal artery and
- Auscultation: presence of bruits at abdominal aorta.
rest and after exercise - Major risk factors: DM, Obesity, cigarette
 Skin, nails and hair smoking, hyperlipidemia and HTN
- Ulcerations, glossy, cold, smooth
skin, pallor III. ETIOLOGY / RISK FACTORS
- Atrophic, delayed capillary refill - Hypertension
- Hair loss - Diet
- Obesity
VIII. DIAGNOSIS AND INTERVENTIONS - Sedentary lifestyle
1. Altered peripheral tissue perfusion ( - Stress
chronic) - DM
- Related to interruption of arterial - Smoking
flow- assess arterial pulses Non- modifiable
- Observe skin color changes and - Age
venous filling - Gender
- Familial predisposition

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 Modifiable
- Smoking II. EPIDEMIOLOGY
- Young males who smoke between the age of
IV. PATHOPHYSIOLOGY 20-40
- This begins with monocyte
adherence to endothelial wall III. ETIOLOGY / RISK FACTORS
following physical damage such as - Cause is unknown but believed to be an
trauma, hypertension, or immune vasculitis
biomechanical process. - Heavy smoking or chewing of tobacco
- A fatty streak develops and results in
production of an atheromatuos IV. PATHOPHYSIOLOGY
plaque in the intima of the artery. - Nicotine is very potent vasoconstrictor
- As the plaques increase in size, the - Results in vasoconstriction, arterial
lumen is narrowed and linear blood circulation to EXs, ischemia ulceration &
flow is impaired. necrosis of soft tissues

V. CLINICAL MANIFESTATIONS
V. CLINICAL MANIFESTATIONS
- Intermittent claudication
- Cold or numb sensation
- Rest pain
- Intermittent claudication
- Pale
VI. DIAGNOSTIC EXAMS
- Rudy or cyanotic
- Segmental Limb Pressure
- Skin and nail changes
- Duplex Ultrasonography
- Ulcerations
- Contrast Angiography
- Gangrene
- Muscle atrophy
VII. Medical Management
- Bruits
- Essentially same as that for Arteriosclerosis
- Unequal pulses between extremities
Obliterans
- Absence of a normally palpable pulse
Goals:
- Reestablish blood flow
VI. DIAGNOSTIC EXAMS
- Preserve the extremity
- Doppler
- Relieve pain
- Ankle- Brachial Index
- Provide sufficient blood flow for wound
- Treadmill testing
healing
- Duplex ultrasonography
- Conservative treatment; modification of risk
factors : walking, weight reduction, smoking
VII. MEDICAL MANAGEMENT
cessation, control of other conditions
- Exercise program
- Pharmacologic treatment with antiplatelet
- Weight reduction and cessation of tobacco
and anticoagulant agents
use
A. Medications
VIII. DIAGNOSIS AND INTERVENTIONS
- Pentoxithylline ( Trental )
1. Altered Tissue Perfusion (peripheral) related
- Anti-platelet aggregating agents
to decrease arterial blood flow
B. Surgery
- Perform neurovascular checks frequently
- Vascular grafting
- Inspect lower extremity or feet for new areas
- Bypass grafts
of ulcerations
- Encourage well-balanced diet
- Encourage walking or performance of ROM
BUERGER’S DISEASE (THROMBOANGITIS
exercises
OBLITERANS)
- Administer pain medications as ordered
I. DEFINITION
2. Sensory / Perceptual Alteration (tactile) of
- Chronic occlusive arterial dse. w/
lower extremity
inflammatory reaction to nicotine
- Avoid tight-fitting socks/shoes
- Manifested initially in the distal aspects of
- Avoid sitting with legs crossed
the extremities and progress proximally.

99 | P a g e
 - Avoid using adhesive tape and harsh soaps
on affected skin
- Instruct patient to check temperature or bath
water
- Perform and teach how to do foot care
3. Risk for infection related to decreased
arterial flow
- Apply lanolin or petrolatum to intact skin of
lower extremities
- Encourage to wear clean hose / socks daily
- Teach patient to:
 Trim toenails straight across after
soaking
 Place wisps of cotton under corner of
great toenail
- Teach patient signs to report:
 Redness, swelling, irritation, blistering,
foul odor
 Itching, burning, rashes
 Bruises, cuts, unusual appearance of skin
 New areas of ulceration
VASOSPASTIC DISORDER (RAYNAUD’S DISEASE)
I. DEFINITION
- Aka 1° Raynaud’s syndrome/ Idiopathic RD
- Chronic, fxnl arterial d/o with digital
vasospasm in small arteries & arterioles of
fingers & toes
- It is characterized by skin color and
temperature changes.
- Raynaud’s phenomenon: 2° complication
assoc. w/ other dses. (scleroderma, SLE,
systemic sclerosis or vasculitis
II. EPIDEMIOLOGY
- F>M (ages 16-40)
- usually in young adults and begins in early
decades of life (1st and 2nd decades)
- most often affecting the arterioles and small
arteries of the fingers.
III. ETIOLOGY / RISK FACTORS
- Caused by abnormality of SNS
- Vasospasm (exposure to cold, vibration or
stress)
- Seen most frequently in cold climates and
during winter months
IV. PATHOPHYSIOLOGY
- Occurrence of vasoconstriction due to the
release of catecholamines
Three phases:
a. Severe constriction
- Results in blanching of the fingers
- Followed by dilatation of the vessels
b. Ischemic Phase
- Fingers turn white and the cyanotic, numb
and cold
c. Hyperemic Phase
- Fingers turn red and patient experiences
throbbing pain
V. CLINICAL MANIFESTATIONS
- Coldness, pain, pallor
- Fingers- asymmetric; thumbs are less often
involved
- Characteristic color changes :
White → Blue → Red
- Ulceration of the fingertips
- Fingers become white due to lack of blood
flow, then turn blue as vessels dilate to keep
the blood in tissues, finally red as blood flow
returns
VII. MEDICAL/ SURGICAL MANAGEMENT
- Avoidance of trigger and aggravating factors
- Calcium channel blockers
- Nitroglycerin or sympatholytics such as:
 Reserpine ( Serpasil)
• guanithidine (Ismelin)
• prasozin ( Minipress)
- Anti- platelet agents
Symphatectomy- removal of sympathetic
ganglia or division of their branches
- Assist patient in avoiding exposure to cold
- Encourage patient to stop smoking
- Let patient understand the need to avoid
stressful situations
- Stress management
- Instruct regarding drug therapy
- Advise patient that episode may be
terminated by soaking hands/feet in warm
water
Pain related to hyperemic stage:
- Explain to the patient when to expect the
occurrence of pain
- Teach about self- administration of
analgesics
- Reassure patient that pain is temporary
VENOUS DISORDERS
I. DEFINITION
 Thrombus
- A composed of platelets, fibrin, clotting
factors, and cellular debris attached to
the interior walls of an artery or vein.
100 | P a g e
  Embolus
- a dislodged thrombus which may IV. CLINICAL MANIFESTATIONS
interfere with tissue perfusion in an - early stages: dull aching or severe pain,
artery or vein swelling
 Phlebothrombosis - changes in skin temp & color (heat &
- Formation of a thrombus in a vein
redness)
 THROMBOPHLEBITIS - edema in vicinity of clot (too deep to palpate)
- A condition in which a clot forms in a vein - clot in calf (distal DVT): pain or tenderness
secondary to phlebitis felt w/ passive DF of affec. foot (Homan’s
1. Superficial veins sign)
- greater or small saphenous veins *Pulmonary Embolism S/Sx
- in calf is small & resolves w/o serious - hallmark: sudden onset of SOB (dyspnea),
Consequences rapid & shallow breathing (tachypnea), pain
2. Deep veins
@ lat aspect of chest ( w/ deep breathing &
- popliteal, femoral, iliac veins
coughing)
 DEEP VEIN THROMBOSIS (DVT) - other s/sx: swelling in LE, anxiety, fever,
- Occurs in calf or more proximally in thigh or excessive sweating (diaphoresis), cough &
pelvic region blood in sputum (hemoptysis).
- Larger & cause serious complications V. MEDICAL MANAGEMENT
- Dislodge & travel proximally as embolus Goals: To prevent propagation of the thrombus,
pulmonary embolism (life-threatening) prevent recurrent thrombus formation, prevent
pulmonary emboli, and limit venous valvular
damage
II. ETIOLOGY / RISK FACTORS
A. Medications
• Pacing wires
- Anticoagulation
• Central venous catheters - For documented cases of DVT
• Local vein damage • Heparin is given IV initially, followed
• Repetitive motion injury by 3 to 6 months of oral
• Venous stasis anticoagulant therapy
• Obesity
• Varicosities VENOUS INSUFFICIENCY/STASIS
• Age (over 65 y/o)
• Coagulopathy CHRONIC VENOUS INSUFFICIENCY
• Pregnancy I. DEFINITION
• Oral contraceptives - a.k.a. postphlebitic syndrome
• Polycythemia - Is a form of chronic venous stasis
• Septicemia - Inadequate venous return over a prolonged
• Post-op or post-fx immob period of time.
• Prolonged bed rest - May begin after severe episode of DVT
• Limb paralysis - Assoc. w/ varicose veins, result of trauma to
• Active malignancy (w/in past 6 mos) LE or blockage by neoplasm
• History of DVT or pulmonary embolism
• Sedentary lifestyle or extensive episode of II. EPIDEMIOLOGY
- Commonly involves iliac and femoral veins
sitting during long-distance travel
and occasionally saphenous vein
• CHF -
III. ETIOLOGY/RISK FACTORS
III. PATHOPHYSOLOGY - Follows most severe cases of deep vein
 Virchov’s Triad thrombosis, although it may also occur as a
- Stasis of blood result of:
- Injury to vessel wall
- Leg trauma
- Altered blood coagulation
- Varicose veins
101 | P a g e
 - Neoplastic obstruction of the pelvic veins
- Valvular incompetence
- Long term sequelae may be chronic leg
ulcers
- Risk factors
• Poor nutrition
• Immobility
• Local trauma
• Previous history of burns
III. PATHOPHYSIOLOGY
- Damaged/destroyed valves in veins →
Decreased venous return → Increased
venous pressure → Venous stasis →
inadequate valve function and absence of
calf muscle pump → Blood flows in veins
bidirectionally → High ambulatory venous
pressures in the calf veins → Dilation of
superficial veins and capillaries → RBCs,
proteins, fluids leak out of the capillaries
into interstitial spaces → Edema and reddish
brown pigmentation
- Chronic pooling inadequate oxygenation
of cells & removal of waste products
necrosis of tissues & venous stasis ulcers
IV.CLINICAL MANIFESTATIONS
 Venous stasis ulceration
 Dermatitis and cellulitis may develop later
in the condition
 dependent peripheral edema w/ long periods of
standing/ sitting
 edema w/ elev
 dull aching or tiredness in affected EX
 w/ varicose veins: venous distention (bulging)
 edema persists: less supple skin & brownish
Pigmentation
V. DIAGNOSTIC EXAMS
1. Doppler ultrasonography
2. Venous Duplex screening/scanning
3. Venography/ Phlebography (invasive)
VI. MEDICAL MANAGEMENT
- Avoid complications that can occur with
vascular ulceration and chronic wounds
- Plan of care essentials:
• Formulating and exercise
prescription
• Collaborating with a
nutritionist
- Gold standard for treatment of venous
insufficiency especially with (+) venous leg
ulcers: Compression therapy
• Goal is to promote venous
return to central circulation
VARICOSE VEINS
I. DEFINITION
- An abnormal dilation of veins leading to
tortuosity of the vessel, incompetence of
the valves and a propensity of thrombosis
II. EPIDEMIOLOGY
- Women > Men (Secondary to pregnancy)
until 70 years old: Men = Women
- Develops between the ages of 30-50 years
III. ETIOLOGY/RISK FACTORS
- Congenital valve or vein wall defects
- Risk factors:
• Heavy lifting
• Prolonged sitting or
standing
• Hormonal changes
(pregnancy, menopause,
hormonal therapy)
o Relaxes vein walls
• Pressure associated with:
o Pregnancy
o Obesity
o Heart failure
o Hemorrhoids
o Constipation
o Esophageal varices
o Hepatic cirrhosis
-Loss of vein elasticity with aging
IV. PATHOPHYSIOLOGY
- Incompetent valve → Unable to withstand
normal pressure → Pooling of blood →
Veins dilate and lose their elasticity → More
blood collects in the veins → Veins become
more swollen and dilated
-Vein dilation → prevents the valve cusps
from meeting → increased backup pressure
in lower vein segments
-The combination of vein dilation and valve
incompetence produces the varicosity
V.CLINICAL MANIFESTATIONS
- May be asymptomatic
- Development of varicosities is usually
gradual
102 | P a g e
 - Most common symptom: dull, aching • Frequent changes in
heaviness, tension or fatigue brought on by posture
periods of standing • Daily exercise program
- Cramps of lower legs may occur especially • Appropriate use of properly
at night; elevation often provides relief fitting elastic stockings
- Visible signs: Dilated, tortuous, elongated - - Surgery for severe cases
veins beneath the skin readily visible when • May be considered for
standing ulceration, bleeding, and
• Secondary tissue changes: cosmetic purposes
Thinning of skin above the A. Sclerotherapy
ankle, swelling around the (injection of hardening solution)
ankles B. Ligation and
- Untreated veins become thick and hard to stripping of the greater and lesser saphenous vein
touch C. Venous
VI. Diagnostic Examinations reconstruction or venous valvular transplant
1. Visual inspection and palpation D. Laser therapy
2. Doppler ultrasonography / duplex scanner (to (non-invasive use of near infrared wavelengths)
detect location of incompetent valves) VII. PROGNOSIS
3. Venous outflow and reflux plethysmography - Early conservative care during initial stages
4. Ascending and descending venography may help condition from worsening
VII. MANAGEMENT - Advanced disease may not be prevented
- Conservative therapies for mild cases from recurring
• Periodic daily rest periods - Surgery can improve appearance but may
• Elevate feet above the level not reduce physical discomfort
of the heart - High mortality associated with ruptured,
• Client education of bleeding esophageal varices
promoting circulation

DIFFERENTIAL DIAGNOSIS FOR PERIPHERAL VASCULAR DISEASES

ARTERIAL VENOUS
Etiology Arteriosclerosis Obliterans Thrombophlebitis
Atheroembolism Trauma, vein obstruction
Risk Factors Smoking Venous hypertension
Diabetes mellitus Varicose veins
Hyperlipoproteinemia Inherited trait
Hypertension
Signs and Symptoms
Pain Severely ischemic (intermittent claudication) Minimal to moderate steady pain
Rest pain = severe involvement Aching pain in lower leg with prolonged
Muscle fatigue, cramping, numbness standing or sitting (dependency)
Paresthesias over time Superficial pain along course of vein

Location of Pain Calf, lower leg or dorsum of foot, thigh, hip or Muscle compartment tenderness
buttock
Skin changes Loss of hair on leg & foot, nails are thickened Brown pigment around ankles (hemosiderin
and ridged, dry skin staining)
Lipodermatosclerosis, fibrosis of the dermis
Temperature Cool Increase in skin temperature of lower legs
Color Pale on elevation; dusky red on dependency Normal or cyanotic on dependency

Peripheral pulse Diminished or absent Normal

Edema Absent or mild Present (U/B), relieved by elevation

103 | P a g e
 Ulcers LEs: lateral malleoli, dorsum of feet, toes or Sides of ankles, especially on medial
areas of trauma malleolus
-necrotic and pale wound base; lacking (+) Granulation tissue in wound bed
granulation tissue wet from large amt of draining exudate
Gangrene May develop (dry)- black mummified Absent
Others itching, fatigue, heaviness

LYMPHATIC DISORDER: LYMPHEDEMA

o Disease Infection
I. DEFINITION and
- Swelling of the soft tissues that results from Inflammation
the accumulation of protein-rich fluid in the
o Chronic Venous
extracellular spaces
Insufficiency
- Caused by decreased lymphatic transport o Tumor
capacity and/or increased lymphatic load o Filariasis
- Seen in the extremities but can occur in the
head, neck abdomen and genitalia
- Obstruction may be in both the lymph IV. CLINICAL MANIFESTATION
nodes and the lymphatic vessels - Swelling distal to or adjacent to the area
II. CLASSIFICATION of impaired lymph system function &
∗ Primary not relieved by elevation
- Congenital or hereditary o Pitting edema
- lymph node or lymph vessel formation is - early stages
Abnormal - Pressure on the edematous
area causes an indentation of
- MC abnormality: hypoplasia, a condition
the skin that persists for several
in which there are fewer lymphatic
seconds after pressure is
vessels and they are smaller than normal
removed.
- One of the more common forms of
o Non-pitting edema
primary lymphedema appears in
- later stages as fibrotic changes
Milroy’s disease.
occur
∗ Secondary
o Brawny edema
- Acquired: surgery and/or radiation
- Pressure on edema feels hard
therapy as part of breast CA tx
with palpation
- More prevalent than primary l.
o Weeping edema
- caused by injury to one or more
- Fluid leaks from cuts and sores
components of the lymphatic
- Feelings of fatigue, heaviness, pressure
system: some portion of the
or tightness in the
lymphatic system has been blocked,
affected region
dissected, fibrosed, or otherwise
- Numbness and tingling
damaged or altered
- Discomfort varying from mild to intense
III. EPIDEMIOLOGY - Fibrotic changes of the dermis
-700,000 people in the Americas - Dermal abnormalities such as cysts,
- 30% of breast cancer survivors fistulas, lymphorrhea,
-Females > Males, 4:1 papillomas, hyperkeratosis
- Incidence increases after surgery and - Increased susceptibility to infection
radiation (first local to affected regionsystemic)
- Loss of mobility
o Trauma and ROM
IV. ETIOLOGY - Impaired wound healing
o Surgical Dissection of Lymph
- Primary Lymphedema: Node
o Unknown V. MEDICAL MANAGEMENT (Radical Mastectomy,
o Hereditary -Bed rest with leg elevation
femoro
o Developmental abnormality -Active and passive exercises
-popliteal by-pass)
-Secondary Lymph Edema: -Complete o Decongestive
Radiation therapy
• Phase I (intensive)
skin care 104 | P a g e
 MLD UE: radial, ulnar & brachial pulses
lymphedema - compare w/ good & bad sides
bandaging
exercise
MLD as needed
compression - normal, diminished, absent
garment at the
- strength rated from 0 to +3
end
• Phase II (self- - (+) pulselessness is a sign of severe
PULMONARY CONDITIONS
management) arterial insufficiency
skin care  Skin Temperature
compression - cool to touch
garment - use electronic thermometer
 Skin Integrity and pigmentation
-External compression o Diminished arterial blood flow
devices causes tropic changes in the
-Elastic stockings skin peripherally characterized
-Diuretics by dryness, diminished color
-Surgical debulking (pallor), hair loss, shiny or waxy
-Excision: Transfer of appearance of skin and
superficial ulcerations
lymphatics to deep lymphatic  Test for rubor/reactive hyperemia
system by buried dermal flap o Patient is supine, noting the
color of the soles of the feet
V.PROGNOSIS o Legs are then elevated 45
Without treatment, the protein- degrees
rich interstitial fluid is replaced by o Pallor or blanching of the skin
fibrinoid material. Inflammatory cells will occur in the feet within 1
accumulate and progressive fibrosis minute or less if arterial

Stage 0 Stages ofStage I

Lymphedema Stage II Stage III
(Latent (Lymphostatic
Lymphedema) Elephantiasis)
Lymph Transport reduced Accumulation of Accumulation of Accumulation of
protein-rich lymph protein-rich lymph protein-rich lymph
with significant
increase in
connective and
scar tissue
Edema (-) Pitting edema Non-pitting with Severe non-pitting
Increases with connective scar fibrotic edema
activity, heat and tissue
humidity
Reversibility of Edema N/A With elevation, Does not resolve Irreversible
may be normal in overnight,
the morning increasingly more
difficult to pit
Skin Changes N/A N/A Present in severe Atrophic
case (hardening of
dermal tissue, skin
folds, skin
papillomas,
hyperkeratosis)
circulation is poor
o Legs then placed to dependent
position
o Pinkish flush appears in the feet
PT EXAMINATION after several seconds
o Color changes may occur more
ARTERIAL than 30 seconds and will be
 Palpation of pulses bright bluish-red or rubor.
- in the distal portion of the extremities: Alternate procedure:
LE: femoral, popliteal, dorsalis pedis & - temporarily restrict blood flow to distal EX
post. tibial

105 | P a g e

w/ BP cuff (accumulation of CO2 & lactic
acid- vasodilators)
- when release cuff, N°: hyperemia/flushing
in
10 secs (Raynaud’s dse. ) w/ AVD: 1-
2mins
of flush to appear
 Claudication time
o Objective is to determine the
amount of time a patient can
exercise before experiencing
cramping and pain in the distal
musculature
o Common test is to have patient walk
on a level treadmill (1-2mph). Period
walk, before claudication prohibits
further activity is recorded
 Ankle-Brachial Index (ABI)
- Results provide useful information
about the potential loss of perfusion in
the LEs.
VENOUS
 Girth measurements of the extremity
- landmarks 8-10cm apart
 Brodie-Trendelenburg test
– determine the competency of the valves in
the deep and superficial veins of the legs in
patients with varicose veins
 Percussion test (competence of greater
saphenous vein)
– for patients with varicose veins
 Homan’s sign
- test for DVT
- pt. supine, knee ext: passively DF ankle &
gently squeeze calf muscles
- (+) pain in calf (DVT)
 Application of blood pressure cuff @ calf
muscle
- inflate cuff slowly ‘til pt. experiences
calf
pain
- w/ acute thrombophlebitis: not
tolerate
40mmHg
LYMPHATIC
 History & Systems Review
- infection, trauma, surgery or radiation
therapy
- onset & duration, delayed wound healing
- occupation & daily axs (long p. sit/stand)
 Exam of Skin Integrity
- visual inspection & skin palpation
- areas of pitting, brawny or weeping edema
- tenderness of nodes
- shiny & red
 Girth measurement
- circumferential measurement
 Volumetric measurement
- immerse limb in tank & measure H2O
displaced
 Palpation to distinguish between pitting or
non-pitting edema
PROBLEM LIST
• Impaired range of motion of involved
extremities
• Edema
• Presence of or risk of skin breakdown
• Impaired mobility
• Impaired endurance
• Impaired respiratory status
• Impaired balance
• Impaired strength
• Knowledge deficit regarding precautions,
activity progression, healing process
• Pain
• Sensation deficits
PT DIAGNOSIS
CP 8: Impaired circulation and anthropometric
dimensions associated with lymphatic system
disorders
INTERVENTIONS WITH RATIONALE
ARTERIAL
 Pt. education
 Putting the extremity on dependent position
to promote gravity assisted arterial blood
flow
- Sleep w/ legs over edge of the bed or
head of bed in slight elevation
 Avoid wearing compressive garments to
prevent obstruction of blood flow
 Wound care for ulcerations and skin
breakage to prevent infections - ES, oxygen
therapy
 Weight control & salt, sucrose, cholesterol
& caffeine intake, quit smoking
 Aerobic conditioning (walking, bicycling)
 Proper nail care, shoe selection & fit
 Avoid hot/cold
 Iontophoresis & reflex heating –
vasodilation
 AROM, gentle stretching
PREVENTION OF DVT & THROMBOPHLEBITIS
1. Prophylactic use of anti-coagulant therapy
(high-
molecular- heparin)
2. Immediate post-op ambulation (X >1 or 2 days)
3. Elevate legs in supine & on footstool/ottoman
if in
sitting
4. No prolonged periods of sitting (w/ long-leg
cast)
106 | P a g e
5. Active ankle pumping ex (DF, PF,
Circumduction)
throughout the day in supine
6. Use of compression stockings to support the
walls
of veins & venous pooling
7. Use Sequential Pneumatic Compression Unit
(bedrest)
PT MANAGEMENT FOR DVT & temp
THROMBOPHLEBITIS
• Bed rest
• Systemic Anti-coagulant therapy
• Elevation w/ knee slightly flexed
• Ambulation w/ legs wrapped in
elastic/non-elastic bandages or pressure
stockings
NOTE: PROM/AROM, moist heat, sequential
pneumatic compression pump are C/I
PT MANAGEMENT FOR CHRONIC VENOUS
INSUFFICIENCY & VARICOSE VEINS
• Pt. education & HEP
• Self skin care, massage (lymphedema)
• Pressure stockings in the morning & all
day
• Support garment during exercise &
ambulation
• Elevate LE after ambulation ‘til heart rate
normalizes
• Avoid prolonged sitting & standing w/
legs in dependent position
• Elevate legs (30-45°) when at rest or
sleep
• Use intermittent mechanical
compression pump & sleeve w/ leg
elevated several hrs. a day
• Manual massage (distal to proximal)
- clear proximal nodes & lymphedema
areas
1stmiddledistal
• Relax & active pumping ex w/ legs
elevated
• Proper skin care (prevent wounds)
PREVENTION OF LYMPHEDEMA
*Avoid static dependent positioning of LE (long
periods of sit/stand)
*Avoid sitting w/ legs crossed
*Elevate involve limb & do repetitive pumping ex
*Avoid carrying heavy loads or weights. during ex
*Wear compressive garments during exercise
*Avoid wearing tight
clothing/jewelries(ring/watch)
*Monitor diet to maintain ideal weight & Na
intake
*Avoid hot environments or use of local heat
*Avoid taking BP/injections on involve EX
Skin Care
*Keep skin clean & supple (moisturizers, avoid
perfumed lotions)
*Avoid infections
*Protect hands & feet (socks, hose, shoes, gloves,
mitts)
*Avoid contact w/ harsh detergents & chemicals
*Caution if cut nails (F: electric razor for legs &
armpit)
*Avoid hot baths, whirlpools & saunas- body
PT MANAGEMENT OF LYMPHEDEMA
(Decongestive LT)
1. Elevation
2. Manual lymphatic drainage (massage)
o direct intervention by PT
o self-massage by pt.
3. Compression
o nonelastic/low stretch bandages or
custom-fitted garments
o intermittent, sequential pneumatic
compression pump
4. Individualized ex program
o AROM (pumping ex)
o Stretching
o Low- intensity resistance ex
o Cardiovascular conditioning
5. Skin care & daily living precautions
EXERCISES FOR MANAGEMENT OF LYMPHEDEMA
1. Deep Breathing & Relaxation Ex
2. Stretching
3. Strengthening & Muscular Endurance Ex
4. Cardiovascular Conditioning Ex
5. Lymphatic Drainage Ex
UE &LE
- Deep breathing & total body relaxation ex
- Posterior pelvic tilts & partial curl-ups
- Cervical ROM
- Bilat Scapular mov’ts
UE
-Active circumduction w/ arm elevated in supine
- Bilat active mov’ts of arms in supine/foam roll
- Shoulder stretches (w/ wand, doorway and
towel) while standing
-Active elbow, FA, wrist & finger ex of involved arm
- Bilat horizontal Abd & Add of shoulder
- Overhead wall press while standing
- Finger ex
- Partial curl- ups
- Rest w/ involved UE elevated
LE
-Alternate knee to chest ex
- Bilat. Knees to chest
- Gluteal setting & posterior pelvic tilts
-Single knee to chest w/ involved LE
- Hip ER in supine w/ both legs elevated & resting on
wedge/wall
-Active knee flexion of involved LE in supine
-Active PF, DF & circumduction of ankles in supine w/
LEs elevated
-Active hip & knee flexion w/ legs in ER & elevated
against wall 107 | P a g e
-Active cycling & scissoring mov’ts w/ legs elevated
-Bilat knee to chest ex then partial curl- ups
-Rest w/ LE elevated
 PULMONARY CONDITIONS
Chronic Lung Diseases
Chronic Obstructive Pulmonary Disorder
Asthma
Cystic Fibrosis
Respiratory Lung Diseases
GENERAL MEDICAL BACKGROUND
Definition
• Ventilation: Movement of air through the
conducting airway
 TLC – full inspiration, lung capacity, lung
contains maximum amount of gas
 Tidal Volume (TV): Amount of air
inspired and expired during normal
resting ventilation
 Inspiratory Reserve Volume (IRV):
Volume of air that can be inspired
when needed, but is usually kept in
reserve
 Expiratory Reserve Volume (ERV):
Kept in reserve, the volume of air
that can be exhaled in excess of tidal
breathing
 Functional Residual Capacity (FRC):
Combination of residual volume and
expiratory reserve volume; volume
of air that remains in the lungs at
the end of a tidal exhalation
 Residual Volume (RV): Volume of air
remaining within the lungs when
ERV has been exhaled
 Inspiratory capacity (IC): Sum of 2 or
more volumes; volume of air that
can be inspired beginning from a
tidal exhalation.
 Vital capacity: Total volume of air
within the lungs that is under
volitional control
 Forced Expiratory Volume in 1 second (FEV):
Important airflow measurement is the volume of
air that can be fully exhaled during the first
second of a first second of a forced vital capacity
 Maximum Inspiratory Pressure (PI max): Reflects
the greatest static inspiratory effort that can be
generated from residual volume; reflects the
strength of muscle of inspiration
 Maximal Sustained Inspiratory Pressure
(SIPmax): A test of inspiratory muscle endurance
• Respiration: Gas exchange within the body
 External Respiration: Exchange of gas that
occurs at the alveolar capillary membrane
between atmospheric air and the pulmonary
capillaries
 Internal Respiration: Takes place at the
tissue and the surrounding capillaries
CO2: Produced at tissue level as a by-product of
metabolism, diffuses out of the working cells
and into the capillaries
Classifications
Chronic Lung Diseases
 Chronic Obstructive Pulmonary Disorder
(COPD)
Definition
- MC chronic pulmonary d/o
- GOLD definition “Disease state
characterized by airflow limitation that
is not fully reversible.”
Epidemiology
- Affecting 14 million adults in the United
States and leading cause of morbidity
- 4th leading cause of morbidity
Risk factors
- Both host factors and environmental
factors
- Hyperactivity of the airways, overall lung
growth and genetics
- Alpha-1 antitrypsin deficiency/well know
genetic cause of COPD
- Environmental factors: Cigarette
smoking (primary and secondary Tabaco
smoking), major environmental
occupation exposures; indoor and
outdoor pollutants
Pathophysiology
- Airway narrowing, parenchymal
destruction and pulmonary vascular
thickening
- Chronic Inflammation: ↑ neutrophils,
macrophages and T-lymphocytes
damages the endothelial lining of the
airways.
- The airways are pulled open wide by
thoracic expansion, allowing air to enter.
During exhalation the airway narrowing
from inflammation, remodeling and
excessive secretions, caused premature
airway closure trapping air in the distal
airways (Hyperinflation)
- MC parenchymal changes in COPD:
dilation; destruction of the respiratory
bronchioles tissue.
- Ventilation in the alveoli and perfusion
in the capillary membrane hypoxemia ↓
amount of oxygen is carried by the
blood to the tissues.
108 | P a g e
 Hypercapnia- ↑ amount of CO2
within the arterial blood
CorPulmonale - ↑ pulmonary
vascular resistance 2⁰ to
capillary wall damage and
destruction and reflex
vasoconstriction in presence of
hypoxemia and hypercapnia →
(R) ventricular blood cells,
another complication of
advance COPD.
Clinical Presentation
- Chronic cough, expectoration and
exertional dyspnea
- Cough and expectoration appear slowly
and insidiously
- Dyspnea: 1st evidence during exertion
- Physical examination
• Thorax appears enlarged
owning to loss of lung elastic
recoil
• A-P diameter of the chest ↑
and dorsal kyphosis is noted.
• Barrel chest appearance
• Diaphragm becomes flatter/ less
domed
- Breath sounds and heart sounds may be
distant and difficult to hear
- Partially obstructed bronchi and
bronchioles may result in expiratory
wheezing
- Hypertrophy of accessory muscles of
ventilation, pursed-lip breathing
cyanosis and digital clubbing
- Lung volumes and capacities are RV and
FRV are increased from the normal
values due to air trapping
- With disease progression:
• Depressed and flattened
diaphragm
• Alteration in pulmonary vascular
markings
• Hyperinflation of the thorax
• Evidence of ↑AP diameter of
the chest
• ↑in size of retro spinal airspace
• Hyperlucency
• Elongation of the heart
• (R) ventricular atrophy
Prognosis
- Insidious onset with a disease
progression that can run for many years.
- Smoking (most relevant risk factor)
 Asthma
Definition
- Common chronic pulmonary disease
- Characterized by episodic periods of
reversible airway narrowing in the
presence of aero allergens, irritants or
exercise
Epidemiology
- Affecting approximately 14.9 million
persons
Etiology
- Airway narrowing is due to
inflammation, smooth muscle,
bronchospasm and increased airway
secretions
- Airway hyper reactivity
- Genetic predisposition
- Indoor and outdoor environmental
irritants
- Infections
- Active airway inflammation
Pathophysiology:
- Cold environment or other irritants,
infections or cigarette smoke.
- Eosinophillic inflammation of bronchial
mucosa, bronchospasm, increase
bronchial secretions→ narrowing of
airways → hyperinflation
Clinical Presentation:
- Cough, dyspnea and wheezing during
quiet or forced exhalation
- Chest is usually held in expanded
position during acute exacerbation
- Use of accessory muscles of ventilation
for breathing
- Intercostal, supraclavicular and
substernal reactions present on
inspiration
- Wheezing during expiration; crackles
may be present
- Breath sounds markedly decrease and
wheezing may be present during
inspiration with severe airway
obstruction.
- Chest radiographs show increase in AP
diameter of chest and hyperlucency of
lung field; may also show areas of
infiltrates or atelectasis
- ↓ FEV1, ↑ residual volume, ↑
functional residual capacity, ↓ VC, ↓
IRV
109 | P a g e
- Mild to moderate hypoxemia which may
lead to hypercapnia and finally to
respiratory failure
Diagnosis
- History of episodic wheezing, SOB,
tightness in chest and or coughing which
may be worse at night in the absence of
any other obvious cause
- FEV1 < 80%
- Inhaled short acting beta2 agonist
improves at least 12% in FEV1
Prognosis
- Children with symptoms of asthma no
longer have the symptoms during
adulthood
- When onset of symptoms begins later in
life, clinical symptoms is usually
progressive
 Cystic Fibrosis (CF)
Definition
- Affects the excretory gland of the body
making secretions thicker. More viscous
affecting pulmonary, pancreatic,
hepatic, sinus and reproductive system
of the body
- Thickened pulmonary secretions will
narrow or obstruct airways leading to
hyperinflation, infection, and tissue
destruction
Etiology
- Autosomal recessive of CF gene ( cystic
fibrosis transmembrane regulator or
CFTD) on the long arm of chromosome 7
- CFTR functions as a chloride channel in
epithelial cells with more than 1000
mutations grouped into 6 different
classes.
- MC defects in class 2 = defective
processing
Epidemiology
- 1 in 2500 live births
- Caucasians make up 94.6% of all cases
of CF in US, less common in Hispanic
and rare African-American population
Pathophysiology
Abnormally viscous
mucus secreted by
tracheobronchial
tree Clinical
airway obstruction uneven ventilation
and hyperinflation and perfusion
reduces ventilation fibrotic changes in
to alveolar units lung parenchyma
Presentation
- Failure to thrive due to gastrointestinal
dysfunction
- Diabetes due to pancreatic dysfunction
- Frequent respiratory secretions
- Thick bronchial secretions
- “Barreled with an increased AP
diameter; ↑ dorsal kyphosis
- Hyperinflation
- ↓ breath sounds with adventitious
sounds of crackles and wheezes
- Hypertrophy of accessory muscle of
ventilation, pursed-lip breathing,
cyanosis and digital clubbing
- ↓ FEV1, ↓ FVC , ↑ RV, ↑ FRC causing
hypoxemia and hypercapnia leading to
destruction of alveolar capillary network
causing pulmonary hypertension and
corpulmonale; may lead to atelectasis
Diagnosis
- Positive family history of the disease
with re-current respiration infections
from staphylococcus aureus and
pseudomonas aeruginosa or with
recurrent respiratory infections from
staphylococcus aureus and
psedumonasaeruginosa or with a dx of
malnutrition and or failure to thrive
- Chloride concentration of 60 mEq/L-
found in sweat or children
- Genotyping of CFTR mutations
Prognosis
- Majority of patients survive into
adulthood since life expectancy
continues to increase due to early
diagnosis and improve medical
management.
- Most frequent COD: respiratory failure
- Treatment includes removal of
abnormal secretions and prompt
treatment of pulmonary infections
110 | P a g e
 - GI dysfunction from CF can be aided by
proper diet, vitamin supplements and
replacement of pancreatic enzymes
- Aerobic fitness is strong correlate with 8
year survival
- Nutritional status is also a powerful
predictor of prognosis
Respiratory Lung Diseases
Definition
- Difficulty in expanding the lungs and a
reduction in lung volume
- Restriction come from diseases of the
alveolar parenchyma and/ or pleura
- Changes in the chest wall or an
alteration in the neuromuscular
apparatus of the thorax
Etiology
- Radiation therapy
- Inorganic dust
- Inhalation of noxious gases
- Oxygen toxicity
- Asbestos exposure
- May be idiopathic
Clinical Manifestation
- Dyspnea
- Non-productive cough
- Weakness and early fatigue
- Rapid, shallow breathing
- Limited chest expansion
- Crackles
- Digital clubbing
- Cyanosis
- Chest radiographs reveal: interstitial
markings with ground glass appearance,
honeycombing, visible interlobular
bronchioles, fibrotic consolidation
- Pulmonary function test reveals: ↓ VC,
FRC and TLC; residual volume may be N⁰
or near normal and expiratory flow rates
remain near N⁰
- Arterial blood studies: hypoxemia and
hypocapnia
- Exercise lowers oxygenation
Prognosis
- Slow onset but is chronic and
progressive in nature
- Survival depends on the type of
restrictive disease, the etiologic factors
and treatment
- Chest radiographs are insensitive
indicators of the extent of the disease
chronic inflammation
ang a thickening of hypoxemia and cor
the alveoli and pulmonale
interstitium
distal airspaces
become fibrosed
reduced lung volumes
- Hypercapnia indicates the terminal
stage of pulmonary fibrosis
Medical management
- Smoking cessation – indicates many
types such as education, behavior
modification, “ cold turkey”, diversion
therapy, aversion therapy, nicotine gum
use
- Pharmacological agents
- Use of supplemental oxygen: Used in
patients with limited ability to exercise
due to dyspnea
Pharmacologic Management
- Maintenance Drugs: Used to reduce or
minimize pulmonary symptoms
throughout the day
• Anticholinergic: Promotes
airway smooth muscle
relaxation, thus promoting
bronchodilation
• Long acting Beta 2 agonist:
Block smooth muscle
constriction promoting
bronchodilation
• Steroids: Mainstay of medical
management of the chronic
eosinophilic inflammation of
asthma
• Cromolyn Sodium: Prevent
inflammatory response by
stabilizing the mast cell within
the alveolar units
• Leukotriene Antagonist: Reduce
airway inflammation and relax
airway smooth muscle
• Rescue Drugs: Used for a more
immediate relief of breakthrough
symptoms
 Short acting beta 2 agonist –
bronchodilation
• Antibiotics: Used to interfere with the
growth and proliferation of bacteria;
bacteriostatic or bactericidal in action
General Healthcare Management
- Surgical Management
111 | P a g e
 • Lung Volume Reduction Surgery:
Removes nonfunctional, over
distended lung tissue to restore
normal biomechanics of the thorax
• Lung Transplantation: Restore
normal lung function, restore
normal exercise capacity and
prolong life
Physical Therapy Management
Goals and Outcomes
- Increase understanding of patient and
family of disease process, expectations,
goals and outcomes
- Increased cardiovascular endurance
- Increased strength, power and
endurance of peripheral muscles
- Improved performance of physical tasks,
both basic activities of daily living and
instrumental ADL
- Increased strength, power and
endurance of ventilator muscle
- Improved independence in airway
clearance
- Decreased work of breathing
- Improved decision making ability
regarding the use of health care
resources
- Enhanced self- management of
symptoms and self-management of
pulmonary disease
Points of Emphasis on Examination
- Patient History
Chief complains – SOB and for loss of
function
Medical History of cough, sputum
production, wheezing, SOB
Occupational, social, medication, and
family histories
- Test and Measures
Vital signs – temperature and resting BP,
HR and RR
Height should be measured as there is a
direct relationship between height and
lung volume
- Weight
- Observation, inspection and palpation
• Use of accessory MS for
ventilation
• Normal configuration of the
thorax
• Cyanosis
• Digital clubbing of fingers and
toes
- Auscultation of the lungs
• Normal and abnormal intensity
of the breath sound, any
additional sounds and vibration
• Adventitious breath sounds and
crackles
- Strength
• Peripheral and/or ventilator
muscle weakness
- Laboratory tests
• Radiology
• Pulmonary function test
• Graded exercise test
• Arterial blood gas analysis
• Oxygen saturation
measurements
• Electrocardiograms
- Exercise testing in patients with
pulmonary disease
• Determine the functional
capacity of the patient
- Graded exercise test
 Provides the following
information:
1. Document a patient’s
symptomatology and
physical impairment
2. Prescribe safe exercise
3. Document changes in
oxygenation during
exercise and determine
the need for
supplemental oxygen
4. Identify any changes in
pulmonary function
during exercise
intervention
 Walk test (6-12 minutes) –
ambulate as far as possible
in the allotted time
 10-M shuttle test – walking
between two markers, 10m
apart at increasing walking
velocities, which are
synchronized to an auditory
signal or metronome
 Cycle Test
- Begin at 100 kpm, increase
100 kpm every minute (Jones)
- Begin at 100 kpm, increase
100kpm every minute or 50
kpm if FEV, is <1 L/S (Berman)
 Treadmill Test
- Begin at 1.7 mph, 10%
treadmill grade; increase both
speed and grade every 3
minutes
112 | P a g e
 - Begin at 1.2 mph, 0% grade;
increase both speed and
grade every 2 minutes
- Begin at constant speed of 3.3
mph, increase grade 3.5 %
every minute
- Exercise Prescription
• Mode
 Sustained aerobic exercise
 Walking, jogging,
throwing, cycling,
swimming
 Arm ergometer,
free weights
• Intensity
 Three parameters; oxygen
consumption, heart rate and a
rating of perceived exertion/
SOB
• Duration
 At least 20-30 minutes
 Varies according to patient
tolerance
 Frequent rest periods can be
interspersed with exercise to
accomplish a total of 20 to 30
minutes of discontinuous
exercise
• Frequency
 Dependent on the intensity that
can be achieved and the
duration that can be maintained
 3-5 evenly spaced workout per
week if 20 to 30 mins. of
continuous aerobic exercise can
be accomplished
 More frequent exercise sessions
are recommended for pt’s with
lower function abilities
 One to two daily sessions for
pt’s with very low functional
work capacities
- Pulmonary Rehabilitation
- Aerobic Training
Components:
 Check in – taking of VS,
resting heart rate,
respiratory rate, and blood
pressure, auscultation and
weight
 Warm-up – slowly increase
HR and BP to prepare
cardiovascular system for
aerobic exercise
 Aerobic exercise – aerobic
activity lasting for at least
20 minutes at an
appropriate intensity
 Cooling down period – 5-10
minutes of low level aerobic
training period to slowly
return the cardiovascular
system to near pre-exercise
levels
- Strength training: Use similar modes of
exercise as the endurance training with
a change to higher resistance and lower
repetitions, or weight training of the
involved muscle
- Exercise Progression: Appropriate when
the individual perceives the intensity of
the exercise session to be easier or
when the same exercise intensity is
performed with a lesser degree of
shortness of breath and lower HR
- Program Duration – conditioning
exercises are conducted up to 3x/
week over a course of 6 to 8 weeks
- Home Exercise Programs
• Can begin with participant is in
outpatient pulmonary
rehabilitation program
• Participant can be assigned
exercise activities to be done at
home
• Patient returns to the clinic with
an exercise log containing HR,
RPE’s, exercise parameters and
any problems that may have
occurred during the home
program.
- Patient education
• Anatomy and physiology of
respiratory disease
• Airway clearance techniques
• Nutritional guidelines
• Energy- saving techniques
• Stress management and
relaxation
• Benefits of being smoke free
• Impact of environmental factors
on COPD
• Pharmacology/ use of MDIs
• Oxygen delivery systems
• Psychosocial aspects of COPD
• Diagnostic techniques
• Management of COPD
• Community resources
113 | P a g e
 • Exercise: Effects,
Contraindications, adherence
- Secretion Removal Techniques
• Postural Drainage
 Positioning a patient so that
bronchus of the involved
lung segment is
perpendicular to the ground
 Gravity assists the
mucociliary transport
system in removing
excessive secretions from
the tracheobronchial tree
• Percussion
 Forced rhythmically applied
with the therapists cupped
hands to patient’s chest wall
 Applied to a specific area on
thorax that corresponds to
an underlying involved lung
segment
 3-5 minutes over each
involved lung segment
• Shaking
 Following a deep inhalation,
a bouncing maneuver is
applied to the rib cage
throughout the expiratory
phase of breathing
 5-7 trials are appropriate to
hasten the removal of
secretions
 Commonly used following
percussion
• Airway Clearance
 Done after secretions are
mobilized
o Coughing
o Huffing
• Active cycle of breathing
techniques
 Independent breathing
exercise program that
includes breathing control
phase, thoracic expansion
exercises, and the forced
expiratory techniques
 Deep inhalations with a 3-
second hold followed by a
passive elongation and
performed next
• Oral airway oscillation devices
 Pt. inhales a breath, approx.
¾ of his or her vital capacity,
and holds it for 2 or 3
seconds
 During active exhalation
through the device, the
exhaled air causes an
intermittent backward air
pressure that jars the
airways
 Exhaled 5 to 10 of these
breaths through the device,
followed by 2 large exhaled
volumes through the device
and finally a huff or cough
to clear mobilized
secretions
• Positive expiratory pressure
 Uses a mask or mouthpiece
with a valve to regulate
expiratory resistance
 Unresisted inhalation with
active exhalation against a
positive expiratory pressure
- Ventilatory Muscle Training
• Pursed lip breathing and pacing:
Used by patient with COPD; ↓
respiratory rate and ↑ tidal
volume
 May delay or prevent
airway collapse, allowing for
better gas exchange
• Activity pacing: Performance of
an activity within the limits or
boundaries of that patient’s
breathing capacity.
SOURCE
Physical Rehabilitation by Sullivan and
Schmitz, 5th Ed.
114 | P a g e
 OBSTETRIC CONDITIONS
Pelvic Floor Dysfunction
Prolapse
Urinary fecal incontinence
Pain and Hypertonus
Pregnancy Induced Pathology
Diastasis Recti
Postural Back pain
Sacroiliac/Pelvic Girdle Pain
Varicose vein
Joint Laxity
Nerve Compression Syndromes
High-Risk Conditions
Definition
- Pregnancy spans for 40 weeks from
conception to delivery and is divided into
three trimesters
Characteristics of Pregnancy and Labor
1. Pregnancy
- First Trimester (0-12 weeks)
• 7-10 days after fertilization –
implantation of fertilized ovum
in uterus
• Mother is fatigued, urinates
frequently and experiences
nausea or vomiting (“morning
sickness’)
• Increased breast size
• Small weight gain of 0-1455 g
(0-3 lb is normal)
• Emotional changes
• End of 12th wk, fetus is 6-7 cm
long; weighs aprox. 20g (2 oz),
fetus can kick, turn head,
swallow and has beating heart
but not yet felt by the mother
- Second Trimester (13-26 weeks)
• Pregnancy is visible to others
• Mother feels movement around
20 wks.
• Nausea and fatigue have usually
disappeared
• Fetus is 19-23 cm (14 inches) in
length; weighs approx. 600 g (1-
2 lb)
• Fetus has eye brows, eyelashes
and fingernails
- Third Trimester (27-40 weeks)
• Uterus is now very large; has
regular contractions felt only
occasionally
• Common complaints are
frequent urination, back pain,
shortness of breath,
constipation
• At time of birth baby will be 33-
39 cm long; weighs approx.
3400g (7 lb, although range of
5-10 lb is normal)
Note: 38-42 weeks of pregnancy is considered
full term
2. Labor
- Divided into 3 stages
- True labor produces palpable changes in
the cervix known as:
• Effacement: Shortening or
thinning of cervix from a
thickness of 5 cm (2 inches)
before onset of labor to a
thickness of a piece of paper
• Dilation: Opening of the cervix
from diameter of a fingertip to
approx. 10 cm (4 inches)
- Labor – Stage 1
• Initial cervical dilation before
true labor
• Cervix is fully dilated
• 3 major phases:
 Cervical Dilation Phase:
Dilates from 0-3 cm almost
completely efface; Uterine
contractions occur from the
top down causing cervix to
open pushing the cervix
downward
 Middle Phase: Dilates 4-7
cm; contractions are
stronger and regular
 Transition Phase: Dilates 8-
10 cm; dilation is complete;
contractions are very strong
- Labor – Stage 2
• “Pushing” and expulsion of the
fetus
• Uterine contractions last for as
long as 90 seconds
• Fetal Descent: Position changes
(cardinal movements) by the
fetus as it pass through the
pelvis
• Engagement: Greatest fetal
head diameter passes the pelvic
inlet
• Descent: Cont’d downward
progression
• Flexion: Fetal chin is brought
closer to its thorax
• Internal Rotation: Turns occiput
toward the mother’s symphysis
pubis
• Extension: Head is extended
bringing occiput in direct
contact with inferior margin of
maternal symphysis pubis; ends
when fetal head is delivered
• External Rotation: Occiput
rotates toward sacrum to allow
fetal shoulders passage
• Expulsion: Fetal anterior
shoulder passes under
115 | P a g e
 symphysis pubis and rest of
body follows
- Labor – Stage 3
• Placental Stage (expulsion of
placenta)
 Placenta detaches from
uterine wall, BV are
constricted, bleeding
slows; occurs 5-30 mins
after delivery
 Hematoma forms to
prevent further
significant blood loss;
mild bleeding for 3-6
wks. after delivery
• Uterine involution
 Uterus continues to
contract and decrease
in size for 3-6 wks.;
remains slightly
enlarged
A. Classification of Pelvic Floor Dysfunction
1. Prolapse
- Descent of any of the pelvic viscera out
of their normal alignment because of
muscular, fascial and ligamentous
deficits and increased abdominal
pressure
- Worsens over time
- Aggravated by constipation and
straining with elimination
2. Urinary or Fecal Incontinence
- Result of neuromuscular and
musculoskeletal impairments
- Occurs in combination with prolapsed
3. Pain and Hypertonus
- Related to delayed healing of perineal
lacerations, trauma to soft tissues or
sacro-coccygeal joint during delivery,
pelvic obliquity, multiple gynecologic/
visceral diagnoses, ms spasm or
guarding
- Pain with ADLs, decreased sitting
tolerance, difficulty with bowel and
bladder elimination
Risk Factors for Dysfunction
- Pregnancy
• Obstetric risk factors: multiple
deliveries, prolonged 2nd stage
of labor, use of forceps or
oxytocin, 3rd degree perineal
tears, birth weight greater than
8 lb
B. Pregnancy-Induced Pathology
1. Diastasis Recti
- Separation of the rectus abdominis
muscles in the midline at the linea alba
- Etiology: unknown
- Separation >2cm or 2 finger widths is
significant
- Incidence: not exclusive to childbearing
women but seen frequently in this
population
- Can occur below or above umbilicus but
less common below umbilicus
Significance:
- Low back pain - due to decreased ability
of abdominal musculature to stabilize
the pelvis and lumbar spine
- Functional limitations
• ex: inability to perform
independent supine to sitting
transitions
- Decreased fetal protection
- Potential for herniation
2. Postural Back Pain
- occurs because of postural changes of
pregnancy, increased ligamentous laxity
and decreased abdominal ms function
- Incidence
• 50-70% of pregnant women
• continue in postpartum in up to
68% of women
- Characteristics:
• Worsens with muscle fatigue
• Relieved with rest or change of
position
- Interventions:
• Low back exercises
• Posture instructions
• improvement in work
techniques
• modality application
3. Sacroiliac/ Pelvic Girdle Pain
Clinical Manifestation:
Sacroiliac pain
- Localized to the posterior pelvis
- Stabbing deep into the buttocks distal
and lateral to L5/S1
- May radiate into posterior thigh or knee
but not to foot
- Pain with prolonged sitting, standing or
walking, climbing stairs, turning in bed,
unilateral standing or torsion activities
- May not be relieved with rest and
worsens with activity
Pubic Symphysis dysfunction
- May occur alone or with SI symptoms
- Tenderness to palpation at the
symphysis
- Radiating pain into the groin and medial
thigh
- Pain with weight bearing
116 | P a g e
4. Varicose Vein
- Aggravated in pregnancy by increased
uterine weight, venous stasis in the legs,
and increased venous distensibility
Manifestations:
- Present in first trimester
- Occur in LE, the rectum (hemorrhoid) ,
or vulva
- Heaviness or aching discomfort specially
with dependent leg positions
- Intensity increases with progression of
pregnancy
5. Joint Laxity
- Joints are at risk during pregnancy
- Tensile quality of ligamentous support is
decreased and can lead to injury
5. Multiple Gestation
- More than one fetus forms
- Complication:
• Premature labor
• Increased incidence of perinatal
mortality
• Lower birth weight infants
• Increased incidence of maternal
complications
6. Diabetes
- Can be present before pregnancy or can
be a result of physiological stress in
pregnancy
- Gestational diabetes - 4-7% of pregnant
women, disappears after pregnancy
General Healthcare Management:

6. Nerve Compression Syndromes A. Prognosis

- CTS and TOS can be caused in pregnancy Depends on:
by: - Characteristic of pregnancy
• Postural changes in neck and - Rehab management
upper quarter - Mother’s lifestyle
• Fluid retention
B. Medical, Surgical Management
• Hormonal changes
- Fetal Presentation
• Circulatory compromise
• Portion of the body that is most
- May also occur in LE caused by: proximal to birth canal
• Weight of the fetus  Vertex / Occiput
• Fluid retention  Face
• Hormonal changes  Sinciput
• Circulatory compromise  Brow
 Breech (Frank Breech,
Complete Breech,
C. HIGH-RISK CONDITIONS Incomplete or Footling)
1. Preterm rupture of membranes - Episiotomy
- Amniotic sac breaks and amniotic fluid is • Incision in perineal body
lost before onset of labor • Common in most pregnancies
- ↑ risk for child infection (33 – 51 % of vaginal deliveries)
• Less common in women who
2. Premature onset of Labor were athletic or active pre –
- Labor that begins before 37 AOG pregnancy
• Divided into 4 degrees:
3. Placenta Previa  1st Degree
- Placenta attaches too low on the uterus, Only skin
near the cervix  2nd Degree
- When cervix dilates, placenta begins to Includes underlying
separate from uterus and may present muscle; normal
before the fetus  3rd Degree
- Primary symptoms: intermittent, Extends to anal
recurrent or painless bleeding that sphincter
increases in intensity  4th Degree
Penetrates into the
4. Pregnancy-related hypertension or rectum
Pre-eclampsia - Cesarean Childbirth
- Characterized by hypertension, protein • Delivery through incision of
in the urine, severe fluid retention abdominal wall and uterus
- Can progress to maternal convulsions, • Aids in prevention of future
coma, and death if it becomes severe pelvic floor dysfunction
(eclampsia) • Possible due to women feeling
- Occurs in third trimester and disappears lethargic during “pushing” of
after birth labor

117 | P a g e
 • Does not spare pelvic - Varicose Veins
musculatures and pudendal Interventions:
nerves • External support
 May create significant • Foot and leg exercises
strain in certain • Cold thermal agents
structures
- Joint Laxity
Physical Therapy Evaluation and Diagnosis: Interventions:
• Exercise modification
A. Points of Emphasis on Examination
• Aerobic exercises
1. Inspection
• Thermal agents
2. Palpation
• Diastasis Recti
- Nerve Compression Syndromes
3. Cardiovascular Assessment
Interventions:
- Vital Signs (BP and RR)
• Postural correction exercises
- Edema
• Manual techniques
4. Musculoskeletal Assessment
• Ergonomic assessment
- Joint Play
- ROM • Splints (for CTS)
- MMT • Thermal modalities
- LGM • TENS
- LLD
C. PT Diagnosis
5. Bowel/Bladder Incontinence
Impaired Joint Mobility, Motor Function, Muscle
6. Posture and Balance (due to shifting of
Performance Associated with Pregnancy
COG)
SOURCES:
B. PROBLEM LIST, PLAN OF CARE, - Therapeutic Exercise: Foundations and
INTERVENTIONS Technique by KISNER
- Diastasis Recti
Problem List:
• Decrease pain
• Maintain muscle strength
• Prevent soft tissue contracture

Interventions:
• TENS
• Corrective Exercise
• BORG Scale
• ROM & MMT exercises
• Thermal modalities

- Postural Back Pain

Problem List:
• Decrease LBP
• Maintain muscle strength

Interventions:
• Low back exercises
• Proper body mechanics
• Posture correction
• Thermal modalities
• TENS

- Sacroiliac Girdle Pain

Problem List:
• Decrease pain
• Maintain muscle strength

Interventions:
• Activity modification
• Exercise modification
• Thermal agents
• TENS

118 | P a g e
 DISORDERS OF THE VESTIBULAR AND BALANCE
SYSTEMS
Central Nervous System pathology
Cerebrovascular Insults
TBI
Demyelinating diseases
Peripheral Nervous System pathology
BPPV
Unilateral Vestibular Hypofunction
Bilateral Vestibular Hypofunction (BVH)
Meniere ’s Disease
Perilymphatic Fistula
Vestibular Schwannoma (VS)
Vestibular Neuritis
Non-Vestibular Disorders
Motion Sickness
Migraine-related Dizziness
Multiple System Atrophy
Cervicogenic Dizziness
Cardiovascular Lightheadedness
Diseases of Unknown cause
GENERAL MEDICAL BACKGROUND
Definition
- Disorder of the body’s
balance/vestibular system in the inner
ear due to various ranges of conditions
Classification
Central Nervous System pathology
- Cerebrovascular insults
• AICA, PICA, Vertebral artery
involvement may cause vertigo
• AICA involvement causes
hearing loss
• TIA may present sudden vertigo
that lasts for minutes and also
hearing loss
- Traumatic brain injury(TBI)
• Due to labyrinthine or skull
fractures
• Pts may complain of vertigo
- Demyelinating diseases
• Multiple sclerosis can affect
cranial nerve 8
Peripheral Nervous System pathology
- Benign Paroxysmal Positional Vertigo
(BPPV)
• A biochemical disorder
• The most common cause of
vertigo
• Symptoms include nystagmus
and vertigo with change in head
position, occasionally nausea
with or without vomiting, and
disequilibrium
• Latency to onset of vertigo and
nystagmus occurs within 15
seconds once the head is in the
provoking position and usually
lasts less than 60 seconds
• Misplaced Otoconia: Caused the
vertigo and nystagmus
• Self-limiting
• Provoked in change of position
with neck extended and rotated
• (+) Tinnitus but no hearing loss
• Occurs in two mechanisms:
Cupulolithiasis and Canalithiasis
• Cupulolitiasis
 Otoconia break away and
adhere to the cupula of one
of the SCCs
 When head is moved into
certain positions, the
weighted cupula is
deflected by the pull of
gravity
 Vertigo and nystagmus
persists as the patient is in
provoking positions
• Canalithiasis
 Otoconia are floating freely
in one of the SCCs
 When head position is
changed, the pull of gravity
causes the free floating
otoconia to move inside the
SCC
 Endolymph movement and
deflection of the cupula
stimulates the ampulla of
the affected canal causing
vertigo
- Unilateral Vestibular Hypofunction
(UVH)
• Decreased or eliminated
receptor input caused by viral
insults, trauma, and vascular
events.
• Pt experiences direct
impairment of vertigo,
spontaneous nystagmus,
oscillopsia during head
movements, postural instability,
and disequilibrium
- Bilateral Vestibular Hypofunction (BVH)
• Most commonly caused by
ototoxicity.
• Less common cause includes
meningitis, autoimmune
disorders, head trauma, tumors
on each CN 8 (including bilateral
vestibular schwannoma),
119 | P a g e
 transient ischemic episodes of
vessels supplying the vestibular
system, and sequential
unilateral vestibular neuritis.
• Pt experiences disequilibrium,
oscillopsia, gait ataxia
• Asymmetric BVH: Nausea,
vertigo, or nystagmus are not
significant
- Meniere’s Disease
• Aka Endolymphatic hydrops
• Common disorder of the inner
ear characterized by episodes of
vertigo and low frequency
hearing loss
• Vertigo lasts for minutes to
hours
• Pt may also complain a sense of
fullness in the ear and tinnitus
• Symptoms gradually increase in
severity and can last several
hours per episode.
• Vestibular exercises are not
recommended during episodes
of attack
- Perilymphatic fistula
• Most commonly caused by
rupture of the oval or round
windows, membranes that
separate the middle and inner
ear
• A rupture of these membranes
results in leakage of the
perilymph into the middle ear
which results to vertigo and
hearing loss
• MOI: Excessive pressure
changes (deep water diving),
blunt head trauma without skull
fracture, extremely loud noise
• Treated first with bed rest in
hopes of allowing the
membrane to heal
• Physical therapy is
contraindicated but can be
beneficial for pts who have
continual disequilibrium
- Vestibular Schwannoma (VS)
• Historically known as
Acoustic neuromas
• Are benign tumors
arising from the
Schwann cell of the 8th
CN, often in the
internal auditory canal
• Symptom presentation
is usually related to
where the tumor arises
• Tumors usually grow
slowly.
• Tumor in the IAC:
Tinnitus and hearing
loss
• Tumor in the
Cerebellar-Pontine
angle: Tumor may
become quite large
before symptoms of
hearing loss are
revealed
• Unilateral hearing loss
– usually the initial sign
of VS
- Vestibular Neuritis
• Inflammation of the
vestibular nerve
• Acute, sustained
dysfunction of the
peripheral vestibular
system with secondary
nausea, vomiting, and
vertigo.
• (+) true vertigo lasting
for days
• Most common self-
limited inner ear
conditions. Usually
preceded by viral
infection of the upper
respiratory and GI tract.
• Intense in 2-3 days &
lasts for 1-2 weeks
Non-vestibular disorders
- Motion sickness
• Is a normal sensation that in
some people becomes
debilitating
• This is because the 3
sensory inputs of
proprioception, vestibular,
and visual information do
not match stored neural
patterns the brain expects
to recognize
- Migraine-related dizziness
• Can be deceptively similar
to a peripheral vestibular
lesion
120 | P a g e
 • Symptoms include vertigo,
dizziness, imbalance, and
motion sickness
- Multiple System Atrophy
• Is a progressive
degenerative disease of the
nervous system involving
four clinical domains:
cerebellar ataxia, autonomic
dysfunction, Parkinson’s
disease-like symptoms, and
corticospinal dysfunction
- Cervicogenic dizziness
• A term meant to imply that
the cause of symptoms such
as dizziness or imbalance
arise from pathology
affecting the cervical spine
or related soft tissue.
- Cardiovascular lightheadedness
• Anemia
• Hyperviscosity
• Hypotension
• Carotid sinus
hypersensitivity
• Cardiac arrhythmia
• Heart failure
• Vertebral artery dissection
- Diseases of unknown cause
• Non-specific dizziness
• Hyperventilation syndrome
• Psychiatric disturbances
Epidemiology
• At an incidence of 5.5%, dizziness in the
United States affects more than 15
million people each year.
• Children have low prevalence of balance
disorders.
• Dizziness: One of the most common
complaints adults report to their
physicians.
• Peripheral vestibular system – most
common origin for patient signs and
symptoms.
Etiology
• Viral infection of the vestibular nerve
and/or labyrinthine is believed to be the
most common cause of vestibular
neuritis
• Head trauma with or without skull
fractures
• Tumors
• Toxics
• Displacement of the otoliths from the
utricle and falling into the semicircular
canal.
Pathophysiology/Pathomechanics
• Meniere’s disease
- Involves an increase in
endolymphatic fluid causing
distention of the membranous
tissues.
Clinical Manifestation
The vestibular system includes the parts of the
inner ear & brain that help control balance &
eye movements. If the system is damaged by
disease, aging or injury, vestibular disorders can
result & are often associated with one or more
of these symptoms, among others:
• Vertigo & dizziness
• Imbalance & spatial disorientation
• Vision disturbance
• Hearing changes
• Cognitive & psychological changes
• Other symptoms
Not all symptoms will be experienced by every
person with an inner ear disorder, & other
symptoms are possible. An inner ear disorder
may be present even in the absence of obvious
or severe symptoms. It is important to note that
most of these individual symptoms can also be
caused by other unrelated conditions.
Vertigo, lightheadedness & dizziness
• Vertigo - a whirling or spinning
sensation; an illusion of movement of
self or the world
• Lightheadedness – fainting is about to
occur
• Dizziness – floating or rocking sensation
Balance & Spatial Orientation
• Imbalance, stumbling, difficulty walking
straight or turning a corner
• Clumsiness
• Difficulty maintaining straight posture:
tendency to look downward to confirm
the location of the ground
• Head may be held in a tilted position
• Tendency to touch or hold onto
something when standing, or touch, or
hold the head while seated
• Sensitivity to changes in walking
surfaces or footwear
• Muscle & joint pain ( due to struggling
with balance)
• Difficulty finding stability in crowds or in
large open spaces
Vision
• Discomfort from busy visual
environments
121 | P a g e
 • Tendency to focus nearby objects; • The ENG oculomotor tests examines
increased discomfort when focusing at a saccadic and smooth pursuit
distance including velocity, latency, and gain
• Poor depth perception - Caloric test
Hearing Changes • The test for the inner ear.
• Hearing loss; distorted or fluctuating • Infuses the external auditory canal
hearing with separate cold and warm air or
• Tinnitus (ringing, roaring, buzzing, water.
whooshing) • The test is particularly useful for
• Sensitivity to loud noises determining the side of the deficit,
• Vertigo, imbalance, dizziness because each labyrinthine is
Cognitive stimulated separately
• Difficulty following speakers in - Rotational chair test
conversations, meetings, especially • Stimulates each SCC by rotating
when there is background noise or subjects in the dark
movement • Considered a standard test for
• Confusion, disorientation, difficulty bilateral vestibular hypofunction
comprehending directions & instruction • Is limited because only the
Other horizontal SCCs are routinely tested
• Nausea, vomiting to determine extent of pathology
• Hangover or sea sick - Vestibular-evoked myogenic potential
• Motion sickness (VEMP)
• Sensation of fullness in ears • A laboratory test that has gained
• Headaches broad clinical used and includes two
• Slurred speech subtypes: cervical and ocular VEMP
• Both types use threshold and
Diagnosis amplitude of a muscle contraction
- Magnetic resonance imaging (MRI) (EMG) to classify pathology
• Reveal the presence of tumors,
stroke damage, and other soft- Differential Diagnosis
tissue abnormalities that might Central vestibular Peripheral vestibular
cause dizziness or vertigo. dysfunction dysfunction
• MRIs of structures in and around • Severe ataxia • Mild ataxia
the inner ear may show problems • Abnormal smooth • Smooth pursuit &
such as an acoustic neuroma. pursuit & saccadic saccadic eye
- CT Scan eye movement movement test
• Is best for studying bony structures. test usually normal;
• Sudden & positional testing
• CT scan of the temporal bone
permanent hearing may produce
(within which the inner ear resides)
loss nystagmus
are often used to look for
• Diplopia, altered • Hearing loss,
abnormalities such as fractures fullness in hears,
consciousness, &
- Hearing test lateropulsion tinnitus
• Audiometry measures hearing • Acute vertigo not • Acute vertigo
function. suppressed by intense, and
• Hearing evaluations are an visual fixation suppressed by
important part of vestibular • Pendular visual fixation
nystagmus • Jerky nystagmus
diagnostics, because of the close
• Pure persistent • Spontaneous
relationship between the inner ear
vertical nystagmus horizontal
hearing and balance organs persist regardless nystagmus usually
- Electronystagmography (ENG) of positional resolves within 7
• Includes a battery of tests that testing days in a patient
measure oculomotor and inner ear • Constant onset with UVH
function. • Severe imbalance • Abrupt onset
• Mild imbalance
• The test also examines for
nystagmus in different positions
Prognosis

122 | P a g e
 • Most patients recover from vertigo and
imbalance
• Conditions like vestibular neuritis and
BPPV are considered self-limiting
• Non-Modifiable:
 Age
 History
• Modifiable:
 Lifestyle: Healthy and active living
would lead to good prognosis
GENERAL HEALTHCARE MANAGEMENT
Medical Management
- Meniere’s disease
• Directed towards reducing or
preventing fluid buildup
• Controlled diet (2g/day or less
sodium diet)
• Avoidance of caffeine and alcohol
• Use of diuretic to control amount of
water in the body
- Perilymphatic fistula
• Strict limitations on activities
• War-ranting good communication
between physician and physical
therapist.
Surgical Management
- Meniere’s disease
• Endolymphatic shunt placement to
prevent fluid buildup in the inner
ear
• Vestibular Nerve Section or
Transtympanic gentamicin injection
to stop the abnormal vestibular
signal
Pharmacological Management
- NSAIDs
- Muscles relaxants
- Anti-histamine drugs
Other Healthcare (Rehabilitative/Supportive)
- Nutritional diet
- Assistive/adaptive devices
PYHSICAL THERAPY EXAMINATION, EVALUATION,
DIAGNOSIS
Points of Emphasis in Examination
- Demographic data
- Subjective data
- Systems Review
- Balance and Tolerance Test
- Balance and Coordination Test
- Gait Assessment
- Functional Assessment
- Examination of Gait and Balance
• Important for determination of a
patient’s functional status.
• Testing should address both static
and dynamic balance.
• Cannot uniquely identify pathology
within the vestibular system.
- Dynamic Visual Acuity Test
• Is the measurement of visual acuity
during horizontal motion of the
head
• To perform the test, static visual
acuity is tested first.
- Tests and Measures
• Visual Analog Scale
 An effective technique to obtain
subjective intensity ratings of
vertigo, lightheadedness,
disequilibrium, and oscillopsia.
• Dizziness Handicap Inventory
 A popular tool used to measure
a patient’s self-perceived
handicap as a result of
vestibular disorders.
 Provides quantification of the
patient’s perception of
disequilibrium and its impact on
daily activities.
• Functional Disability Scale
 Developed to determine the
patient’s response to physical
therapy administered before
and after rehabilitation.
• Motion Sensitivity Quotient
 Developed to provide a
subjective score of an
individual’s sensitivity to
motion.
 The test involves placing
patients into positions
incorporating head or entire
body motion to determine
whether the movement
reproduces dizziness.
• Examination of Eye Movements
 Observation of nystagmus.
 Nystagmus is the primary
diagnostic indicator used in
identifying most peripheral and
central vestibular lesions
• Head Impulse Test (Examination of
the VOR at High Acceleration)
 A widely accepted clinical tool
used to examine semicircular
canal function.
 Cervical ROM should be
determined before performing
HIT and the PT should explain
why the head must be moved
quickly.
• Head Shaking Induced Nystagmus
Test
123 | P a g e
  A useful aid in the diagnosis of a sated: to
unilateral peripheral vestibular normal perform
defect
 Vision is occluded during this - Vestibular Function Tests
test. • Semicircular Canal Tests
- Positional Testing - Electronystagmography (ENG),
• Commonly used to identify videonsytagmography (VNG), caloric
whether otoconia have been test, rotational chair test
displaced into the SCC, causing a • Otolith Tests
condition referred to as BPPV. - Vestibular-evoked myogenic potential
• Dix-Hallpike Test: The most (VEMP), Subjective visual vertical (SVV),
common positional test used to Subjective visual horizontal (SVH)
examine for BPPV
• Dix Hallpike Test: Problem List
A. Patient is positioned in long- - Risk for falls
sitting position with head - Nsytagmus
turned 45° horizontally - Vertigo & dizziness
B. Patient is quickly brought to - Imbalance & spatial disorientation
supine position with the - Vision disturbance
neck extended 30° and - Hearing changes
maintained 45° rotation - Cognitive & psychological changes
C. Check for nystagmus and
vertigo
Physical Therapy Diagnosis
D. Patient is brought back to NM1 – Primary Prevention/Risk Reduction for
sitting position Loss of Balance and Falling
E. The other side is tested
F. The side that reproduces Physical Therapy Prognosis
nystagmus and vertigo is Plan of Care
the side that has the BPPV - Pt. will demonstrate reduced vertigo
associated with head motion.
Test BPPV UVL BVL Central - Pt. will demonstrate improved balance.
Lesion - Pt. will demonstrate improved stability
Romberg Negative Acute: Acute: Often of gaze during head movements
Positive Positive negative - Pt. will demonstrate diminished
Chronic: Chronic:
sensitivity to motion.
Negative Negative
Tandem Negative Positive, Positive Positive - Pt. will demonstrate improve static and
Romberg eyes dynamic postural stability.
closed
Single- Negative May be Acute: May be Intervention
legged positive Positive unable - Canalith repositioning maneuver (CRM)
stance Chronic: to - Liberatory (Semont) maneuver
Negative perform - Brandt-Daroff exercises
Gait Normal Acute: Acute: May
- Vestibular adaptation exercise (x1 and
wide- wide- have
x2)
based, based, pronoun
slow, slow, ced - Postural stability exercises incorporate
decrease decrease ataxia with head movements
d arm d arm - Habituation training
swing swing and - Balance exercises
and trunk
trunk rotation
rotation Compens
Compen ated: mild
sated: gait
normal deviation
Turn May Acute: May not May not
head produce may not keep keep
while slight keep balance balance,
walking unsteadi balance or slows increase
ness Compen cadence d ataxia

124 | P a g e
 Intervention Volume Rationale
To get the
involved
Sitting Exercises muscles to
with slight 5 reps x 3sets contract to
perturbation keep the COG
between the
BOS
To help patient
Sitting Exercises
maintain
with one-leg 5 reps x 3sets
balance while
raise
sitting
Sitting Exercises
with upper To help patient
extremity maintain
movements or 5 reps x 3 sets balance even
lighter weights when there are
on the upper UE motions
extremities
To help patient
maintain
March in Place balance in the
5 reps x 3 sets
while sitting presence of
continuous
motions
In preparation
Sit-to-Stand
5 reps x 3 sets for standing
Exercises
exercises
Standing To help
exercises with a 15 seconds maintain
wide BOS; then hold x 3 sets x balance in the
proceed to a 5 sec rest standing
narrow BOS position
Standing To help patient
Exercises with maintain the
5 reps x 3 sets
slight COG within the
perturbation BOS
In preparation
for Gait
Weight-shifting 4 reps x 3sets
Training
Exercises
4 reps back For safe
Gait Training and forth x 10 ambulatory
with Parallel sec rest or as training with
bars tolerated by less tendency
the patient to fall
Gait Training 20 steps back For safe
with Crutches and forth x 5 ambulatory
(4-point Gait) sec rest training
In preparation
20 steps back
Gait training for ambulation
and forth x 5
using a cane without any
sec rest
assistive device

30 steps up
For endurance
Stair Climbing and down x 5
purposes
sec rest

Source
- Physical Rehabilitation 5th edition by
Susan B. O’Sullivan & Thomas J. Schmitz
- Seminar 1 notes

125 | P a g e
 HIV/AIDS • Health Care Professionals and Laboratory
Workers
• Human Immunodeficiency Virus (HIV)
o Caused by a lentivirus, which is a slow Etiology
retrovirus • Etiologic agent is HIV
o Entails a condition wherein there is a o Subfamily: Lentivirus
progressive failure of the immune o Family: Human retrovirus
system o Retrovirus depend on a unique enzyme
 Allows other life-threatening called Reverse Transcriptase to replicate
conditions and agents to propagate using host DNA
and thrive. o 4 Recognized Human retroviruses
• Acquired Immunodeficiency Syndrome  Human T Lymphotropic Virus
(AIDS) • HTLV I
o Results or is “acquired” from HIV o Associated with lymphoma
 Not inherited or genetic • HTLV II
o A condition characterized by a defect in o In circulating cells of
natural immunity against diseased monocytes / macrophages
 Human Immunodeficiency Viruses
Terms • HIV I
• Antigen o Classic AIDS virus
o Foreign molecule that elicits the immune o More pathogenic
response o Closely related to Simian
• Antibodies / Immunoglobins Immunodeficiency Virus
o Proteins that engages to ‘tag’ antigens • HIV II
• Lymphocytes o Restricted to a few countries
o Primary cells of the immune system of West Africa
o T and B Lymphocytes o Less pathogenic, most are
• Macrophages asymptomatic
o Accessory cells that process and present o Has 40% nucleotide
antigens to lymphocytes sequence homology with
• Cytokines HIV I
o Molecules that link immune cells with
other tissues and organs Modes of Transmission
• CD Molecules • Direct
o Master regulator o the immune response o Sexual contact
• Major Histocompatibility (MHC) Membrane o Exposure to infected blood
Molecules o IV Drug Users / Needle sharing
o Recognition of foreign threats from self • Indirect
o Perinatally
Epidemiology • No evidence of transmission by ‘casual
• WHO estimates that contact’
o 1M of children have AIDS
o 22M people were infected with HIV Pathophysiology
worldwide • Hallmark of HIV is profound
• AIDS was the leading cause of death of immunodeficiency
Americans aged 25 – 44 y.o. o ↓ of CD4+ T lymphocytes
• ♂ > ♀ at 6:1  Average is 700 – 1400 / mL
o However, rate of infected women is • After infection, virus has 3 stages
growing faster o Early Asymptomatic Stage
• Asia has lowest number of cases  >500 / mL CD4+ T lymphocytes
• America has the highest number of cases  Cells start to get destroyed
 Drain to lymphoid organs
Risk Groups  Initial Virema
• Homo and bisexuals  Acute HIV Syndrome
• Sexually active people • 3 – 6 weeks
• Intravenous drug users • ↑ circulating antibodies
• Blood transfusion recipients • ↑ cytotoxic / suppressor cells
• Organ transplantation recipients  Decreased Viremia
• Dialysis recipients o Intermediate Stage
• Hemophiliacs  200 – 500 / mL CD4+ T lymphocytes
o Blood disease where blood does not clot  Asymptomatic Stage – Clinical
Latency
• Mother -> Baby
• ~ 10 years

126 | P a g e
 • ↑ virus in lymph nodes
• Progressive ↓ of CD4+ T
lymphocytes
• ↓ trapping function of cells
o Advanced Stage
 0 – 200 / mL CD4+ T lymphocytes
 Advanced Stage
• (-) trapping function of cells
• Virus spills to circulation
o Defensive cells
outnumbered by HIV virus
• Opportunistic Infection
• DEATH
Clinical Manifestations
• Acute HIV Syndrome
o Approx. 50 – 70% of cases
o Symptoms persists for 1 -2 weeks
o Gradually subside as immune response
to HIV
o Opportunistic infections reported
o Clinical findings:
 General
• Fever
• Pharyngitis
• Lymphadenopathy
• Headache
• Retro-orbital Pain
• Arthralgias / Myalgias
• Lethargy / Malaise
• Weight Loss / Anorexia
• Nausea / Vomiting / Diarrhea
 Neuropathic
• Meningitis
• Encephalitis
• Peripheral neuropathy
• Myelopathy
 Dermatologic
• Erythematous maculopapular
rash
• Mucocutaneous ulceration
• Asymptomatic Stage – Clinical Latency
o Initial symptoms associated with first
manifestation of opportunistic disease
o Varying degrees of intermittent
symptoms
o High risk opportunities & clinically
apparent disease
• Early Symptomatic Disease (ARC or AIDS
Related Complex)
o Generalized lymphadenopathy
 >1cm
 Extra-inguinal sites
 >3 months
 Idiopathic
 Early symptoms
o Oral Lesions
 Thrush
 Oral Hairy Leukoplakia
 Aphthous ulcers of posterior
oropharynx
o Reactivation of “Herpes zoster” or
“shingles”
 10 – 20% of all cases
 1st clinical indication of
immunodeficiency
 5 years after primary infection
o Thrombocytopenia
 ↓ platelet count
• AIDS (Full Blown)
o Opportunistic infection
are Complications
• Affect virtually every organ
o General approach is to quickly diagnose
treatable conditions rapidly
• Gynecologic Complications
o Vaginal Candidiasis
o Cervical Dysplasia
o Neoplasia
• HIV-related Malignancies
o Kaposi’s Sarcoma
• Endocrinologic Complication
o Adrenal gland most commonly affected
• Skin Complications
o Dermatitis
• GI Complications
o Candidal Esophagitis
o Hepatic Diseases
o Malabsorption
• CNS Complication
o Toxoplasmosis
o AIDS dementia complex
• Sinopulmonary Complications
o Pneumonia
o Sinusitis
• Oral Lesions
• Rheumatologic Manifestations
Diagnosis
• Licensed tests for diagnosis HIV infection
• Enzyme-Linked Immunosorbent Assay
(ELISA)
o Standard screening test
o Extremely sensitive
o Disadvantage: Low Specificity
• Western Blot Asay (WBA)
o Most common confirmatory test
 CD4 + T-cell Count
 P24 Antigen Capture Assay –
simplest test
 Plasma HIV RNA Assay – most
sensitive and reliable measurement
of plasma viral load
Prognosis
• From time of seroconversion, 10 – 20% of HIV
infected individuals will progress to AIDS in 3
– 6 years
• Once patient has constitutional symptoms,
herpes zoster, thrush or a lowered CD4+ T-
cell Count, chances are >40% of progressing
to AIDS after 3 years and >50% after 5 years
• Can be modified by antiretroviral therapy
and general medical support
127 | P a g e
Medical / Surgical Management • Impaired mobility, difficulty with self-care,
• Medical impaired cognition, and uncontrolled pain
o Supportive, as there are no known cure o Therapeutic exercise
for HIV or AIDS o Gait aids
• Pharmacologic o Orthosis
o Antiretroviral Therapy o Pain management
 Nucleoside Analog Reverse o Whirlpool treatment
Transcriptase Inhibitors (NARTI) o Assistance, especially in areas of:
• Zidovudine  Stair climbing
• Zalcitabine  Ambulation
• Lamivudine  Bowel management
• Didanosine  LE dressing
• Stavudine • For Cancer pain and pain
 Protease Inhibitors o TENS
• Saquinavir  Conventional is most effective
• Ritonavir o NSAIDS
• Indinavir o Opioid Meds
 Non-Nucleoside Reverse o CAUTION for Cancer patients
Transcriptase Inhibitors  Heat modalities may ↑ circulation
• Acvirapine and ↑ potential for metastatic
 Must be taken within 24 hours upon spread, and this must only be used
exposure, preferably within the first for non-cancer patients
2 – 4 hours  US is contraindicated
• Take CBC Count and use CD4+ as
baseline
• Take the test every 2 weeks
• Surgical
o Preparations for post-surgical rehab can
be made in advance

PT Evaluation
• Assessment
o Asses the general condition
o Usual assessment includes:
 Pulmonary Test
 UE and LE Instability Test
 ROM
 MMT
 Motor and Sensory Tests
• Usual problems
o Impaired mobility
o Difficulty with self-care
o Impaired cognition
o Uncontrolled pain
• Check for deconditioning problems
o Contractures
o Adhesions
o Atrophy
o LOM
o Weakness
o Instability
o Edema / Swelling
• Specific tests for complications should be
done

PT Management
• Most important aspect is to keep patient
mobile
• Improve Function
o Gait and functional training
o Prevention of deconditioning effects
o Adaptive equipment and strategies

128 | P a g e
 CANCER & NON-MALIGNANT TUMORS • Carcinoma
o From epithelial cells
• Malignant neoplasm o Most common cancers in
• Group of various disease with the general the age
characteristic of unregulated cell growth  Breast
• Cells divide and grow uncontrollably  Prostate
o Form tumors  Lung
o Invade other nearby body parts • Sarcoma
o May spread to other body parts through o From connective tissue
circulatory system o Originate in mesenchymal
• 200+ kinds of causes cells outside the bone
 Bone
Neoplasm  Nerve
• Abnormal mass of tissue • Lymphoma / Leukemia
• Due to neoplasia o Two types that originate
from the blood cells
Neoplasia o Leukemia is the most
• Abnormal proliferation of cells common type of cancer in
• Often undergo an abnormal pattern of children by 30%
growth • Germ Cell Tumor
o Metaplasia o From pluripotent cells
o Dysplasia  Testicles or Seminoma
 Not all metaplasia or dysplasia  Ovary or Dysgerminoma
progress into neoplasia • Blastoma
• Growth exceeds normal tissue growth o From immature ‘precursor’
around it cells or embryonic tissue
• Growth persists in the same excessive o More common in children
manner even after the cessation of the o Classified by their organ or tissue of
stimuli origin
 - Carcinoma
• Usually causes a lump or tumor
• Hepatocarcinoma
Tumor o Cancer in liver originating
from malignant epithelial
• From the Latin word tumor, which means
cells
swelling
 - Sarcoma
• Traditionally means an abnormal swelling of
• Liposarcoma
flesh
 - Blastoma
• In contemporary English, often synonymous
• Hepatoblastoma
for
o Classified by the organ
o Cysts
 Has no neoplastic cells  An example of which is Ductal
o Solid Neoplasm (may or not be Carcinoma of the Breast
cancerous) • Most common type of Breast
• In modern English, means a neoplasm that cancer
has formed a limp o Classified by size and shape under
microscope
• Can be caused by other non-cancerous
 Giant Cell Carcinoma
conditions
 Spindle Cell Carcinoma
• Not all tumors are cancerous
 Small Cell Carcinoma
o Benign tumors do not grow, invade or
• Benign Tumors
spread
o Named using -oma with organ name as
the root
Classification
 Leiomyoma
• Neoplasms
o Confusingly, some cancers end with –
o Benign
oma
o Pre-malignant
 Carcinoma in situ
Epidemiology
o Malignant
 Cancer • ♂
o Most common is Prostate cancer
• Cancers
o Most common cancerous cause of death
o Classified by the type of cell that the
is Lung and Bronchus cancer by 29%,
tumor cells resemble
followed by Prostate cancer by 9%
 Presumed to be the origin of the
tumor Men 848,170
 Types include: Prostate 29%

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 Lung and Bronchus 14% • Local Effects
Colon and Rectum 9% o May occur due to either
Urinary Bladder 7%  Mass of tumor
Melanoma of skin 5% • In lung cancer, can cause
Kidney and renal 5% blockage
pelvis 4% • In esophageal cancer, can cause
Non-Hodgkin 3% narrowing of esophagus
lymphoma 3% • In colorectal cancer, can cause
Oral cavity 3% narrowing
Leukemia 18% • Masses in breasts / testicles may
Pancreas be easily felt
All other sites  Ulceration of tumor
• Can cause bleeding
• ♀ • In lungs, hemoptysis is likely
o Most common is Breast cancer • In bowels, rectal bleeding may
o Most common cancerous cause of death happen
is Lung and Bronchus cancer by 26%, • In bladder, blood in the urine
followed by Breast cancer by 14% • In uterus, vaginal bleeding
Women 790,740 o Initial swelling is painless
Breast 29% o Can cause build-up of fluid in chest or
Lung and Bronchus 14% abdomen
Colon and Rectum 9% • Systemic Symptoms
Uterine Corpus 6% o General symptoms, such as
Thyroid 5%  Unintentional weight loss
Melanoma of skin 4%  Fever
Non-Hodgkin Lymphoma 4% • Leukemia, Liver cancer and
Kidney and Renal pelvis 3% Kidney cancer can cause a
Ovary 3% persistent fever of unknown
Pancreas 3% origin
All other Sites 20%  Fatigue
 Skin changes
Etiology o Specific symptoms, termed as
• Chemicals paraneoplastic phenomena, may occur
• Diet and exercise  Myasthenia Gravis in thymoma
• Infection  Clubbing in lung cancer
• Radiation • Metastasis
• Hereditary o Due to spread of cancer to other
• Physical agents locations
• Hormones  Enlarged lymph nodes
 Hepatomegaly
Pathophysiology  Pain / Fracture of affected bones
1.) Mutation inactivates tumor suppressor gene  Neurological symptoms
2.) Cells proliferate
3.) Mutation inactivates DNA repair gene Complications
4.) Mutation of proto-oncogene • Pain
5.) Mutation inactivates more tumor suppressor o Acute
genes  Has a beginning and an end
6.) Cancer  <6 months
Clinical Manifestations  Can be readily described
• Initially  Controlled with meds
o “Great Imitator” o Chronic
 Not uncommon for people with  Most frequently seen in cancer
cancer to have been treated for patients
other diseases  No definite beginning or end
o Invariably produces no symptoms or  >6 months
signs  Difficult to describe
 Sometimes only as growing or  Not easily controlled
ulcerating mass • Fatigue
o Finding depends on type and location of o Manageable
cancer o Associated with chemo or radiation
o Few symptoms are specific therapy
 Many occur in individuals with other  Temporary
conditions • Difficulty in breathing

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 o Treatments may bring relief
• Nausea
o Doctors can often predict if treatment
can cause it
o Meds may help prevent or relieve it
• Diarrhea / Constipation
• Weight loss
• Unusual Immune System Reactions
o Paraneoplastic Syndromes
o In some cases, the body’s immune
system will attack healthy cells
• Recurrence
o All survivors have a risk for cancer
recurrence
o Some cancers more likely to recur than
others
General Diagnosis
• Cancer screening
o Diagnosing at its earliest stages can
provide best chances of cure
o Recommended screening:
 Cervical cancer in ♀ at least until the
age 65
 Colorectal cancer from age’s 50 – 75
y.o.
 Prostate cancer screening >75 y.o.
 Mammography for breast cancer
every 2 years for 50 – 74 y.o.
• Genetic Testing
o BRCA1 and BRCA2 genes
 Breast, ovarian, pancreatic cancers
o HNPCC, MLH1, MSH2, MSH6, PMS1 and
PMS2 genes
 Colon, uterine, small bowel, stomach
and urinary tract cancers
• Cancer Warning Signs
o CAUTION
 Changes in bowel / bladder habit
 A sore that does not heal
 Unusual bleeding / discharge
 Thickening or lump in body parts
 Indigestion or difficult in swallowing
 Obvious change in wart or mole
 Nagging cough / hoarseness
• Cancer Diagnostic Procedures
o Physical examination
o Blood / Urine test
o Medical imaging
o Biopsy
• Cancer Stages
o Overall stage grouping
 Referred as Roman Numeral Staging
 Stage 0
• Carcinoma in situ
 Stage I
• Localized cancer to one part
 Stage II
• Locally advanced cancer
 Stage III
• Locally advanced
• Sometimes dependent on kind
of cancer
 Stage IV
• Cancer have metastized
• Tumors
o Tumor Grading
 Grade 1
• Well differentiated
o Appears normal
o Growing slowly
o Not aggressive
 Grade 2
• Moderately differentiated
o Semi-normal
o Growing moderately fast
 Grade 3
• Poorly differentiated
o Abnormal
o Growing quickly
o Aggressive
o Benign Tumors
 Generally self-contained, localized,
have a well -defined perimeter
 Grow slowly, expanding outwardly
 Dangerous when they compress
surrounding tissues
 Restrict flow of blood if near a blood
vessel
• In abdomen, can impair
digestion
• In brain, can cause paralysis
o Malignant Tumors
 Not self-contained and usually do
not compress surrounding tissues
 Growth is irregular
 Invasive of adjacent cells
• Can grow either slowly or rapidly
• Not localize
• Can establish malignant growth
in a different type of tissue
Prognosis
• Reputation for being a deadly disease
o About 50% of people who receive
treatment for invasive cancer die from it
or its treatment
• Survival is worse in developing countries
• Survival rate vary dramatically between types
of cancers
o Range from all surviving to almost none
• Those that survive are at increased risk to
develop a second primary cancer at twice the
rate of those never diagnosed with cancer
o Believed to be due to the same risk
factors that produced the 1st cancer
• Predicting either short or long term survival
is difficult and depends on many factors
o Most important factors are the particular
kind of cancer and the patient’s age and
health
Risk Factors
• Age
• Habitat / Lifestyle
• Family history
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• Health conditions Problem List
• Environment • Pain
• Easy fatigability
General Health Care Management • Deconditioning
• Goals • Functional limitations
o Treat to kill / remove cancer cells • Lymphedema
 Primary
o Treatment to kill any remaining cancer PT Interventions
cells • Pain Management
 Adjuvant • Therapeutic Exercises
o Manage side effects and its treatment • Manual Therapy Techs
 Palliative care • Lymphedema Management
• Functional Training / Retraining
Cancer Treatments • Pulmonary Rehabilitation
• Surgery • Endurance / Strength Training
• Chemotherapy • Prescription / Fabrication / Training-devices
• Radiation Therapy
• Stem Cell Transplant Role of In-patient PT
• Biological Therapy • Multidisciplinary Care
• Hormone Therapy • Order Equipment
• Targeted Drug Therapy • Transfer Training
• Clinical Trials and Other Treatments • Family Education
• Discharge Planning
Other Management
• Breathing Difficulties / Cough Role of Out-patient PT
o PT / OT • Patient-centered Care
• Fatigue / Tiredness • Return to Prior Level of Function
o PT / OT / Dietician • Return to Work
• ↓ mobility / exercise tolerance / weakness • Assistive Device
o PT / OT • Out-patient services for:
• Pain o Lymphedema
o PT / OT / Dietician o Myofascial Release
• Dysphagia o Head and Neck Program
o SLT / Dietician o Therapeutic Exercise Program for
• Cachexia / weight loss / ↓ appetite  UE
o PT / Dietician  LE
• Specific info needs  Cardio
o PT / OT / Dietician / SLT
• Difficulties č ADL / Leisure / Work Role of PT in Palliative Care
o PT / OT • Work with the following conditions
• Specific Functional Impairments o Respiratory
o PT / OT o Neurological
• Equipment Needs o Lymphatic
o PT / OT o Orthopedic
• Anxiety / Stress o Musculoskeletal
o OT o Hematological
• Communication Difficulties o Pain
o SLT • Education and Training of MDT as well as
patients and caregivers
4 Levels of Rehabilitation • Dissemination of information to MDT
• Preventive • Communication and collaboration between
• Restorative primary and secondary care
• Supportive
• Palliative Re-evaluation Tests
Karnofsky Scale
PT Examination Able to carry on normal activity; no special care
• Focus depends on patient’s specific condition is needed
• Usual components are: 10 Normal; no complaints, n evidence of
o Pain disease
o Cardiovascular / Pulmonary 9 Able to carry on normal activity; minor
o Musculoskeletal signs or symptoms of disease
o Neuromuscular
o Functional

132 | P a g e
 8 Normal activity with effort; some signs
or symptoms of disease
Unable to work; able to live at home; cares for
most personal needs; varying amounts of
assistance is needed.
7 Cares for self; unable to carry on normal
activity or do active work
6 Requires occasional assistance, but is
able to care for most of own needs
5 Requires considerable assistance and
frequent medical care
Unable to care for self; requires equivalent of
institutional or hospital care; disease may be
progressing rapidly.
4 Disabled; requires special care and
assistance
3 Severely disabled; hospitalization is
indicated, although death is not
imminent
2 Very sick; hospitalization necessary;
active supportive treatment necessary
1 Moribund, fatal process progressing
rapidly
0 Dead

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GERIATRIC REHABILITATION & DECONDITIONING - Physiologic
SYNDROME • Cognitive Deficits
• Depression
Dementia
• Atypical presentations
Alzheimer’s disease
Osteoporosis • Motivation
Immobilization - Social
• Negative views of aging
Definition • Less frequent referrals
- The process of growing old • Financial barriers
- Describes a wide array of physiological
changes in the body systems; complex Pathophysiology
and variable Theories of Aging
I. Aging changes
Categories of Elderly A. Cellular changes
- Young Elderly : Ages 65 – 74 (60% of the a. Inc. in size; fragmentation of
population) golgi apparatus &
- Old Elderly: Ages 75 – 84 mitochondria
- Old, Old Elderly or Old Frail Elderly: Ages b. Decrease cell capacity to
>85 divide & reproduce
c. Arrest of DNA synthesis &
Epidemiology cell division
- 1990, more than 30 million Americans B. Tissue changes
or 12.7% of the U.S population of 65 a. Accumulation of pigmented
years age or older materials, lipofuscins
- Will increase to 17.3% by the year 2020 b. Accumulation of lipids &
and to 21.8% by the year 2050 fats
- Whites represent about 90% of persons c. Decrease elastic content,
over 65; only 10% are non-whites (8% degradation of collagen;
black) presence of pseudoelastins
- Leading Causes of Death in persons over C. Organ changes
65, in order of frequency: a. Decrease functional
• Coronary heart disease, accounts capacity
for 31% of deaths b. Decrease in homeostatic
• Cancer, 20% of deaths efficiency
• Cerebrovascular disease (stroke) II. Biological theories
• Chronic obstructive pulmonary A. Genetic: Genes are programmed to
disease (COPD) modulate aging changes, overall rate of
• Pneumonia/flu progression
- Leading Causes of disability/chronic Premature aging syndromes
conditions in persons over 65, in order a. Hutchinson-Gilford syndrome:
of frequency: progeria of childhood
• Arthritis, 49% b. Werner’s syndrome: progeria
• Hypertension, 37% of young adults
• Hearing impairments, 32% B. Doubling/Biologic Clock: Functional
• Heart impairments, 30% deterioration within cells is due to
• Cataracts & chronic sinusitis, 17% limited number of genetically
each programmed cell replication
C. Free radicals: highly reactive & toxic
• Orthopedic impairments, 16%
form of oxygen
• Diabetes & visual impairments, 9%
a. Causes damage to cell
each
membranes & DNA cell
• Most older persons (60-80%) report
replication
having on or more chronic
b. accumulation of aging
conditions
pigments
c. interfere c cell transport &
Etiology
diffusion
- Biologic
d. trigger pathologic changes:
• multiple diseases
cell mutations, atherosclerosis
• Deconditioning D. Cell mutation
• Contractures E. Hormonal theory: fxnal decrements in
• Polypharmacy neurons & associated hormones
• Subclinical organ dysfunction F. Immunity theory: becomes less fxnal

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Physiologic Changes & Adaptation in Older Adult
- Muscular
• Changes due to hypokinesis rather than
aging
• Decreased strength
• Loss of power
• Atrophy
• Fatigue more rapidly
- Skeletal System
• Cartilage changes: decreased H2O
content
• Loss of bone mass & density
• IVD: flatten, less resilient due to loss of
water content
• Senile postural changes
o Forward head
o Kyphosis
o Flattening of lumbar spine
o Hip & knee contractures
- Neurological System
• Atrophy of nerve cells
• Changes in brain form and structures
• Decreased cerebral blood flow and
energy metabolism
• Decreased synaptic transmission
• Neuronal loss, atrophy, slowed
conduction of spinal cord/peripheral
nerves.
• Tremors
- Sensory System
• Loss of function of the senses
• Vision
o General decline in visual acuity
o Cataracts, glaucoma, diabetic
retinopathy
o Small, irregular pupils
• Hearing
o Hearing loss, change in sound
sensitivity, understanding
speech, and maintenance of
equilibrium
• Vestibular/ balance control
o Diminished acuity, delayed
reaction time & longer response
time.
• Somatosensory
o Decreased sensitivity to touch
o Proprioceptive loss
o Loss of joint sensitivity
• Taste & Smell
o Decreased in taste & smell
sensitivity
- Cognition
• Decline in intellectual abilities
o Perceptual speed
o Numeric ability
o Verbal ability
o Memory
o Learning
- Cardiovascular system
• Degeneration of heart muscle
• Decreased blood flow
• Valves thicken and stiffen
• Decline of conduction system
• Blood pressure changes
• Decreased blood volume
• Increased blood coagulability
- Pulmonary System
• Chest wall stiffens & declining strength
of respiratory muscles
• Changes in lung parenchyma, blood
vessels
• Decline in total lung capacity
- Integumentary System
• Skin loss of elasticity, easily bruised,
dehydration, wrinkled, aging spots,
general thinning, slowed healing,
decreased sensitivity & sweat
production.
• impaired thermoregulation
• Appearance: skin appears dry, wrinkled,
yellowed, and inelastic; age spots
appear (clusters of melanocyte
pigmentation); increase with sun
exposure
• General thinning and graying of hair due
to vascular insufficiency and decreased
melanin production
• Nails grow more slowly, become brittle
and thick
- Gastrointestinal System
• Decreased salivation, taste & smell
• Inadequate chewing
• Poor swallowing
• Reduced motility and control of
esophagus
• Reduced motility, emptying, digestion &
absorption of stomach
- Renal System
• Kidney loss of mass, atrophy, decreased
blood flow & filtration
• Bladder reduced capacity
- Body Composition
• Gradual loss of lean tissue
• Increase in fat by 30% of body weight at
age 80
• Loss of bone mineral
• High prevalence of osteoporosis and
osteoarthritis
- Postural & Gait Changes
• Accentuated thoracic kyphosis
• Straightening of lumbar spine
• Increase hip and knee flexion
• Decrease ankle dorsiflexion
• Hand deformities
• Diminished arm swing
• Shorter step length
• Men: Widening of standing base; in
women: knee varus deformity with
narrow standing base
• Shift of center of gravity
• Increase postural sway
• Impaired balance
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 • Decreased righting reflexes
• Increased reaction time
- Immunologic System
• Increased autoantibodies and immune
complexes
• Decreased antibody production
- Endocrine-Metabolic System
• Gradual decrease in glucose tolerance
• Risk for untreated hyperglycemia,
osmotic diuresis, dehydration,
hyperosmolar nonketoic coma or
ketoacidosis
• Decrease production rate and metabolic
clearance rate of thyroid hormone
• Progressive decrease in cortisol
production
• Decreased estrogen levels in
postmenopausal women
• Altered male libido, potency, and sexual
arousal
Pathological Conditions Associated with the
Elderly
1. MUSCULOSKELETAL DISORDERS & DISEASE
A.OSTEOPOROSIS
– Examination
• Medical record review
• Physical activity/fall history
• Assess dizziness: Dizziness Handicap
Inventory
• Sensory integrity: vision hearing,
somatosensory, vestibular; sensory
integration
• Motor function: strength, endurance,
motor control
• ROM/flexibility/Postural deformity:
o Feet: hammer toes, bunions lead to
antalgic gait
o Postural kyphosis, forward head
position
o Hip and knee flexion contractures
• Postural hypotension
• Gait and balance assessment
– Maintain bone mass: regular weight-
bearing exercise
– Postural/balance training
– Safety education/fall prevention
B. FRACTURES:
High risk of fractures in the elderly:
associated with low bone density and
multiple risk factors; e.g., age, comorbid
diseases, dementia, psychotropic
medications
C. DEGENERATIVE ARTHRITIS (OA)
A non-inflammatory, progressive
disorder of joints; typically affects
hips, knees, fingers, and spine
M>F up to age 45
F (5x) > M by age 65
Characteristics:
• Pain, swelling, and stiffness,
worse early morning or with
over-use
• Muscle spasm
• Loss of ROM and mobility;
crepitus
• Bony deformity
• Muscle weakness secondary to
disuse
Goals, Outcomes and Intervention
• Medical management: NSAIDs,
corticosteroid injections, topical
analgesics, joint replacements
• Reduction of pain and muscle
spasm: modalities, relaxation
training
• Exercises (ROM, Aerobic,
Aquatic)
• Patient education and
empowerment
• Teach patients about disease,
taking an active role in care
• Teach joint protection, energy
conservation strategies
• Provide assistive devices for
ambulation and activities of
daily living
• Promote healthy lifestyle:
weight reduction to relieve
stress on joints
2. NEUROLOGICAL DISORDERS AND DISEASES
A.STROKE
– Sudden, focal neurological deficit
resulting from ischemic or hemorrhagic
lesions in the brain
– Most common cause of adult disability
in the United States
B. DEGENERATIVE DISEASE
– PARKINSON’S DISEASE
– Chronic, progressive disease of nervous
system
3. COGNITIVE DISORDERS
A. DELIRIUM
– Fluctuating attention state causing
temporary confusion and loss of mental
function; an acute disorder potentially
reversible
Characteristics:
• Acute onset, often at night;
fluctuating course with lucid
intervals; worse at night
• Duration: hours to weeks
• May be hypoalert or hyperalert,
distractible; fluctuates over course
of day
• Orientation usually impaired
• Illusions/hallucinations, periods of
agitation
• Memory deficits: immediate and
recent
• Disorganized thinking, incoherent
speech
• Sleep/wake cycle always disrupted
Goals, Outcomes and Intervention
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 • Provide safe and soothing - Informed consent
environment - Advance care medical directive (Living
• Support individual’s remaining Will)
function
• Provide regular physical activity Common Problems Areas for Geriatric Clients
• Participate in restraint reduction • Immobility – Disability
programs - Impaired mobility and disability
• Educate / Support family, caregivers - Limitations in function
• Present a realistic, consistent team - immobility
approach to management • Falls and Instability
B. DEPRESSION • Medication errors
– A disorder characterized by depressed • Nutritional deficiency
mood and lack of interest or pleasure in
all activities, and other associated Physiologic Benefits of Physical Activity
symptoms, lasting for at least 2 weeks • Aerobic/Cardiovascular Endurance
EXAMINE FOR DEPRESSIVE SYMPTOMS • Muscle strength
1. Nutrition problems • Flexibility
2. Sleep disturbances • Balance/coordination
3. Psychomotor changes • Velocity of movement
4. Fatigue or loss of energy
5. Feelings of worthlessness, low self-esteem, DECONDITIONING
guilt • Due to prolonged bed rest
6. Inability to concentrate, slowed thinking, • Results in a reduced functional capacity
impaired memory, indecisiveness of multiple body systems (especially
7. Withdrawal from family and friends, self- musculoskeletal system)
neglect • Causes numerous physiologic
8. Recurrent thoughts of death, suicidal adaptations in all organ systems, often
ideation with negative consequences
9. Decline in cognitive function • Levels of deconditioning
- Mild difficulty with Maximal
GOALS, OUTCOMES, AND INTERVENTIONS Activity – i.e. swimming,
 Medical treatment running, exercising
 Avoid excessive cheerfulness - Moderate difficulty with normal
 Assist patient in adjustment process to activity – 1.e walking down the
losses, coping strategies street, shopping, mowing the
 Encourage activities, exercise program lawn
 Assist in improving/maintaining - Sever difficulty with minimal
independence activity & self-care
4. CARDIOPULMONARY & INTEGUMENTARY
DISORDERS AND DISEASES Staircase to Dependence
A. Hypertension Weak, wobbly legs
B. Coronary artery disease More muscle weakness DEPENDENCE
C. Peripheral vascular disease Less ability to perform A steep and
D. Chronic bronchitis More muscle weakness rapid
E. Asthma Less ability to perform descent
Disuse atrophy
F. Chronic obstructive pulmonary disease
No ability to perform
G. Pneumonia
H. Lung cancer Staircase to Independence
I. Pressure ulcers PROGRESSIVE MOBILIZATION
A Slow long climb Stair Climbing
Patient Care Concepts Walking
- Recognize variability of older adults Standing
- Focus on careful and accurate clinical Transfering
examination Sitting
- Focus on functional goals Bed activities
- Promote optimal health
- Restore/maintain Common Causes of Immobility
- Holism • Multiple trauma/Orthopedic injury
- Recognize demands • Spinal Cord Injury
• Stroke
Ethical and Legal Issues • Prolonged hospitalization
- Professional practice

137 | P a g e
 • Multiple medical problems/Multiple
organ failure
• Myocardial Infarction
Muscle Weakness and Atrophy
• Cause: Disuse
Pathophysiology
• Loss of strength: total inactivity >10-20%
decrease in muscle strength pero week
(1.3% per day); in 305 weeks of
complete immobilization can lead to a
50% decrease in muscle strength
Involvement
• Greatest in the postural muscles (i.e low
back and weight bearing lower
extremity muscles quadriceps and
gastrocnemius soleus muscle groups)
• Contractures
• Disuse osteoporosis
CRITERIA FOR DIAGNOSIS/DIFFERNTIAL
DIAGNOSIS
- Medical History
• Drug history
• Dietary history
• Incontinence history
- Physical Examination
• Pelvic and breast
examinations in women
• Rectal exam in both male
and female
• Check urinary incontinence,
distended bladder, perineal
sensation and
• Bulbocavernososus reflexes
in male
- Laboratory Examinations
• Sedimentation Rate
• Fasting Glucose Test
• Serum Creatinine
Complications
THE FIVE I’S GERIATRICS/ THE GRIATRIC
QUINTET/ “O”COMPLEX
1. Intellectual impairment
2. Impaired mobility
3. Incontinence
4. Impaired homeostasis
5. Iatrogenic drug reaction
OTHER COMMON COMPLICATIONS
- Amputation
- Arthritis
- Burns
- Cancer
- Cardiovascular disorders
- Chronic pain
- Chronic pulmonary disease
- Contractures
- Deconditioning
- Disc disorders
- Fracture
- Head injury
- Trauma
- Joint replacement
- Lymphedema
- Neuropathy
- Osteoporosis
- Pain syndromes
- Parkinson’s Disease
- Postural disorders
- Pressure sores
- Spinal cord injury
- Spinal stenosis
- Stroke
Prognosis
Framing the definition of the outcome is
very important for the success and
professional rewards of the geriatric
rehabilitation. Their quality of life can
be maintained or improved through
appropriate rehabilitation
methodologies and social support from
family and community. Most elderly
patients live in the community with ages
85 and above, only 15% of men and 25%
of women live in a nursing home.
Discharge data reveal that over 85% of
these patients are discharged to a non-
institutional setting
Medical/Surgical Management
GENERAL PRINCIPLES OF GERIATRIC
MEDICINE
1) Individuals become more dissimilar
as they age, bellying any stereotype
of aging.
2) An abrupt decline in any system or
function is always due to disease
and not to “normal aging”.
3) “Normal aging can be attenuated to
some extent by modification of risk
factors.
4) “Healthy old age” is not oxymoron.
5) The onset of new disease in the
elderly generally affects the most
vulnerable organ system.
6) Disease in older patients often
presents at an early stage because
of their impaired compensatory
mechanism.
7) Homeostatic mechanisms are often
compromised, multiple
abnormalities are amenable to
treatment, and small improvements
in each may yield dramatic effects.
8) Many findings that abnormal in
younger patients are relatively
common in older people and may
not be responsible for a particular
symptom.
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 9) The diagnostic “law of parsimony”
often does not apply because
symptoms in older people are due
to multiple cases.
10) Treatment and prevention are
more effective in an older patient
who is more likely than a younger
one to suffer the adverse
consequences of the disease.
Drug Therapy
- Female Atropic Vaginitis: Estrogen
- Incontinence: Oxybutinin,
Anticholingergics, Calcium Channel
Blockers, Imipramine
- Sleep Disorders: Tricyclic
Antidepressants
- Depression: Tricyclic Antidepressants
- Agitation: Alprazolam, Imipramine, and
Buspirone, Tricyclic Antidepressants,
Antipsychotics
- Pain: Opiate Analgesics
- Hypotension: High Sodium diet and
Fludrocortisone Aceate, NSAIDs,
Clonidine, Midodrine, Propranolol,
Pindol, Phenylpropanolamine
Surgery
- Surgical techniques of creating artificial
urinary bladder sphincters
Physical Therapy Assessment
In the elderly, assessment tools measure
ADL and independent ADL. It is also
used to determine the cognitive status
of the patient. The Mini-Mental State
Examination (MMSE) is an example of a
screening tool to detect and assess
dementia, and delirium. The Geriatric
Depression Scale was developed to
screen for the common symptoms of
depression in the elderly. Gait and
balance instruments are also used for
both diagnostic assessment and
longitudinal of patient function.
FUNCTIONAL DISABILITY TESTING
A = Performed easily
B = Performed with some difficulty
C = Unable to perform
1. Touch first metacarpophalangeal
joint to top of head
2. Touch waist in back
3. Place fingertips to palmar crease; if
abnormal, test
4. Place palm of hand on contralateral
trochanter
5. Touch index finger pad to thumb pad
6. Sitting, touch toe or shoe
7. Stand unassisted; step over a 6-in
block
INSTRUMENTAL ACTIVITIES OF DAILY LIVING
(IADL)
- Shopping
- Cooking
- Cleaning
- Using the telephone
- Writing
- Reading
- Taking medications
- Climbing stairs
- Walking outdoors
- Using public transportation
- Managing
- Money
Dementia
Definition
- An organic and global
deterioration of intellectual
functioning without clouding of
conscience
Epidemiology
- Occurs most often in old age
- One million Americans over age
(5% of the aged population)
have a significant degree of
dementia and are unable to
care for themselves.
- Another two million ( 10% of
the aged ) have mild dementia,
and about 60% of persons in
nursing homes have some
dementia
- The prevalence of dementia
increases with age; it is 5 times
more common in 70 and
younger
- By year 2030 an estimated 20%
of the population will be over
age 65.
Etiology
- Primary degenerative dementia of the
Alzheimer type.
• The most common cause of
dementia
• 65% of all cases
- Multi-infarct Dementia
• Second most common
- Dementia related to human
immunodeficiency virus (HIV)
OTHER RELATED CAUSES OF DEMENTIA
- Parenchymatous diseases of the CNS
• Alzheimer’s disease (Primary
degenerative dementia)
• Pick’s disease (Primary
degenerative dementia)
• Huntington’s disease
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 • Parkinson’s disease
• Multiple sclerosis
- Systemic Disorders
• Endocrine and Metabolic
Disorders
 Thyroid disease
 Parathyroid disease
 Pituitary – Adrenal
disorders
 Posthypoglycmic states
• Liver Disease
 Chronic progressive
hepatic encephalopathy
• Urinary Tract Disease
 Chronic uremic
encephalopathy
 Progressive uremic
encephalopathy
(dialysis dementia)
• Cardiovascular Disease
 Cerebral Hypoxia or
Anorexia
 Cardiac Arrhythmias
 Inflammatory disease of
blood vessels
- Pulmonary States
• Respiratory encephalopathy
- Deficiency States
• Cyanocobalamin Deficiency
• Folic Acid Deficiency
- Drugs and Toxins
- Intracranial Tumors and Brain Trauma
- Infectious Processes
• Creutzfeldt-Jacob Disease
• Cryptococcal Meningitis
• Neurosyphilis
• TB and Fungal meningitis
 Viral Encephalitis
 Human
Immunodeficiency Virus
- Miscellaneous Disorders
• Hepatolenticular Degeneration
• Hydrocephalic Dementia
• Sarcoidosis
• Normal Pressure Hydrocephalus
Pathophysiology
Multiple neuropathologic processes
underlie dementia, including both
neurodegenerative diseases and
vascular disease. Most common in
elderly individuals, with advancing age
being the strongest risk factor.
Furthermore, comorbidity (the presence
of more than one disease process) is the
rule rather than the exception for
dementia in elderly persons
Clinical Manifestation
- Defects in orientation, memory
perception, intellectual function,
reasoning, and judgement
Complications
- Difficulty in learning new information
(short-term memory loss) and in
recalling personal data or commonly
known facts ( long-term memory loss)
- Impaired orientation for time may
appear early and always precedes
spatial disorientation for place and
person
- Language may be vague, stereotyped,
imprecise, and circumstantial
- Severely demented persons may
actually be mute
- Disturbance in constructional ability
- Agnosias and apraxias are present
- Abstract attitude
- Difficulty in generalizing from a single
instance, in forming concepts, and in
grasping similarities and differences
among concepts
- The ability to solve problems, to reason
logically, and to make sound judgments
is compromised
- Catastrophic reaction which is marked
by agitation secondary to subjective
awareness of one’s intellectual deficits
under stressful events
- Patients compensate for defects by
changing the subject, mak9ng jokes or
diverting the interviewer
- Lack of judgment and poor impulse
- Neglect for personal appearance and
hygiene
- General disregard for conventional rules
social conduct
- Sundowner’s syndrome characterized by
drowsiness, confusion, ataxia, and
accidental falls and occurs in demented
person when external stimuli such as
light and interpersonal cues are
diminished
Prognosis
The prognosis is good in acute
(reversible) cases, fare in moderate
cases, and poor in deteriorated states.
The average patient with dementia lives
7-10 years after early symptoms but
lifespan changes from 3-20 years.
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About 10-15% of all patients who exhibit
symptoms of dementia have potentially
treatable conditions. The treatable
conditions includes systemic disorders,
such as heart disease, renal disease, and
CHF; endocrines disorders such as
hypothyroidism; vitamin deficiency;
medication misuse; and primary mental
disorders, most notably depressive
disorders.
Osteoporosis
Definition
- A bone disease characterized by a
reduction of bone tissue relative to the
volume of anatomical bone which
increases susceptibility to fracture
Epidemiology
- Middle-aged and elderly people
- Postmenopausal women, and women in
the third decade of life.
- W>M
Etiology
- Osteoporosis presents when bone mass
lies more than 2 SD below the mean.
The bone is of normal size but contains
less bone tissue without change in the
ratio of mineral component to organic
material
- It may also present from immobility and
lack of normal weight bearing
Pathophysiology
- Bone loss occurs after the age of early
30’s, resulting to increase fracture risk
with normal or moderate trauma. The
main determinant of Osteoporosis are
the peak bone mass level reached at
skeletal maturity and the subsequent
rate of bone loss.
- Low bone mass may be due to multiple
causes, including failure to achieve
adequate bone mass at skeletal maturity
and postmenopausal bone loss.
Immobility
Definition
- Immobilization syndrome refers to the
effects of inactivity or immobility. There
is reduced functional capacity of all
systems including musculoskeletal,
cardiovascular and pulmonary
Epidemiology
- People who are chronically ill, aged or
disabled who are subjected to
prolonged bed rest are prone to the
effects of immobility
Etiology
- Inactivity of the body system due to
prolonged bed rest or after trauma, or
other, cases wherein there is no
movement of the body for extended
periods
Pathophysiology
- With contractures, there is shortening
of the muscle belly and loose CT
becomes dense. Muscles atrophy due to
disuse, and osteoporosis is due to loss of
weight-bearing
Complications
- Musculoskeletal
• Contractures
• Muscle weakness and atrophy
• Immobilization osteoporosis
• Immobilization hypercalcemia
- Cardiovascular and Pulmonary
• Redistribution of body fluids
• Orthostatic hypotension
• Reduction of cardiopulmonary
functional capacity
• Thromboembolism
• Mechanical resistance to
breathing
• Hypostatic pneumonia
- Genitourinary and Gastrointestinal
• Urinary stasis, stones and
urinary infection
• Loss of appetite
• Constipation
- Metabolic and Endocrine
• Electrolyte alteration
• Glucose intolerance
• Increased parathyroid hormone
production
• Other hormone alteration
- Congestive and Behavioral
• Sensory deprivation
• Confusion and disorientation
• Anxiety and depression
• Decrease intellectual capacity
• Impaired balance and
coordination
General Physical Therapy Management
PRINCIPLES OF GERIATRIC PRESCRIPTION
- Ascertain level of function (functional
assessment)
- Ascertain available resources and
options
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 - Avoid immobilization • Sleep disturbance
- be aware of altered physiological • Loss of appetite
reactions • Constipation
- Determine patient’s goals, motivation • Impaired concentration
- Determine family’s expectations • Poor memory
• Psychomotor
(psychosocial issues)
• Retardation
- Differentiate between delirium,
• Electroconvulsive
dementia, and depression
- Emphasize function; management not Agitation
diagnosis; cure • Develop social contracts for the
- Emphasize task-specific exercise; patient
simplify program • Physical modalities (heat, cold,
- Encourage socialization and stimulation massage)
• TENS
- Minimize medications
• Biofeedback
- Realize that function may not be
• Hypnosis
regained • Distractive techniques
- Recognize that patients have multiple • Encourage physical mobility and
interacting impairments activities
- Understand that improvement occurs in
slow increments Hypotension
- Symptomatic Orthostasis
Incontinence • Discontinue any prescribed or
- Timed voiding program over the counter medication to
• Initially intervals are very short the
(every 15-20 minutes) • Hypotension
• Then with progressive increases • Exercises (ankle dorsiflexion)
• Patterned urge-response before arising
toileting • Stand up slowly while holding
- Overflow incontinence due to detrusor on to a support
decompensation • Wear thigh-high elastic
• Long term and intermittent stockings or an abdominal
indwelling catheters blinder to minimize lower
• Cholinergic drugs extremity pooling
- Bowel incontinence secondary to diffuse
brain disease Preventive Medicine
• Biofeedback • Avoid smoking
- Bowel incontinence secondary to diffuse • Maintenance of an active and
brain disease challenging lifestyle
• Behavioral approach with bowel • Eat a well-balanced relatively
movements induced by low in cholesterol and saturated
• Suppositories intervals fat
• Immunizations
Sleep Disorders • Elimination of environmental
- Insomnia hazards
• Simple reassurance • Preservation of adequate
• Good sleep hygiene practices activity, nutrition, and
• Patients should avoid watching socialization
the clock during the night • Annual assessment by a
• Avoid day naps except if physician
absolutely needed briefly after
lunch

Depression
- Maintain a high index of suspicion for its
presence and vegetative signs of more
severe depression which include

142 | P a g e
 AMPUTATION foot ulceration or gangrene than the non-
diabetic population.
I. GENERAL MEDICAL BACKGROUND • A person who has diabetes or smokes is
A. Definition 3-4 times more likely to develop PAD compared
- It is the surgical cutting of a limb or outgrowth of to their non-diabetic or non-smoking
counterparts.
the body. The word amputation is reserved for
surgical, traumatic and disease created limb D. Etiology
loses. 1. Congenital Anomaly
- Refers to the absence or abnormality of a limb
B. Classification evident at birth or no etiology.
1. Acquired Amputation - I.e. polydactyl, congenital absence of a distal
- Loss of part or all of an extremity as the direct part
result of trauma or by surgery. It is also done to 2. Peripheral Vascular Disease (PVD)
- Berger’s Disease or Arteriosclerosis
revise a congenital limb amputation or alter a
- Emboli or thrombus may cause a loss of blood
deformity secondary to burns or trauma. supply to extremity resulting to ischemia,
2. Congenital Amputation ulceration, or gangrene requiring amputation
- Loss of a limb in uterus and are believed to - Mostly involve lower limbs and the level of
result from such stimuli as drug toxicity. There is amputation depends on the adequacy or
failure of formation or strangulation of limb remaining circulation
buds by the umbilical cord. 3. Trauma
- Amputation is done where blood supply or
tissues are so destroyed, gangrene is inventible
C. Epidemiology or reconstruction is impossible
- 5:1 Ratio of lower limb to upper limb - I.e. blast injuries
amputees, majority are men than women 4. Infection
• 90% lower extremity - I.e. chronic osteomyelitis, gas gangrene of high
• 5% partial foot and ankle virulence
• 50% below knee 5. Tumor
• 35% above the knee - For primary malignant tumors not possible to
• 7 - 10% at the hip resects or irradiate without heavy risks or
- Peripheral Vascular Disease (PVD) recurrence or dysfunction
• PVD without diabetes ranges 2-5% among * Without metastasis – amputation is curative
individuals * With metastasis – it is palliative (relieves pain;
• PVD with diabetes ranges 6-25% in acute or chronic infections that can’t be
• 7-13% usually is associated with other medical controlled by medical or ordinary surgical
problems such as cardiac dose and stroke treatment and has local or systemic sequelae or
-Trauma prevents and pathological fracture; enhance
• 75% of acquired amputation in UE chemotherapy; improve systemic status)
• primarily men aged 15-45 yrs. Old 6. Thermal, Chemical, Electrical Injuries
• Next most common cause for LE amputation - Excess of these creates severe tissue damage
- Disease and Tumors resorting to amputation
• responsible for about equal number of the
remaining acquired UE amputations E. Levels of Amputation
Two factors are considered:
• in LE, it accounts approximately 75% of all
acquired amputations among 60 years and • Circulation
above • Functional usefulness
• it is the most frequent cause of all amputation in SURGICAL PRINCIPLES
both the UE and LE among children aging 10-20 Level – sites of Election versus sites of Emergency
yrs. old Amputation Optimum Shortest Longest
Statistics Levels
• It is believed that every 30 seconds a Transradial Junction prox 3cm 5cm above
lower limb is lost somewhere in the world as a (forearm) 2/3 & distal below wrist joint
consequence of diabetic foot. 1/3 biceps
• The life time risk of an individual with insertion
diabetes developing a foot ulcer could be as high Transhumeral Middle third 4cm 10cm
as 25%. (arm) below above
• Amputations are preceded by foot axillary olecranon
ulcers in 75-85% of cases, usually in association fold
with infections and gangrene. Transfemoral Middle third 8cm 15cm
• Individuals with diabetes are 15X more (thigh) below above knee
likely to have PAD and 22X more likely to have joint

143 | P a g e
 pubic
ramus
Transtibial 8cm for every 7.5cm
(leg) metre of below
height knee joint
(12cm)
Amputation of the LEs
a. Foot & Ankle
A.1. Lisfranc’s Amputation/Distraction
- Amputation through tarsometarsal joint that
allows function of the foot distorts muscle
balance of foot creating intractable equinos
deformity.
A.2. Chopart Amputation
- Through the talonavicular and calcaneocuboid
joints
- A supracondylar amputation
- Equinos deformity of stump develops
C.2. Kirk’s Amputation
- Similar to a foot of the gorse and difficult to - A supracondylar tendoplastic
have a satisfactory prosthesis amputation
A.3. Symes Amputation C.3. Callander Amputation
- involves disarticulation at the ankle joints and - A supracondylar amputation with minimum
may include removal of the medial and lateral tissue dissection
malleoli and distal/fibular flares C.4. Roger’s Amputation
- Knee joint disarticulation with arthrodesis
A.4. Body Amputation and Pirogoff Amputation
(surgical fusion of the patella in anatomical
- Amputation done which include tibio-calcaneal position of the patella to the front of femur)
fusion C.5. Knee disarticulation
A.5. Partial Toe - Through the knee joint
-through the metatarsophalangeal joint C.6. Long Above Knee
A.6. Toe Disarticulation - Amputation of more than 60% femoral
length
- Through metatarsophalangeal joint
A.7. Partial Foot/Ray Resection
- Resection of 3rd, 4th and 5th metatarsal and
digits
A.8. Transmetatarsal
- Through midsection of all metatarsals
b. Below Knee Amputation (BKA)
- Transtibial amputation
- Best done at the junction of the middle and
upper thirds of the tibia, between 8 and 18 cm.
below the tibial plateau.
B.1. Short Below Knee
- Less than 20% of tibial length
B.2. Long Below Knee
- More than 50% of tibial length
d. Above Knee Amputation
B.3. Non-ischemic Limb
- Because patient’s knee joint is lost, it is
- The ideal level for amputation below the knee
extremely important that stumps be long as
is at the musculo-tendinous junction of the
possible to provide a strong lever arm for
gastrocnemius muscle. The distal third of the leg
control of prosthesis. The conventional, constant
is not satisfactory because there the tissues are
friction knee joint used in the most AK
relatively avascular and soft tissue padding is
prosthesis extends for 9-10cm distal to end of
scanty.
prosthetic socket and the bone must be
B.4. Ischemic Limb
amputated this for proximal to the knee to allow
- Amputations performed in ischemic limbs are
room for the joint.
customarily at a higher level, for example 10-
- Transfemoral amputation most commonly seen
12.5 cm distal to the joint line, than are
in the elderly
amputations in non-ischemic limbs
- Ideal length is 10-12 inches below the greater
c. Amputations through or just above the knee
trochanter
joint
e. Hip disarticulation
C.1. Gritti-Strokes

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- Amputation through the hip joint, pelvis intact
- Should be avoided because there is no
substitute for anatomical joint
f. Hemipelvectomy (Hind Quarter Ablation)
- Resection of lower half of the pelvis and bears
weight on soft tissues and chest cage
g. Hemicorporectomy (Humpty-Dumpty)
- Amputation of both lower limbs and pelvis
below L4/L5
2. Amputation of Upper Extremity
a. Forearm and Hand
- The optimal length is 7 inches below the tip of
olecranon and it shouldn’t exceed it
b. Krukenberg Amputation
- The forearm stump after a below – elbow
amputation is converted into a crude pinching
mechanism by separating the lower ends of
radius and ulna and cover them with soft tissues
c. Partial Hand Amputation
- Creates significance functional limitation and
special prosthetics and orthotic problems.
d. Amputation throughout the wrist
- with adequate palmar skin, the carpal bones
should be retained when possible to be useful
for a patient with or without prosthesis
e. Wrist Disarticulation
- Although carpus disarticulation has occasionally
been possible, this is not often practical.
Disarticulation at the radio-carpal joint is the
much more common site for total head
amputation.
f. Forearm Amputation
- as much length as possible should be preserved
g. Short Below Elbow Amputation
- The most proximal useful stump measure 1.5”
below the insertion of the biceps tendon. The
prosthesis for this stump must be short to allow
elbow flexion yet long enough to hold the stump
securely.
h. Long Below Elbow Amputation
i. Elbow Disarticulation
- This is uncommon. When the forearm is
disarticulated at the elbow or amputation occurs
at a higher level, a mechanical elbow joint is
required to place the forearm and terminal
device is use.
j. Supracondylar Amputation
- Above elbow amputation are most satisfactory
at this level, because above this functional
efficiency becomes less as shoulder ids
approached and at least 2” of bone stump
should remain below anterior axillary fold.
k. Short Arm Stump
- Amputation may be carried out within 2.5”
above the anterior axillary fold.
l. Forequarter or Interscapulothoracic Amputation
- Severe deforming procedure with removal of
scapula and most of clavicle required for
treatment of malignant disease
m. Cineplastic Amputation
- the power of one or more of the patient’s
muscle transmitted by means of a small peg
traversing a muscle tunnel lined by the skin used
to activate prosthetic hand mechanism
F. Complications
- Hematoma
- Infection
- Necrosis of stump end
- Neuroma at the cut nerve ending
- Phantom pain
- Terminal overgrowth (children)
- Contractures (due to muscle imbalance)
Level of Typical Method of Prevention
Amputat Contractu
ion re
Above Extend When supine in bed, the patient
Knee should be positioned with sand
bags to prevent external rotation
Abductio ROM exercises and resistive
n exercises to the hip abductors
are useful
Flexion The patient spent large portions
of each day in the position
Below Hip Method of prevention are
Knee Flexion identical to those listed under
above knee amputation
Knee When sitting, the leg should be
Flexion positioned on board so that knee
is in full extension
Pain
• In the postoperative period must distinguish
between normal postoperative (i.e., surgical)
pain and phantom limb pain.
• Surgical pain usually responds well to opioids.
• Phantom limb pain usually is like a burning,
stinging, electric pain, and it can be increased
with anxiety and stress.
• Phantom pain is quite common initially,
• If it is still present at 6 months post-surgery, the
prognosis is unfavorable.
• Phantom limb sensation also must be
differentiated from phantom limb pain.
• Phantom limb sensation is the sensation that the
amputated limb is still present
• Patients usually report that the absent
hand/arm/limb is itching, tickling, or moving
through space.
• Phantom sensation is perceived as a "funny" or
"different" feeling but usually is not perceived as
painful.
PHANTHOM LIMB PAIN THEORIES

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• Three theories as to why patients experience II. GENERAL HEALTHCARE MANAGEMENT
phantom limb pain and sensation exist. A. Medical, Surgical, and Pharmacological
• One theory is that the remaining nerves 1. Medical Management
continue to generate impulses. Goal: non-tender & healthy residual limb for
prosthetic use.
• A second theory is that the spinal cord nerves
Promote healing:
begin excessive spontaneous firing in the
• Careful handling
absence of expected sensory input from the
• Controlling edema
limb.
• Preventing infection
• The third theory is that there is altered signal
Types of Dressing
transmission and modulation within the • Closed rigid dressing
somatosensory cortex.
• Removable rigid dressing
• Soft dressing
PAIN MANAGEMENT
• Difficult to treat; no “gold standard”
• First line: antidepressants & anticonvulsants.
• Some success using N-methyl-D-asparate
antagonists, gabapentin, calcitonin, mexiletine,
& opiates.
• Little to no success using NSAIDs, paracetamol,
beta-blockers, capsaicin, local anesthetic blocks.
TELESCOPING
• Another common phenomenon is telescoping.
• Telescoping is the sensation that the distal part
of the amputated extremity has moved
proximally up the arm.
• A patient might report that it feels like the entire
extremity has shrunk so that the hand is now up 2. Surgical Management
at the elbow. A. Basic Surgical Procedures of Amputation
• This is a normal part of the nerve healing General Procedure:
process and usually fades with time. 1. Surgeon removes part or all of the limb
- Type of amputation is at the discretion of the
G. Criteria for Diagnosis surgeon and the state of the extremity at the
* General Indications for Amputation time of the amputation.
1. Irreparable loss of blood supply in a disease or 2. Allow for 1 or 2 wound healing.
injured limb
3. Construct a resident limb for optimum
2. Injury that is so severe that function would be
better after amputation prosthetic fitting and function.
3. To save life when infection is uncontrollable B. Types of Surgical Amputation
4. To remove part or all of a congenital abnormal 1. Open Amputation (Guillotine Amputation)
limb for cosmoses or improving functions - Often indicated for infection.
2. Closed Amputation (Flap Amputation)
H. Prognosis - Amputation in which the stump is closed or
There are number of factors that may affect
covered by a flap of skin sutured over the bone
healing. Postoperative infection, whether from
external or internal sources is a major concern. end of the stump. This type of amputation is
Individual with contaminated wounds, from preferred when there is no evidence of infection
injury, infected foot ulcers, or other causes are and consequently no need for extensive open
at greater risk. Research indicates that smoking drainage.
is major deterrent to wound healing, with one 3. Minor Amputation
study reporting that cigarette smokers had a 2:5
- Amputation done through or distal to the
higher rate of infection and reamputation than
metacarpus or the metatarsus
non – smokers. There is some indication that
failed attempts at limb revascularization may 4. Major Amputation
negatively influence healing at below – knee - Amputation is done proximal to the metatarsal
levels. Other factors influencing wound healing or metacarpal bones and they are designed to
are the severity of the vascular problems, produce a stump suitable for an artificial limb
diabetes, renal disease, and other physiologic 5. Joint Amputation
problems such as cardiac disease.
- Amputation done at the joint

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 C. Other Healthcare(Rehabilitative/Supportive) IV. PHYSICAL THERAPY PROGNOSIS
A. Plan of Care
III. PHYSICAL THERAPY EXAMINATION, EVALUATION B. Intervention
& DIAGNOSIS
A. Points of Emphasis in Examination 1. Ultraviolet Irradiation – has a physiological
effect on the skin. Depending on the dosage,
a. Pre-prosthetic Management
they increase circulation, cause erythema, and
1. Pre-operative Care: Education and prevention
kill bacterial growth.
of further adversity
2. Whirlpool Bath – stimulates stump circulation,
b. Acute Post-Operative Care
help de sensitize the tender stump, provide
1. Healing without complication
gentle rinsing debridement of the wound,
Goals:
disinfect the wound, contribute to a general
• Reduce edema
feeling of well-being
• Prevent Contractures
3. Wound taping – indicated for suture line splits
• Prevent cardiopulmonary and
and small open wounds
general body conditioning
4. Stump immobilization – in early post-
• Educate the patient and family operative stages, when it becomes evident that
• Provide psychological support healing will not occur by primary intention, the
c. Immediate Post-operative dressing rigid dressing is reapplied. This non-weight
d. Immediate Post-operative prosthesis bearing resting cast promotes healing by
e. Pre-prosthetic Assessment Guide protecting the wound from external trauma,
1. General Medical Information controlling edema, and preventing tissue
• cause of amputation mobility.
• associated diseases and symptoms 5. Topical medications – like hygeol, saylon,
• current physiologic state (postsurgical providine, hydrogen peroxide, cicatrin. These
cardiopulmonary status, vital signs, can be used to further stimulate wound healing
duration of time out of bed, pain) and/or oral antibiotics to combat any infection.
2. Skin
• scar (healed, adherent, invaginate, flat) Management for Patients with Phantom Pain
• other lesions (size, shape, open scar 1. Pre-operatively, inform patient about
tissue) phantom sensation which is normal and not
• moisture (moist, dry, scaly) harmful.
• sensation (absent, diminished, 2. Post-operatively, examine the stump’s
hyperesthesia) appearance, sensation and function.
• grafts (locations, type, healing) 3. Observe proper post-operative care.
• dermatologic lesion (psoriasis, eczema, 4. For a healed stump wound, instruct patient to
cysts) massage it with an emollient lotion and apply
3. Residual Limb Length tincture of benzoin afterward to toughen the
4. Vascularity skin. Patient can also do gentle pounding or
• pulses slapping of the stump or use a mechanical
• color vibrator without traumatizing the scar.
• temperature 5. Exercise the stump muscles through
• edema imaginary movement of phantom limb.
• pain 6. Provide a functional as well as cosmetic
• trophic changes prosthesis as soon as possible to reduce or
5. ROM relieve phantom pain.
6. MMT 7. A number of measures may block neural
7. Neurologic conduction and relieve the phantom pain e.g.
• pain (phantom) ethyl chloride spray
• neuropathy
Treatment Goals
• cognitive status
1. Reduce edema and shape limb for prosthetic
• emotional status
fit
8. Functional Status
A. Intermittent compression pump therapy
B. Elevation with active exercise
B. Problem List
C. Elastic wrapping of the residual limb
- Edema or Swelling
D. Commercially made stump shrinkers
- Altered sensation
*elastic bandage not only help control edema
- LOM
but also shrink and shape the residual limb prior
- Decreased muscle strength
to prosthetic casting.
- Phantom pain
2. Instruct patient in stump hygiene
3. Increase strength of all extremities and trunk.
D. PT Diagnosis
Maintain ROM and prevent contractures.

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 A. Dynamic stump exercises
B. Conventional progressive resistive
exercise
C. Proprioceptive neuromuscular
facilitation
D. Sling suspension techniques
4. Teach independence in ambulation (with and
without prosthesis)

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 FRACTURES disease such as tumor, cysts,
osteomyelitis, or osteoporosis
I. GENERAL MEDICAL BACKGROUND
Classifications
Definition - According to site
- A fracture is defined as any break in A. Diaphyseal
the continuity of a bone. B. Metaphyseal
- C. Epiphyseal
Epidemiology D. Intra-articular
- Trauma causes more than 140,000
- According to extent
deaths per year in the United States.
A. Complete
- Extremity fractures are most
B. Incomplete
common in men younger than 45 yo
- According to configuration
and women over 45 yo
A. Transverse
- Most common fracture prior to age
B. Oblique or spiral
75 is wrist fracture; most common
C. Comminuted
after the age of 75 is hip fracture
- Relationship of the fragments
- Traumatic fractures > Pathological
A. Undisplaced
fracture
B. Displaced
- Most common cause of traumatic
- Relationship to the environment
fracture: sports/recreational
A. Closed (skin intact)
activities > MVA > falls
B. Open (fractured or object
- Most common cause of pathologic
penetrate the skin)
fracture: primary metabolic
diseases/conditions > neoplastic
Pathophysiology
diseases Stress placed on a bone, exceeds the
bone’s ability to absorb it
Etiology
- Traumatic Fracture
Injury in the bone
• Direct trauma – direct
application of force to Disruption in the continuity of bone
fracture site; tapping
fractures, crush Disruption of muscles and blood vessels
fractures, penetrating attached to the ends of bone
fractures (eg. Fracture
of metatarsal bone by a Tissue debris and blood clotting
heavy weight dropped
on the foot) Inflammatory reaction occurs
• Indirect trauma – force
acting at a distance STAGES OF HEALING:
from fracture site; - Reactive Phase
traction fracture, • Fracture and Inflammatory
angulation fracture, Phase
rotation fracture,  After fracture, there
compression fracture is the presence of
(eg. Radial head blood cells within
fracture by FOOSH) the tissues adjacent
- Stress Fracture: Result of bone to injury site
fatigue from repeated,  Blood Vessels would
unaccustomed loading and then constrict to
inadequate muscular support prevent further
- Common sites: metatarsal, fibula, bleeding
tibia, femur  Blood clot
- Pathological Fractures: occur in formation
bones weakened by preexisting  All of the cells
within the blood

149 | P a g e
 clot degenerate and
die
- Granulation Tissue Formation
• Fibroblasts survive and
replicate
• Form the granulation tissue
- Reparative Phase
• Cartilage Callus Formation
1. Periosteal cells replicate and
transform
Periosteal cells closest to
fracture gap  Chondroblast 
Hyaline Cartilage
Periosteal cells further from
fracture gap osteoblast
Woven bone
2. Fibroblasts in granulation
tissue Chondroblast
Hyaline Cartilage
• Lamellar Bone Deposition:
Replacement of hyaline
cartilage and woven bone with
lamellar bone
1. Bony Substitution: Replacement
of woven bone
2. Endochondral Ossification:
replacement of hyaline cartilage
3. Lamellar bone mineralized and
forms the mineralized matrix
4. Lamellar bonetrabecular
bone
- Remodeling Phase
• Remodeling the original bone
contour
1. Trabecular bone resorption
by osteoclasts osteoblast
deposit compact bone
TIME FOR HEALING
- Varies with age, location and type of
fracture, whether it was displaced,
and the blood supply to the
fragments
- Generally, children heal within 4 to
6 weeks; adolescents within 6 to 8
weeks; adults within 10 to 18 weeks
Clinical Manifestations
• Pain and tenderness
• Decrease function of the part
• Swelling
• Visible or palpable deformity
• Abnormal movement and
crepitus
• Visible bruising
Complications
• Swelling that is contained within
a compartment leading to nerve
and circulatory compromise
• Fat embolism that migrates to
the lungs and blocks pulmonary
vessels
• Problems with fixation devices
such as displacement of screws
and breakage of wires
• Infection that may occur locally
or systematically
• Refracture
• Delayed or malunion
TYPES OF ABNORMAL HEALING OF FRACTURES
• Malunion: Fracture heals in
unsatisfactory position resulting
in a bony deformity
• Delayed Union: Fracture takes
longer than normal to heal
• Nonunion: Fracture fails to unite
with a bony union
Diagnosis
- History
• Details of the injury or accident
should be recorded
• Record of the time and place of
the injury
• Age of the patient (certain
fractures predominate in
particular age groups)
• History of pain or deformity
preceding fracture
• In patients with open fractures,
ask for any immunizations for
tetanus
• History of recent respiratory
infection or of cardiac or renal
difficulty may modify the
treatment
• Allergies in medications in
connection with anesthesia and
antibiotics
- Physical Examination
• Respiratory difficulties –
obstructions produced by
edema and accumulated
secretions in respiratory tract;
include tension pneumothorax,
open wounds on chest, and an
unstable or flail chest
150 | P a g e
 • Acute hemorrhage –arterial and shaft fractures and cervical spine
venous bleeding injuries
• Shock – cold, clammy skin, rapid • Open surgery – used when fracture
and thread pulse segments are caught within soft tissues
- Roentgenographic examination 2. Maintenance of reduction
• X-ray films • External fixation by cast or splint – most
• CT Scan in diagnosing the more common; plaster cast fixation is
difficult injuries, particularly especially applicable where bones are
fractures of the pelvis, spine and close to the surface and can be held
complex intra-articular fracture efficiently by the cast; cast are less
effective for immobilizing fractures
Differential Diagnosis bones that lie deep in the muscles;
Traumatic Stress Pathologic usually effective in controlling
Fracture Fracture Fracture angulation and rotation in long bone
Presence of None None Yes fractures
underlying • Traction – used in fractures that cannot
disease be immobilized efficiently by casts;
Magnitude Maximal Submaximal Usually muscles act as internal splint to protect
of force minimal
the fracture; disadvantage: patient is
Speed of Quick Repetitive Usually
required to remain in bed and usually in
force quick
hospital
Prognosis • Internal fixation by nail, plate, or screws
FACTORS IDEAL PROBLEMATIC – used when other methods of
Age, Years Youth Advanced age maintaining the reduction of the
(>40 yo) fracture is unreliable or impractical;
Comorbidities None Multiple disadvantage: converts a close fracture
medical
into an open fracture and may lead to
comorbidities
infection
Medications None NSAIDS,
3. Preservation and restoration of function –
corticosteroids
patient develops joint stiffness and muscle
Social Factor Nonsmoker Smoker
atrophy after the period of immobilization;
Nutrition Well nourished Poor nutrition measures to preserve the strength of muscles
Fracture Type Closed fracture, Open fracture and the mobility of joints should be started early
neurovascularity with poor in the period of fracture healing; active
intact blood supply movement of the joints above and below the
Trauma Single limb Multiple cast should be done; muscle setting, or
traumatic isometrics of the muscles covered by the cast
injuries can usually be started a day or two after the
Local factors No infection Local infection application of cast and increased as the fracture
stabilizes; joints should be kept in functional
II. GENERAL/ HEALTHCARE MANAGEMENT position
Medical & Surgical Approach
Pharmacological Approach
THREE PRINCIPLES OF FRACTURE TREATMENT - Analgesics for pain relief
1. Reduction: Manipulation of the bone to - Biphosphonates – bone density-enhancing
restore correct alignment OTHER HEALTHCARE MANAGEMENT
• Reduction by manipulation – most • Occupational Therapy
common; may involve longitudinal • Nursing care
• Orthotist
traction to restore length, angulation to
allow locked fragments to disengage
III. PHYSICAL THERAPY EXAMINATION,
and slide past one another, and manual EVALUATION, AND DIAGNOSIS
pressure of the bone fragments into
proper position A. Points of Emphasis on Examination
• Traction – applied over a period of • Patient History
several hours or days; sustained - Relevant Demographic Data
o Age
traction is generally used when the
o Sex
traction will also be used to maintain o Medications
reduction; commonly used in femoral

151 | P a g e
 - Chief complaint IV. PHYSICAL THERAPY PROGNOSIS (Plan of care
- History of present injury & Intervention)
(pathomechanics) • Period of Immobilization
- Past medical history PLAN OF CARE INTERVENTION
- Patient’s lifestyle 1. Educate the 1. Teach functional
- Home situation patient adaptations
- Patient’s Goal Teach safe
• Physical Examination ambulation, bed
- Ocular inspection mobility
o Skin 2. Decrease effects of 2. Ice, elevation
inflammation
o Bony landmarks and
3. Decrease effects of 3. Intermittent
deformities
immobilization muscle setting;
- Palpation AROM on joints
o Bone above and below
o Skin immobilized region
o Muscles
o Peripheral vasculature 4. if patient is 4. Resistive exercises
- Crepitus confined to bed, to major muscle
- Cardiopulmonary Assessment maintain strength groups not
o Check for probable and ROM in major immobilized,
cardiopulmonary muscle groups especially in
complications preparation for
future ambulation
- Neurologic Assessment
o Check for probable • Post-immobilization
neurologic affectation PLAN OF CARE INTERVENTION
o Sensations 1. Educate the patient 1. inform patient’s
limitations until
- Balance and coordination
fracture site is
- Musculoskeletal Assessment
radiologically
o Joint play healed; teach home
o ROM exercise
o Muscle strength 2. Provide protection 2. use partial weight
o Limb Girth until radiologically bearing in LE and
o Muscle Bulk healed nonstressful
o Limb Length activities in the UE
- Postural Assessment 3. Initiate active 3. AROM; gentle
- Gait Assessment exercise multiangle
- Functional Assessment isometrics
4.increase joint and 4. initiate joint play
soft tissue mobility stretching
Problem List
techniques
• Period of Immobilization 5. increase strength 5. as ROM increases
 Initially, inflammation and and muscle and bone heals,
swelling endurance initiate resistive and
repetitive exercises
 In the immobilized area, 6. improve 6. initiate safe
progressive muscle atrophy, cardiorespiratory aerobic exercises
contracture formation, cartilage fitness that do not stress
degeneration, and decreased the fracture site
until it is healed
circulation
 Potential overall body
weakening if confined to bed
 Functional limitations
• Post-immobilization
 Pain with movement
 Decreased ROM
 Decreased joint play
 Scar tissue adhesions
 Decreased strength and
endurance
PT Diagnosis
Impaired joint mobility, muscle performance,
and range of motion associated with fracture

152 | P a g e
 JOINT REPLACEMENT PROCEDURES
Orthopedic surgery or Orthopedics
• (Also spelled orthopaedic surgery and
orthopaedics in British English) is the branch of
surgery concerned with conditions involving the
musculoskeletal system.
• Orthopedic surgeons use both surgical and
nonsurgical means to treat musculoskeletal
trauma, sports injuries, degenerative diseases,
infections, tumors, and congenital disorders.
The Need for Surgical Intervention
• Injuries, diseases, and disorders of the
musculoskeletal system that affect muscles,
tendons, ligaments, cartilage, fascia, joint
capsules, or bones can cause impairment of the
upper or lower extremities or the spine,
resulting in functional limitation and disability to
such an extent that surgical intervention is
required
Statistics/Epidemiology
2008 -National Interview Survey
110 million adults (50% of the adult population)
are having disabling musculoskeletal condition
2002-2004
Average annual direct costs is estimated @
$510billion
Average annual indirect costs is estimated @
$840 billion
CLASSIFICATIONS:
Muscle Repair
Definition: It is surgery to repair damaged or
torn muscles.
Indications: complete tear or rupture of a muscle
Procedure: The muscle is reopposed, sutured,
and immobilized so it is initially held in a
shortened position as it begins to heal. Patient
can achieve a more satisfactory outcome with a
late repair (approx 48 to 72 hrs after injury) after
acute symptoms have decreased
Tendon repair
Definition: It is surgery to repair damaged or
torn tendons.
Indications: Tendon laceration
Procedure: The surgeon makes a cut on the skin
over the injured tendon. The damaged or torn
ends of the tendon are sewn together. If the
tendon has been severely injured, a tendon graft
may be needed. In this case, a piece of tendon
from the foot, toe, or another part of the body is
often used. If needed, tendons are reattached to
the surrounding tissue. The surgeon examines
the area to see if there any injuries to nerves
and blood vessels. When complete, the wound is
closed. After the tendon is sutured, the repaired
muscle-tendon unit is maintained in a shortened
position, as with complete tear of a muscle.
Complete tear or laceration of a tendon
should be repaired immediately or within a few
days after injury = tendon begins to retract,
making reattachment difficult.
Ligament Repair or Reconstruction
Definition: It is a surgery to repair damaged or
torn ligaments. Repair involves approximating
and suturing the torn ligament. Reconstruction
is accomplished with a tissue graft taken from a
donor site.
Indication: Ligament tear or laceration, recurrent
instability, px who expect to return to relatively
high levels of fxnl activity (athletes)
Procedure: There are several surgical procedures
that involve ligamentous repair or
reconstruction. Common among these surgeries
is that postoperatively, the joint is held in a
position that places a safe level of tension on the
sutured or reconstructed ligament during the
healing process.
Capsule Stabilization & Reconstuction
Definition: A surgical procedure done to restore
the appropriate stability of joints that have
become unstable unstable (ranging from
subluxation to gross instability and recurrent
dislocation)
Indication: traumatic dislocation with associated
capsular or labral avulsion or fracture, recurrent
dislocation, symptomatic subluxation despite a
course of nonoperative tx, irreducible (fixed)
dislocation.
Procedure:
a.) Capsulorrhaphy (capsular shift): using an
arthroscopic or an open approach, a specific
portion of the capsule is incised and tightened
by overlapping and then suturing the redundant
tissue.
b.) Capsulolabral reconstruction: involves
arthroscopic or open repair of a capsular lesion
and labral tear by reattaching the labrum to the
rim of the glenoid combined with stabilization of
the capsule.
c.) Electrothermally assisted capsulorrhaphy. For
electrothermally: assisted capsulorrhaphy, using
an arthroscopic approach, thermal energy(laser
or radiofrequency)
Tendon Transfer or Realignment
Definition: A surgery wherein a tendon is shifted
from its original attachment to a new one to
restore the action that has been lost. The
transfer of realignment of a muscle-tendon unit
alters the line of pull of a muscle
Indication: to improve the stability of an
unstable joint
Procedure: During tendon transfer or
realignment procedure, usually the distal
attachment of the muscle-tenon unit is removed
from its bony insertion and reattached to a
different bone or a different tendon. The
muscle-tendon unit is then immobilized in a
shortened position for a period of time. After its
153 | P a g e
insertion has been moved, when the muscle
fires, it will produce a different action,
depending on where it has been inserted.
Myotomy
Definition: A surgery in which a muscle is cut
(myo- denotes muscle). While many surgeries
may involve the cutting of some muscles, the
term myotomy is reserved for a procedure with
the specific intent of cutting a muscle. Common
example is the Heller myotomy.
Indications: achalasia, a disorder in which the
lower esophageal sphincter fails to relax
properly, making it difficult for food and liquids
to reach the stomach. (e.g. Heller Myotomy)
Procedure: During the procedure (Heller
Myotomy), the patient is put under general
anesthesia. Five or six small incisions are made
in the abdominal wall and laparoscopic
instruments are inserted. The myotomy is a
lengthwise cut along the esophagus, starting
above the LES (lower esophageal sphincter) and
extending down onto the stomach a little way.
The esophagus is made of several layers, and the
myotomy only cuts through the outside muscle
layers which are squeezing it shut, leaving the
inner muscosal layer intact.
Tenotomy
Definition: The cutting of a tendon. This and
related procedures are also called tendon
release, tendon lengthening, and heel-cord
release (for tenotomy of the Achilles tendon)
Indications: infants w/ clubfoot, older patients
who develop contractures or subluxations from
neuromuscular disease, the upper motor neuron
syndrome, or other disorders
Procedure: During a tenotomy, the tendon is cut
entirely or partway through, allowing the muscle
to be stretched. Tenotomy may be performed
through the skin (percutaneous tenotomy) or by
surgically exposing the tendon (open tenotomy).
The details of the operation differ for each
tendon.
During a percutaneous lengthening of
the Achilles tendon, a thin blade is inserted
through the skin to partially sever the tendon in
two or more places. This procedure is called a Z-
plasty, and is very rapid, requiring only a few
minutes. It may be performed under local
anesthesia. More severe contracture may be
treated with an open procedure. In this case, the
tendon may be cut lengthwise, and the two
pieces joined lengthwise to form a single longer
tendon. This procedure takes approximately half
an hour. This type of tenotomy is usually
performed under general anesthesia. If multiple
joints are to be treated (for example, ankle,
knee, and hip), these are often performed at the
same time.
Fasciotomy (Fasciectomy)
Definition: A surgical procedure where
the fascia is cut to relieve tension or pressure
commonly to treat the resulting loss
of circulation to an area of tissue or muscle.
Indications: Compartment syndrome is one of
the conditions where a fasciotomy may be
indicated. People who are likely to suffer injuries
needing a fasciotomy include the following:
• Victims of vehicular accidents or crush injuries
• Athletes who have sustained one or more
serious impact injuries
• People with severe burns
• Persons who are severely overweight
Procedure: Fasciotomy in the limbs is usually
performed by a surgeon under general or
regional anesthesia. An incision is made in the
skin, and a small area of fascia is removed where
it will best relieve pressure.
Synovectomy
 Involves surgical removal of the synovium (lining
of the joint)
 Synovectomy of a joint is usually performed
using an arthroscopic approach and is most
commonly performed on the knee, elbow, wrist
and MCP joints.
 When synovium proliferates in the synovium
sheaths of tendons, it is referred to as
tenosynovitis.
 Removal of excessive synovium from tendon
sheaths is known as tenosynovectomy.
Indications:
• Rheumatoid Arthritis
• Joint Infection
• Joint Trauma
• Exposure to toxins
• Hemophiliac Arthritis
• Pigmented villonodular synovitis (an idiopathic
joint disorder resulting from brownish-colored
nodular growth in the villi of the synovium)
Procedure:
In an open procedure, the joint capsule is
exposed through an incision over the affected
joint (arthrotomy). The lining is identified and
removed by scraping and cutting. A soft
pressure dressing is applied to control swelling.
Early limited joint motion is encouraged to
prevent scar tissue (adhesions) from forming in
the joint that would limit range of motion.
More often, a synovectomy is performed
arthroscopically. A thin, fiberoptic surgical and
viewing instrument (arthroscope) is inserted into
the joint space through a small skin incision to
visualize the interior of the joint. Instruments
are then inserted into the joint through 4 or 5
other tiny incisions (portals) to cut away the
synovium. An irrigation solution is infused into
the joint to help clear the area of debris created
during the procedure. The arthroscopic
approach is generally less invasive and requires
only a few small incisions.
154 | P a g e
 Arthroscopic Debridement
 Surgical removal of fibrillated cartilage, unstable
chondral flaps, and loose bodies (fragments of
cartilage or bone) in a joint.
Indications:
• Acute Effusion
• Earlier stages of degenerative joint disease
• Well localized joint line tenderness
• patients with imaging studies confirming loose
bodies
• A ragged meniscus or cruciate ligament
Abrasion Arthroplasty
• Also known as abrasion chondroplasty
• It is performed first by debriding the damaged
articular cartilage remnants and any fibrous
tissue within the defect back to the demarcation
of the surrounding healthier cartilage to allow
clot binding to the edges of the normal
remaining cartilage. The surface of the exposed
subchondral bone is then abraded with an
arthroscopic burr to create a bleeding bony
surface.
Subchondral Drilling
• Involves abrasion or drilling of an articular
surface to the superficial layer of subchondral
bone with a motorized, arthroscopic burr or
drill.
Microfracture
Indications:
• Full thickness articular cartilage lesion on either
a weight bearing surface (femur or tibia) or a
contact lesion on either the patella or trochlear
surfaces of the patellofemoral joint.
• Unstable cartilage overlying subchondral bone
• Degenerative changes in knees
Chondrocyte Transplantation, also known as
autologous chondrocyte implantation
• Is designed to stimulate growth of hyaline
cartilage for repair of focal defects of articular
cartilage and prevention of progressive
deterioration of joint cartilage.
Indications:
• Symptomatic, large full-thickness chondral
lesions
• Osteochondritis Dessicans
Osteochondral Autografts and Allografts
• Involve transplantation of intact articular
cartilage along with some underlying bone,
resulting in a bone-to-bone graft
• Autogenous osteochondral graft (an autograft)
procedure or osteochondral allograft procedure
Arthroplasty
It is commonly called joint replacement. It
involves the reconstruction of a diseased,
damaged, or ankylosed joint by natural
modification or artificial materials.
It is a reconstructive joint procedure, with or
without joint implant, designed to relieve pain
and improve function.
Indications:
• OA
• RA
• Inflammatory Arthritis
• Post-traumatic Arthrtitis
• Osteonecrosis
• Arthritis associated with polio, Parkinson’s
Disease, and hemophilia
Contraindications:
• Active infection
• Chronic osteomyelitis
• Systemic infection
• Substantial loss of bone or malignant tumors
• Significant paralysis of muscles surrounding the
joint
• Neuropathic joint
• Inadequate patient motivation
Excision Arthroplasty
• Also known as resection arthroplasty, involves
removing periarticular bone from one or both
articular surfaces
• Disadvantages:
o Possible joint instability
o In the hip, significant leg length discrepancy and
poor cosmetic result because of shortening of
the operated extremity
o Persistent muscular imbalance and weakness
Excision Arthroplasty with Implant
• For excision arthroplasty with implant, after
removing the articular surface, an artificial
implant is fixed in place to help in the
remodelling of a new joint.
• This is sometimes called implant resection
arthroplasty
Interposition Arthroplasty
• Essentially is biological resurfacing of a joint to
provide a new articulating surface.
• After the involved joint surface is débrided, a
foreign material is placed (interposed) between
the two joint surfaces
Joint replacement arthroplasty includes total
joint replacement arthroplasty and
hemireplacement arthroplasty
• Total joint replacement procedures involve
resecting both affected articulating surfaces of a
joint and replacing them with artificial
components
• Hemireplacement arthroplasty involves
resection and replacement of just one of the
articulating surfaces of a joint
Arthrodesis
• Surgical fusion of the surfaces of a joint
155 | P a g e
• Fusion of joint surfaces in the position of • Congenital dysplasia
maximum function is achieved with internal • Leg length discrepancy
fixation (i.e., pins, nails, screws, plates, bone
grafts)
• It is used most frequently in the cervical and PHYSICAL THERAPY EXAMINATION, EVALUATION
lumbar spine, wrist, thumb, and ankle but in AND DIAGNOSIS
some instances in the shoulder and hip. • Points of Emphasis in Examination

Indications: Subjective Information

• Severe joint pain
- Chief complaint
• Late stage arthritis
- HPI
• Joint instability
• Significant weakness of muscles - Lifestyle
• Peripheral neuropathy Objective Information
• Severe brachial plexus injury - Inspection
signs of inflammation
Extra-Articular Bony Procedures - Palpation
note for muscle spasm & tenderness
Open Reduction and Internal Fixation of
- Integumentary Assessment
Fractures
Scar
• During surgery after the fracture site is exposed,
any number of internal fixation devices, such as - Sensory Assessment
pins, nails, screws, plates, or rods, may be used Superficial sensations are more likely affected
to align and stabilize the bone fragments. - Musculoskeletal Assessment
• ROM
Indications: • MMT
• LGM
 Absolute
1. Unable to obtain an adequate reduction • MBT
2. Displaced intra-articular fractures • LLD
3. Certain types of displaced epiphyseal fractures • Joint play (not replaced/repaired joint)
4. Major avulsion fractures where there is loss of - Chest expansion (for surgical procedures of
function of a joint or muscle group spine and thorax)
5. Non-unions - Postural Assessment
6. Re- implantations of limbs or extremities - Gait Assessment (for surgical procedures of LE)
 Relative - Functional Assessment
1. Delayed unions
2. Multiple fractures to assist in care and general • Problem List
management - Wound
3. Unable to maintain a reduction - Post op pain
4. Pathological fractures - Signs of inflammation (swelling, hyperthermia,
5. To assist in nursing care erythema)
6. To reduce morbidity due to prolonged - Altered superficial sensations
immobilisation - Limitation of motion due to immobilization by
7. For fractures in which closed methods are cast or splint
known to be ineffective - Contracture due to immobilization by cast or
 Questionable splint
1. Fractures accompanying nerve of vessel injury - Edema
2. Open fractures - Hypertrophic and keloid scar formation
3. Cosmetic considerations - Atrophy due to prolonged immobilization
4. Economic considerations - Muscle weakness
- Decreases functional independence
Osteotomy
• The surgical cutting and realignment of bone—is • Physical Therapy Diagnosis
an extra-articular procedure indicated for the - Impaired joint mobility, motor function, muscle
management of impairments associated with a
performance and range of motion associated
number of musculoskeletal disorders
with joint replacement
Indications:
• Congenital deformities

156 | P a g e
- Impaired joint mobility, motor function, muscle - Functional movement patterns increasing speed
performance and range of motion associated and resistance
with soft tissue repairs - Functional activities
- Plyometrics
PHYSICAL THERAPY PROGNOSIS AND
INTERVENTION
• Plan of Care
- Prevent infections
- Relieve pain
- Reduce swelling
- Reduce edema
- Retard atrophy
- Prevent onset of contracture
- Restore ROM
- Restore/maintain muscle strength
- Prevent hypertrophic and keloid scar formation
- Restore functional independence

• Intervention (in general)

Pre-operative management:
- Evaluate pt’s ROM and MMT
- Teach basic precautions
- Teach ankle pumping
- Teach use of assistive device (if needed)

Post-operative management:
Maximum Protection Phase (duration depends
on procedure)
- Immobilization to promote healing
- Proper wound care
- PRICE
- Modalities for pain
- Cryotherapy
- PROM –pain free
- AROM exercises of adjacent joints
- Ankle/wrist pumping
- Gentle muscle setting

Moderate Protection Phase (duration depends

on procedure)
- ES
- Cross friction massage of scar
- Gentle stretching
- AAROM to AROM
- Begin isometric exercises
- Multiple angle isometrics
- Gentle resistance exercises
- Initiate functional exercises
- Initiate ambulation (for LE procedures)

Minimum Protection Phase

- Attain optimal function
- Progressive resistive exercises using Therabands
or weights (implemented slowly and cautiously)
- Close and open chain exercises
- Stretching using hold relax technique

157 | P a g e
 SOFT TISSUE INJURY AND PROCEDURES
GENERAL MEDICAL BACKGROUND
Definition
• Soft tissue injury
- Is the damage of muscles,
ligaments, and tendons throughout
the body
Classification
• Sprain
- Severe stress, stretch, or tear of a
ligament, tendon or joint capsule
- Grade:
First degree: mild
Second degree: moderate
Third degree: severe
• Strain
- Overstretching, overexertion,
overuse of soft tissue especially the
muscles.
- Less severe than sprain
• Dislocation
- Complete malalignment of a joint
- Displacement of a part, usually the
bony partners in a joint resulting in
loss of the anatomical relationship
and leading to soft tissue damage,
inflammation, pain and muscle
spasm
• Subluxation
- An incomplete or partial dislocation
of the bony partners in a joint that
often involves secondary trauma to
surrounding soft tissue
• Muscle/tendon rupture or tear
- Found commonly in sports injury
- Partial tear: pain is experienced in
the region of the breach when the
muscle is stretched or contracting
against a resistance
- Complete tear: does not cause pain
during stretching or contraction as
the muscle does not pull against the
gravity
• Tendinous lesions/tendinopathy
- Tenosynovitis: inflammation of the
synovial membrane covering a
tendon
- Tendinitis: inflammation of a tendon
- Tenovaginitis: inflammation and
thickening of a tendon sheath
- Tendinosis: degeneration of the
tendon due to repetitive micro
trauma
• Synovitis
- Inflammation of a synovial
membrane
- An excess of normal synovial fluid in
a joint or tendon sheath caused by
trauma or disease
• Hemarthrosis
- Bleeding into a joint usually due to
severe trauma
• Ganglion
- Ballooning of the wall of a joint
capsule or tendon sheath.
- May arise after trauma
- Sometimes occur with rheumatoid
arthritis
• Bursitis
- Inflammation of a bursa
- Most common in the elbow, hip,
and knee
• Contusion
- Bruising from a direct blow resulting
in capillary rupture, bleeding,
edema, and inflammatory response
• Overuse syndromes, cumulative trauma
disorders, repetitive strain injury
- Repeated, submaximal overload
and/or frictional wear to a muscle or
tendon resulting in inflammation
and pain
Epidemiology
- Incidence is quite high because
some level of soft tissue
involvement is present in nearly
every traumatic incidence
- 5th leading cause of nonfatal injuries
in all age group
Etiology
• Direct trauma
– Right after an activity
– E.g. Sports accidents and other
accidents, being struck by an
object, and falling
• Indirect trauma
– chronic injuries:
• Repetitive movements,
body mechanics, stress,
level of fitness, and
prior injury
Pathomechanics
Episode of trauma or a continued mechanical
stress
Tear or stress in the soft tissues involved or
stretching or a small tear of other ligaments that
support and limit the mobility of joints
Insult to connective tissue
158 | P a g e
 - Stage last for 6 months to 1 year
Stage of repair follows (refer to prognosis) depending on the tissue involved
and amount of tissue damage
Clinical manifestation
• Pain (dolor) GENERAL HEALTHCARE MANAGEMENT
• Swelling (tumor) Medical & Surgical management
• Redness (rubor) 1. Tenolysis
• Heat (calor) o Surgical release of a tendon
• Loss of function (function laesa) affected by adhesions
• Stiffness o Commonly done on hands
• Bruising and wrists
Complications o Done to return movement
1. Overuse, cumulative trauma, repetitive of the affected body part
trauma 2. Tenorraphy
- Results in structural weakening, or o The union of torn or divided
fatigue breakdown of connective tendons by means of a
tissue with collagen fiber crosslink suture
breakdown and inflammation o Commonly done on a
2. “old scar” reinjury – scar adhesions near lacerated Achilles tendon
surrounding tissues or not properly 3. Myotomy
aligned to the stress imposed to the o The surgical cutting of a
tissue can make the area susceptible to muscle
injury o For decompression, muscle
3. Contractures or poor mobility – due to repair, and presence of
faulty postural habits or prolonged contractures
immobility 4. Fasciotomy
o A surgical procedure where
Diagnosis the fascia is cut to relieve
• Arthrography – used to help diagnose tension or pressure
the cause of unexplained joint pain commonly to treat the
• Bone scan resulting loss of circulation
• CT Scan to an area of tissue or
• Discography muscle
• Electromyography o E.g. Myofascial
• Flexibility test compartment syndrome
5. Tenotomy
• Joint aspiration and analysis
o The surgical cutting of a
• Magnetic Resonance Imaging
tendon
• Muscle Test
o Aka tendon release, tendon
• Palpation
lengthening, and heel-cord
release
Prognosis
o Eg. Clubfoot, contractures
 Stages of Soft Tissue Injury:
6. Capsulotomy
o Acute Stage (Inflammatory Reaction)
o Creation of an opening
- Inflammation is present
through a capsule;
- Pain before tissue resistance
frequently done to gain
- Stage lasts for 4 to 6 days unless
entry into a joint.
insult is perpetuated
7. Tenodesis
o Subacute Stage (Repair and Healing)
o Stabilizing a joint by
- Inflammation decreases and
anchoring the tendons that
eventually are absent
move that joint, thereby
- Pain synchronous with tissue
preventing any excursion of
resistance
the tendons
- Stage lasts for 10 to 17 days
8. Capsulorraphy
- May last up to 6 weeks for tissues
o Suture of a tear in a capsule,
with limited circulation like tendons
especially of a joint capsule
o Chronic Stage (Maturation and
to prevent recurring
Remodeling)
dislocation.
- Absence of inflammation
o Common in knee joint
- Pain after tissue resistance

159 | P a g e

9. Capsulectomy
o The surgical excision of a ca
psule, usually the capsule of
a joint or of the lens of the
eye
10. Synovectomy
o A type of surgery done to
remove inflamed synovial
tissue that is the source of
much pain and limited
mobility
o Eg. Rheumatoid Arthritis
11. Osteotomy
o Surgical cutting of a bone
o Used to encourage healing
o E.g. in a poorly aligned heal
ed fracture, or to reduce pai
n in osteoarthritis.
12. Meniscectomy
o Excision of the meniscus
o Common in the knee joint
13. Tenoplasty
o Plastic repair/surgery of a
tendon
14. Chrondroplasty
o Plastic repair/surgery of a
cartilage
o the most common being
corrective surgery of the
cartilage of the knee
15. Arthrodesis
o Surgical fusion of a joint
o Aka artificial ankyloses
o Eg. Osteoarthritis,
rheumatoid arthritis, post-
traumatic arthritis
16. Arthroplasty
o Plastic repair/surgery of a
joint
o Joints are being replaced
with plastic
to restore the function of a
stiffened joint and relieve p
ain.
o Eg. Osteoarthritis,
rheumatoid arthritis
PHYSICAL THERAPY EXAMINATION, EVALUATION
& DIAGNOSIS
Points of emphasis in examination
• Patient/Client history
• Systems review
• Integumentary assessment
• Sensory assessment
• Musculoskeletal assessment
• Chest expansion measurement for
surgical procedures in the spine and
thorax area
• Postural assessment
• Gait assessment
Problem list
• Wound and signs of inflammation
• Pain
• Altered sensation
• Limitation of motion
• Mm weakness
• Contractures
• Edema
• Hypertrophic and keloid scar formation
• Mm atrophy
• Postural deviations
• Gait deviations
• Decreased functional independence
Physical therapy diagnosis
• MS2 – Impaired posture
• MS3 – Impaired muscle performance
• MS5 – Impaired joint mobility, motor
function, muscle performance, and ROM
associated with localized inflammation
• MS9 – Impaired joint mobility, motor
function, muscle performance, and ROM
associated with bony or soft tissue
surgery
PHYSICAL THERAPY PLAN OF CARE &
INTERVENTION
 Acute Stage – Protection phase
o Impairments:
1. Inflammation, pain, edema,
mm spasm
2. Impaired movement
3. Joint effusion (if joint is
affected)
4. Decreased used of
associated areas
o Precautions:
1. Proper dosage of rest and
movement must be used
during the inflammatory
stage.
2. Signs of too much
movement – increased pain
& increased inflammation
o Contraindications:
1. Stretching
2. Resistance exercises
PLAN OF CARE INTERVENTION RATIONALE
(up to 1 week post
injury)
1. Patient • Information of • To give patient
education anticipated reassurance
recovery time
160 | P a g e
 • Protection of that acute sx but it should not last longer
affected part are short-lived than a couple of hours.
while • To learn safe PLAN OF CARE INTERVENTIO RATIONALE
maintaining movements
N (up to 3
appropriate during this
functional stage of healing weeks post
activities injury)
2. Control pain, • PRICE • To minimize 1. Patient • Information • To give
edema, • Immobilization musculoskeletal education of patient an
spasm (splint, tape, pain anticipated idea if
cast) • To promote healing he/she is
• Avoidance of healing time pushing
stress position • HEP beyond
• Gentle (grade I) tissue
joint oscillation tolerance
with joint in pain • Giving of
free position HEP helps
3. Maintain • PROM • To avoid patient to
soft tissue • Intermittent development become an
and joint muscle setting of adhesions active
integrity and • Electrical and participant
mobility stimulation contractures in the
• Grade I or II • To decrease recover
distraction and pain process
glide techniques • Assist the 2. Promote • Adaptive or • To prevent
• Gentle massage circulation to healing of assistive further
give nutrients to injured devices injuries
the affected tissues • Splints,
part tapes,
4. Reduce joint • Provide • To prevent wraps
swelling if sx protection further injury 3. Restore soft • AAROM to • To increase
are present through splints tissue, AROM ROM
and casts muscle, • Scar • To increase
5. Maintain • AAROM/AROM • To maintain and/or joint mobility functional
integrity and • PREs joint integrity mobility • Stretching activities
function of • Modified aerobic and prevent 4. Develop • Multiple- • To initiate
associated exercise development of neuromuscul angle, control and
areas • Adaptive or contractures ar control, submaximal strengthenin
assistive devices • To improve mm isometric g of the
functional endurance, exercise muscles of
activities and strength • AROM the affected
in involved • Protected part in a
 Subacute Stage – Controlled motion and related weight nonstressful
muscles bearing manner
phase
exercise • To give
o Impairments: • Stabilization patient
1. Pain at end of ROM exercise awareness
2. Decreasing soft tissue of using the
edema correct
muscles
3. Decreasing joint effusion (if
joints are involved)
5. Maintain • PREs • To maintain
4. Developing soft tissue, integrity and ROM and
• Stabilizatio
muscle, and/or joint function of n exercises strength for
contractures associated functional
5. Developing mm weakness areas activities
6. Decreased functional use of
the affected part and  Chronic Stage – Return to Function
associated areas Phase
o Precautions: o Impairments:
1. Too much activity and 1. Soft tissue and/or joint
motion causes resting pain, contractures and adhesions
fatigue, increased weakness 2. Limitation of range of
and spasm. motion and joint play
2. Discomfort usually occurs as 3. Decreased muscle
the activity is progressed, performance, weakness,

161 | P a g e
 poor endurance, poor • Progression of • To increase
neuromuscular control parameters until functional
4. Decreased functional usage the muscles are activities
strong enough
of the involved part
and are able to
5. Inability to function respond to the
normally in an expected required
activity. functional
o Precautions: demands.
1. There should be no signs of
inflammation
2. Some discomfort will occur
as activity level is
progressed but is should not
last longer than a couple of
hours
PLAN OF CARE INTERVENTION (>3 RATIONALE
weeks postinjury)
1. Patient • Instructions on • For
education safe progression continuance
of exercises and of a safe
stretching recovery
• Monitor
understanding
and compliance
• Teach ways to
avoid reinjuring
the part
• Provide
ergonomic
counseling
2. Increase • Stretching • To increase
soft tissue, exercises ROM
muscle, • PJM • To increase
and/or joint • Cross-fiber functional
mobility massage activities
• Neuromuscular
inhibition
3. Improve • Progression of • To increase
neuromusc exercise: strength
ular control, - Submaximal to
strength, maximal
muscle resistance
endurance - Resisted
concentric and
eccentric
exercise
- Weight bearing
and non-weight
bearing
- Single plane to
multiplane
motions
- Simple to
complex
motions
- Increase speed
and time

4. Improve • Progression of • To increase

cardiovascul aerobic exercises endurance
ar endurance using safe of doing
activities the
activities
5. Progress • Continuance of • To increase
functional using assistive muscle
activities devices strength

162 | P a g e
 CONGENITAL DEFECTS
I. GENERAL MEDICAL BACKGROUND
A. Definition:
Abnormalities of development present at birth
B. Classification:
> Original (Classic) Classification:
This includes classic terms that include the
following:
• Amelia - absence of a limb
• Meromelia - partial absence of a limb
• Hemimilia - absence of half of a limb
• Phocomelia - flipper like appendage
attached to the
trunk
• Acheiria - missing hand or foot
• Adactyly - absent metacarpal or
metatarsal
• Aphalangia - absent finger or toe
• Camptodactyly - flexion contracture of
the little finger usually (B), involving the
FDP
• Syndactyly - union of 2 digits (simple -
skin and connective tissues, complex -
includes bones)
• Polydactyly - supernumerary digits
> Frantz Classification:
• Terminal - representing the complete
loss of the distal extremity
• Intercalary - denoting the absence of
intermediate parts with preserved
proximal and distal parts of the limb.
(E.g., Intercalary fibular deficiency)
> ISPO Classification System (International
Society for Prosthetics and Orthotics)
• Transverse deficiency - Named after the
segment beyond which there is no
skeletal portion. All elements beyond a
certain level are absent, and the limb
resembles an amputation stump
• Longitudinal deficiency - has distal
portions, name the bones that are
affected. Involve specific
maldevelopments (E.g., complete or
partial absence of the radius, fibula, or
tibia).
** Radial ray deficiency is the most common
upper-limb deficiency
** Hypoplasia of the fibula is the most common
lower-limb deficiency
C. Epidemiology:
• 5-9.7/10,000 live births
• ratio of 3:1 UE:LE
• The National Birth Defects Prevention
Study has reported that 6% of all types
of birth defects are limb deficiencies.
D. Etiology:
Conditions with implied vascular disruption:
• Adams-Oliver Syndrome - a rare
condition that is present at birth. The
primary features are an abnormality in
skin development (called aplasia cutis
congenita) and malformations of the
limbs.
• Klippel-Feil Syndrome - a bone disorder
characterized by the abnormal joining
(fusion) of two or more spinal bones in
the neck (cervical vertebrae)
• Moebius Syndrome - an extremely rare
congenital neurological disorder which
is characterized by facial paralysis and
the inability to move the eyes from side
to side and limb deficiencies.
• Maternal Diabetes - Diabetes is
characterized
by hyperglycemia and disturbances of
carbohydrate,
fat, and protein metabolism associated
with absolute or relative deficiencies in
insulin secretion and/or insulin action.
These disturbances alter molecular
signaling pathways and adversely affect
embryogenesis. (Information regarding
the teratogenicity of diabetes has been
obtained from animal models and
human studies)
• Thalidomide - anticonvulsant
• Uterine Abnormalities - may compress
the body parts of the fetus altering its
developing anatomical shape
• Amniotic Band Syndrome - is a
congenital disorder caused by
entrapment of fetal parts (usually a limb
or digits) in fibrous amniotic bands while
in uterus
E. Pathophysiology:
• The first trimester is crucial for the
genesis of limb production. Congenital
limb deficiency occurs as a result of
failure of formation of part or all of the
limb bud.
• The mesodermal formation of the limb
occurs at 26 days gestation and
continues with differentiation until 8
weeks gestation.
• The various limb segments develop in a
proximal-to-distal order so that the arm
and forearm appear before the hand,
and the thigh and leg before the foot.
• Limb development is a complex process
that involves orchestration of a number
of genes; some are well known and
studied, and account for various
syndromes and abnormalities.
F. Clinical Manifestation:
Common Upper Limb Deficiencies
1. Digital Deficiencies
163 | P a g e
 • Digital deficiencies are common but
rarely present in isolation.
• Removal of additional digits or
intervention with Z-plasty procedures
produce acceptable results for the
children with polydactyly and
syndactyly, respectively.
• Etiologies such as Moebius syndrome
and Poland syndrome (sequence) result
in digital deformities associated with a
more serious underlying condition.
• Moebius syndrome often affects the
sixth and seventh cranial nerves, which
compromises the child’s ability to
visually follow objects, swallow, and
communicate.
• In addition to hand anomalies, Poland
syndrome involves a partial absence of
the ipsilateral pectoralis muscle and
hypoplastic chest.
2. Partial Hand and Wrist Disarticulation
Deficiencies
• Partial hand deficiencies are quite
common and are often treated as wrist
disarticulation–level limbs.
• Nubbins (very small underdeveloped
vestigial digits) are present in a majority
of these cases, as are shortening of the
ipsilateral radius and ulna.
• Nubbins are rarely problematic or
surgically removed. The child can be
quite functional with no intervention.
• The major functional drawback of this
particular limb length is the inability to
perform prehensile tasks with the
involved limb.
3. Transverse Deficiencies of the Forearm
• Transverse deficiency of the upper third
of the forearm is the most common
(major) upper limb deficiency.
• The clinical presentation of these
children is similar to that of children
with longer, transradial residual limbs.
• Ipsilateral humeral shortening and the
presence of smaller nubbins are
common to this level.
• The proximal radius in these shorter
residua is often unstable, subluxing
anteriorly during full extension. This
creates a challenge to prosthetic fitting.
• The longer residual limbs, in the middle
third of the forearm, tend to be more
easily fit with prostheses, as they have
more surface area over which to
distribute the forces of the socket
interface.
• They also have longer lever arms with
which the patient can control the
prosthesis. If prosthetic intervention is
not attempted or accepted, bimanual
tasks will be performed via grasping of
objects in the cubital fold, between
one’s legs, in the axilla region, or under
the chin.
4. Elbow Disarticulation and Transhumeral
Deficiencies
 The more articulations that are involved,
the greater is the functional deficit.
 When the elbow joint is compromised or
absent, the child has fewer options to assist
in prepositioning his or her distal limb in
space. The child relies solely on the muscles
and range of motion of the shoulder
complex.
 The true elbow disarticulation limb has the
distal epiphysis present, which is important
to overall growth of the residuum.
 A drawback of any disarticulation is the lack
of room to fit prosthetic components and
maintain humeral length equality.
 Transverse deficiencies of the humerus are
analogous to acquired transhumeral
amputations in children.
5. Shoulder Disarticulation and
Intrascapulothoracic Deficiencies
• It becomes increasingly difficult to restore
the functions of the anatomical arm as the
level of deficiency reaches the shoulder and
higher.
• Children with remnant humeri have the
ability to use these segments to assist in
their activities.
• Often, the axilla will be used to assist these
individuals to grasp and manipulate objects.
• If the child has unilateral limb deficiencies,
the contralateral noninvolved limb will be
the dominant side for grasping, with holding
for manipulation taking place between the
knees, in the mouth, or trapped between
chin and chest or chin and shoulder.
• When the child has bilateral deficiencies at
the shoulder level, the latter method is all
that is possible to grasp objects. In these
cases, the child will be strongly encouraged
to use his or her feet to grasp and
manipulate objects.
• When the child has an intrascapulothoracic
(forequarter) level of involvement, as they
only have uniscapular motion to capture for
prosthetic limb control.
Common Lower-Limb Deficiencies
6. Longitudinal Deficiency of the Fibula
• The clinical presentation of longitudinal
deficiency of the fibula, which is a
completely absent fibula, generally has a
foreshortened tibial section, and
frequently has ipsilateral femoral
shortening.
• This tibial section appears shorter than
it is as a result of kyphoscoliotic bowing.
• This anterior bowing of the tibia
shortens the segment longitudinally and
164 | P a g e
 creates an anterior prominence of the
tibia. This anterior prominence is
indicated by a subcutaneous dimple,
which can range from superficial to
invaginated.
• Proximally, the limb is often in genu
valgum or drifts into genu valgum as the
child grows.
• The distal involvement is usually an
equinus position and a valgus posture
during weight bearing due to lack of
lateral support.
• On physical examination, the degree of
internal hip rotation is often less than
that of external hip rotation.
7. Femoral Abnormalities
• Proximal femoral focal deficiency (PFFD)
- PFFD has been the acronym of choice
for many femoral anomalies.
• Congenital short femur differs from
PFFD by having the proximal aspect of
the femur and intact ipsilateral
acetabulum.
• Although the skeletal structures are
quite variable, the clinical presentation
for these limbs is similar.
• The femoral section is shorter, with a
larger mass of soft tissue, which includes
musculature, between the pelvis and
the involved knee.
8. Longitudinal Deficiency of the Tibia
• The clinical presentation of a
longitudinal tibial deficiency may include
a varus foot and lower leg, a short leg,
and an unstable knee and ankle (or
both).
• The foot may have medial tarsals,
metatarsals, and rays missing as well.
Deformities
9. Arthrogryposis Multiplex Congenital
• Comprises nonprogressive conditions
characterized by multiple joint
contractures found throughout the body
at birth.
• The involved extremities are fusiform or
cylindrical in shape, with thin
subcutaneous tissue and absent skin
creases.
• Deformities are usually symmetric, and
severity increases distally, with the
hands and feet typically the most
deformed
10. Metatarsus Varus
• Characterized by adduction of the
forefoot on the hindfoot, with the heel
in normal position or slightly valgus
11. Club foot
• Consist of 3 associated deformities,
equinus/Plantar flexion of the foot at
the ankle, varus or inversion deformity
of the heel, forefoot varus
12. Talipes Calcaneovalgus
• Excessive dorsiflexion at the ankle and
eversion of the foot
13. Carvus foot
• High longittudinal arch.
• Usually associated with contractures of
toe extensors.
14. Blount’s Disease (tibia vara)
• Most common morphologic cause of
bowing in the young child and is found
most commonly in obese children who
walks at 9-10 mos.
15. Developmental Dysplasia of the Hip (DDH)
• Preferred term for congenital
dislocation of the hip.
• It includes hip subluxation, hip
dislocation, and acetabular dysplasia, all
of which implies instability of the hip.
Complications
>Contractures
>Immobility
>Terminal Overgrowth - spiking at the
transected end of a long bone
>Appositional Growth - the distal bone begins to
form in the shape of an icicle.
>Bone Spur Formation
>Development of Adventitious bursae - Occurs
to protect the distal residuum
>Stump Scarring
Diagnosis
Early identification of limb anomalies occurs
with routine ultrasound. A detailed level 3
ultrasound, as well as echo 3-D,
amniocentesis, and cordocentesis to
anticipate syndromes, is recommended if
limb deficiencies are detected.
Prognosis
Good as long as the complications are
addressed.
II. GENERAL HEALTHCARE MANAGEMENT
Surgical Procedures:
General principles: to preserve length, preserve
growth plate, perform disarticulation rather
than transosseous amputation, preserve the
knee joint whenever possible, stabilize and
normalize proximal portions of the limb.
1. Revision amputation
For centralization and reconstruction of the
deformed structure
165 | P a g e
A. Krukenberg Procedure: Decrease the residual Desensitization of the
Reconstructs the forearm and creates a sensate limb pain residual limb through
prehensile surface for children with absent wrapping and massage.
hands by separating the ulna and radius in the Prevent postural Educate the pt. about
forearm. Because of cosmetic appearance, the deviation the proper posture
with visual assistance
procedure is used rarely with unilateral
from a mirror for the
conditions. Indications: absent hands, visual
pt to picture out the
impairment correct posture and for
him/her to get used to
B. Vilkke Procedure: that position.
Attaches a toe to the residual limb to create a Improve balance and Gentle rocking
pincher grip with the transferred great toe. tolerance techniques in sitting -
standing position, with
2. Plastic surgery for reconstruction of skin flaps progression from
or with complicated repairs of residual limb. unilateral standing
using the good leg to
using the prosthetic
3. Rotationplasty
limb.
A type of autograft wherein a portion of a limb is
Prevent gait deviation Strengthening of the
removed, while the remaining limb below the in ambulation using the residual limb to
involved portion is rotated and reattached. This prosthetic device prevent gait deviation
procedure is used when a portion of an due to the weak
extremity is injured or involved with a disease, muscles. (PREs)
such as cancer. It is also performed to patiend Achieve a modified Task modifications for
with PFFD given that the affectation is unilateral dependent status from the pt. to cope up with
and the ankle joint is in good condition. complete dependence the ADLs in a most
efficient way
III. PHYSICAL THERAPY EXAMINATION,
EVALUATION, AND DIAGNOSIS

A. Points of Emphasis in Examination

1. Maternal Hx
2. ROM
3. MMT
4. Posture
5. Balance and Tolerance
6. Gait
7. ADLS

B. Problem List
1. Contractures
2. Muscle weakness
3. Residual limb pain
4. Postural deviations
5. Poor balance and tolerance
6. Gait deviations 20 poor prosthetic training
7. Dependent in some ADLs

C. PT Diagnosis: Impaired posture; impaired joint

mobility, motor function, muscle performance,
& ROM associated with bony or soft tissue
surgery.

(PLS REVIEW ORTHOPROS)

IV. PHYSICAL THERAPY PROGNOSIS

A. PLAN OF CARE B. INTERVENTION
Decrease the severity Rhythmic rotation with
of contractures deep tendon pressure
followed by prolonged
stretching x 30 secs x 5
sets for
Increase muscle PREs through play
strength therapy

166 | P a g e
 AUTISM AND DOWN’S SYNDROME
Autism Spectrum Disorders
GENERAL MEDICAL BACKGROUND
Definition
- Previously known as the pervasive
developmental disorders, is a
phenotypically heterogeneous
group of neurodevelopmental
syndromes, with polygenic
heritability, characterized by a wide
range of impairments in social
communication and restricted and
repetitive behaviors.
Classification
- Autistic Disorder
- Asperger’s syndrome (characterized
by impairment and oddity of social
interaction and restricted interest
and behavior; no significant delays
in language or cognitive
development)
- Childhood disintegrative disorder
(characterized by marked regression
in several areas of functioning after
at least 2 years of apparently normal
development. Childhood
disintegrative disorder, also called
Heller’s syndrome and disintegrative
psychosis)
- Rett Syndrome (a progressive
condition that has its onset after
some months of what appears to be
normal development. Head
circumference is normal at birth and
developmental milestones are
unremarkable in early life. Between
5 and 48 months of age, generally
between 6 months and 1 year, head
growth begins to decelerate)
- Pervasive developmental disorder
not otherwise specified (condition
with severe, pervasive impairment
in communication skills or the
presence of restricted and repetitive
activities and associated impairment
in social interactions)
Epidemiology
- Believed to occur at a rate of about 8
cases per 10,000 children (0.08
percent).
- 4x more in boys
Etiology
- Genetric factors
• Current evidence supports a genetic
basis for the development of autistic
disorder in most cases, with a
contribution of up to four or five
genes
• High rates of cognitive difficulties,
even in the nonautistic twin in
monozygotic twins with perinatal
complications, suggest that
contributions of perinatal insult
along with genetic vulnerability may
lead to autistic disorder.
- Immunological factors
• Several reports have suggested that
immunological incompatibility (i.e.,
maternal antibodies directed at the
fetus) may contribute to autistic
disorder. The lymphocytes of some
autistic children react with maternal
antibodies, which raise the
possibility that embryonic neural or
extraembryonic tissues may be
damaged during gestation.
- Prenatal and Perinatal factors
• A higher-than-expected incidence of
perinatal complications seems to
occur in infants who are later
diagnosed with autistic disorder.
Maternal bleeding after the first
trimester and meconium in the
amniotic fluid have been reported in
the histories of autistic children
more often than in the general
population. In the neonatal period,
autistic children have a high
incidence of respiratory distress
syndrome and neonatal anemia.
• Prenatal risk factors: advanced
maternal and paternal age at birth,
maternal gestational bleeding,
gestational diabetes, and first-born
baby.
• Perinatal risk factors: umbilical cord
complications, birth trauma, fetal
distress, small for gestational age,
low birth weight, low 5-minute
Apgar score, congenital
malformation, ABO blood group
system or Rh factor incompatibility
and hyperbilirubinemia.
- Biological Factors
• Autistic disorder is also associated
with neurological conditions,
notably congenital rubella,
phenylketonuria (PKU), and
tuberous sclerosis. Autistic children
have higher than expected histories
167 | P a g e
 of perinatal complications
compared with the general
population and also compared with
children with other psychiatric
disorders. The finding that autistic
children have significantly more
minor congenital physical anomalies
than expected suggests abnormal
development within the first
trimester of pregnancy.
- Immunological Factors
• Several reports have suggested that
immunological incompatibility (i.e.,
maternal antibodies directed at the
fetus) may contribute to autistic
disorder. The lymphocytes of some
autistic children react with maternal
antibodies, which raise the
possibility that embryonic neural or
extraembryonic tissues may be
damaged during gestation.
- Biochemical Factors
• A number of studies in the last few
decades have demonstrated that
about one third of patients with
autistic disorder have high plasma
serotonin concentrations. This
finding, however, is not specific to
autistic disorder, and persons with
mental retardation without autistic
disorder also display this trait. In
some autistic children, a high
concentration of homovanillic acid
(the major dopamine metabolite) in
cerebrospinal fluid (CSF) is
associated with increased
withdrawal and stereotypes.
- Psychosocial and Family Factors
• Studies comparing parents of
autistic children with parents of
normal children have shown no
significant differences in child-
rearing skills.
• Children with autistic disorder, as
children with other disorders, can
respond with exacerbated
symptoms to psychosocial stressors,
including family discord, the birth of
a new sibling, or a family move.
Some children with autistic disorder
may be excruciatingly sensitive to
even small changes in their families
and immediate environment.
Clinical Manifestations
- It is distinguished not by a single
symptom but by a characteristic triad of
symptoms:
A. Impairments in social
interactions
B. Impairments in communication
C. Restricted interests and
repetitive behavior
- Associated Physical Characteristics:
• Exhibit higher rates of minor
physical anomalies, such as ear
malformations
• May reflect abnormalities in fetal
development of those organs along
with parts of the brain
• Do not show early handedness and
lateralization, and remain
ambidextrous at an age when
cerebral dominance is established in
most children.
- Associated Behavioral Symptoms that
May Occur in Autism Spectrum
• Disorder Disturbances In Language
Development and Usage
• Intellectual Disability
• Irritability (Broadly defined,
irritability includes aggression, self-
injurious behaviors, and severe
temper tantrums)
• Instability of mood and affect
• Response to stimuli
• Hyperactivty and inattention
• Precocious skills
• Insomnia
• Minor Infections and
Gastrointestinal Symptoms
(excessive burping, constipation,
and loose bowel movements. Also
seen is an increased incidence of
febrile seizures)
Complications
- Mental Retardation: up to 75% of
autistic individuals are cognitively
impaired
- Seizures: 1 in 4 children develop
epileptic seizures, typically during
adolescence
- Tuberous Sclerosis: rare genetic
disorder that causes benign tumors to
grow in many different organs including
the brain, eyes, heart, lungs, and skin.
Around 3-4% of children with autistic
disorder have tuberous sclerosis
Diagnosis
168 | P a g e
 - According to APA, an individual must childhood schizophrenia, intellectual
show some mild to severe impairment disability syndromes with behavioral
in all three of the following areas: symptoms, and language disorders
• Communication (there may be a total - Social (pragmatic) communication
lack or delay in the development of
disorder-difficulty in conforming to
speech and the individual does not
sustain or initiate conversation, or uses typical storytelling, understanding the
language in a stereotyped and repetitive rules of social communication through
manner) language, exemplified by a lack of
• Socialization (may not use or conventional greeting others, taking
understand nonverbal behavior or turns in a conversation, and responding
develop peer relationships that are to verbal and nonverbal cues of a
appropriate to his developmental level,
listener. This disorder does not include
or may appear aloof and indifferent to
other people) restricted or repetitive behaviors and
• Imaginative thought (Repetitive motor interests, as autism spectrum disorder
mannerisms may be observed. Often does
there is lack of make-believe or social
imitative play) - Schizophrenia with childhood onset
- “Red Flags”
Criteria Autism Schizophrenia
• No big smiles or other warm, joyful
Spectrum with
expressions by 6 months or thereafter.
Disorders childhood
• No back-and-forth sharing of sounds, onset
smiles or other facial expressions by 9
months or thereafter. Age of onset Early Rarely under 5
• No babbling by 12 months. developmenta y.o
• No back-and-forth gestures such as l period
pointing, showing, reaching or waving Incidence 1% <1 in 10,000
by 12 months. Sex ratio(M:F) 4:1 1.67:1 (slight
• No words by 16 months. preponderanc
• No two-word meaningful phrases e on males)
(without imitating/repeating) by 24 Family hx of Not increased Likely
months. Schizophrenia increased
• Any loss of speech, babbling or social Prenatal and increased Not increased
skills at any age. perinatal
- Medical Tests complications
• Audiograms and tympanograms: to Behavioral Poor social Hallucinations
check for hearing impairments characteristics relatedness, and delusions,
• Blood tests: to show any abnormalities may be thought
in the genes that could cause a aberrant disorder
developmental disability language
• Electroencephalogram (EEG): to detect speech or
tumors and other brain abnormalities echolalia,
and to measure brain waves that can stereotyped
show seizure disorders. phrases, may
• Blood and urine lab tests (Metabolic have
screening): to measure how a child stereotypies,
metabolizes food and its impact on repetitive
growth and development behaviors
• Magnetic Resonance Imaging (MRI) Adaptive impaired Deterioration
• Computer-assisted axial tomography functioning in functioning
(CAT-scan): useful in diagnosing Level of Wide range, Usually within
structural problems in the brain intelligence may be the normal
intellectually range, may be
Differential Diagnosis disabled low to
Classic Autism Asperger’s syndrome (30%) average
IQ can be anywhere IQ is at least average normal
in the scale and there and there is no Pattern of IQ Typically More even
is language delay language delay higher
- It is difficult to make the diagnosis of performance
autism spectrum disorder because of its than verbal
potentially overlapping symptoms with Grand Mal 4%-32% Low incidence
seizures

169 | P a g e
 - Congenital deafness or severe hearing Sex ratio (M:F) 4:1 Equal or
disorder almost equal
Autism Spectrum Congenital deafness or Family hx of <25% of cases <25% of cases
Disorders severe hearing speech delay
disorder or language
problems
Infants with autism History of relatively Associated Very Not
spectrum disorder may normal babbling that deafness infrequent infrequent
babble only then gradually tapers Nonverbal Impaired Actively
infrequently off and may stop at 6 communicatio utilized
months to 1 year of n
age Language Present in a uncommon
May ignore loud or Generally respond only abnormalities subset
normal sounds and to loud sounds Articulation Infrequent frequent
respond to soft or low problems
sounds Intellectual Impaired in a Uncommon,
Usually seek out level subset (about least
nonverbal social 30%) frequently
communication with severe
regularity and seek Patterns of IQ Typically Often verbal
social interactions with tests lower on scores lower
peers and family verbal scores than
members more than performance
consistently than performance
children with autism scores
spectrum disorder. Impaired Present Absent or if
- Intellectual Disability with Behavioral social present, mild
Symptoms Children with intellectual communicatio
n, repetitive
disability
and restricted
Autism spectrum Intellectual disability behaviors
disorder Imaginative Often Usually intact
Relatively weak in Generally display play impaired
social interactions global impairments in
compared to other both verbal and Prognosis
areas of performance nonverbal areas - Best prognosis: Children with autism
Generally relate
spectrum disorder and IQs above 70
verbally and socially to
adults and peers in with average adaptive skills, who
accordance with their develop communicative language by
mental age, and they ages 5 to 7 years
exhibit a relatively - Prognosis of a given child with autism
even profile of spectrum disorder is generally improved
limitations.
if the home environment is supportive
- Psychosocial deprivation
Autism Spectrum Psychosocial
Disorders deprivation GENERAL HEATLHCARE MANAGEMENT
Severe neglect, maltreatment, and lack of Medical, Surgical, and Pharmacologic
parental care can lead children to appear - The goals of treatment for children with
apathetic, withdrawn, and alienated. Language autistic disorder are to target
and motor skills may be delayed. behaviours that will improve their
No Improvement. Children with these
abilities to integrate into schools,
signs generally
improve when placed develop meaningful peer relationships,
in a favorable and and increase the likelihood of
enriched psychosocial maintaining independent living as
environment adults.
- Language disorder
Criteria Autism Language
Spectrum disorder Pharmacologic
Disorders - Antipsychotic drugs
Incidence 1% 5 of 10, 000 • Risperidone (Risperdal),
olanzapine(Zyprexa), aripiprazole

170 | P a g e
 (Abilify), andquetiapine (Seroquel)- treat
irritability, aggression, and self-injurious
behaviors in children and adolescents
with autism.
- Antidepressants
• Selective serotonin reuptake inhibitors
(SSRIs)- fluoxetine (Prozac),
fluvoxamine (Luvox), sertraline
(Zoloft),paroxetine (Paxil), citalopram
(Celexa), and escitalopram (Lexapro)-
reduce repetitive behaviors, depression,
irritability, tantrums, and aggression.
- Stimulants
• Methylphenidate (Ritalin, Concerta),
dexmethylphenidate (Focalin), as well as
amphetamines (amphetamine and
dextroamphetamine[Adderall],
dextroamphetamine [Dexedrine], and
lisdexamfetamine[Vyvanase])- used to
treat attention-deficit/hyperactivity
disorder (ADHD) may help some people
with autism. These drugs work by
increasing the person's ability to
concentrate and pay attention and by
reducing impulsivity and hyperactivity.
- Nonstimulant medications
• Atomoxetine (Strattera) and guanfacine
(Intuniv)- equally effective as stimulants
in their ability to increase the
individual's ability to focus, manage
their impulses and activity level.
- Anticonvulsants
• Buspirone(Buspar) and propanolol-
frequently used to manage seizures in
people with autism and may also be
used to stabilize mood and/or behavior.
Alpha-2 adrenergic agonists (for
example, clonidine[Catapres]) are also
sometimes used to manage
hyperactivity and behavioral problems
in some individuals with autism
Other Healthcare (Rehabilitative/Supportive)
- Main Goal: target core behaviors to
improve social interactions,
communication, broaden strategies to
integrate into schools, develop
meaningful peer relationships, and
increase long-term skills in independent
living.
- Psychosocial Interventions (aim to help
children with autism spectrum disorder
to develop skills in social conventions,
increase socially acceptable and
prosocial behavior with peers, and to
decrease odd behavioral symptoms)
• UCLA/Lovaas-based Model- utilizes
techniques derived from applied
behavior analysis, which is administered
on a one-to-one basis for many hours
per week. A therapist and a child will
work on practicing specific social skills,
language usage, and other target play
skills, with reinforcement and rewards
provided for accomplishments and
mastery of skills.
• Early Start Denver Model (ESDM)
Interventions are administered in
naturalistic settings such as in day care,
at home, and during play with other
children. Parents are typically taught to
be co-therapists and provide the
training at home while educational
settings also provide the interventions.
The focus of the interventions is on
developing basic play skills and
relationship skills, and applied behavior
analysis techniques are integrated into
the interventions. This approach is
focused on training for very young
children and is applied within the
context of the child’s daily routine.
• Parent Training Approaches- includes
Pivotal Response Training, in which
parents are taught to facilitate social
and communication development within
the home and during activities by
targeting gateway or pivotal social
behaviors for mastery by the child with
the expectation that once these central
social skills were mastered, a natural
generalizing of social behaviors would
follow.
- Social Skills Approaches
• Social Skills Training- Typically provided
by therapeutic leaders to children of
various ages in a group setting with
peers; children are given guided practice
in initiating social conversation,
greetings, initiating games, and joint
attention.
- -Behavioral Interventions (BIs) and
Cognitive-Behavioral Therapy (CBT) for
Repetitive Behaviors and Associated
Symptoms
• Behavioral Therapy- Early intervention
is recommended for repetitive
behaviors that are self-injurious;
behavioral interventions may need to be
combined with pharmacologic
treatments to adequately manage the
symptoms.
• Cognitive-Behavioral Therapy.
- Interventions for comorbid symptoms in
autism spectrum disorder 1.
Management of insomnia in autism
spectrum disorder- The most common
behavioral intervention for insomnia in
autism spectrum disorder is based on
changing the parents behavior first
toward the child at bedtime and
throughout the night, such that there is
a removal of reinforcement and
attention for being awake, leading to a
gradual extinction of the “staying
171 | P a g e
 awake” behavior. Several studies using
massage therapy before bedtime in
children with autism spectrum disorder
between the ages of 2 years and 13
years provided an improvement in
falling asleep and a sense of relaxation.
- Educational interventions for children
with autism spectrum disorder
• Treatment and Education of Autistic and
Communication-related Handicapped
children (TEACCH)- involves structured
teaching based on the notion that
children with autism spectrum disorder
have difficulty with perception, and so
this teaching method incorporates many
visual supports and a picture schedule
to aid in teaching academic subjects as
well as socially appropriate responses.
• Broad-based approaches- These
educational plans include a blend of
teaching strategies that use behavioral
analysis and also focus on language
remediation.
• Computer-based approaches and virtual
reality- are centered on using computer-
based programs, games, and interactive
programs to teach language acquisition
and reading skills.
PHYSICAL THERAPY EXAMINATION, EVALUATION
AND DIAGNOSIS
Points of Emphasis in Examination
- MMT
- Coordination test
- Functional assessment
Problem List
- Decreased muscle strength,
coordination and skills
Physical therapy Diagnosis:
- NM2. Impaired neuromotor
development
PHYSICAL THERAPY PROGNOSIS
Plan of Care
- Increase muscle strength, coordination
and skills
Intervention (including rationale)
- Physical therapist may work with very
young children on basic motor skills
such as sitting, rolling, standing, and
playing.
- As children grow older, PTs are more
likely to come to a child’s preschool or
school. There, they may work on more
sophisticated skills such as skipping,
kicking, throwing, and catching. These
skills are not only important for physical
development but also for social
engagement in sports, recess, and
general play.
- In school settings, PTs may pull children
out to work with them one-on-one, or
“push in” to typical school settings such
as gym class to support children in real-
life situations.
- It’s not unusual for a PT to create groups
including typical and autistic children to
work on the social aspects of physical
skills
- PTs may also work with special
education teachers and aides, gym
teachers and parents to provide tools
for building social/physical skills.
DOWN’S SYNDROME
GENERAL MEDICAL BACKGROUND
Definition
- Most common chromosomal cause of
moderate to severe intellectual
disability.
Classification
- Nondisjunction (error in cell division)
• About 95 out of 100 children with
DS have an extra chromosome in
pair 21. The extra cell creates three
chromosomes.
- Translocation
• A child may have the normal
number of 46 chromosome but
chromosome 21 has an extra part.
When this abnormal chromosome
21 changes location or translocate,
DS develops.
• Accounts for 4%-5% of DS cases.
- Mosaicism
• Cells contain mixed numbers of
chromosomes, some may have 46
and some have 47.
• Accounts for 4%-5% of DS cases.
Epidemiology
- Occurs approximately one in every 740
live births.
- M=F
Etiology
- Caused by an overexpression of genes
on human chromosome 21.
Pathophysiology/Pathomechanics
- DS is a part of human genetics.
• The human body is made up of cells.
There are message centers in the
cells called Genes which include all
the details and characteristics of a
172 | P a g e
 human being. Genes are located in
parts of cell called Chromosomes.
Normally, there are 46
chromosomes in every human cell,
they are arranged into 23 pairs. The
pair works together to help cells
divide and multiple into different
parts of a body. Sometimes an
accident occurs during cell division
when chromosomes copy
themselves, sometimes the copy
ends up with an extra chromosome.
Babies born with this extra or 47th
chromosome in each of their cells
have Down syndrome.
Clinical Manifestations
- Head and Face features:
• Head is somewhat smaller than
usual.
• Excessive skin at the nape of the
back
• Epicanthic folds
• (+) Brushfield spots on the outer rim
(white dots on iris)
• Almond-shaped eyes
• Ears may appear smaller, misshapen
or set lower than the head
• Flat nasal bridge
• Small mouth
• Upward slanting palpebral fissures
- Craniofacial impairments: (frequently
results to feeding difficulties at birth)
• Shortened palate
• Midface hypoplasia
• Oral hypotonia
• Tongue thrusting
• Poor lip closure
• -Hands and feet:
• Short, thick hands and feet (fifth
finger on each hand may curve
inward)
• Larger space than normal may
develop between the 1st and 2nd toe
• Single transverse palmar crease
- Muscles and joints
• Hypotonia
• Weak muscles and joints
• -Musculoskeletal anomalies:
• Metatarsus primus varus
• Pes planus
• Thoracolumbar scoliosis
• Patellar instability
• ↑ risk for Atlantoaxial dislocation
(has been observed through
radiography in up to 10%-30% of
individuals with DS)
Complications
- -Congenital heart problems (half of all
children with down syndrome have this)
- Respiratory infection
- Leukemia
- ↑ tendency for premature cellular aging
- Alzheimer’s disease
- Impairments of visual and sensory
systems (common in individuals with
DS))
- (+) refractive error (myopia, hyperopia),
astigmatism or problems in
accommodation (as many as 77% of
children with DS)
- Hearing loss that interfere with
language development (reportedly
present in 80% of children with DS)
- Obstructive sleep apnea
- High risk for Obesity or overweight (may
be, in part a result of the retarded
growth and endocrine and metabolic
disorders associated with DS)
- Mental retardation
Diagnosis
- Screening test
• First trimester combined test
• Blood test. (Measures the levels of
pregnancy-associated plasma protein-A
(PAPP-A) and the pregnancy hormone
known as human chorionic
gonadotropin (HCG). Abnormal levels of
PAPP-A and HCG may indicate a
problem with the baby.)
• Ultrasound. (Used to measure a specific
area on the back of your baby's neck.
This is known as a nuchal translucency
screening test. When abnormalities are
present, more fluid than usual tends to
collect in this neck tissue)
• Integrated screening test (done in two
parts during the first and second
trimesters of pregnancy)
• First trimester. Part one includes a blood
test to measure PAPP-A and an
ultrasound to measure nuchal
translucency.
• Second trimester. The quad screen
measures your blood level of four
pregnancy-associated substances: alpha
fetoprotein, estriol, HCG and inhibin A.
• Cell-free fetal DNA analysis. (Checks for
fetal DNA circulating in the mother's
blood. This test is usually recommended
for women who have a higher risk of
having a baby with Down syndrome or
in response to risk detected by one of
the previous tests. The mother's blood
can be tested during pregnancy after 10
weeks gestation)
- Diagnostic test during pregnancy:
• Amniocentesis. (A sample of the
amniotic fluid surrounding the fetus is
withdrawn through a needle inserted
into the mother's uterus. This sample is
then used to analyze the chromosomes
of the fetus. Doctors usually perform
this test in the second trimester, after
173 | P a g e
 15 weeks of pregnancy. The test carries constipation, dry
a slight risk of miscarriage, but risk skin, fatigue.
increases if it's done before 15 weeks)
Prognosis
• Chorionic villus sampling (CVS). (In CVS,
- Down syndrome patients tend to age
cells are taken from the placenta and
used to analyze the fetal chromosomes. more quickly and are prone to
Typically performed in the first developing Alzheimer’s, often as young
trimester, after 10 weeks of pregnancy, as age 40.
this test appears to carry a somewhat - Those patients who maintain their
higher risk of miscarriage than second mental capacity tend to have a longer
trimester amniocentesis.)
life span.
• Cordocentesis. (In this test, also known
- A poorer prognosis is found in those
as percutaneous umbilical blood
sampling or PUBS, fetal blood is taken patients who develop dementia, lose
from a vein in the umbilical cord and their ability to perform daily physical
examined for chromosomal defects. activities, and those who have
Doctors can perform this test between decreased vision.
18 and 22 weeks of pregnancy.)
- After pregnancy:
• Physical exam (initial diagnosis of Down GENERAL HEATLHCARE MANAGEMENT
syndrome is often based on the baby's
appearance. But the features associated Medical, Surgical, and Pharmacologic:
with Down syndrome can be found in Surgical:
babies without Down syndrome) - Systemic surgery
• For confirmation: • Congenital cardiac malformations may
• Chromosome analysis—also known as require early cardiovascular surgery
karyotype—is a test to find the size, - Ocular surgery
shape, and number of chromosomes in • Patients may benefit from strabismus
a sample of body cells. Chromosome surgery; corneal surgery; cataract
surgery; phacoemulsification (refers to
analysis can be done on blood, tissue, or
modern cataract surgery in which the
cells from amniotic fluid (the fluid that
eye's internal lens is emulsified with an
surrounds the baby in the womb). ultrasonic hand piece and aspirated
from the eye)
Differential Diagnosis
Differentiating Differentiating Other Healthcare (Rehabilitative/Supportive):
Condition signs/symptoms tests - Primary care pediatrician to coordinate
and provide routine childhood care
Isolated Hypotonia during Normal • Pediatric cardiologist
hypotonia infancy but no karyotype.
• Pediatric gastroenterologist
associated
dysmorphic • Pediatric endocrinologist
features or • Developmental pediatrician
congenital • Pediatric neurologist
defects. • Pediatric ear, nose and throat (ENT)
specialist
Zellweger's Peroxisomal Elevated very
• Pediatric eye doctor (ophthalmologist)
syndrome disorder with long chain fatty
hypotonia, flat acids in plasma. • Audiologist
occiput and face, • Speech pathologist
epicanthal folds, Normal • Occupational therapist
Brushfield spots, karyotype.
cataracts, single PHYSICAL THERAPY EXAMINATION, EVALUATION
palmar crease, AND DIAGNOSIS
seizures. Points of Emphasis in Examination
- History taking
Difficult to - Physical examination
distinguish - Cardiovascular system
clinically. • Regular vital signs assessment
Congenital Poor feeding, Normal - Neurologic assessment
hypothyroidism poor growth, karyotype. - Musculoskeletal assessment
hypotonia, • ROM
• MMT

174 | P a g e
 • Joint play - Umphred’s Neurological Rehabilitation 6th
- Functional assessment edition.
- Gait assessment - Autism Spectrum Disorders by Ana Maria
- Postural assessment Rodriguez
- Autism Spectrum Disorders: The complete
guide to understanding Autism, Asperger’s
Problem List
syndrome, Pervasive Developmental Disorder
- Hypotonia
and other ASDs by Chantal Sicile-Kira
- Decreased strength - Down Syndrome by Marlene Targ Brill
- Decreased postural stability - Kaplan and Saddock’s Synopsis of Psychiatry
- Clinodactyly 11th edition.
- Delayed fine and gross motor skills http://www.webmd.com/children/tc/down-
- Decreased functional activities syndrome-exams-and-tests#

Physical therapy Diagnosis:

- NM2. Impaired neuromotor
development

PHYSICAL THERAPY PROGNOSIS

Problem list Plan of Care Intervention
- Hypotonia - To facilitate - Roods/ PNF
movement facilitation
techniques
- Decreased - To improve - Strengthening
strength muscle exercises:
strength dumbbells,
theraband,
ankle weights
- Decreased - To increase - Static: PNF
postural ability to alternating
stability maintain static isometrics,
and dynamic Rhythmic
position stabilization

- Dynamic:
Weight bearing
with forward
backward or
side reaching
of the
extremities
- Clinodactyly - To increase - Manual
range of stretching;
motion and Paraffin wax
tissue bath x 15 mins.
extensibility
- Delayed fine - To improve - Fine motor
motor skills fine motor activities
skills (to teach
patients how
to properly
hold objects)
- Delayed gross - To improve - Grasping
motor skills gross motor activities (big
skills objects to
small objects)
- Decreased - To improve - Refer to OT
functional ADLs
activities

Sources:

175 | P a g e
 MUSCULAR DYSTROPHIES
Muscle Dystrophy
Duchenne Muscular Dystrophy (DMD)
Becker Muscular Dystrophy (BMD)
Limb Girdle MD
Facioscapulohumeral MD
Myotonic MD
Emery Dreifuss MD
Endocrine Myopathy
Steroid Myopathy
Hyperthyroid myopathy
Hypothyroid myopathy
Cushing's disease
Excess parathyroid hormone
Inflammatory Myopathy
Polymyositis (PM)
Dermatomyositis (DM)
I. GENERAL MEDICAL BACKGROUND
A. DEFINITION
- Myopathy is a neuromuscular disorder
in which the muscle fibers do not
function for any one of many reasons
resulting to muscular weakness.
- -”Myopathy” means muscle disease
(myo- Greek meaning “muscle” +
pathos- Greek meaning “suffering”
B. EPIDEMIOLOGY
- 14% worldwide incidence of all
inheritable myopathies
- Muscular dystrophy incidence: 63 per 1
million
- Worldwide incidence of inflammatory
myopathies: 5-10 per 100,000 people
- >women
C. ETIOLOGY
- Infection
- Muscle injury due to medications
- Inherited diseases affecting muscle
function
- Disorders of electrolyte levels
- -thyroid diseases
- -idiopathic inflammatory myopathies
D. CLASSIFICATIONS
• Hereditary Muscle Diseases
- Muscle Dystrophies
- Muscle Channelopathis
- Mitochondrial Myopathies
- Metabolic Myopathies
• Acquired Muscle Diseases
- Inflammatory Myopathies
- Endocrine and Toxic Myopathies
- Infectious Muscle Diseases
• X-linked Recessive
- Female carries the abnormal gene
which is
- Located at the short arm of the x
- Chromosome. (-) Family hx
- Ex: Duchenne, Becker, Emery-
Dreifus
• Autosomal Dominant
- Defect is seen in every generation
of those affected.
- (+) family hx
• Autosomal Recessive
- Affected gene non-dominant
- One of the parents carries the
abnormal recessive gene but does
not manifest the disease
- (-) family hx
• X-linked Dominant
- -Defective Gene is x-chromosome
- (+) family hx
1. MUSCLE DYSTROPHY
Definition
- Heterogenous group of hereditary
myopathies often presenting in
childhood
- Characterized by progressive
degeneration of
muscle fibers leading to muscle
weakness,
wasting and atrophy.
- Genetic defect of proteins constituting
the
sarcolemma-associated cytoskeleton
system
- Histologically, in advanced cases, muscle
fibers are replaced by fibrofatty tissue
- This distinguishes dystrophy from
myopathies which also present muscle
weakness
Pathophysiology:
- Xp21 defect or deletion (DMD or BMD)
results in the absence of the specific
427-kd
cytoskeletal protein labelled
“dystrophin”
- This protein provides structural stability
to the
dystroglycan complex in cell membrane
- Absence of dystrophin results in ongoing
cell
membrane depolarization due to
calcium
176 | P a g e
 entering the cell
- This causes ongoing degeneration and
regeneration of muscle fibers
- Dystrophin - deletions appear to
represent
large proportion of the genetic
abnormalities,
with frameshift and point mutations
accounting for the rest
A. Duchenne Muscular Dystrophy (DMD)
Definition
- DMD is the most severe and the most
common form of muscular dystrophy,
with an incidence of about 1 per 3500
live male births.
- Most common MD
- DMD becomes clinically evident by age
of 5, →progressive weakness leading to
wheelchair dependence by age 10 to 12
years →death by the early 20s.
Onset:
- 3-5 years
Etiology:
- Deficiency of dystrophin, resulting in
progressive loss of muscle fibers
Clinical Manifestations:
- Difficulty getting up from deep position
and climbing steps, waddling gait
- Skeletal deformities & Cardiomyopathy
- Markedly elevated creatine kinase
- Inability to walk by 9-11 years
- Death occurs usually in the 3rd decade, from
respiratory insufficiency
- Pain in muscles: calves (m.c.) w/
enlargement
- Earliest weakness @ NECK FLEXORS;
generalized but predominantly proximal =
pelvic girdle > shoulder girdle
- Half of these children are somewhat
mentally retarded (slow learners); some are
very intelligent.
B. Becker Muscular Dystrophy (BMD)
Definition
- Benign pseudohypertrophic muscular
dystrophy is an X-linked recessive
inherited disorder characterized by
slowly progressive muscle weakness of
the legs and pelvis
- Occurs in approximately 3 to 6 in
100,000 male births
- Less common and much less severe than
DMD
Etiology: same gene that causes the Duchenne
form is responsible, but its defects are less
damaging to muscle.
Clinical Manifestations:
- Same as those of Duchenne muscular
dystrophy, but begin later in life and
progress more slowly.
- Most affected men must eventually use
a wheelchair, but some do not, and
many live past middle age.
Pathophysiology (DMD &DMD)
- DMD and BMD are caused by
abnormalities in the dystrophin gene
- The role of dystrophin in transferring
the force of contraction to connective
tissue has been proposed as the basis
for the myocyte degeneration that
occurs with dystrophin defects, or with
changes in other proteins that interact
with dystrophin
C. Limb Girdle MD
- Erb's muscular dystrophy is an
autosomal class of muscular dystrophy
that is similar but distinct from
Duchenne muscular dystrophy and
Becker's muscular dystrophy.
- LGMD isn't a fatal disease; it may
eventually weaken the heart and lung
muscles, leading to illness or death due
to secondary disorders.
Onset: between 10 and 30.
Prevalence: Men=Women
Clinical Manifestations:
- Most severely affected are generally those
of the hips and shoulders -- the limb girdle
muscles.
- Muscle weakness- symmetric, proximal, and
slowly progressive
- Myoglobinuria
- Pain
- Myotonia
- Cardiomyopathy
- Elevated serum CK
- Rippling muscles
- (-) MR
D. Facioscapulohumeral MD
- aka Landouzy-Dejerine
- autosomal dominant form of muscular
dystrophy that initially affects the
skeletal
muscles of the face (facio), scapula
(scapulo)
and upper arms (humeral)
Onset: infancy to middle age
177 | P a g e
 - Symptoms may develop in early
childhood and
are usually noticeable in the teenage
years with
- 95% of affected individuals manifesting
disease
- by age 20 years.
- Life expectancy is normal, but up to 15%
of
- affected individuals become severely
disabled
- and eventually must use a wheel chair.
Clinical Manifestations:
- A progressive asymmetrical skeletal muscle
weakness usually develops in other areas of
the body as well
- Facial muscle weakness: eyelid drooping,
inability to whistle, decreased facial
expression, depressed or angry facial
expression, difficulty pronouncing the letters
M, B, and P
- Shoulder weakness: difficulty working with
the arms raised, sloping shoulder
- Abnormal heart rhythm
- Unequal weakening of the biceps, triceps,
deltoids, and lower arm muscles
- Loss of strength in stomach muscles and
eventual progression to the legs
- Foot Drop
E. Myotonic MD
- Dystrophia myotonica DM is a chronic,
slowly
progressing, highly variable inherited
multisystemic disease.
Prevalence: 1 in 8000; occur in patients of any
age; males=females
Etiology: CTG repeat expansion in a gene on
chr. 19
Clinical Manifestations:
- Myotonia: hyperexcitability of muscle
membrane ,inability of quick muscle
relaxation
- Progressive muscular weakness and
wasting, most prominent in cranial and
distal muscles
- Cataracts, frontal balding, testicular
atrophy
- Cardiac abnormalities, mental
retardation
F. Emery Dreifuss MD
- An x-linked recessive progressive
dystrophic
myopathy with a gene identified at Xq28
that
affects an estimated 1 in 100,000
people.
Etiology: deficient muscle protein - EMERIN
- chiefly affects muscles used for
movement
(skeletal muscles) and heart (cardiac)
muscle.
- TRIAD:
 Slowly progressive muscle weakness and
wasting in a scapulohumeroperoneal
distribution (beginning in muscles of the
upper arms and lower legs and
progressing to muscles in the shoulders
and hips)
 Early contractures of the elbow, ankle,
and posterior neck
 Cardiac conduction defects,
cardiomyopathy, or both
- Hallmark: early presence of contractures
of the elbow flexors w/ LOM of full
elbow extension.
2. ENDOCRINE MYOPATHY
- Caused by underlying conditions caused
by the
over or underproduction of hormones.
- Can develop in children and adults and
usually
respond well to treatment.
A. Steroid Myopathy
- Most common endocrine muscle
disease
- Steroid excess, whether caused by an
adrenal gland disorder (e.g., Addison
disease) or chronic administration of
glucocorticoid drugs, causes muscle
weakness and wasting.
B. Hyperthyroid myopathy
- Caused by the thyroid gland producing
too much thyroxine.
- Symptoms: weakening and wasting of
the muscles, especially in the shoulders
and hips, and sometimes the eyes
C. Hypothyroid myopathy
- Caused by the underproduction of
thyroxine
- Muscle weakening in the legs and arms.
The muscles may become enlarged.
D. Cushing's disease
- Overproduction of hormones produced
by the pituitary and adrenal glands,
cause myopathy.
E. Excess parathyroid hormone
- Results to Hypercalcemia
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 - Causes proximal muscle pain and - Breathing difficulties and increased risk for
weakness pneumonia, flu, and other respiratory
- infections
3. INFLAMMATORY MYOPATHY - Dysphagia → choking and malnutrition
- Autoimmune disorder - Contractures: severe in DMD patients
- Body's immune system attacks healthy - Decreased mobility
muscle fibers and causes inflammation, - Scoliosis, Osteoporosis → Fractures
which in turn damages the muscle. - Decreased strength
-
A. Polymyositis (PM) G. DIAGNOSIS
- Occur at any age in either sex - Complete medical history and physical
- More common in children and in examination
women - Blood Tests
between 40 and 60 years old. - Urinalysis
Clinical Manifestations: - Gene Studies / Genetic testing
- Muscle aches, cramping, and tenderness - Electrocardiogram (ECG)
- Muscle weakness is often worse in the - Muscle Biopsy
neck, arms, and thighs, making it
difficult to stand up from a sitting H. DIFFERENTIAL DIAGNOSIS
position Autosomal Dominant:
- Fever, general discomfort (malaise), and • FSH
loss of appetite. • LGMD
Autosomal Recessive:
B. Dermatomyositis (DM) • LGMD
- Characterized by a skin rash and all of • Metabolic myopathies
the muscle X-Linked:
- Symptoms of PM. • Duchenne’s MD
- The rash is a purple discoloration • Becker’s MD
around the • Emery
eyes and on the cheeks but may also • Dreifuss MD
appear on
other parts of the body. Characteristic PM DM
- Skin becomes thin and fragile
Onset >18 y.o. Childhood or
- Most commonly develops in children
adult
between
Location of Proximal Proximal
the ages of 5 and 14 years.
weakness
- People who have DM have an increased
Distribution Symmetrical Symmetrical
risk for
of weakness
developing cancer.
skin findings None Yes
Association No Yes
E. GENERAL SIGNS AND SYMPTOMS
with
- Skeletal muscle weakness (proximal
malignancy
muscles> distal)
Creatine Elevated level Normal or
- Aching, Cramping, Pain, Stiffness, -
Kinase elevated
Tenderness, and Tightness
- Initially, individuals may feel fatigued doing
I. PROGNOSIS
very light physical activity.
- Underlying cause of the disorder can be
- Walking and climbing stairs may be difficult.
treated successfully
- Muscle Wasting
- Endocrine myopathies: prognosis is
- Myopathic face
usually good
- Tendon reflexes are normal or depressed
- Progressive myopathies that develop
- Waddling gait
later in life
- Usually have a better prognosis than
F. COMPLICATIONS
conditions that develop during
- Abnormal heart rhythms or cardiomyopathy,
childhood.
CHF

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 - Duchenne MD: rarely live beyond their Muscle Increase muscle Strengthening
middle to late 20s. Becker MD: may live weakness strength exercises to
until middle age. repetition
maximum to
II. GENERAL HEALTH CARE MANAGEMENT progressively
increase strength
A. MEDICAL, SURGICAL, PHARMACOLOGIC and delay muscle
- Deflazacort – has more bone-sparing atrophy
and carbohydrate-sparing properties LOM Increase range Passive
with less weight-gain effects and of motion stretching to
improves strength and function proximal
- Oxazoline muscles->distal
- Creatine monohydrate muscles to
supplementation- enhance athletic increase range of
performance of healthy individuals in up motion
to 10% Fatigues conserve energy Teach energy
- Functional testing; physical therapy; use easily conservation
of orthoses; fracture management; soft- techniques and
tissue, bone, and spinal surgeries; use of activity pacing
a wheelchair when indicated; and wheelchair/ prevent Frequent
genetic and/or psychological testing. bedbound pressure sores position changes
in sitting (every
III. PHYSICAL THERAPY EXAMINATION,
30 mins) and
EVALUATION, AND DIAGNOSIS
lying down
(every 2 hrs)
A. Points of Emphasis in Examination
Contractur Prevent Daily AAROME to
• Observation – look for muscle atrophy,
es contractures all major joints in
deformities
the body to
• Strength testing – manual muscle test
prevent
• ROM testing
contracture
• Functional testing formation.
• Stand up from a chair Decrease Increase Aerobic exercise:
• Posture & Gait endurance cardiovascular aquatic
• Balance capacity endurance programs; bike
• Step up on a low stool ergometer to
• REFLEXES and SENSATION provide a
beneficial
B. Problem List training stimulus
• Muscle weakness to the
• LOM cardiopulmonary
• Contractures and muscular
• Decreased endurance capacity system
• Pain Pain Decrease pain Heating
• Balance problems modalities like
• Swallowing problems US, TENS, IFC,
• Respiratory and cardiac complications Hot moist packs
to decrease the
sensation of pain
C. Physical Therapy Diagnosis through the
- Impaired muscle performance, range of counter irritant
motion, posture and balance associated with effect.
genetic and neuromuscular disorder. Poor Promote perturbation
balance balance training
IV. PHYSICAL THERAPY MANAGEMENT

Problem Plan of Care Intervention

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Postural Correct posture Stretching and
problems strengthening
(scoliosis) ex; postural
training
Gait Improve gait Gait training
deviations
Respiratory Prevent Postural
and cardiac blockage of drainage and
complicatio respiratory tract ankle pumps to
ns and circulation prevent
thrombus
formation and
promote
clearance of
secretion and
predisposal to
pulmonary
infections.

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 CEREBRAL PALSY 2. Severe and prolonged
intrapartum asphyxia – injuries
I. GENERAL MEDICAL BACKGROUND more global & more likely to
cause a more severe disability
A. DEFINITION 3. Chorioamnionitis
- a disorder of movement and posture 4. Maternal autoimmune disease
caused by a non-progressive injury to the and coagulation disorders
immature brain 5. Hyperbilirubinemia
Kernicterus - a form of brain damage
B. CLASSIFICATION caused by excessive jaundice.
a. By tone abnormalities
I. Spastic (75% - - athetoid CP (injury to the basal
decerebrate or ganglia); associated with hearing loss
decorticate) C. Postnatal Causes
II. Dyskinetic 1. CNS infection
- Athetoid 2. Vascular causes
- Choreiform 3. Head injury
- Ballistic 4. Others include anoxia, ischemia,
- Ataxic and inflammation
III. Hypotonic
IV. Mixed E. PATHOPHYSIOLOGY
b. By body parts involved A.
I. Diplegia 1. Brain injury occurring in children
II. Quadriplegia born prematurely
III. Triplegia 2. Immaturity, fragile brain vasculature,
IV. Hemiplegia and the physical stresses of
c. Gross Motor Functional prematurity
Classification 3. Results to compromised cerebral
Level 1: walks without restriction, blood flow
limitations in high-level skills 4. Intraventricular hemorrhage in
Level 2: walks without devices, differing degrees
limitations walking outdoors B.
Level 3: walks with devices, 1. Very low birth weight
limitations walking outdoors 2. Increased incidence of periventricular
Level 4: limited mobility, power hemorrhagic infarction
mobility outdoors
Level 5: very limited self-mobility, F. CLINICAL MANIFESTATION
even with assistive technology 1. Hypotonia and motor delay – early
signs of CP
C. EPIDEMIOLOGY 2. UMNL – (+) increased tone and
- One of the most common disabling reflexes, Babinski’s reflex
conditions affecting children 3. Spasticity
- approximately 1-2.3 per 1000 live births; 4. Retention of primitive reflexes
M>F 5. Muscle weakness
- 5.2 per 1000 live births at 1 year of age 6. Abnormal posture – children with
- Premature low birth weight (<2500g) to spasticity
extremely low birth weight (<1000g) 7. Sensory issues – hypersensitivity;
infants have higher CP risk decreased ability to distinguish 2-point
discrimination in UE
D. ETIOLOGY 8. Deformity of the spine
- Brain injury that leads to CP can occur in
the prenatal, perinatal, or postnatal G. COMPLICATIONS
period 1. Contractures
- Most causes of CP occur in the prenatal 2. Bony deformity – increased
period anteversion of femoral neck; increase in
- APGAR score of <7 hip FADDIR
A. Prenatal Causes 3. Respiratory function is compromised
1. TORCH infections 4. Visual sequelae – Strabismus
2. Intrauterine stroke (exotropia or esotropia)
3. Genetic malformation 5. Abnormalities of oral motor function –
B. Perinatal Causes drooling, dysphagia, and dysarthria
1. Severe anoxic or ischemic brain 6. Feeding difficulties – due to the
injury increase or decrease in tone

182 | P a g e
 7. Gastrointestinal symptoms – •
Gastroesophageal reflux (constipation)
8. Seizure disorders – 1/3 of children
9. Osteporosis – calcium and Vit D
deficiency
10. Cognitive impairments – ability to
interact with peers, physical ability and
mobility, tube feeding, incontinence, and
seizures
H. DIAGNOSIS
- The diagnosis of CP has historically rested
on the patient’s HISTORY and PHYSICAL
EXAMINATION
- CT and MRI Imaging – neuroimaging is
warranted when the etiology of a patient
has not been established
- An MRI is preferred over CT scan due to
diagnostic yield and safety
- Furthermore, an abnormal neuroimaging
study indicates a high likelihood of
associated conditions, such as Epilepsy
and Mental Retardation
I. DIFFERENTIAL DIAGNOSIS
CVA in the young – affectation of the mature
brain
Traumatic Brain Injury
J. PROGNOSIS
- CP is not a progressive disorder in which
actual brain damage does not worsen,
but the symptoms can become worse
over time due to subdural damage.
- People who have CP to develop Arthritis
at a younger age than a normal person
because of the pressure placed on joints
by excessively toned and stiff muscles.
- The full intellectual potential of a child
born with CP will often be unknown until
the child starts school. Intellectual level
among with CP varies from genius to
mentally retarded.
- The ability to live independently with CP
also varies depending on the severity of
the disability.
- However, in most cases persons with CP
can expect to have a normal life
expectancy; survival has been shown to
be associated with the ability to
ambulate, roll and self-feed.
- As the condition does not directly affect
reproductive function, some persons
with CP have children and parent
successfully.
- According to OMIM, only 2 % of CP is
III. PHYSICAL THERAPY EXAMINATION,
inherited (with Glutamate
decarboxylase-1 as one known enzyme
involved). There is no evidence of an
increased chance of a person with CP
having a child CP.
II. GENERAL HEALTHCARE MANAGEMENT
A. MEDICAL/PHARMACOLOGIC
Muscle relaxants – relax hyperspastic or
hypertonic muscle
Ex: Baclofen, Dantrolene Sodium (for
liver function complications; check every
3 months)
Side effects: sedation, weakness,
drowsiness, dry mouth
• Stimulants – given upon awakening in the
morning and at noon
Ex: Methyl Phrenidate
• Anticonvulsants
• Phenothiazines – for hyperactive and
emotionally disturbed children for
tranquilization without sedation
• Diazepam – the most effective control
for athetosis and spasticity
B. SURGICAL
Surgery usually involves one or
combination of:
• Loosening tight muscles and releasing
fixed joints, most often performed on the
hips, knees, hamstrings and ankles. In
rare cases, this surgery may be used for
people with stiffness of the elbows,
wrists, hands and fingers.
• Insertion of a baclofen pump usually
during the stages while a patient is a
young adult
• Peripheral Nerve Block (3-6 months)
• Straightening abnormal twist of the leg
bones i.e. femur (termed femoral
anteversion or antetorsion)
 This is a secondary complication
caused by spastic muscles
generating abnormal force on bones,
and often results in tiptoeing
(pigeon-toed gait). The surgery is
called Derotation Osteotomy, in
which the bone is broken or cut and
then set in the correct alignment.
• Cutting nerves on the limbs most
affected by movements and spasms, this
procedure is called a Rhizotomy, “rhizo”
meaning root and “tomy” meaning
cutting of. Reduces spasms and allows
more flexible control of the affected
limbs and joints
• Botolinum Toxin A (Botox) injections into
muscles that are either spastic or have
contractures, the aim being to relieve the
disability and pain produced by the
inappropriately contracting muscle (4-6
months)
•
EVALUATION AND DIAGNOSIS
A. EXAMINATION/EVALUATION
a. Patient’s interview
1. Mother’s pregnancy and birth
history
183 | P a g e
 2. Medical history (diagnoses, 1. Sensorimotor assessment ( ages
intubated and on ventilator, 4-9 having mild to moderate
surgeries and medications) learning impairment)
3. Family history, caretakers, 2. Includes tests of balance,
current home situations, proprioceptive and tactile
support to family, sensation and control of specific
socioeconomic status. movements
b. Preterm infant examination
1. Neurological assessment of h. Pediatric Functional Assessment
preterm and full term newborn 1. Pediatric Evaluation of Disability
infants Inventory (scale of ADL with or
2. Assessment of infant motor without modification completed
performance by caregiver)
c. Full term newborn/child 2. weeFIM (functional
examination independence measure;
1. APGAR screening function in self-care mobility,
2. Neurological examination; locomotion, communication and
reflexes and consciousness social recognition)
3. Skeletal system examination
4. Rom B. PROBLEM LIST
5. Posture 1. Abnormal muscle tone
6. Movements (reflexive) (spastic/hypotonic)
7. Neonatal review 2. Asymmetry of movement
d. Screening tests 3. Abnormal postures
1. Denver Development Screening 4. Weakness
Test (developmental delays, 5. Contractures
social, fine and gross motor 6. Sensory issues
skills, and language skills) 7. Retention of primitive reflexes
2. Alberta Infant Motor Scale
(assess gross motor milestones C. PHYSICAL THERAPY DIAGNOSIS
from birth through independent 1. Delayed developmental milestones
walking) 2. Decreased muscle strength and ROM
e. Standardized Motor Test 3. Abnormal muscle tone
1. Movement assessment (identify 4. Sensory issues
motor dysfunction) 5. Abnormal posture
2. Peabody Developmental Motor 6. Asymmetry of movement
Scale (assess gross and fine
motor development from birth- IV. PLAN OF CARE AND INTERVENTION
42 mos) – includes spontaneous, A. PLAN OF CARE
elicited, reflexes and automatic 1. Prevention of contractures and
reactions deformities
3. Gross and motor function test 2. Maximal functional movement
(measure change in gross motor 3. Utilization of dynamic patterns of
functions, includes 5 movement
developmental dimensions: 4. Developmental activities
prone & supine, sitting, crawling 5. Improve blood flow and improve muscle
& kneeling, standing & walking, growth and strength
jumping) 6. Increase proprioceptive input to the
f. Comprehensive Developmental neuromuscular system and improve
Assessment motor function
1. Bayley Scales of infant
development revision (norm- B. INTERVENTION
referenced motor and mental 1. Contractures and deformities
scales from birth-42 mos of age) - PNF stretching techniques
g. Sensory Integration and Praxis Test (ex.HR,HRAC)

184 | P a g e
 - Sensory stimulation (ROODS)-
inhibition of spastic ms
- Splinting
- TRAFOs (tone-reducing ankle-foot
orthosis)
- Serial Casting
- Bracing (W.M. Phelps)
2. Maximal functional goals and utilization
of dynamic patterns of movement
- PNF movement patterns techniques
( mass movement patterns)
- Synergistic movement patterns
(Brunnstrom)- primitive and reflex
responses
- Neurodevelopmental approach
(Bobath) – reflex inhibition and
facilitation of functional movements
3. Developmental activities
- Implementation of ontogenetic
developments (progressive pattern
movement)
- Neuromotor development (Eirene
Collis) – strict developmental
sequence is followed; placing
children in normal postures in order
to stimulate normal tone
4. Functional Electrical Stimulation and
Biofeedback
- Training specific muscles and
improving blood flow
- Low-voltage, high-frequency ES
- Used together with the exercises
5. Compression garments
6. Reflex creeping and other reflex
reaction (Vaclav Vojta)
- Touch, pressure, stretch and muscle
action against resistance are used in
triggering mechanisms or in
facilitation in creeping

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 CEREBROVASCULAR ACCIDENT - Ischemic Strokes
o Lack of cerebral blood flow
Definition deprives the brain of needed
- Stroke (Cerebrovascular Accident) is the oxygen and glucose, disrupts
sudden loss of neurological function cellular metabolism, and leads to
caused by an interruption of the blood injury and death of tissues.
flow to the brain.  Thrombus
• Formation or
Classification development of a
- Etiological Category blood clot within the
• Thrombosis cerebral arteries of
• Embolus their branches.
• Hemorrhage • Results from
- Vascular Territory platelet adhesion
• Anterior Cerebral Artery and aggregation on
Syndrome plaques.
• Middle Cerebral Artery • Thrombi lead to
Syndrome ischemia, or
• Posterior Cerebral Artery occlusion of an
Syndrome artery with resulting
• Internal Carotid Artery cerebral infarction
Syndrome or tissue death
• Lacunar Stroke (atherothrombotic
• Vertebrobasilar Artery brain infarction)
Syndrome  Embolism
- Management Categories • Composed of bits of
• Transient Ischemic Attack matter (blood clot,
• Minor Stroke plaque) formed
• Major Stroke elsewhere and
• Deteriorating Stroke released into the
bloodstream,
• Young Stroke
traveling to the
cerebral arteries
Epidemiology
where they lodge in
- Stroke is the fourth leading cause of
a vessel, producing
death and the leading cause of long-term
occlusion and
disability among adults.
infarction.
- Each year approximately 795,000
individuals experience a stroke in the US. • The most common
Stroke accounts for 1 of every 18 deaths source of Cerebral
in the US. Embolism is disease
- Sex: Women have a lower age-adjusted of the
stroke incidence than men. However, cardiovascular
this is reversed in older ages; women system.
over 85 years of age have an elevated risk  Hemorrhagic Stroke
compared to men. • Abnormal bleeding
- Race: Compared to whites, African into the
Americans have twice the risk of first- extravascular areas
ever stoke; rates are also higher in of the brain, are the
Mexican Americans, American Indians, result of rupture of a
and Alaska Natives. cerebral vessel or
- Age: Incidence of stroke increases with trauma.
age, doubling in the decade after 65 • Intracerebral
years old. Hemorrhage is
- Previous History: Survival rates are caused by rupture of
dramatically lessened by increased age, a cerebral vessel
hypertension, heart disease, and with subsequent
diabetes. bleeding into the
- Hemorrhagic stroke accounts for the brain.
largest number of deaths. • Primary Cerebral
Hemorrage
Etiology (nontraumatic
- Atherosclerosis is a major contributory spontaneous
factor. hemorrhage)

186 | P a g e
 typically occurs in Clinical Manifestations
small blood vessels
weakened by Clinical Manifestations of Anterior Cerebral Artery
atherosclerosis Syndrome
producing an Signs and Symptoms Signs and Symptoms
aneurysm. Structures Involved Structures Involved
• Subarachnoid Contralateral Primary motor area,
hemiparesis involving medial aspect of cortex,
Hemorrhage occurs
mainly the LE (UE is internal capsule
from bleeding into more spared)
the subarachnoid Contralateral Primary sensory area,
space typically from hemisensory loss medial aspect of cortex
a saccular or berry involving mainly the LE
aneurysm affecting (UE is more spared)
primarily large Urinary incontinence Posteromedial aspect of
blood vessels. superior frontal gyrus
Problems with imitation Corpus callosum
Pathophysiology and bimanual tasks,
Figure 1 Ischemic Cascade apraxia
Abulia (akinetic Uncertain localization
Release of excess neurotransmitters mutism), slowness,
(eg. Gulatamte and Asparate) delay, lack of
spontaneity, motor
Progressive disturbance of energy
Contralateral grasp Uncertain localization
matabolism and anoxic reflex, sucking reflex
depolarization
Can be asymptomatic if
circle of Willis is
Inability of brain cells to produce
competent.
energy (ATP)

Clinical Manifestations of Middle Cerebral Artery

Syndrome
Excess influx of Calcium Ions Signs and Symptoms Signs and Symptoms
Structures Involved Structures Involved
Contralateral Primary motor cortex
hemiparesis involving and internal capsule
Release of Nitric Oxide and mainly the UE and face
Formation of Free Radicals
Cytokines
(LE is more spared)
Contralateral Primary sensory cortex
hemisensory loss and internal capsule
involving mainly the UE
and face (LE is more
spared)
Brain cell damage Motor speech Broca’s cortical area
impairment: Broca’s or (third frontal
nonfluent aphasia with convolution)
Figure 2 Cerebral Edema limited vocabulary and in the dominant
slow, hesitant speech hemisphere, typically
the left
Tissue necrosis hemisphere
Receptive speech Wernicke’s cortical
impairment: Wernicke’s area (posterior portion
Widespread rupture of or fluent aphasia with of the
cell membranes impaired auditory temporal gyrus) in the
comprehension and dominant hemisphere,
fluent speech with typically the left
Movement of fluid from normal rate and melody
blood into brain tissues Global aphasia: Both third frontal
nonfluent speech with convolution and
poor comprehension posterior portion of
Significant edema the superior temporal
gyrus
Perceptual deficits: Parietal sensory
Elevated intracranial unilateral neglect, depth association cortex in
pressure (ICP) perception, spatial the nondominant
hemisphere, typically
the right
Intracranial hypertension Limb-kinetic apraxia Premotor or parietal
& neurologic detoriation cortex

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Contralateral Optic radiation in Medial medullary Occlusion vertebral
homonymous internal capsule syndrome artery, medullary
hemianopsia branch
Loss of conjugate gaze Frontal eye fields or Ipsilateral to lesion CN XII, hypoglossal, or
to the opposite side their descending tracts Paralysis with atrophy nucleus
Ataxia of contralateral Parietal lobe of half the tongue with
limb(s) (sensory ataxia) deviation to the
Pure motor hemiplegia Upper portion of paralyzed side when
(lacunar stroke) posterior limb of tongue is protruded
internal capsule Contralateral to lesion Corticospinal tract
Paralysis of UE and LE
Clinical Manifestations of Posterior Cerebral Artery Impaired tactile and Medial lemniscus
Syndrome proprioceptive sense
Signs and Symptoms Signs and Symptoms Lateral medullary Occlusion of posterior
Structures Involved Structures Involved (Wallenburg’s) inferior cerebellar
Peripheral Territory syndrome artery or vertebral
Contralateral Primary visual cortex artery
homonymous or optic radiation Ipsilateral to lesion Descending tract and
hemianopsia Decreased pain and nucleus of CN V,
Bilateral homonymous Calcarine cortex temperature sensation trigeminal
hemianopsia with some (macular sparing is in face
degree of macular due to occipital pole Cerebellum or inferior Cerebellar ataxia: gait
sparing receiving collateral cerebellar peduncle and limbs ataxia
blood supply from Vertigo, nausea, Vestibular nuclei and
MCA) vomiting connections
Visual agnosia Left occipital lobe Nystagmus Vestibular nuclei and
Prosopagnosia (difficulty Visual association connections
naming people on sight) cortex Horner’s syndrome: Descending sympathetic
Dyslexia (difficulty Dominant calcarine miosis, ptosis, tract
reading) without lesion and posterior decreased sweating
agraphia (difficulty part of corpus Dysphagia and CN IX, glossopharyngeal,
writing), color naming Callosum dysphonia: paralysis of and CN X, vagus, or
(anomia), and color palatal and laryngeal nuclei
discrimination problems muscles, diminished
Memory defect Lesion of inferomedial gag reflex
portions of temporal Sensory impairment of Cuneate and gracile
lobe bilaterally or on ipsilateral UE, trunk, or nuclei
the dominant side only LE
Topographic Nondominant primary Contralateral to lesion Spinal lemniscus—
disorientation visual area, usually Impaired pain and spinothalamic tract
bilaterally thermal sense over
Central Territory 50% of body,
Central post-stroke Ventral posterolateral sometimes face
(thalamic) pain nucleus of thalamus Complete basilar artery Basilar artery, ventral
Spontaneous pain and syndrome (locked-in pons
dysesthesias; sensory syndrome)
impairments (all Tetraplegia Corticospinal tracts
modalities) (quadriplegia) bilaterally
Involuntary movements; Subthalamic nucleus Bilateral cranial nerve Long tracts to cranial
choreoathetosis, or its pallidal palsy: upward gaze is nerve nuclei bilaterally
intention tremor, connections spared
hemiballismus Coma Reticular activating
Contralateral hemiplegia Cerebral peduncle of system
midbrain Cognition is spared -
Weber’s syndrome Third nerve and Medial inferior pontine Occlusion of
Oculomotor nerve palsy cerebral peduncle of syndrome paramedian branch of
and contralateral midbrain basilar artery
hemiplegia Ipsilateral to lesion Pontine center for
Paresis of vertical eye Supranuclear fibers to Paralysis of conjugate lateral gaze paramedian
movements, slight third cranial nerve gaze to side of lesion pentine reticular
miosis and ptosis, and (preservation of formation (PPRF)
sluggish pupillary light convergence)
response Nystagmus Vestibular nuclei and
connections
Clinical Manifestations of Vertebrobasilar Artery Ataxia of limbs and gait Middle cerebellar
Syndrome peduncle
Signs and Symptoms Signs and Symptoms Diplopia on lateral gaze CN VI, abducens, or
Structures Involved Structures Involved nucleus

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Contralateral to lesion Corticobulbar and Cerebellar ataxia of cerebellum, dentate
Paresis of face, UE, and corticospinal tract in limbs and gait, falling nucleus
LE lower pons to side of lesion
Impaired tactile and Medial lemniscus Dizziness, nausea, Vestibular nuclei
proprioceptive sense vomiting
over 50% of the body Horizontal nystagmus Vestibular nuclei
Lateral inferior pontine Occlusion of anterior Paresis of conjugate Uncertain
syndrome inferior cerebellar gaze (ipsilateral)
artery, a Loss of optokinetic Uncertain
Ipsilateral to lesion branch of the basilar nystagmus
Horizontal and vertical artery Horner’s syndrome: Descending sympathetic
nystagmus, vertigo, miosis, ptosis, fibers
nausea, vomiting decreased sweating on
Facial paralysis CN VII, facial, or nucleus opposite side face
Paralysis of conjugate Pontine center for Contralateral to lesion Spinothalamic tract
gaze to side of lesion lateral gaze (PPRF) Impaired pain and
Deafness, tinnitus CN VIII, cochlear, or thermal sense of face,
nucleus limbs, and trunk
Ataxia Middle cerebellar Impaired touch, Medial lemniscus
peduncle and cerebellar vibration, and position (lateral portion)
hemisphere sense, more in LE than
Impaired sensation Main sensory nucleus UE (tendency to
over face and descending tract of incongruity of pain and
fifth nerve touch deficits)
Contralateral to lesion Spinothalamic tract
Impaired pain and
thermal sense over half Diagnosis
the body (may include - History and Examination
face)
- Test and Measures
Medial midpontine Occlusion of
- Cerebrovascular Imaging
syndrome paramedian branch of
the mid-basilar artery • Computed Tomography
Ipsilateral to lesion Middle cerebellar • Magnetic Resonance Imaging
Ataxia of limbs and gait peduncle • Magnetic Resonance
(more prominent in Angiography
bilateral involvement) • Doppler Ultrasound
Contralateral to lesion Corticobulbar and • Arteriography and Digital
Paralysis of face, UE, corticospinal tract Subtraction Angiography
and LE
Deviation of eyes Abducent nerve
Differential diagnosis
nucleus, medial
longitudinal fasciculus Seizures
Lateral midpontine Occlusion of short Space-Occypying Lesions (e.g. Subdural
syndrome circumferential artery Hematonoa, Cerebral Abscess/Infectiom,
Ipsilateral to lesion Middle cerebellar Tumor)
Ataxia of limbs peduncle Syncope
Paralysis of muscles of Motor fibers or nucleus Somatization
mastication of CN V, trigeminal Delirium secondary to sepsis.
Impaired sensation Sensory fibers or
over side of face nucleus of CN V, Prognosis
trigeminal The initial grade of paresis, measured on initial
Medial superior pontine Occlusion of hospital admission is an important predictor of
syndrome paramedian branches of
motor recovery.
upper basilar artery
Cerebellar ataxia Superior or middle
- Complete paralysis on admission,
cerebellar peduncle complete motor recovery occurs in less
Internuclear Medial longitudinal than 15% of patients.
ophthalmoplegia fasciculus
Contralateral to lesion Corticobulbar and No significant difference in potential for motor
Paralysis of face, UE, corticospinal tract recovery between type of stroke (hemorrhage vs
and LE infarction) and location (brainstem vs
Lateral superior pontine - hemispheric infarction).
syndrome (occlusion of
superior cerebellar Patients who demonstrate less successful
artery, a branch of the
rehabilitation outcomes tended to include those
basilar artery)
with:
Ipsilateral to lesion Middle and superior
cerebellar peduncles,
- Advanced Age
superior surface of - Severe Motor impairments

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 - Persistent medical problems
- Impaired cognitive function - Summarized table for medications –
- Severe language disturbances Sullivan pp. 664, table 15.2.
- Severe visuospatial hemi neglect
- Other less well-defined social and - Thrombolytic
economic problems - Anticoagulants
- Antiplatelet Therapy
GENERAL HEALTHCARE MANAGEMENT - Antihypertensive Agents
- Angiotensin II receptor antagonists
Medical Management - Anticholesterol Agents/Statins
- Improve cerebral perfusion by - Antispasmodics/Spasmolytics
reestablishing circulation and - Antispastics
oxygenation and assist in stopping - Anticonvulsants
progression of the lesion to limit deficits - Antidepressants
- Maintain adequate blood pressure
- Maintain sufficient cardiac output PHYSICAL THERAPY EXAMINATION, EVALUATION
- Restore/maintain fluid and electrolyte AND DIAGNOSIS
balance
- Maintain blood glucose levels within the Points of Emphasis on Examination
normal range - Summarized table – Sullivan pp. 668, box
- Control seizures and infections 15.3
- Control edema, intracranial pressure,
and herniation using anti-edema agents. Patient/Client History
Ventriculostomy may be indicated to - Age
monitor and drain cerebrospinal fluid. - Location and Severity of stroke
- Maintain bowel and bladder function. - Stage of Recovery
- Maintain integrity of skin and joints by - Data from Initial Screenings
instituting protective positioning. - Phase of Rehabilitation
- Decrease the risk of complications such - Home/Community/Work Situation
as DVT, aspiration, decubitus ulcers, and Systems Review
so forth. - Neuromuscular
- Musculoskeletal
Neurosurgical Management - Cardiovascular/Pulmonary
- In hemorrhagic stroke, surgery may be - Integumentary
indicated to repair a superficial ruptured Tests and Measures
aneurysm or AVM, prevent rebleeding, - Level of Consciousness
and evacuate a clot. Larger, deeper - Emotional Status
intracranial or brainstem vascular - Behavioral Style
lesions are generally not amenable to - Communication and Language
surgery. Surgery may also be indicated - Circulation
for resection of a superficial unruptured - Ventilation and respiration/gas
AVM when there is high risk of rupture exchange
and stroke. - Anthropometric
- Merci Retriever System – this device is - Integumentary Integrity
threaded via a catheter into a large - Pain
artery just beyond the site of occlusion. - Cranial and Peripheral nerve Integrity
It uses a tiny corkscrew-shaped device - Sensory Integrity and Integration
that wraps around and traps the clot. - Perceptual Function
The clot is then retrieved and slowly - Joint Integrity, alignment, and mobility
removed from the artery. Blood flow is - Motor Function
successfully restored. This system is not - Muscle Performance
effective for smaller arteries and more - Postural Control and Balance
distance locations. - Gait and Locomotion
- The Penumbra System – uses a catheter - Wheelchair Management and Mobility
and separator that is threaded to the - Aerobic capacity and endurance
site of the clot. It suctions and grabs the - Orthotic, Protective, and Supportive
clot and aspirates the site. This system devices
can be used effectively within an 8-hour - Functional status and Activity level
window of symptom onset.
- Carotid Endarterectomy is a surgical Problem List
procedure used to remove fatty - Sensation
deposits from the carotid artery. - Cranial Nerve Impairments
- Flexibility and Joint Integrity
Pharmacological Management - Motor Function

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 o Tone Risk for falls -Decrease risk -Balance and
o Reflexes for falls proprioceptive
o Voluntary Movements training to
o Coordination decrease risk for
falls
o Motor Programming
-Assistive devices
- Muscle Strength
for pts with
- Postural Control and Balance persistent activity
- Gait and Locomotion limitations
- Integumentary Integrity Sleep -Improve sleep -Proper sleep
- Aerobic Capacity and Endurance disturbance hygiene
- Functional Status (avoidance of
caffeine, nicotine,
Physical Therapy Diagnosis alcohol, and
NM5 - Impaired motor function and sensory medications with
integrity associated with non-progressive stimulants)
-Simple exercises
disorders of the central nervous system -
and stretching
congenital origin or acquired in adolescence or may also improve
adulthood. sleep quality

PHYSICAL THERAPY PROGNOSIS

SOURCES:
PROBLEM LIST POC INTERVENTION
Sensation -Improve -Pt. and family
Physical Rehabilitation 5th edition by O’Sullivan
ability to cope education about
and Schmitz
with pain chronic pain
-Teach non -HMP, paraffin
pharmacologic wax, ice massage,
al pain topical rubs, and
management TENS to decrease
techniques pain
-Decrease pain -Lumbar and
cervical traction
to decompress
spinal structures
and decrease pain
Fatigue -Decrease Relaxation
fatigue techniques
(diaphragmatic
breathing,
biofeedback,
progressive
relaxation,
stretching,
aerobic exercise,
imagery,
autogenic
training) to relax
overactive
muscles
Deconditioning -Increase -Aerobic
physical conditioning to
strength, improve overall
endurance, function
and -Graded
cardiovasvular exercise(starting
fitness from a level that
-Improve the pt can
mobility, perform and
independence, gradually
and functional increased) to
ability increase strength
-Return to and endurance
previous levels -Postural
of activity at exercises to
home, improve posture
workplace and and decrease
leisure muscular
pursuits imbalances

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 TRAUMATIC BRAIN INJURY
GENERAL MEDICAL BACKGROUND
I. DEFINITION
Insult to the brain caused by an
external physical force possibly
leading to permanent or temporary
impairment of cognitive, behavioral,
emotional or physical functioning
with an associated diminished or
altered state of consciousness.
II. CLASSIFICATION
ACCORDING TO THE SEVERITY OF
INJURY
1. Mild or Minor TBI: No loss of
consciousness or only a very brief
period of altered consciousness.
2. Moderate TBI: loss of consciousness
lasting for a brief period of time to a
few hours.
3. Severe TBI: defined as coma lasting
for 6 hours or longer.
III. EPIDEMIOLOGY
• Incidence of TBI requiring
hospitalization: 95 per 100,000
population in the United States. 230,000
individuals hospitalized and survive with
TBI annually.
• Substantially fewer cases being
hospitalized due to managed care
practices and changes in admission
policies, rather than a drop in incidence
of TBI.
• Approximately 5.3 million Americans are
living with a TBI-related disability.
• The age distribution is bimodal, with
young adults (between the ages of 15 to
24 years, 145 per 100,000) and the
elderly (75 years and older, 191 per
100,000) showing the highest incidence.
• Elderly patients have a much slower and
less certain recovery process, compared
with the young adult population
• Men > Women 3:1
• Mortality rate: adults > children
• Most individuals who experienced TBI
are from a lower socioeconomic status
and are single.
IV. ETIOLOGY
1. DIRECT
• MVA
• Violence
• Falls or hits by falling debris
• Pedestrian accidents
• Sport accidents
2. INDIRECT
• Primary
– drunk driving/alcohol
abuse
• Secondary: drugs
• Tertiary: low economic
status
MECHANISMS OF INJURY
Acceleration - Deceleration
• Coup: the affectation is
ipsilateral, same side to
where the shear forces
were applied.
• Countercoup: the
affectation is contralateral
to the application of the
shear force.
V. PATHOPHYSIOLOGY
• TBI can be caused by a
penetrating injury (open) or a
non-penetrating injury (closed)
• Head trauma includes both
immediate, impact-related
(primary injury) and delayed brain
injury (secondary injury).
• Open brain injury typically is
caused by a gunshot wound or
fragments from exploding objects.
Focal neurological symptoms and
post traumatic seizures are more
common in penetrating injuries.
• Closed brain injury occurs when
there are rotational acceleration
and deceleration forces applied to
the head. The momentum to the
head causes diffuse shearing of
white matter fiber. Often seen in
patients who are involved in MVA.
• Both primary and secondary
damage may result from a closed
brain injury.
1. PRIMARY DAMAGE
• Occurs at the time of injury
• Caused by localized
contusions and diffuse
axonal injury.
A. Contusions and Bruises
 Are usually bilateral but
asymmetric in their
severity
 Occurs in the frontal
and temporal regions,
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 where bony structures b. Intracranial hematomas
are prominent, when – hematoma occurring
the brain slides and within the cranium
b.1 Epidural –
strikes the rough skull
situated upon or
and scrapes over bony
placed outside the
irregular structures
dura mater.
 May be associated with
b.2 Subdural –
depressed skull
occur between the
fracture, intracerebral,
dura mater and
subdural or epidural
arachnoid in the
hemorrhage or tentorial
subdural space
herniation
b.3 Intracerebral –
B. Focal Brain Injury
 Caused by a direct blow situated within or
to the head, a administered by
penetrating injury, and entering the
the collision of the brain cerebrum
with the inner tables of
the skull : Concussion
(Closed-head injury)
and Contusion (Open-
head injury)
C. Diffuse Axonal Injury
 Acceleration/Decelerati
on and Rotational
Forces that commonly
result from MVA
produce diffuse axonal
disruption
- Acceleration: e.g. head on
collision; Deceleration: e.g.
gunshot wounds
- Most severe in the upper c. Hypoxic ischemic injury-
brainstem and corpus callosum results from a lack of
and is primary responsible for the oxygenated blood flow
initial loss of consciousness. to brain tissue.
- The mechanism of axonal damage Can caused by systemic
includes microscopic hemorrhage hypotension, anoxia, or
and retraction bails of extruded damage to specific
axoplasm in white matter.
vascular territories of
- When axonal damage is severe,
coma is induced. When the axonal the brain.
fibers are stretched but not torn Can lead to global
and most fibers escape damage; associated
permanent structural damage, a with poorer cognitive
concussion, or brief loss of function and lower
consciousness, can occur. expected outcomes.
2. SECONDARY DAMAGE
• May evolve over time VI. CLINICAL MANIFESTATIONS
a. Increased Intracranial 1. PHYSICAL STATUS
Pressure –Due to  TBI patients may exhibit a variety of
swelling or abnormality symptoms depending on the type,
of brain fluid dynamics. severity, and location of the injury.
Can cause decreases in a. Rigidity- is the presence of increased
cerebral perfusion resistance to passive movement
pressures and throughout the most of the range
subsequent ischemic that is independent of stretch
damage. velocity.

193 | P a g e
 • Decorticate Rigidity - results
from damage to the
cerebral hemispheres
(particularly the internal
capsules), causing an
interruption in the
corticospinal tracts – those
that emerge from the
cortex and send voluntary
motor messages to all
extremities.
- The UE are in spastic
flexed position with internal
rotation and adduction. The
Les are in a spastic
extended position but also
internally rotated and
adducted.
• Decerebrate Rigidity - occurs
as a result of damage to the
brainstem and
extrapyramidal tracts – the
tracts that send involuntary
motor messages from the
brainstem to the
extremities. Individuals with
decerebrate rigidity have a
poorer prognosis than do
those exhibiting decorticate
rigidity.
- both the UEs and Les are
in a position of spastic
extension, adduction, and
internal rotation. The wrist
and fingers flex, the plantar
portions of the feet flex and
invert, the trunk extends,
and the head retracts.
b. Abnormal Reflexes
• Typical reflexes seen in the
low level TBI adult
include the ATNR and STNR.
• Treatment is focused
not only on inhibiting
these brain stem
reflexes but also on
replacing them with
new motor programs to
facilitate improvement
in function.
c. Abnormal Muscle Tone
• Varies from hypotonus
(flaccidity) to hypertonus
(spasticity)
• When muscles are flaccid
the resistance to passive
movement is diminished
and the stretch reflexes are
dampened.
• When an entire UE is
hypotonic, such as in the
early days post injury, the
arm appears floppy.
d. Spasticity
• One of the most common
and damaging physical
problems
• May range from minimal to
severe in any particular
muscle or muscle group
• Patient emerging from
coma usually exhibits severe
spasticity throughout the
body.
• Patients who are
functioning at a higher
cognitive level generally
exhibit a combination of
both flaccidity and
spasticity.
• Fluctuates as a result of
changes in the patient’s
position, volitional
movement, medication, any
infections or illness, an
increase in pain or
discomfort, or a change in
emotions.
• Long term consequences of
spasticity: compromised
function in ADL, difficulty
with transfer, difficulty in
positioning the patient in
bed/wheelchair, gait
deviations, poor speech and
breath control, painful
spasms, and contracture
formation.
e. Muscle Weakness
• A decrease in muscle
strength without the
presence of spasticity.
• When a TBI patient exhibits
impaired strength in the UE
without spasticity: MMT is
indicated
194 | P a g e
 • When present in both UE,
impaired coordination will
be evident
f. Ataxia
• An abnormality of
movement and disordered
muscle tone seen in
patients with damage to the
cerebellum or the sensory
pathways.
• A close correlation exists
between ataxia, hypotonia
and impaired sensation.
• The normal flow of a
smooth voluntary
movement is destroyed by
errors in the direction and
speed of movement
• Patient with ataxia has a
lack of postural stability in
sitting and standing, has
difficulty maintaining the
trunk in a stable position
• Patient attempts to
compensate for this deficit
by holding onto a fixed
surface such as a mat w/
one or both extremities
and/or tensing or fixing the
proximal muscle.
• If present in the elbow
and/or shoulders,
movement impairments
occur when the patient
attempts to lift the UE away
from the body and off a
stable surface such as table.
g. Impaired Motor Control
• Occurs in both UE and LE as
a result of an imbalance in
muscle tone and muscle
weakness
• Usually one side of the body
is more involved than the
other
h. Postural Deficits
• Developed as a result of an
imbalance in muscle tone
throughout the body,
impaired motor control,
delayed or absent righting
reactions and impaired
vision, cognition, and
perception.
• Abnormal postures
frequently exhibited in
adults with moderate to
severe TBI include the
following:
Head/Neck – Forward flexion or
hyperextension, head may be
laterally flexed to one side
Scapula – Depressed, Protracted,
Retracted, and/or downwardly
rotated
UE – Bilateral involvement w/
asymmetry between sides or
unilateral involvement
Trunk - Kyphosis, Scoliosis, and loss
of lordosis
Pelvis – Posterior pelvic tilt,
retraction of one side of the pelvis
and a pelvic obliquity, in which one
side of the pelvis sits lower than the
other side
LE – Severe extension patterns, hip
adduction, knee flexion, plantar
flexion, and inversion of the feet
i. Limitation of Joint Motion
• Possible causes of
decreased ROM: increased
muscle tone, myostatic
contracture, heterotrophic
ossification, an undetected
fracture or dislocation, pain
or lack of patient
cooperation
j. Loss of Sensation
• Loss of light touch, sharp or
dull differentiation,
proprioception, kinesthesia,
and/or stereognosis in the
extremities.
• Loss of light touch, sharp or
dull sensation: evident in
the face
• Impaired sense of taste and
smell: result of cranial nerve
involvement
k. Decreased Functional Endurance
• Medical complications such
as pneumonia or infections,
as well as prolonged bed
rest, also affect the
patient’s ability to
participate in therapy
programs
l. Loss of Total Body Function
• Total body function skills:
head and trunk control,
sitting and standing
balance, reaching, bending,
stooping, and functional
ambulation
• Patient with severe physical
involvement usually has
poor sitting and standing
balance, may not even
retain the ability to maintain
the head in the upright
position
• Total body function skills
are necessary for
195 | P a g e
 performing different levels
of ADL
2. DYSPHAGIA
 A difficulty in the four stages of chewing
and swallowing, is caused by cranial
nerve damage.
 There is a higher incidence of oral
preparatory, oral, pharyngeal stage
dysphagia than esophageal stage
dysphagia.
 The cognitive, behavioral and linguistic
problems evident in TBI patient further
complicate the ability to manage the
intake of food and liquids
 If impulsivity is a behavioral
manifestation of TBI, px will have
difficulty monitoring the amount and
rate of bringing the hand to the mouth,
resulting in coughing and increasing the
risk of aspiration.
a. Self- Feeding
• Clients with a TBI may be
unable to sustain attention
long enough to feed
themselves.
3. COGNITIVE STATUS
 Cognitive deficits frequently seen are
decreased levels of attention, impaired
memory, impaired initiation, safety
awareness, decreased ability to process
information accurately, and difficulty
with executive functions and abstract
thinking.
a. Reduced Attention and Concentration
• Seriously affects functional
independence
• Patient with a brain injury
often loses not only the
ability to concentrate for
any length of time, but also
the ability to filter out
distraction
• Evidence of deficits are
often noted for months or
years post-injury
b. Impaired Memory
 One of the most devastating problems
 Types of memory impairment:
• Immediate Memory-
inability to recall a few
words just heard
• Short-term Memory-
forgetting what happened
in the last treatment
session
• Long-term Memory-
remembering events that
occurred 24 hours ago or
years before the injury
 Manifested in the inability to
learn and carry over new tasks and
contributes to confusion and inability to
interact effectively with the
environment.
c. Impaired Initiation
• Inability ir difficulty in beginning
the first actions, steps, or stages
of a task
• Affects the patient’s ability to
live independently
d. Decreased Safety Awareness
• Displays unsafe behavior
• A result of impulsiveness,
decreased insight into the
disability, impaired judgement,
or a combination if all these
• Decreased insight,
disorientation, and impaired
memory can contribute to the
patient’s inability to recognize
limitations for specific situations
or analyze the consequences of
his/her actions.
e. Delayed Processing Information
• Difficulty in processing visual
and auditory information within
a normal time frame.
• The delay may be only a few
seconds or persist for a few
minutes.
f. Impaired Executive Functions and
Abstract Reasoning
• Executive function skills are
composed of the ability to set
goals, plan, and complete tasks
effectively.
• Requires patient to perform
high level problem solving,
reasoning, and judgement.
• Patients tend to analyze
problems in concrete terms,
interpreting all information at
the most literal level.
• Able to recognize errors but
unable to resolve the errors
without external cueing. Unable
to determine more than one
solution to a problem.
4. BEHAVIORAL STATUS
 Common behaviors observed include
agitation, combativeness manifested by
kicking, biting, grabbing, spitting, or
striking when overstimulated,
disinhibition and refusal to cooperate.
 A disinhibited patient may lack
awareness of the external environment.
Examples of socially inappropriate and
disinhibited behavior are shouting
obscenities or making indiscriminate
sexual advances to a stranger in the
community.
196 | P a g e
 – Transcortical Sensory
5. VISUAL STATUS – Conduction
 Damage to the visual system is the – Anomic
result of cranial nerve damage or direct • Dysprosody/Aprosodia
trauma to the orbital content – Executive Dysprosody
 Visual problems frequently noted – Receptive Dysprosody
include:
• Strabismus with diplopia 8. FUNCTIONAL STATUS
• Convergence insufficiency  Patients with brain injury may have
• Accommodative dysfunction problems in almost all performance
(blur up clos) areas. Possible areas of performance
• Nystagmus deficit are:
• Oculomotor Dysfuntion (poor 1. Self-Care
tracking) 2. Mobility
3. Home Management
• Field defects
4. Communication
• Reduced blink rate
5. Transportation
• Lagopthalmus(incomplete lid
6. Community Function
closure)
7. Work Skills
8. Leisure Activities
6. PERCEPTUAL MOTOR SKILLS
 Patients may experience impairments in
the following areas: VII. COMPLICATIONS
• Visual Perception - Deep Vein Thrombosis
- R-L - Heterotopic Ossification
- Pressure Ulcers
discrimination,
- Pneumonia
figure-ground - Chronic Pain
discrimination, - Contractures
form constancy, - Decreased endurance
position in - Muscle atrophy
space, - Fracture
- Peripheral nerve damage
topographical
orientation, VIII. DIAGNOSIS
visual agnosia, a. History and Examinations
prosopagnosia b. Clinical Rating Scales
• Perceptual-Motor Dysfunction 1. Glasgow Coma Scale
- Ideational - defines the severity of a TBI
Apraxia within 48 hours of injury.
- Ideomotor Scoring & Interpretation:
Apraxia • Severe TBI = 3-8
- Constructio • Moderate TBI = 9-12
nal Apraxia • Mild TBI = 13-15
• Praxis Assess 3 behavioral areas
• Body Scheme • motor responses
- Anosognosi • verbal responses
a • eye opening
- Unilateral
Neglect
Syndrome
• Figure-Ground
• Position in Space
• Size and/or Shape
Discrimination
• Unilateral Spatial Inattention
• Part-Whole Integration
• Visual Organization

7. COMMUNICATION DEFICITS
• Aphasia
– Wernicke’s
– Broca’s 2. Ranchos Los Amigos Level of Cognitive
– Transcortical Motor Functioning

197 | P a g e
The RANCHOS LOS AMIGOS SCALE uses the
following eight levels:
1. No response
- Pt. appears to be in deep sleep and
is completely unresponsive to any
stimuli
2. Generalized response
- Pt. reacts inconsistenly and
nonpurposefully to stimuli in a
nonspecific manner. Responses are
limited and often the same regardless
of stimulus presented. Responses
may be physiological changes, gross
body movements, and/or
vocalization.
3. Localized response
- Pt. reacts specifically but
inconsistently to stimuli. Responses
are directly related to the type of
stimulus presented. May follow
simple commands such as closing
eyes or squeezing hand in an
inconsistent, delayed manner.
4. Confused – agitated
- Pt. is in a heightened state of
activity. Behavior is bizarre and
nonporpuseful reactive to immediate
environment. Does not discriminate
among person or objects; is unable to
cooperate directly with treatment
efforts. Verbilizations frequently are
incoherent and/or inappropriate to
the environment; confubation may be
present. Gross attention to
environment is very brief; selective
attention is often nonsexist. Pt. lacks
short and long term recall.
5. Confused – inappropriate,
nonagitated
- Pt. is able to respond to simple
commands fairy consistenly. However,
with increased complexity commands or
lack of any external structure, responses
are nonpurposeful, random, fragmented.
Demonstrates gross attention to the
environment but is highly distractable and
lacks ability to focus attention on a
specific task. With structure, may be able
to converse on a social autonomic level
for short periods of time. Verbalization is
often inappropriate and confabulatory.
Memory is severely impaired; often
shows inappropriate use of objects; may
perform previously learned tasks with
structure but unable to learn new
information.
6. Confused – appropriate
- Pt. shows goal-directed behavior but
is dependent on external input or
direction. Follows command
inconsistently and shows carryover
for relearned tasks such as selfcare.
Responses may be in correct due to
memory problems, but they are
appropriate to situation. Past
memories show more depth and
detail than recent memory.
7. Automatic – inappropriate
- Pt. appears appropriate and oriented
within hospital and home settings; goes
through daily routine automatically, but
frequent robot-like. Pt. shows minimal to
no confusion and has shallow recall of
activities. Shows carryover for new
learning but a decreased rate. With
structure is able to initiate social or
recreational activities; judgement remains
impaired.
8. Purposeful – appropriate
- Pt. is able to recall and integrate past
and recent events and is aware of and
responsive to environment. Shows
carryover for new learning and needs no
supervision once activities are learned.
May continue to show a decreased ability
relative to premorbid activities, abstract
reasoning, tolerance to stress, and
judgement in emergencies or unusual
circumstances.
3. Duration of Post-Traumatic Amnesia
and Severity of Injury
- Measurement of PTA is
performed with the Galveston
Orientation and Amnesia Test (GOAT)
- Score of 78 or more on three
consecutive occasions is considered to
indicate that patient is out of post-
traumatic amnesia (PTA)
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 Progression Progressive Non-
progressive

X. PROGNOSIS
Mild Mod TBI Severe
TBI TBI
LOC 0- >30mins >24hr
30min and
<24hr
AOC Brief >24hrs >24hrs
>24hr
s
PTA 0-1day >1 and >7 days
4. Rappaport’s Disability Rating Scale <7days
- intended to accurately GCS 13-15 9-12 <9
Neuroimagin norma Normal Normal
measure general functional changes
g l or or
over the course of recovery after TBI abnorma abnorma
l l
Legend: LOC- loss of consciousness
AOC- alteration of consciousness
PTA- Post-traumatic amnesia
GCS- Glasgow Coma Scale

GENERAL HEALTHCARE MANAGEMENT

I. Medical, Surgical, and Pharmacologic

5. GALVESTON ORIENTATION AND
Surgical Management:
AMNESIA
1. Craniotomy- surgical removal of part of
- This is the most commonly
the bone from the skull to expose the
accepted test to assess PTA. The GOAT
brain.
is a series of ten questions that are
given to a patient, usually on a weekly
Pharmacological management:
basis. The patient is then scored on a
NAME PURPOSE
scale of 0 to 100. The patient id
1. ELAVIL Antidepressant
described as being out of PTA after the
Level 2/3 to
patient reaches a score of greater than
heighten arousal;
75.
with higher levels
to decrease
6. Functional Independence Measure
agitation
- This is a ten item,
multidisciplinary assessment that is 2. TOFRANIL Antidepressant
generally completed on admission and 3. RITALIN Stimulation to
discharge from an inpatient program. heighten
The categories included self-care, alertness
mobility, psychosocial function, and 4. PHENOBARBITAL Anticonvulosant
cognitive function. This assessment tool (seizure
is used in many facilities throughout the prevention)
United States. 5. THORAZINE Tranquilization
Management of
Psychotic
c. Laboratory Examinations
Disorder
- X-ray
6. MELLARIL Tranquilization
- CT Scan
- MRI 7. HALDOL Tranquilization
- MRA Management of
Psychotic
IX. DIFFERENTIAL DIAGNOSIS Disorder
TBI CVA 8. DILANTIN Anticonvolusant
Cause Trauma by Brain 9. DANTRIUM Control of
/Mechanism external infarction Spasticity
forces 10. BACLOFEN Control of
Involvement Bilateral Uni or Spasticity
Bilateral General CNS
depressant

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 16. Ventilation and respiratory/gas
II. Other Healthcare exchange
(Rehabilitative/Supportive) 17. Work/leisure/community reintegration
Interdisciplinary team
- Family members II. Problem List
- Physician 1. Complications (Pressure Sores, DVT, HO,
- Speech-Language etc)
pathologist 2. Pain (Chronic pain)
- Occupational therapist 3. Decreased Aerobic Capacity
- Rehabilitation Nurse 4. LOM
- Case Manager 5. Muscle weakness
- Social Worker 6. Impaired motor function
- Neuropsychologist 7. Abnormal tone
8. Impaired posture
PHYSICAL THERAPY EXAMINATION, EVALUATION 9. Impaired gait, locomotion and balance
AND DIAGNOSIS
III. Physical therapy Diagnosis
I. Points of Emphasis in Examination (Focus) NM6- Impaired motor function and sensory
1. Aerobic capacity integrity associated with non-progressive
2. Arousal, attention, and cognition disorders of central nervous system.
3. Behavioral status
4. Cranial nerve integrity
5. Gait, locomotion, and balance
6. Integumentary integrity
7. Joint integrity and mobility
8. Motor function (motor control and
learning)
9. Muscle performance: strength, power,
and endurance
10. Pain
11. Posture
12. ROM
13. Reflex integrity
14. Self-care and ADL skills
15. Sensory integrity
PHYSICAL THERAPY PROGNOSIS

Problem list Plan of Care Intervention with rationale

1. Complications (DVT, HO, To prevent secondary complications - Proper bed/wheelchair positioning

Pressure Ulcers, Pneumonia,
Contractures, Atrophy, etc.)
2. Pain (Chronic pain)
due to immobilization.
To decrease pain on the affected
extremities
(head should be in neutral, hips and
knees should be slightly flexed.
- Splints are used to assist in
positioning (Multi-podus boot used
for ankle and foot positioning to
prevent skin breakdown on the heel)
- Repositioned every 2hrs in bed and
Specialized mattresses to prevent
pressure sores
- Serial Casting to improve ROM from
contractures ( 2 to 5 days the cast is
removed)
-Hot packs
-TENS
-IFC

3. Decreased aerobic capacity
To increase cardiopulmonary The mode of training can vary from
endurance traditional exercises (walking,
jogging, treadmill, elliptical
machines, and ergometers) to circuit
training (obstacle training).
Intensity: 60% to 90% of age
predicted maximal heart rate
Duration: 20 to 40 minutes

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4. LOM
5. Muscle weakness
6. Impaired motor function
7. Abnormal Tone
8. Impaired posture
9. Impaired gait, locomotion
and balance.
To increase ROM and improve
functional independence.
To increase strength
Improve motor function
To increase or decrease abnormal
tone.
To improve posture and self-
awareness.
To improve gait and balance.
Frequency: 3 to 4 times a week
-Functional Electrical Stimulation or
FES (esp. for foot drop) to increase
active DF during swing phase of gait.
-PNF D1D2 flexion and extension,
and techniques (Rhythmic Initiation:
PROM-> AAROM-> RROM ->AROM).
Resistance training with improved
force production, functional abilities,
and quality of life.
Duration: 3 sets of 8 to 12
repetitions
Frequency: 2 to 3 days a week
Motor Relearning Strategies
- Random practice schedule
- Explicit or Augmented
Feedback
Practice should be distributed with
frequent rest periods.
Facilitatory Techniques to facilitate
flaccid muscle. (Roods or PNF)
Inhibitory Techniques to inhibit
spastic muscles (Roods or PNF )
Biofeedback techniques.
High level, task oriented balance and
gait training.
Activities that are challenging to the
vestibular system :
-Walking with head turns and on
uneven or varied surfaces.
-Sport specific skill training.
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 SPINAL CORD INJURY E. Spinotectal tract
Vascular Supply
I. GENERAL MEDICAL BACKGROUND A. Spinal arteries
ANATOMY a. anterior
Bony Tissue Components b. posterior
1. Regions of the spinal column B. Vertebral artery
 Cervical C. Vessel of Adamkiewicz
 Thoracic - Largest segmental artery from aorta
 Lumbar - Between T8 & L4
 Sacral - One of the vessels related to the cause
 Coccygeal why tuberculosis spreads rapidly to the
2. Typical vertebrae lungs
3. Atypical vertebrae Spinal Nerves
 C1,C2 C7 & first and last - 31 pairs; forms a single cord segment
vertebrae of each regions - consists of:
4. Joints A. dorsal root
B. ventral root
Soft Tissue Components
1. intervertebral discs (shock absorption, DEFINITION:
cushions, gives height to spinal column) Traumatic insult to the spinal cord that can
2. capsules result in alteration of normal motor, sensory &
3. ligaments (ALL, PLL for stabilization) autonomic functions
4. muscles
5. spinal cord CLASSIFICATION:
1. Topography
Cross Section A. Tetraplegia
A. White matter - peripheral; composed of  Due to lesions at the cervical level
myelin sheath  Involves all 4 limbs, trunk & respiratory
B. Gray matter – central; composed of cell muscles
bodies; forms an “H” or butterfly shape
B. Paraplegia
C. Anterior column, horn & fissure (deep)
 Due to lesions at the thoracic, lumbar or
D. Posterior column, horn & furrow
(shallow) cauda equina
E. lateral horn  Involves all or part of the trunk & the
F. Conus medullaris – between L1 and L2 lower limbs
G. Cauda equina (horsetail-like structure)  May refer to CAUDA EQUINA & CONUS
MEDULLARIS
Tracts 2. Broad Functional Categories
I. Motor or Descending A. Complete
A. Corticospinal tracts – primarily involved  (-) S4 and S5 = motor & sensory
in voluntary movements
 Determined by anal sensation &
1. anterior – (10%-20%) does not
cross voluntary external anal sphincter
2. lateral – (80%-90%) cross; aka contraction
pyramidal tract B. Incomplete
B. Reticulospinal tract  (+) residual brain influence on spinal
C. Rubrospinal tract cord function below the level of lesion
D. Tectospinal tract including S4, S5
E. Vestibulospinal tract  Zone of partial preservation = areas of
II. Sensory or Ascending
intact motor and/ or sensory function
A. Spinothalamic tracts
a. anterior – crude touch and below neurological level
pressure
b. lateral – pain and temperature Types of Incomplete Lesions:
sensation A. Anterior cord syndrome
B. Dorsal columns  usually due to flexion injuries
C. Spinocerebellar tract  bone and cartilage spicules compromise
D. Spinoreticular tract anterior spinal artery
 features:

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 1. Bilateral loss of motor function,  43% experience thoracic, lumbar or
pain & temperature sensation sacral lesions = paraplegia
below lesion level  Incomplete tetraplegia>complete
2. Prognosis is extremely poor for paraplegia >incomplete
return of bowel and bladder, hand paraplegia>complete tetraplegia
function & ambulation ETIOLOGY
B. Brown-Sequard syndrome Categorized as:
 usually due to stab or gunshot wounds A. traumatic (direct or indirect forces)
 only ½ of SC is damaged 1. Motor vehicle accidents (MVA)
 features: 2. Falls
1. Contralateral loss of pain, 3. Acts of violence
temperature & light touch below 4. Falling objects
neurological level 5. Sports injuries
2. Ipsilateral loss of motor, B. non traumatic
proprioception, vibration & kinesthesia 1. Vascular malfunctions
3. Hyporeflexia 2. Vertebral subluxations
4. (-) superficial reflexes 3. Infections
5. Prognosis: good recovery 4. Spinal neoplasms
C. Central cord syndrome 5. Neurological diseases
 usually due to hyperextension injuries & 6. Syringomyelia – tube like cavities in
 degenerative or congenital anomalies of the spinal cord seen usually at birth
the spinal canal 7. Abscesses of the spinal cord
 UE > LE
 features: Mechanisms of Injury
1. Walking SCI – cervical region is only I. Flexion
affected; the lumbar and sacral region is  head on collision or
spared  rapid deceleration
2. Intact sexual, bladder & bowel  frequent at C4 – C7 & T12 – L2
functions  may result in:
3. Ambulation prognosis is good A. anterior dislocation of the vertebra
4. Intrinsic hand function is last to return B. teardrop or wedge fracture due to
D. Posterior cord syndrome compressive forces anteriorly
 rare C. fractures may impinge neural tissue
 resulting from compression by tumor or D. soft tissue tears due to distractive
infarction of the posterior spinal artery forces posteriorly
 features: II. Vertical compression
1. Preservation of motor function  with related sports such as diving &
2. (+) pain, temperature & light touch  impact of falling objects
3. (-) proprioception, stereognosis, 2  frequent at C4 – C5
point discrimination and vibration  may result in:
below lesion level A. fractures
4. Wide based gait pattern B. neurological damage
E. Cauda Equina Syndrome III. Hyperextension
 occurs with injuries at or below L1  with rear end collision
 LMNL that is incomplete  frequent at C4 – C5
 features:  also common among the elderly
1. Results to flaccid paralysis  may result in:
2. (-) spinal activity present A. fractures due to compressive forces
posteriorly
F. Conus Medullaris Syndrome B. soft tissue tears due to distractive
 injury of the sacral cord and lumbar forces anteriorly
nerve roots C. neurological damage
 LE motor & sensory loss IV. Lateral flexion
 rare
 Areflexic bowel & bladder
 usually referred & involves the brachial
plexus
EPIDEMIOLOGY
 56% experience cervical lesions = V. Flexion with rotation
tetreplegia

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  may result in fractures & soft tissue  center for bowel/ bladder & sexual
tears due to compressive & distractive dysfunctions: S2-S4 & Conus Medullaris
forces respectively
VI. Shear Types of Bladder dysfunction:
 falls on uneven surfaces 1. Reflex, spastic or automatic bladder
 impact from behind  lesion above S2-S4
 reflexively empties upon reaching a
Regional Involvement certain level of filling pressure
A. cervical region With intact reflex arc:
 all of the above mentioned mechanisms  may be triggered by:
B. thoracic o stroking
 usually due to MVA, gunshots & falls: o kneading
1. unto upper back & one shoulder o tapping the suprapubic region,
2. unto buttocks or feet thigh & lower abdomen
C. lumbar o pinching
 usually neurological damage is o hair pulling
incomplete due to: 2. Non reflex, flaccid or autonomous bladder
1. A good vascular supply &  lesions of the conus medullaris or cauda
2. Large vertebral bodies equina (sacral nerve roots)
 Lesion below S2-S4
PATHOPHYSIOLOGY  can be emptied by:
flexion injury - increasing intra-abdominal pressure
 - Manually compressing the
fracture & soft tissue tears lower abdomen (Crede
 maneuver)
vasodilation
 Types of Bowel dysfunction:
Na & K ions derangement 1. Spastic bowel
  above the center for defecation
edema  with intact defecation reflex
  with spastic contraction of anal
neurological damage
sphincters
 maybe addressed by:
CLINICAL MANIFESTATIONS
 regularly scheduled evacuation
1. spinal shock
 use of laxatives & suppositories
- shutting down of the CNS to prevent
 digital stimulation
further damage (results after 24 hrs of
2. Flaccid bowel
trauma/injury)
 lesions in the conus medullaris or in the
- Initial period = 24 hrs
cauda equina (sacral nerve roots)
- Gradual return of reflexes= 1-3 days
 with loss of spinal defecation reflex
after injury
 maybe addressed by:
- Increasing hyperreflexia = 1-4weeks
 regularly scheduled evacuation
after injury
 manual removal of stool straining with
- Final hyperreflexia = 1-6mos after
available musculature
injury
- Bulbocavernosus reflex - a reflex
7. Sexual dysfunction
testing method which indicates when a
- characterized by physiological
spinal shock has resolved
dysfunction, sensory & motor
- Procedure: Insert a gloved finger in the
impairments
anus and squeeze the glans penis/ glans
- With the males:
clitoris; positive result: anal contraction
a. UMNL
or anal winking
 lesions above conus medullaris
2. spasticity – due to UMNL
b. LMNL
3. impaired or loss of sensation
 lesions at the conus medullaris or
4. respiratory impairment
cauda equina
5. thermoregulation
6. bowel & bladder dysfunction
As to erectile capacity:
 center for micturition: S2 – S4
- Incomplete SCI > complete SCI

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 - UMNL > LMNL 8. Vasodilation above the lesion
Reflexogenic erection: 9. Pupil constriction
- UMNL > LMNL 10. Nasal congestion
Psychogenic erection: 11. Piloerection
- LMNL > UMNL 12. Blurred vision
As to ejaculation: COMPLICATIONS AND INDIRECT IMPAIRMENTS
- Incomplete SCI> complete SCI 1. Pressure ulcers
- LMNL > UMNL  major complication of SCI
 frequent with complete &
Types of erection tetraplegia
1. Reflexogenic 2. Orthostatic hypotension
 erection in response to external  aka postural hypotension
physical stimulation of the genitals  due to loss of sympathetic
or perineum vasoconstriction control
 mediated through S2 – S4  characterized by
2. Psychogenic lightheadedness & dizziness
 response to cognitive activity 3. Edema
 mediated from cerebral cortex through 4. Heterotopic ossification
the thoracolumbar or sacral cord  aka ectopic ossification
centers  usually below the level of the
lesion
Orgasm Vs. Ejaculation  idiopathic
 the former being a cognitive,  extra capsular & extra-articular
psychogenic event  LE: hips & knees
 the latter being a physical occurrence  UE: elbows, shoulders

Female Issues Heterotopic ossification

 vaginal lubrication, labial engorgement Manifestations:
& clitoral erection:  swelling
UMNL > LMNL  decreased ROM
 psychogenic response:  erythema
LMNL > UMNL  local warmth near the joint
 menstruation is interrupted from 1 – 3  increased serum alkaline phosphatase
months
 fertility & pregnancy under close 5. Contractures
medical supervision  hip: flexion, adduction & IR
 shoulder: flexion/extension,
Autonomic Dysreflexia adduction & IR
 aka autonomic hyperreflexia/crisis 6. DVT
 with lesions above T6  due to loss of muscle tone
7. Osteoporosis & renal calculi
Stimuli  below the level of the lesion
 bladder distention  due to immobilization, loss of
 rectal distention sensation and paralysis
 pressure sores 8. Pain
 urinary stones Includes:
 bladder infections  traumatic pain
 noxious cutaneous stimuli  nerve root pain
 kidney malfunction  musculoskeletal pain
 environmental temperature changes  spinal cord dysesthesias
Manifestations
1. Increased BP Spinal Cord Dysesthesias
2. Bradycardia  present below the level of the lesion
3. Severe pounding headache  described as burning or numbness, pins
4. Profuse sweating & needles & tingling sensation
5. Increased spasticity  diffuse distribution
6. Restlessness
7. Vasoconstriction below the lesion DIAGNOSIS

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  MRI B. vital signs
 CT scan C. integumentary assessment
 X-rays D. sensory assessment
 myelography E. musculoskeletal examination
F. muscle tone & DTRs
PROGNOSIS G. functional examination
 degree of pathological changes due to
trauma FIM
 precautions taken to prevent further  7 point scale
damage  covers 18 items
 prevention of additional compromise of  measure of physical, psychological &
neural tissue social functions
 complete vs. incomplete
 early appearance of reflex activity FIM Grading

II. GENERAL HEALTHCARE MANAGEMENT 7 – Complete independence, no helper

SURGICAL MANAGEMENT 6 – Modified independence (device)
1. decompression
 anterior Helper – Modified Dependence
 posterior 5 – Supervision (subject = 100%)
2. bony fusion 4 – Min assistance (subject = 75% of >)
3. myotomy 3 – Mod assistance (subject = 50% or >)
4. neurectomy
5. tenotomy Helper – Complete Dependence
2 – Max assistance (subject = 25% or >)
POST SURGICAL MANAGEMENT 1 – Total assistance (subject = 25%)
1. fracture stabilization
 use of orthosis Functions
1. Knight – Taylor A. self-care:
2. Jewett 1. Eating
3. Halo 2. Grooming
 use of skeletal traction devices 3. Bathing
 use of turning frames & beds 4. Dressing – upper
5. Dressing – lower
PHARMACOLOGIC MANAGEMENT 6. Toileting
A. steroids B. sphincter control:
 methylprednisolone 1. Bladder
B. antispasticity 2. Bowel
 baclofen C. transfers:
 dantrolene 1. Bed, chair, wheelchair
 diazepam 2. Toilet
 peripheral nerve blocks 3. Tub, shower
 intrathecal injections D. locomotion:
C. laxatives & suppositories 1. Walk/wheelchair
D. ephedrine 2. Stairs
E. diphosphates E. communication:
F. anticoagulants 1. Comprehension
G. analgesics 2. Expression
F. social cognition:
III. PHYSICAL THERAPY EXAMINATION, 1. Social interaction
EVALUATION & DIAGNOSIS 2. Problem solving
PT ASSESSMENT 3. Memory
A. respiratory function exam
 chest expansion Consider
measurement A. mat & bed abilities
 breathing pattern - Even & uneven transfers
 coughing B. wheelchair skills
 vital capacity - Distance

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 - Capabilities  motor or sensory function below the
- Time required to propel neurological level
- Obstacle negotiation  does not include S4 – S5
- Pressure relief
C. ambulation Levels of Function
- Distance I. C1 – C3
- Gait patterns A. intact:
- Level of assistance 1. Facial muscles
- Donning & doffing orthosis 2. Pharyngeal muscles
D. instruction of others for assistance 3. Laryngeal muscles
E. needs for any equipment 4. Neck muscles
F. home & environment modification 5. Partial SCM
 Needs a respirator or phrenic nerve
ASIA Impairment scale stimulator
A B. transfers, mat & bed activities, self-
– Complete: care:
(-) motor & sensory function is  Dependent
preserved in the sacral segments S4-S5  full time attendant required
C. wheelchair mobility:
B  powered wheelchair
– Incomplete: (+) sensory with no motor controlled by breathing
function below the neurological level motions such as:
including the sacral segments S4- S5  sip & puff or head, chin,
C power reclining for pressure
– Incomplete: motor function preserved relief
below the neurological level & > ½ of  with a portable respirator,
the key muscles below the neurological seatbelt & trunk support
level have a grade of < 3 II. C4
D A. intact:
– Incomplete: motor function preserved 1. Diaphragm
below the neurological level & at least ½ 2. Trapezius
of the key muscles below the 3. midcervical flexors &
neurological level have a grade of 3 or extensors
more 4. scalenes
E 5. Partial rhomboids
– Normal: motor & sensory function are 6. Partial levator scapulae
normal B. transfers, mat & bed activities, self-
care:
Terminology:  dependent
a. Neurological level  limited self-feeding with adaptive
 most caudal level of the spinal cord with equipment such as a mobile arm
normal motor & sensory function on support
both the right & left sides C. wheelchair mobility:
1. Motor level  electric with head, mouth & chin,
 most caudal segment of spinal cord with breath or sip & puff controls
bilateral normal motor function III. C5
 MMT of key mm & myotomes adjacent  highest level for independent
to suspected level of impairment transfers
2. Sensory level A. intact:
 most caudal segment of spinal cord with 1. Biceps brachii
bilateral normal sensory function 2. Brachialis
 key dermatomes which focuses on light 3. Brachioradialis
touch & pinprick 4. Deltoids
b. Zone of partial preservation 5. Infraspinatus
 partially innervated segments located 3 6. Supinator
segments below the neurological level 7. Rhomboids
 applies to complete injuries only B. transfers:

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  dependent with the use of the B. transfers
sliding board  indep in all transfers
 use of overhead frames with  indep self-care
hanging loops  manual wheelchair with
 use of overhead swivel bar standard handrims
C. self-care: VII. T4 – T6
 able to self-feed, facial hygiene A. intact:
 limited upper extremity dressing 1. Upper half of intercostals
D. wheelchair mobility: 2. sacrospinalis
 independent pressure relief with 3. Semispinalis
power tilt in space wheelchair  indep in all transfers
 manual with plastic coated hand rim  indep in all self-care
projections  (+) physiological standing
IV. C6  requires bilateral KAFOs with spinal
A. intact: attachment
1. Infraspinatus VIII. T9 – T12
2. latissimus dorsi A. intact:
3. Pronator teres 1. All intercostals
4. teres minor 2. Abdominals
5. Clavicular part of pectoralis  (+) household ambulation
major  requires bilateral KAFOs with
6. Serratus anterior crutches or walker
7. ECR IX. L2 – L4
B. transfers: A. intact:
 independent on level 1. gracilis
surfaces with sliding board 2. Iliopsoas
C. mat & bed activities: 3. quadratus lumborum
 independent with side rails 4. Rectus femoris
or overhead triangle 5. sartorius
D. self-care:  (+) functional ambulation
 independent with adaptive  requires bilateral KAFOs & crutches
equipment X. L4 – L5
E. wheelchair mobility: A. intact:
 projections/friction surface 1. ED
hand rims 2. Low back muscles
 2” curb 3. Medial hamstrings
V. C7 4. tibialis posterior
A. intact: 5. tibialis anterior
1. Triceps 6. Quadriceps femoris
2. EPL & EPB  (+) functional ambulation
3. FCR  requires bilateral AFOs with crutches or
B. transfers: canes
 indep with or without
sliding board PROBLEM LIST
C. mat & bed: - Loss of sensation
 indep - Motor impairment and weakness
- Complications
D. wheelchair mobility: - Contractures
 uneven terrain - Respiratory problem
 4” curb - Pain
 manual with friction surface - Dependence in ADLs
hand rims - Pressure sores
VI. C8 – T1 - Bladder and bowel problems
A. intact:
1. Extrinsic & intrinsic finger IV. PHYSICAL THERAPY PROGNOSIS INCLUDING
flexors PLAN OF CARE & INTERVENTION
2. FCU PT GOALS
3. FPL & FPB A. Patient education regarding:

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 1. Condition 4. Stopped late in the day to reduce the
2. Common complications need for catheterization at night
3. Means to address the 5. Initially, catheterization every 4 hours
complications 6. Patient attempts to void prior to
B. Prevention of secondary catheterization
complications 7. Maintain a record of voided &
C. Maintenance or improvement of: residual urine
1. Flexibility
2. ROM B. Non reflex bladder
3. Strength 1. Timed voiding
D. Develop cardiorespiratory endurance - Establish the pattern of incontinence
E. Alleviate pain, edema, and - Check residual volume
contractures - Compare between intervals & a new
F. Promote independence in ADLs pattern of intake & voiding is
G. Facilitate learning of using orthotic established
devices & adaptive equipment’s
H. Home & environmental modifications  BOWEL
A. Diet
PT INTERVENTION B. Fluid intake
• ACUTE C. Stool softeners
A. Respiratory D. Regular pattern of evacuation
- Improve ventilation E. Suppositories
- Increase effectiveness of cough F. Digital stimulation
- Prevent chest tightness G. Manual evacuation
- Prevent ineffective substitute
breathing SPINAL DYSRAPHISMS
*DBE
*Glossopharyngeal breathing GENERAL MEDICAL BACKGROUND
*Airshift maneuvers
*Assisted coughing I. Definition:
*Abdominal support
*Stretching exercises Multiple structural anomalies due to abnormal
*Strengthening of intact embryonic development of the neural tube and
respiratory mm its surrounding structures. Failure of the neural
*Postural drainage tube to fuse may allow spinal cord to pass
B. ROM & positioning through the opening of vertebral bones and may
* Selective stretching cause spinal cord defects.
C. strengthening ex
* Bilateral motions II. Classification
D. Bed positioning 1. Spina Bifida Occulta
E. Orientation to vertical position - Splits in vertebrae are so small so
* Use of abdominal binders
spinal cord does not protrude
* Use of elastic stockings
* Monitor BP - Muscle or skin covers the lesion
- (+) dimple or tuft of hair or birthmark
 SUB ACUTE overlying the defect
A. Consider functional expectations - Usually asymptomatic
B. Re-evaluation - Other cases: (+) back pain
C. Skin inspection
D. Continuing activities
2. Spina Bifida Aperta / Cystica
E. Mat programs
-contents of the spinal canal herniate
 BLADDER MANAGEMENT through the posterior vertebral opening.
A. Reflex bladder a. Meningocele – least common
1. Intermittent catheterization - Only meninges protrude
2. Fluid intake pattern ~ 2000 mL/d b. Meningomyelocele
3. Monitored at 150-180 mL/hour from – Meninges and spinal cord
am – early pm protrude
- Most severe complications

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 c. Myeloschisis
- Worst type of
meningomyelocele
- No overlying membrane
covering the spinal cord

• Neurulation of the anterior and

posterior neuropores occurs during the third to
fourth week after conception. The post
neurulation phase takes place during the fourth
through seventh post conceptional weeks.
Defects occurring at this phase are skin covered
lesions.
• Normal neural tube closure starts in the
third week of gestation from the mid-cervical
level and proceeds in both the cephalad and
*REFER TO TABLE (LAST PAGE) caudad directions.
III. Epidemiology • Defect of neural tube closure is thought
• increased rate in: to occur around day 26 and accounts for most
a. females lesions through mid-lumbar.
b. midspring conceptions • The more distal caudal cell mass forms
c. families with low socioeconomic between days 26 and 30 eventually resulting in
class formation of the central canal in the embryonic
d. in siblings tail.
e. use of Valproic acid during • Caudal regression with rostral extension
resulting in fusion with the neural tube results in
pregnancies
formation of the spinal cord by day 53.
i. valproic acid is a medication
• Lesions of the lumbo-sacral levels occur
for epileptics to reduce before day 53.
seizures
• Recurrence rate is 2.5 to 5% after the VI. Clinical Manifestation
birth of one child with spina bifida and doubles 1. Primary (Organic) Functional Deficits
after two affected children.  paraplegia – with motor and sensory
problems
IV. Etiology  mental retardation
1. genetic  neurogenic sphincter dysfunction
2. environmental – Folic acid and vit.B12
production, transport, and metabolism 2. Acquired Secondary Disabilities
 progressive development of
musculoskeletal complications and
V. Pathophysiology
deformities
1. neural tube fails to close at the 28th day of
• hip dislocation, scoliosis,
embryonic development
progressive deterioration of
2. neural tube opens due to focal necrosis
renal function, significant
emotional maladjustment
3. Musculoskeletal Deformities

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VII. Complications
• Arnold Chiari Malformation Type II
• Hydrocephalus
• Osteoporosis
• Malformations forebrain and hindbrain
• Tethered cord—abnormal attachment
of spinal cord at distal end.
• Benign lumbosacral tumors
• Syringomyelia
• Scoliosis/kyphosis
• Central respiratory dysfunction
• Impaired fine hand coordination, ataxia
• Impaired visual function (Strabismus,
lateral rectus palsy and nystagmus)
• Ureteral or lower tract anomalies
• Neurogenic bladder
• Neurogenic bowel
• Obesity
VIII. Diagnosis
• Maternal serum measurement of alpha-
fetoprotein (AFP) and acetyl cholinesterase in
the maternal serum and amniotic fluid and fetal
ultrasound are methods of prenatal diagnosis.
AFP is reliable in 80% of open neural tube
deficits in weeks 13 through 15.
• Amniocentesis done by week 16
T6-T12 Kyphosis, scoliosis, hip & knee flexion
contracture (frog leg position), equinus
foot
L1-L3 Scoliosis, lordosis, hip flexion & add
contractures, early hip dislocation,
knee flexn contracture &equinus foot
L4-L5 Scoliosis, lordosis, hip flexion
contractures, late hip dislocation, knee
ext contractures, calcaneovarus,
clubfoot
S1 Cavus foot
S2 Clawing of toes
S3-s4 Sphincter control
through 18 is nearly 100% accurate for detecting
elevated amniotic fluid AFP. Amniocentesis does
not detect closed neural tube defects without
leakage of fetal cerebrospinal fluid (CSF).
• Fetal ultrasound between 16 to 24
weeks gestation is reported to have > 90%
reliability
• Cranial Ultrasound – neonates & infants
• CT scan, MRI, BAER, VER, EEG
IX. Prognosis
• Nonprogressive neurologic lesion
• Changing function and dysfunction over
long years of growth and development
• 1st few years: developmental delay; later
age: secondary sequelae of long
standing neuromuscular deficit
• The employment rate among those with
spina bifida is 25%–50%
GENERAL HEATLHCARE MANAGEMENT
Medical, Surgical, and Pharmacologic:
1. Neurosurgical repair of cystic lesion is
usually performed on the first day of life,
with resultant lower mortality.
• 75%–85% require shunting for
hydrocephalus.
2. Urologic Treatment - Intermittent
catheterization should begin, Pharmacologic
management includes anticholinergics
3. Orthopaedic Management
a. Mild scoliosis—Thoraco Lumbar
Sacral Orthosis (TLSO) with regular
follow-up
b. At the knees, soft tissue releases of
flexion or extension contractures
may increase mobility and allow
sitting and/or bracing.
c. Equinus deformity is often treated
with Achilles tendon lengthening.
d. Flexor tenodesis or transfer and
plantar fascia fasciotomy is used to
correct severe claw toe deformity
and pescavus.
PHYSICAL THERAPIY EXAMINATION, EVALUATION
AND DIAGNOSIS
I. Points of Emphasis in Examination
a. Patient& Maternal History
b. Physical Examination
1. Early (Predective) Signs
a. Tone abnormalities of limbs,
neck, trunk
b. Weak cry, weak suck
2. Suspicion:
a. (+)neuromuscular deficit
b. Motor delay
3. Ocular inspection
4. Muscle Tone
5. Sensory Assessment
6. MMT
7. MBT
8. Reflexes
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 a. DTR
b. Developmental
9. Balance & Coordination
10. Posture
11. Gait
12. Functional status

II. Problem List

1. Tone Abnormalities
2. Reflex Abnormalities
3. Postural Abnormalities
4. Atypical Motor performance

III. Physical therapy Diagnosis

Impaired Motor Function, Peripheral Nerve
Integrity, and Sensory Integrity Associated With
Spinal Dysraphism.

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213 | P a g e
 MULTIPLE SCLEROSIS
I. GENERAL MEDICAL BACKGROUND
A. Definition:
• Multiple sclerosis (MS) is an autoimmune
disease characterized by inflammation,
selective demyelination, and gliosis.
• It causes both acute and chronic symptoms
and can result in significant disability and
impaired quality of life.
• Characterize by Charcot’s triad: (SIN)
a. Scanning speech
b. Intention tremor
c. Nystagmus
B. Classification
- Relapsing-Remitting MS (RRMS)
•Characterized by discrete attacks of
neurological deficits (relapse) with
either full or partial recovery (remission)
in subsequent weeks to months.
•The periods between relapses are
characterized by lack of disease
progression.
•The stable patient may have local
inflammatory activity that is clinically
silent.
•Affects approximately 85% of patients
with MS at diagnosis.
- Secondary-Progressive MS (SPMS)
•Characterized by an initial relapsing-
remitting course, followed by a change
in clinical course with progression to
steady and irreversible decline with or
without continued acute attacks.
•Result of progressive axonal loss rather
than new lesions.
•Before newer treatments, the majority
of patients with RRMS progressed to
SPMS.
- Primary-Progressive MS (PPMS)
•Characterized by disease progression
and steady functional decline from
onset; patients may experience modest
fluctuations in neurological disability but
discrete attacks do not occur.
•PPMS is associated with later onset
(mean age 40 years) and more equal
gender distribution. •Affects
approximately 10% of patients with MS.
- Progressive-Relapsing MS (PRMS)
•Characterized by a steady
deterioration in disease from onset
(similar to PPMS) but with occasional
acute attacks.
•Intervals between attacks are
characterized by continuing disease
progression.
•Affects approximately 5% of patients
with MS.
- Benign MS
•Mild disease, pt is fully functional in all
neurological systems 15 years after
disease onset
- Malignant MS
•Marburg’s variant
•Rapid progression leading to significant
disability or death within a relatively
short time after onset
C. Epidemiology
- Affects approximately 400,000 persons
in the U.S
- Worldwide: 2.1 million people.
- Onset typically occurs between ages 20
and 40 years.
- MS is rare in children, as is the onset of
symptoms in adults older than age 50
years.
- The disease is more common in woman
than in men by a ratio of 2:1 to 3:1.
Ethnic differences:
- Affects predominantly white
populations
- African Americans demonstrate
approximately half the risk of acquiring
the disease.
- Low rates in Asians and Native
Americans.
Geographical pattern of MS:
High-frequency areas:
Temperate zones of the northern U.S
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Scandinavian countries
Northern Europe
Southern Canada
New Zealand
Southern Australia.
Medium frequency closer to the equator
include:
Southern U.S and Europe
Rest of Australia
Low-frequency tropical areas include:
Asia
Africa
South America
***Migration studies indicate that the
geographical risk associated with an individual’s
birthplace is retained if emigration occurs after
age 15 years.
***Individuals migrating before this age assume
the risk of their new location.
D. Etiology
- The risk of MS is increased in persons
with an affected family member.
- The risk is 3.0% for a sibling
- 5.0% for a fraternal co-twin
- 25.0% for an identical co-twin
- Autoimmune BUT implicated viruses
which is under investigation include the
Epstein-Barr virus, measles, canine
distemper, human herpesvirus-6, and
Chlamydia pneumonia, though none
have been definitely proven to trigger
MS.
- The viruses may be retained in the body,
resulting in a self-perpetuating
autoimmune process.
- Risk of MS may also be increased with
vitamin D deficiency and smoking
E. Pathophysiology
1. Immune response triggers activation of
immune cells (e.g., T cells, CD4+ helper T
cells, B cells) that cross the blood–brain
barrier.
2. Activation of autoantigens, producing
autoimmune cytotoxic effects within the
central nervous system (CNS) (this process
can be viewed as a form of “friendly fire”)
3. Phagocytic activity of macrophages may
also contribute to demyelination.
4. Myelin serves as an insulator, speeding up
the conduction along nerve fibers from one
node of Ranvier to another (termed
saltatory conduction). It also serves to
conserve energy for the nerve because
depolarization occurs only at the nodes.
5. Disruption of the myelin sheath and active
demyelination slows neural transmission
and causes nerves to fatigue rapidly.
6. With severe disruption, conduction block
occurs with resulting disruption of function.
An acute inflammatory event emerges.
7. Edema and infiltrates (e.g., monocytes,
macrophages, and microglia) surround the
acute lesion and can cause a mass effect
(abnormally high pressures), further
interfering with the conductivity of the
nerve fiber.
8. Conceivably, this inflammation (which
gradually subsides) may, in part, account
for the pattern of fluctuations in function
that characterize this disease.
9. With repeat attacks, the antiinflammatory
processes become less effective and are
unable to keep up.
10. During the early stages of MS,
oligodendrocytes (myelin-producing cells)
survive the initial insult and can produce
remyelination. This process is often
incomplete and, as the disease becomes
more chronic, stalls altogether.
11. Eventually the oligodendrocytes become
involved and myelin repair cannot occur.
One form of MS, primary-progressive MS,
appears to be associated exclusively with
disease of the oligodendrocytes.
12. Demyelinated areas eventually become
filled with fibrous astrocytes and undergo a
process called gliosis. Gliosis refers to the
proliferation of neuroglial tissue within the
CNS and results in glial scars (plaques). At
this stage, the axon itself becomes
interrupted and undergoes
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 neurodegeneration. This is believed to be Speech and Swallowing
the main cause of permanent neurological - Dysarthria
disability. - Diminished verbal fluency
13. Type 1 lesion location: White matter (early), - Dysphonia
gray matter (later stage) - Dysphagia
Type 2: Small perivascular areas of Bladder Symptoms
demyelination - Spastic bladder
Type 3: Pial surface - Flaccid bladder
** Areas of predilection: optic nerves, - Dyssynergic bladder
periventricular white matter, spinal cord - Constipation
(corticospinal tracts, posterior white - Diarrhea and incontinence
columns), and cerebellar peduncles. Sexual Symptoms
- Impotence
F. Clinical Manifestation - Decreased libido
Sensory Symptoms - Impaired ability to achieve orgasm
- Hypoesthesia, numbness
- Paresthesias ** Pattern of Symptoms
- Pain •Varies greatly from person to person
- Paroxysmal limb pain, dysesthesias •Varies over time in each individual affected
- Headache •First symptoms usually transient; typically
- Optic or trigeminal neuritis sensory and visual
- Lhermitte’s sign •Diagnosis involves evidence of damage
- Hyperpathia occurring in at least two separate areas of CNS
- Chronic neuropathic pain and at two separate points in time at least one
Visual Symptoms month apart (dissemination of lesions in space
- Blurred or double vision (diplopia) and time)
- Diminished acuity/loss of vision
- Scotoma G. Complications:
- Nystagmus Musculoskeletal
- Lateral gaze palsy - Osteoporosis
Cognitive Symptoms - Fibrosis/ankylosis
- Short-term memory deficits - Decreased contractile strength
- Diminished attention, concentration - Decreased muscle endurance
- Diminished executive functions - Atrophy
- Diminished information processing Digestive
- Diminished visual– spatial abilities - Loss of appetite
Affective Symptoms - Constipation
- Depression - Poor nutrition/delayed healing
- Anxiety Respiratory
- Pseudobulbar affect - Decreased vital capacity
- Anxiety - Decreased respiratory endurance
Motor Symptoms - Impaired coughing
- Paresis or paralysis - Increased respiratory infections
- Fatigue Neuromuscular
- Spasticity, spasms - Decreased sensory input
- Ataxia: incoordination, intention tremor - Decreased motor control
- postural tremor - Poor coordination
- Impaired balance and gait Autonomic ability

216 | P a g e
- Renal Urinary stasis of MS)
- Increased urinary infections • Multifocal areas of increased intensity
- Renal calculi (plaques) on T2 weighted images are abnormal
Cardiovascular in 85% of the cases
- Decreased physical work capacity • These ovoid-appearing plaques are located in
- Thrombophlebitis the periventricular white matter (corpus
- Orthostatic hypotension callosum)
Psychosocial • Enhancement with gadolinium may precede
- Anxiety/depression the onset of deficits and identify active disease •
- Detachment May visualize subclinical lesions
- Intellectual deficit • Contrast-enhanced T1weighted images
Integumentary (gadolinium-enhanced) are used to
- Skin atrophy detect more long-term disease activity
- Decubiti (i.e., loss of myelin and axons, gliosis).
These lesions are seen as “black holes”
H. Diagnosis on the MRI; the darker the lesion, the
• Made by the neurologist based on a more extensive the tissue damage.
careful medical history, a complete  CT Scan
neurological examination, and • Not effective in visualizing lesion of brainstem,
supportive laboratory tests. cerebellum, and optic nerve.
• Cerebral atrophy is most common sign.
 Cerebral Spinal Fluid (CSF) Examination
• Increased in Protein (myelin basic, 25%), Simplified Diagnostic Criteria for MS
Oligoclonal IgG bands (greatest sensitivity), IgG 1. Possible MS
and WBCs - history of relapsing and possible remitting
 VEP (Visual Evoked Potentials) (high signs (-)
sensitivity along with MRI) prior neurogenic symptoms
• P100 latency is abnormal (slowing secondary - 1 site of involvement in the CNS
to plaques) in 75% 2. Probable MS
 BAER (Brainstem Auditory Evoked Response) - 2 documented attacks with clinical evidence
• Investigates the pontine area displaying an of 1
absence or delay of wave formation secondary lesion OR
to the demyelinating process - 1 documented attack, 2 lesions
 SEP (Sensory Evoked Potentials) 3. Definite MS
• Prolongation of absolute peak or interpeak - 2 attacks separated by 1 month, 2 separate
latency lesions
 EMG/NCS
• Sensory Nerve Action Potentials (SNAPs), I. Differential Diagnosis
Compound Motor Action Potentials (CMAPs), 1. SLE
Conduction Velocity (CV) worsens as the myelin 2. Sjogrens Syndrome
thins 3. Lyme Disease
• EMG may show abnormal activity: Fibs, 4. AIDS
Positive Sharp Waves (PSW), Facial myokymia 5. Sarcoidosis
and a decrease Motor Unit Action Potentials
(MUAP) J. Prognosis
• Single Fiber Electromyography (SFEMG) Factors Good Poorer
• Blink Reflex: May be abnormal prognosis prognosis
 MRI (Greatest sensitivity for the diagnosis

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 Age of onset < 40 years old > 40 years old Tegretol - for paroxysmal spasm
(sudden, sharp onset
Symptoms Monosympto Polysymptom Phenol - causes a motor point block
matic atic Dantrolene Sodium
Onset Sudden, good Rapidly Anticholenergics: Regulates bladder emptying
recovery with progressive Propantheline
long remission Imipramine (Tofranil)
Findings at Sensory Motor (1st Amantadine Fatigue
onset Optic Neuritis sign) Pemoline ** edema, dec. Concentration,
Ataxia and insomnia
tremor Isoniazid Tremors
Ambulation Yes No Clonazepam
Remission Longer, more Higher Prozac Depression
and Relapse complete relapse rate Paxil
remissions
Disability Low current High disability
disability Surgical Management for severe spasticity:
Benign and PPMS 1. Tendonotomy - severing tendons
RRMS 2. Neurectomy - nerves
Cerebellar 3. Rhizotomy - nerve roots
and
pyramidal III. PHYSICAL THERAPY EXAMINATION,
signs (+) EVALUATION, AND DIAGNOSIS
multiple sites
involvement A. Points of Emphasis in Examination
1. History: symptoms, disease progression,
functional deficits
II. GENERAL HEALTHCARE MANAGAMENT 2. Cognitive/behavioral status: mild-to-
(MEDICAL, SURGICAL, & PHARMACOLOGIC) moderate cognitive impairment are common;
also euphoria, emotional dysregulation
Pharmacologic Management 3. Communication: dysarthria and scanning
Drugs Indication speech are common; dysphasia
4. Sensation
Interferon Drugs: Slow down immune system Common findings: Paresthesias, hyperpathia,
Betaseron response reducing dysesthesias, trigeminal neuralgia, Lhermitte’s
Avonex inflammation, and swelling. sign
Rebif Also block T cells from crossing
5. ROM and deformities
the BBB damaging myelin 6. Vision: diplopia and blurred vision are
Corticosteroids: For acute disease relapses, common
Prednisone shortening the duration of the
7. Skin integrity and condition
Methylprednisolone episode. Diminish swelling 8. Muscle tone and DTRs: spasticity and
within the CNS. Doesn’t hyperreflexia are common due to pyramidal
modify disease course. tract lesions
Anti-Spasticity 9. MMT: paresis is common, if spasticity is
Baclofen severe, MMT may be invalid
Dantrium 10. Coordination: ataxia is common, intention
Valium - causes too much sedation tremors, dysmetria, dysdiadochokinesia

218 | P a g e
11. Balance: vestibular involvement with vertigo, - AAROM - AROM
dizziness, unsteadiness, paroxysmal or sudden exercises
onset of symptoms
12. Gait: Ataxic gait is common Muscle Increase - Submaximal intensity
13. Fatigue: (number one complaint) weakness muscle exercises
14. Respiratory status (Paresis) strength - resistance exercises
15. Functional status: FMS, ADLs using elastic band
16. Standardized Test and Measures: - circuit training,
a. Expanded Disability Status Scale (Kurtzke) alternating UE and LE
b. Minimum Record of Disability work
c. Modified Fatigue Impact Scale by Fisk ** balance ex with
rest periods
B. Problem List Spasticity Decrease - Rhythmic rotation
1. Sensory deficits / changes spasticity with deep tendon
2. LOM pressure then
3. Muscle weakness prolonged stretching
4. Spasticity - PNF stretching
5. Pain exercises
6. Decrease cardiorespiratory function Pain Decrease pain - stretching and
7. Impaired motor control and coordination, and exercise
balance - hydrotherapy using
8. Easy fatigueability lukewarm water
9. Gait abnormalities (ataxic)
10. Dependence in ADLS Decrease Increase Cycling, walking,
cardiorespirat cardiorespirat swimming, circuit
C. PT Diagnosis ory ory function training
Impaired motor function and sensory integrity function/deco ** lmtd to 60-75 peak
associated with progressive CNS disorders nditioning HR
Impaired Promote - Holding in weight
IV. PHYSICAL THERAPY PROGNOSIS postural, and static postural bearing, antigravity
motor control as postures. Progress by
Goals: To manage the effects of this progressive control, baseline varying BOS.
disease and prevent/minimize indirect coordination, protocol - Joint approximation
impairments associated with disuse and and balance - Hydrotherapy
inactivity
Problem list A. Plan of care B. Intervention Easy Decrease Activity pacing and
fatigueability fatigue during exercise modifications
Sensory Improve - Sensory integration exercise
deficits / sensory techniques; (initiation Gait Slow down - PNF dynamic
changes awareness; of different of stimulis abnormalities the ataxic reversals ( slow
teach sensory depending on the (ataxic gait) movement reversals)
compensation affected senses) and promote - Hydrotherapy
s to prevent - Use eye patch with postural - coordination
injury diplopia stability and exercises (Frenkel’s
Loss of Increase - PJM of specific joints proprioceptio exercise)
Motion Motion to loose adhesions n -

219 | P a g e
 Flaccid Crede maneuver
bladder

Please refer to the following sources for more

comprehensive explanation of the topic:
 Physical Rehabilitation by Sullivan, Schmitz
 NPTE Review and Study Guide by O’Sullivan,
Sigelman
 Physical Medicine and Rehabilitation Board
Review by Sara J. Cucurullo

220 | P a g e
 PARKINSON’S DISEASE AND OTHER MOVEMENT disulfide, CO, cyanide, &
DISORDERS methanol
 Common among miners
I.GENERAL MEDICAL BACKGROUND
• Pharmacological
Definition  Drugs that interfere with
dopaminergic mechanisms
PARKINSONISM either presynaptically or post-
- Refers to a group of disorders that produce synaptically such as
abnormalities of the basal ganglia neuroleptics: ex.
Haloperidol/haldol
BASAL GANGLIA
 Also antidepressants ex.
- Damage to the basal ganglia can either result in
a hyperkinetic or hypokinetic motor disturbance amitriptyline & antihypertensive
- There are two pathways of the signals: ex. Methyldopa especially with
• Direct pathway which facilitates the flow of high doses
signals to the thalamus thus allowing • Metabolic
movement  Disorders of Ca metabolism that
• Indirect pathway which inhibits information causes basal ganglia calcification
flow & thus suppresses other movements
 Disorders such as
- The neurotransmitters involve in the flowing of
signals include the: hypothyroidism,
• Gamma amino butyric acid (GABA) hyperparathyroidism,
• Dopamine hypoparathyroidism & Wilson’s
• Glutamate disease
• Acetylcholine - AKINETIC/CLASS III/MULTISYSTEM ATROPHY
• Aka rigid syndromes with
PARKINSON’S DISEASE parkinsonism, parkinsonian plus
- Aka primary parkinsonism syndromes
- Aka paralysis agitans • Neurodegenerative diseases that
- Most common affect the substantia nigra &
- True PD produce parkinsonian symptoms
- A chronic, progressive disease of the nervous along with other neurological signs
system characterized by the cardinal features of • Includes: striatonigral
rigidity, akinesia, bradykinesia, tremors & degeneration(SND), Shy Dragger
postural instability syndrome, progressive supranuclear
- Was described as “shaking palsy” by James palsy(PSPO), olivoponto cerebellar
Parkinson in 1817 atrophy(OPCA), cortical basal
- Has two subgroups: ganglionic degeneration
• Postural Instability Gait disturbance • During the early stages, there’s
 The dominant symptoms rigidity & bradykinesia then with
include postural instability & cognitive impairment
gait disturbances • Parkinson- plus syndromes don’t
• Tremor predominant improve from L-dopa
 With tremors as the dominant therapy(apomorphine test)
feature - SHY DRAGER SYNDROME
• Manifested by seborrhea,
Classification sialorrhea, hyperhydrosis, penile
- PRIMARY PARKINSONISM/CLASS I dysfunction & orthostatic
• Idiopathic hypertension
- SECONDARY PARKINSONISM/CLASS - PROGRESSIVE SUPRANUCLEAR PALSY
II/ACQUIRED PARKINSONISM • Loss of upward or vertical gaze &
• Post infectious Parkinsonism then latter part of the disease loss
 Viral infection of lateral gaze
- HYPERKINETIC DISORDERS
 Influenza epidemics of
• Chorea
encephalitis lethargica
 Associated with Huntington’s
• Toxic Parkinsonism disease
 Industrial poisons & chemicals  Characterized by rapid, involuntary,
which includes Mn, carbon irregular & jerky movements

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 - Types:
1. Huntington’s disease
- An autosomal dominant
disorder of
chromosome 4p
2. Tardive dyskinesia
- Secondary to prolonged
use of neuroleptic drugs
3. Sydenham’s
- Common among
children & is related
with rheumatic fever
due to streptococcal
infection
• Athetosis
 Slow, writhing, sinusoidal
movements due to affectations of
the globus pallidus
• Ballismus
 Flinging, hurling & ballistic
movements of the extremities
 Primarily axial & proximal
 Due to involvement of the
subthalamic nucleus
• Dystonia
 Twisting, bizarre movements & if
prolonged contraction occurs, this
results in dystonic posturing
• Tremors
• Tics
 Characterized as repetitive,
intermittent & stereotypical
movements
 Usually involves males
 Gilles de la Torrette (smacking,
puckering or barking, there’s also
coprolalia & palilalia
Epidemiology
- Age: > 55 year old
- Mean age of onset: 58-62 y/o
- Onset: insidious with slow rate of
progression
- Gender: Males > Females
Etiology
- Based on classification
Pathophysiology
- Degeneration of dopaminergic neurons that
produce dopamine
- These neurons have their cell bodies in the
substantia nigra pars compacta & send their
axons to the striatum (caudate nucleus &
putamen)
- At least 80% of neurons degenerate before
symptoms show up
- Loss of dopaminergic neuron results in
reduction of spontaneous movement
- There can also be a decrease of the binding sites
for dopamine in the basal ganglia
- Develops a characteristic cytoplasmic inclusion
known as Lewy’s bodies
AREAS OF PREDILECTION
- Dorsal motor nucleus of the vagus,
hypothalamus, locus ceruleus, cerebral cortex, &
autonomic ganglia
Clinical Manifestations
• Rigidity
 One of the clinical hallmarks
 Refers to resistance to passive motion
 Typically unequal in distribution
 Patient complaints of heaviness & stiffness
of the limbs
 Initially proximal muscles
 Types include:
1. Cogwheel
2. Leadpipe
• Akinesia & Bradykinesia
 Moments of freezing can occur, deficit in
the preparation phase of movement
 The latter is the most disabling symptom
• Micrographia
• Tremor
 Initial symptom
 Slow frequency of about 4-7 cycles/second
 “Pill rolling” of the hand but can also involve
the feet, lips, tongue & jaw
 (+)Postural tremor which disappears during
sleep
• Postural instability
 (+) Ability to maintain a steady position but
can’t with dynamic activities
Complications
- Poverty of movement
A. As tasks become more complex, the
difficulty increases
B. Can also be caused by fatigue, &
loss of motivation
- Fatigue
A. Performance decreases with great
physical effort
- Masked face
A. There’s infrequent blinking & lack of
expression
B. (+) Blepharoclonus with eyelids
closed
C. (+) Blepharospasm which is
involuntary
- Musculoskeletal changes
A. loss of flexibility
B. Contractures are common
C. Deformities also include kyphosis,
some also with scoliosis
D. There’s also (+) Myerson’s sign
which characterized by a sustained
blink response with repetitive
tapping over the glabella
- Gait disturbances
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 A. Decreased velocity
B. Hip, knee, ankle motions are
decreased
C. Decreased stride length & reciprocal
arm swing
D. (+) Small shuffling steps with (-) heel
to toe progression
E. (+) Festinating gait characterized by
progression in speed & shortening
of stride
F. There can also be a propulsive gait
or retropulsive gait
- Swallowing & communication dysfunction
A. Dysphagia
B. Sialorrhea
C. Hypokinetic dysarthria & with
advanced cases there is mutism
- Visual & sensorimotor disturbances
A. Blurred vision
B. Impaired conjugate eye movements
& saccadic eye movements
C. Decrease blinking
D. Numbness & paresthesia
E. Postural stress syndrome can cause
pain
F. Akathisia which is extreme motor
restlessness that interferes with
relaxation
- Cognitive & behavioral changes
A. Dementia
B. Loss of executive functions
C. Bradyphrenia
D. Perceptual deficits especially with
spatial organization
E. Depression
F. Dysthmic disorder which is atypical
depression with intermittent
episodes of severe anxiety
G. Hallucinations & delusions
H. Insomnia
- Autonomic dysfunction
A. Excessive perspiration, greasy skin,
thermoregulatory abnormalities &
bladder dysfunction
B. Decreased GIT motility
- Cardiopulmonary
A. Orthostatic hypotension
B. Cardiac arrhythmias
C. Decreased forced expiratory
volume, forced vital capacity, with
higher residual volume
D. Edema
Diagnosis
- No single definitive test
- Based on history & clinical exam
- At least two of the four cardinal features are
present
- CT scan & MRI
Differential diagnosis
- Parkinson's disease must be differentiated
from other conditions, especially those
presenting with tremor. Parkinsonism refers
to any condition that causes a combination
of the movement abnormalities seen in
PD—such as tremors, slow movement,
impaired speech, or muscle stiffness—
resulting from the loss of dopamine-
containing neurons. Not everyone who has
Parkinsonism has Parkinson's disease.
- Other diagnoses that you should consider:
• Essential tremor - An essential tremor
produces tremors, or uncontrolled shaking,
in the hands and sometimes the head, that
progress over time. The tremor is not
associated with other Parkinson's disease
symptoms. Progressive supranuclear palsy
(PSP) - loss of vertical eye movements
• Progressive supranuclear palsy (PSP). PSP is a
brain disorder that affects walking and
balance, often resulting in falls. The
condition can also cause problems with
vision and eye movement. PSP does not
usually respond to medication.
• Multiple system atrophy (MSA) - MSA is a
rare, progressive nervous system disorder
that may share some of the same symptoms
as Parkinson's disease. Other symptoms of
MSA may include poor coordination, slurred
speech, problems with breathing and
swallowing, and constipation.
• Corticobasal degeneration (CBD) - alien limb,
spasticity, cortical sensory loss
• Diffuse Lewy body dementia (LBD) - early
dementia presenting within 2 years of motor
symptoms
- Early clinical features that suggest an
atypical Parkinsonism rather than Parkinson
disease include the following:
• Falls at presentation or early in the disease
• Poor response to levodopa
• Symmetry at disease onset
• Rapid disease progression
• No tremor
• Dysautonomia (eg, urinary incontinence,
fecal incontinence, catheterization for
urinary retention, persistent erectile failure,
prominent symptomatic orthostatic
hypotension)
Prognosis
- An estimate of the stage and severity of the
disease can be made by using the Hoehn-
Yhar Classification of Disability Scale. It
provides a useful measure for charting the
progression of the disease. Stage 1 is used
to indicate minimal disease involvement,
whereas stage 5 is indicative of severe
deterioration in which the patient is
confined to bed or a wheelchair.
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 - Patients who have a young age at onset or
who are tremor predominant typically
demonstrate a more benign progression and
a relatively good prognosis.
- Rapid progression is a poor prognosis.
II.GENERAL HEALTHCARE MANAGEMENT
Medical, Surgical, and Pharmacological Management
- No direct cure
PHARMACOLOGICAL MANAGEMENT
- Monoamine oxidase B
A. Reduce oxidative stress on neurons
or inhibit toxins on neurons
- Dopamine replacement
A. Aka L-dopa, Levodopa, Carbidopa
B. Mainstay treatment
C. Is a precursor of dopamine, raises
the dopamine levels in the basal
ganglia
D. -L- dopa & Carbidopa are combined
to allow greater amount of the L-
dopa to enter BBB
E. The initial improvement seen
among PD patients is known as
“honeymoon period”
F. “Wearing off” or end of dose
deterioration is characterized by
worsening of symptoms during the
expected time frame of medication
effectiveness
G. There’s dyskinesias which are
presented as facial grimace, lip
twitching or tongue protrusion
H. “Drug holidays”
- Anticholinergics
A. tremors
- Antiviral
A. has antiparkinson effects
- Dopamine Agonists
A. may improve the function of
dopamine receptors
NUTRITIONAL MANAGEMENT
- No high CHON diet
SURGICAL MANAGEMENT
- Stereotaxic surgery
• Surgical lesioning of the brain
- Pallidotomy
• Producing a destructive lesion in the
basal ganglia that tends to reduce
globus pallidus internus excessive
activity
- Thalamotomy
- Deep brain stimulation
• Implantation of electrodes in the
brain that block the signals that
cause symptoms
- Transplantation
• Of cells capable of delivering
dopamine into the striatum of the
patients with advanced PD
PHYSICAL THERAPY EXAMINATION, EVALUATION &
DIAGNOSIS
Points of Emphasis in examination
- Cognition
• MMSE
- Affective & psychosocial
• Geriatric Depression Scale/ Beck
Depression Inventory
- Sensory integrity
- Pain
• McGill Pain Questionnaire & VAS
- Visual function
- ROM
- Posture
- MMT
- Motor function
• Rigidity, bradykinesia with slowed
reaction time & prolonged
movement time, tremors, postural
instability
- Gait
- Dysphagia & speech impairments
- Autonomic changes
- Cardiorespiratory
- Skin integrity & condition
- Functional status
• FIM
• Katz Index of Independence in ADLs
- General & disease specific health measures
• Unified PD Rating Scale, Sickness
Impact Profile, PD Questionnaire-39
• The former documents the overall
effects of the disease while the
latter is a subjective report of the
impact of PD on daily life & points
out on mobility, ADLs, emotional
well-being, stigma, social support,
cognition, communication, & bodily
discomfort
HOEHN & YAHR CLASSIFICATION OF DISABILITY
SCALE
- STAGE I
• Minimal/absent; unilateral
involvement if (+)
STAGE II
• Minimal bilaterally/ but
independent in ADL & (-) postural
instability
- STAGE III
• Bilateral; independent in ADL with
postural instability
- STAGE IV
• Bilateral involvement; needs
assistance with ADLs; independent
with ambulation
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- STAGE V
• Confined to bed or wheelchair
Problem list
- Rigidity
- Contractures
- Postural Instability
- Impaired Balance
- Impaired coordination
- Impaired Gait and gait disturbances
- Decreased daily functional activities
- Fatigue
Physical Therapy Diagnosis
- Decreased functional activities 2 to impaired
muscle performance
- Impaired muscle performance 2 to damage
of the basal ganglia
PHYSICAL THERAPY PROGNOSIS & INTERVENTION
Plan of care
- To decrease rigidity
- To prevent contractures
- To promote body awareness for postural
instability
- To improve balance and coordination
- To increase participation in daily functional
activities
- To conserve energy
Intervention
- Motor learning strategies
• In the early stage, practice can be
expected to improve learning and
performance.
• Large number of repetitions to develop
procedural skills
• Long and complex movement sequence
should be broken down into component
parts
• In favor of a blocked practice order,
thereby reducing the effects of
contextual interference
• Task should be modified and minimize
- Relaxation Exercises
• Gentle rocking to produce generalized
relaxation of excessive muscle tension
due to rigidity.
• PNF technique of Rhythmic Initiation
helps overcome the effects of rigidity.
• Diaphragmatic breathing during
exercise.
• Stress management techniques are an
important adjunct to relaxation training.
• Jacobson progressive relaxation
techniques
- Flexibility
• AROM and PROM exercises are used to
improve flexibility. AROM exercises
emphasize active motions and PROM
exercises work within the patient’s
available ROM to maintain range.
• Stretching techniques to elongate
muscles. Can also be combined with
joint mobilization techniques to reduce
tightness of the joint capsule or of
ligaments around a joint. Stretch should
maintain at least 20-30 sec/3-5x/20-30
min.
• Passive positioning can also be used to
stretch tight muscles and soft tissues.
• Address Contractures
- Mobility
• As well as controlled mobility
• Include the muscles of the face
- Balance
• ‘Kitchen sink exercises’ consists of heel-
rises and toe-offs, partial wall squats
and chair rises, single limb stance with
side-kicks or back-kicks, and marching in
place.
- Gait training
• Designed to lengthen stride, broaden
BOS, improve stepping, improve heel-
toe gait pattern, increase contralateral
trunk movement and arm swing,
increase speed and provide a program
of regular walking.
• For improving upright alignment: have
the patient walk with vertical poles (pole
walking) and verbal cues to ‘walk tall’.
• PNF patterns can be used
• Provide visual cues as well as auditory
cues
- Motor learning strategies
• With advanced cases, compensatory
strategies are utilized
- Functional Adaptations
• Of assistive devices
• Appropriate shoes
- Respiratory Exercises
• DBE
- Aerobic Conditioning
• Submaximal intensities (50-70% of heart
rate reserve)
• Frequency: 3-5 days/week
- Group and Home exercises
• Low impact aerobics
- Patient and Family Education
• Clinical presentation of the disease
225 | P a g e
• Strategies to manage symptoms
• Preventative measures to minimize the
secondary complications and
impairments
• Strategies for energy conservation and
ensuring activity participation

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 PERIPHERAL NERVE INJURIES CLASSIFICATION
(Anatomy and Physiology)
CN XI Injury
Bell’s Palsy - The nervous system is divided into two:
Upper Lesions of the Brachial Plexus o central nervous system
Lower Lesions of the Brachial Plexus o peripheral nervous system
Long Thoracic Nerve Injury
Terminologies:
Phrenic Nerve Injury
a. Dermatome - an area of skin innervated by
Dorsal Scapular Nerve Injury
Suprascapular Nerve Injury spinal segment
Nerve to Subclavius Injury b. Myotome - muscle or group of muscles
Subscapular Nerve Inury innervated by a spinal nerve
Thoracodorsal Nerve Injury c. Peripheral nerves
Axillary Nerve Injury
Radial Nerve Injury Functional classification specific to PNS only:
Injuries of the Radial Nerve in the Axilla a. Sensory Division
Injuries of the Radial Nerve in the Spiral - Carries info from skin, skeletal muscles &
Groove
joints (somatic)
Arcade of Frohse
Injuries to the Superficial Branch of the Radial - Carries info from viscera (visceral)
Nerve
b. Motor Division
Musculocutaneous Nerve
- Divided into the somatic & autonomic
Musculocutaneous Nerve Tunnel Syndrome
Median Nerve nervous systems
Injuries of the Median Nerve at the Shoulder - The significance of having the knowledge of
Injuries of the Median Nerve above the the pathways is to point out specific nerve
Elbow involved
Pronator Teres Syndrome
Anterior Interosseous Nerve Syndrome Supporting Structures:
Carpal Tunnel Syndrome - Referred to as the connective tissue sheaths
Injuries to the Ulnar Nerve a. Epineurium - primarily resists compression
Injuries of the Ulnar Nerve at the Shoulder b. Perineurium - strongest connective tissue;
Injuries of the Ulnar Nerve at the Elbow
serves as a barrier for diffusion
Cubital Tunnel Syndrome
Injuries to the Ulnar Nerve at the Wrist c. Endoneurium
Injuries to the Femoral Nerve
Nerve Roots:
Injuries to the Sciatic Nerve
- More prone to be injured than the
Sciatica
Injuries to the Common Peroneal Nerve peripheral nerve due to lack of perineurial &
Injuries to the Tibial Nerve epineurial protection.
Tarsal Tunnel Syndrome - The fibers are also less slack & supported by
Injury to the Medial Plantar Nerve less amount of collagen.
Injuries to the Obturator Nerve
Injury to the Lateral Femoral Cutaneous Nerve of the
Thigh Nerve Parts:
Nerve Parts Functions
I. GENERAL MEDICAL BACKGROUND Cell Body
Axon - Long cellular processes of both motor
DEFINITION & sensory nerves
- aka peripheral neuropathy - Has an excitable membrane
- Any disorder of the peripheral nervous -Each segment of an axon must reach
system either involving the axon or the a threshold of electrical excitation
myelin sheath due to trauma, metabolic (depolarized) to be able to propagate
an impulse
disorders or genetic problems which can
Myelin Sheath - Serves as an insulator
either be localized or generalized; proximal
or distal affectation that results in motor Unmyelinated - Poorly insulated
and sensory problems. - Usually for functions that do not
- Usually with chronic stages, both the myelin need faster transmission
sheath & the axon are involved
Myelinated - Usually larger in diameter with less
electrical resistance
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Nodes of - Gaps between individual Schwann 2nd Degree - (+) Axonal damage
Ranvier cells - (+) Wallerian degeneration
Saltatory - Faster impulse transmission with less - Intact supporting structures
Conduction energy consumption - intact endoneurial tube
- good prognosis
Type of Definition = axonotmesis
Neuropathy 3rd Degree - (+) Axonal and Endoneurium
Demyelination - Involves the myelin sheath discontinuity
- Tends to ↓nerve conduction - (+) Hemorrhage, Edema & Fibrosis
which can be localized or inside the fascicle
generalized - Intact perineurium
- ex. CTS, GBS - Prognosis: the more proximal the injury,
Axonopathy - Involves the axon that are due to: the less likelihood of nerve re-
a. nerve toxicity innervation
b. metabolic disorders abberant innervation:
c. trauma - axonal regrowth into a different
endoneurial tube
CLASSIFICATION SYSTEM - results in synkinesis
- According to the degree of severity - ex. crocodile tears with Bell’s palsy
SEDDON’S Definition - ex. with respiration, arm mm contract
Neuropraxia - A localized nerve damage 4th Degree - (+) Axonal, Endoneurial & Perineurial
- (-) Wallerian degeneration damage
- Commonly caused by - (+) Neuroma formation
compression 5th Degree - Axon + all supporting structures are
- characterized by: damaged
1.decreased vibratory sense - Results from stretch, compression or
2.proprioceptive sensation nerve laceration
impairment - Prognosis is good with surgery
3. impaired light touch
4. paresthesias ETIOLOGY
- with transient motor loss - Compression
- with myelin sheath recovery, - Toxic exposure
impulse conduction across - Metabolic derangements
affected segment is restored - Neoplasm
Saturday night’s palsy - Infection
- a severe form of neuropraxia
- Inflammation
- a compression injury to the
myelin sheath leading to a - Amyloidosis
localized nerve conduction block - Autoimmune problems
Axonotmesis - Axonal injury - Genetic
- (+) Wallerian degeneration
- Supporting structures are intact PATHOPHYSIOLOGY
- Schwann cells are also intact
- Due to fractures & dislocations Nerve Injury 2° Compression
- (+) sensory, motor & sudomotor ↓
problems Conduction Block
Neurotmesis - Complete transection of the
axon as well as the supporting PROGNOSIS OF AXONOPATHY
structures
- Possibility of neuroma - The course of time & completeness of
formation which can be recovery depends on:
addressed by surgical excision of a. location of the injury
the damaged segment & re- b. age & overall condition of the pt
anastomosis c. with delayed recovery
- Poor Prognosis
- The endoneurial sheath can deteriorate
permanently & recovery may never be
SUNDERLAND’S Definition complete
1st Degree - Intact axon - Rate of regeneration: 1.5-2mm/day
- (+) Focal conduction block
= neuropraxia CN XI INJURY

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ETIOLOGY Tic Doulouruex
- Cervical rib - Idiopathic neuralgia affecting CN 5.
- Spasm of the scalenius muscle - (+) Chronic pain in the face
- Fractures in the cervical region - Suspected causes:
- Dislocations  Degeneration of the nerve
- Stab injuries  Compression
- Gunshot injuries - Manifested by neurogenic pain
- Surgical procedures in the cervical area - Normal motor control
Brachial Plexus Injuries
MANIFESTATIONS - The roots, trunks & divisions are situated in
- With injuries at the anterior triangle, the the lower part of the posterior triangle of
SCM is affected the neck
- With injuries at the posterior triangle, the - The cords & most of the branches are
trapezius is affected located in the axilla
- Sliding door deformity (lateral winging of - Complete lesions affecting all the roots are
scapula) rare
BELL’S PALSY - Incomplete injuries are common usually due
- An idiopathic facial paralysis affecting CN 7. to
- Inability to control facial muscles on the  Traction
affected side both upper and lower  Pressure
- Named after Sir Charles Bell  Stab wounds

ETIOLOGY (suspected) 1. UPPER LESIONS OF THE BRACHIAL PLEXUS

- Viral or bacterial infection - Aka Erb Duchenne palsy
- Nerve compression ETIOLOGY
- Frequent exposure to cold temperature - Excessive traction or tearing of C5, C6 nerve
- Trauma to the nerve roots
- Tumor PATHOPHYSIOLOGY

CLASSIFICATION Excessive displacement of head to opposite side and

depression of shoulder on the same side
Site of Injury Result ↓
Outside Stylomastoid - (+) Bell’s phenomenon Excessive Traction of C5 C6 nerve roots
Foramen - Muscle paralysis ↓
Facial Canal involving - (+) Bell’s phenomenon Motor and Sensory Impairments
Chorda Tympani - Muscle paralysis MANIFESTATIONS
- Loss of taste sensation - (+) Muscle paralysis
- ↓Saliva production of the - (+) Waiter’s Tip Deformity (Radial Nerve
submandibular and sublingual glands Palsy)
Facial Canal involving - Manifestation of first two sites - Limp on the upper limb, medial rotation and
Stapedius muscle - (+) Hyperacusis pronation
Involving Geniculate - (+) Ramsey Hunt Syndrome
- Nerves affected:
Ganglion - Manifestation of first 3 sites
 Axillary nerve
- (+) pain behind ear
Involving Internal -Manifestations of the previous sites  Suprascapular nerve
Auditory Meatus - (+) Deafness  Nerve to the Subclavius
- (+) Tinnitus in one or both ear  Musculocutaneous nerve
- Defective vestibular responses
2. LOWER LESIONS OF THE BRACHIAL PLEXUS
COMPLICATIONS - Aka Klumpke’s palsy
- Eye problems ETIOLOGY
- Crocodile tears - Traction injuries of T1 nerve root (usually),
- Contractures also includes C8 nerve roots
- Breathing problems due to nasal obstruction - Presence of a cervical rib
- Aesthetic issues - Malignant metastases from the lungs to the
lower deep cervical lymph nodes
DIFFERENTIAL DIAGNOSIS
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PATHOPHYSIOLOGY - Rarely injured
MANIFESTATIONS
Excessive arm ABD - (+) Muscle paralysis
↓
Excessive traction of T1 Nerve root 8. SUBSCAPULAR NERVE INURY
↓ - Nerve roots C5 – C6
Motor and Sensory Impairment
MANIFESTATIONS
MANIFESTATIONS
- (+) Muscle paralysis
- (+) Clawing Of hands
9. THORACODORSAL NERVE INJURY
- (-) Sensation along medial side of the
- Nerve Roots C7 – C8
forearm, hand and medial two fingers when
MANIFESTATIONS
C8 is also affected - (+) Muscle paralysis
Nerves Affected:
1. Median nerve 10. AXILLARY NERVE INJURY
2. Ulnar nerve - aka circumflex nerve; nerve roots C5 – C6
ETIOLOGY
3. LONG THORACIC NERVE INJURY - Pressure from crutches towards the armpit
- Aka external respiratory nerve of Bell - Shoulder dislocations (inferior displacement)
- Aka knapsack nerve - Fracture of the surgical neck of the humerus
ETIOLOGY MANIFESTATIONS
- Blows or pressure on the posterior triangle - (+) Muscle paralysis
- During radical mastectomy - (+) Loss of sensation over the lower half of
MANIFESTATIONS the deltoid muscle
- (+) Muscle paralysis -
- (+) Scapular Winging with vertebral scapula 11. RADIAL NERVE INJURY
protruding posteriorly
- Difficulty raising the arm above the head A. Branches in the axilla:
 Posterior cutaneous nerve to the arm
4. PHRENIC NERVE INJURY B. Branches in the spiral groove:
- From nerve roots C3 – C5  Lower lateral cutaneous nerve of the arm
ETIOLOGY  Posterior cutaneous nerve of the forearm
- Rarely injured  Nerve to the lateral head of the triceps
- Gunshot wounds  Nerve to the medial head of the triceps &
MANIFESTATIONS anconeus
- (+) muscle paralysis C. Branches in the anterior compartment of the arm
- May need a ventilator above the lateral epicondyle:
 Nerve to a small part of the brachialis
5. DORSAL SCAPULAR NERVE INJURY  Nerve to the brachioradialis
- Nerve root C5  Nerve to ECRL
ETIOLOGY  Nerve to the elbow joint
- Pressure on the nerve D. Branches in the cubital fossa:
MANIFESTATIONS  A deep branch
- (+) Paralysis of the rhomboids  A superficial branch
- (+) Weakness of the levator scapulae (upper NOTE: Radial nerve is commonly damaged in the
part receives branches from C3 & C4) axilla & the spiral groove
- (+) Scapular drooping
6. SUPRASCAPULAR NERVE INJURY INJURIES TO THE RADIAL NERVE IN THE AXILLA
- Nerve root C5 – C6 - Nerve roots C5 – T1
ETIOLOGY ETIOLOGY
- Penetrating wounds & surgical procedures - Pressure from crutches toward the armpit
MANIFESTATIONS - Fractures & dislocations of the proximal end
- (+) Muscle paralysis of the humerus, at the spiral groove
- Stretch from inferior dislocations of the
7. NERVE TO SUBCLAVIUS INJURY humerus
- Nerve Root C5 MANIFESTATIONS
ETIOLOGY
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 - (+) paralysis of the muscles innervated by
the radial nerve MUSCULOCUTANEOUS NERVE TUNNEL SYNDROME
- Inability to extend the elbow, wrist joint & ETIOLOGY
fingers - Compression under the distal biceps tendon
- Loss of sensation down the posterior surface - Due to forced elbow hyperextension or
of the lower part of the arm & a narrow strip repeated pronation
on the back of the forearm MANIFESTATIONS
- Sensory loss over anterolateral forearm
- Loss of sensation in the hand & fingers
(radial nerve distribution)
13. THE MEDIAN NERVE
-
- Gives no branches at the level of the axilla &
INJURIES OF THE RADIAL NERVE IN THE SPIRAL
arm
GROOVE
ETIOLOGY - At the proximal 3rd in the anterior aspect of
- Fractures of the humerus the forearm: gives off the anterior
- Excessive pressure to the back of the arm interosseous branch that supplies all the
- “Honeymoon’s palsy” or “bridegroom’s muscles in the anterior compartment of the
palsy” forearm
MANIFESTATIONS - At the distal 3rd of the forearm:
- Inability to extend the wrist & the fingers - Gives off palmar cutaneous branch that
(wrist drop) crosses in front of the flexor retinaculum
- Loss of sensation of the hand & the fingers supplying the skin on the lateral half of the
supplied by the radial nerve palm
- In the palm:
ARCADE OF FROHSE - Innervates the thenar muscles & the 1st two
- Aka canal of Frohse lumbricals
- Aka radial tunnel syndrome - Also supplies the skin of the palmar aspect
ETIOLOGY of the lateral three & a half fingers as well as
- Spasm of the supinator mm
the nail beds
- Hypertrophy of the supinator mm
MANIFESTATIONS
INJURIES OF THE MEDIAN NERVE AT THE SHOULDER
- (+) Injury to the posterior interosseous
- Nerve roots C5 – C8 & T1
branch (wrist drop) ETIOLOGY
- (-) Sensory loss - TOS due to a cervical rib
- Spasm of the scalenes
INJURIES TO THE SUPERFICIAL BRANCH OF THE MANIFESTATIONS
RADIAL NERVE - Muscle paralysis
ETIOLOGY - (apelike hand)
- Stab wounds
- Forearm in a supinated position
- Compressed under the tendon of the
- Thumb is adducted
brachioradialis
- Weak wrist flexion with UD
MANIFESTATIONS
- Weak flexion at the IP joints by the
- Loss of sensation of the hand & the fingers
interossei
(radial nerve distribution)
- When making a fist, the ring & the little
- Aka “cheiralgia paresthetica” or
fingers flex while the middle & the index
“Wartenberg’s disease”
fingers remain straight (Benediction’s sign or
12. MUSCULOCUTANEOUS NERVE bishop’s sign)
- Nerve roots C5 – C6 - Loss of skin sensation of the lateral half of
ETIOLOGY the palm & palmar aspect of the lateral 3 &
- Rarely injured ½ fingers up to the nail beds
- Due to trauma - The skin areas involved are warmer & drier
MANIFESTATIONS than normal due to arteriolar dilatation
- (+) Muscle paralysis - There’s absence of sweating due to loss of
- Loss of sensation over the anterolateral side sympathetic control
of the forearm (antebrachial cutaneous - Nails crack easily
nerve)
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 - Atrophy of the pulp of the fingers involved
over time
INJURIES OF THE MEDIAN NERVE ABOVE THE ELBOW
ETIOLOGY
- (+) ligament of Struthers
- A rare anomalous structure
- Is attached from a bony spur to the medial
epicondyle
- Aka humerus supracondylar process
syndrome
MANIFESTATIONS
- Weakness or paralysis of the muscles
innervated by the median nerve
- Sensory involvement
14. PRONATOR TERES SYNDROME
ETIOLOGY
- An injury to the median nerve at the elbow
- Compression of the median nerve between
the two heads of the pronator teres muscle
MANIFESTATIONS
- Motor & sensory involvement
15. ANTERIOR INTEROSSEOUS NERVE SYNDROME
- Aka Kiloh Nevin syndrome
ETIOLOGY
- Forearm fractures (Monteggia fracture)
MANIFESTATIONS
- Pulp to pulp “ok sign”
- Paralysis of the:
a. Pronator quadratus
b. FPL
c. Lateral half of the FDP
d. 1st two lumbricals
- (+) Atrophy of the thenar muscles
16. CARPAL TUNNEL SYNDROME
- Carpal tunnel is formed by the concave
anterior surface of the carpal bones &
closed by the flexor retinaculum
ETIOLOGY
- Compression
- With Colle’s fracture
- Lunate dislocation
MANIFESTATIONS
- Weakness of the thenar muscles
- Burning pain or pins & needles sensation
worst @ night
- Normal sensation over the thenar eminence
since it is supplied by the palmar cutaneous
branch of the median nerve
17. INJURIES TO THE ULNAR NERVE
- No cutaneous or motor branches in the
axilla or the arm
- Enters the forearm behind the medial
epicondyle
- Supplies the FCU & medial half of the FDP
Palmar cutaneous branch
- In the distal 3rd of the forearm
- Supplies the skin of the hypothenar
eminence
- Passes in front of the flexor retinaculum &
enters the palm
Superficial branch
- Supplies the skin of the medial 1 & ½ fingers,
the nail beds & the palmaris brevis muscle
Deep branch
- Innervates all muscles of the hand except
the muscles of the thenar eminence & 1st
two lumbricals
INJURIES OF THE ULNAR NERVE AT THE SHOULDER
ETIOLOGY
- TOS
MANIFESTATIONS
- Motor problems
- Sensory affectation
INJURIES OF THE ULNAR NERVE AT THE ELBOW
- Aka cubital tunnel syndrome
ETIOLOGY
- Fractures of the medial epicondyle
MANIFESTATIONS
- Paralysis of the FCU & medial half of the FDP
- Flattening of the anterior aspect of the
forearm (medial)
- Wrist flexion will be accompanied by
abduction
- Inability to abduct & adduct the fingers
- Inability to grip a piece of paper placed
between the thumb & the index finger; to
hold the paper there will be substitution
from FPL & flexing the terminal phalanx
- (+) “claw hand deformity” (main en griffe) or
“intrinsic minus hand” due to paralysis of
the lumbricals & the interossei
- MCP hyperextension & IP flexion deformities
are more prominent in the ring & little
fingers
- Flattening of the hypothenar eminence;
dorsal part of the hand will exhibit hollowing
between the metacarpal bones
- Loss of skin sensation over the anterior &
posterior surfaces of the medial 3rd of the
hand & medial 1 & ½ fingers
- Skin areas affected will be warmer & drier
than normal due to arteriolar dilatation &
absence of sweating due to loss of
sympathetic control
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 - Pain is felt in the posterior aspect of the
18. CUBITAL TUNNEL SYNDROME thigh, posterior & lateral sides of the leg as
- Leads to “tardy nerve palsy” well as the lateral part of the foot
ETIOLOGY
19. INJURIES TO THE ULNAR NERVE AT THE WRIST - Prolapse of an IV disc
- At the Guyon’s canal or pisohamate canal - Intrapelvic tumors
ETIOLOGY - Inflammation of the sciatic nerve & its
- Hook of the hamate fractures
branches
- Pressure from handle bars (crutches)
- Frequent use of pneumatic jackhammers
23. INJURIES TO THE COMMON PERONEAL NERVE
MANIFESTATIONS - Nerve roots L4 – L5 & S1 – S2
- Paralysis & atrophy of the small muscles of
ETIOLOGY
the hand except for the 1st two lumbricals & - Fibular neck fractures
the thenar muscles - Pressure from casts or splints
- Claw hand deformity is more marked - “Cross leg palsy”
- Palmar cutaneous branch is commonly MANIFESTATIONS
involved - Muscle paralysis
- Equinovarus
20. INJURIES TO THE FEMORAL NERVE - Sensory loss in the anterior & lateral sides of
- Nerve Roots L2 – L4 the leg, dorsum of the foot & toes as well as
ETIOLOGY the 1st web space
- Stab wounds
- Gunshot wounds 24. INJURIES TO THE TIBIAL NERVE
MANIFESTATIONS - Nerve roots L4 – L5 & S1 – S3
- Paralysis of the quadriceps femoris muscle ETIOLOGY
- Action is compensated by the adductor - Rarely injured
muscles - Compression
- Sensory loss on the anterior & medial sides MANIFESTATIONS
of the thigh, Medial side of the leg, medial - Calcaneovalgus deformity
border of the foot until the ball of the big - Sensory loss on the sole of the foot
toe (saphenous nerve) - Possible complications: trophic ulcers

21. INJURIES TO THE SCIATIC NERVE 25. TARSAL TUNNEL SYNDROME

- Nerve roots L4 – L5 & S1 – S3 - Formed by the medial malleolus, calcaneus,
ETIOLOGY talus & deltoid ligament
- Piriformis syndrome ETIOLOGY
- Penetrating wounds - Compression due to valgus deformity
- Fractures of the pelvis - Chronic inversion
- Dislocations of the femur - Swelling
- Badly placed IM injections in the gluteal MANIFESTATIONS
region - Inability to invert & PF with inability to
MANIFESTATIONS abduct, flex & adduct the toes
- Paralysis of the hip extensors & knee flexors - Sensory loss over the sole of the foot, lateral
knee surface of the heel, & plantar surface of the
- Flexion is possible thru the sartorius & toes
gracilis
- Foot drop 26. INJURY TO THE MEDIAL PLANTAR NERVE
- Loss of sensation in the posterior aspect of - Aka jogger’s foot
thigh & below - Associated with hindfoot valgus
- Possible complications: trophic ulcers in the ETIOLOGY
sole of the foot - Compression in the medial longitudinal arch
of the foot
22. SCIATICA MANIFESTATIONS
- Refers to the condition wherein there’s pain - (+) burning, aching pain in the heel & sole of
along the sensory distribution of the sciatic the foot
nerve
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 - (+) paralysis of FDB, adductor hallucis, FHB & - Difficulty with activities of daily living (ADLs)
1st lumbrical
DIAGNOSIS
27. INJURIES TO THE OBTURATOR NERVE - NCV tests
- Nerve roots L2 – L4 • The conduction times for both motor &
ETIOLOGY sensory are slowed
- Rarely injured • Possibility of a complete conduction block
- Due to: - EMG
a) Penetrating wounds • Evidence of spontaneous fibrillation
b) Anterior dislocations of the hip joint potentials which is an indication of
c) Abdominal hernia through the obturator denervation atrophy
foramen • Sign of reinnervation presents a low
- “Obstetric palsy” amplitude, short duration, polyphasic motor
MANIFESTATIONS potentials
- Muscle paralysis
- Sensory loss on the medial aspect of the MEDICAL MANAGEMENT
thigh - Surgery: Such as surgical excision of a
neuroma formation
28. INJURY TO THE LATERAL FEMORAL CUTANEOUS - Nerve grafting or suturing
NERVE OF THE THIGH - Tendon resection
- Aka meralgia paresthetica
- Medications
- Nerve Roots L2 – L3
o Analgesics
ETIOLOGY
o Anti-inflammatory (corticosteroids)
- “Fat wallet syndrome”
- Antidepressants
MANIFESTATIONS
- Sensory loss on the anterolateral aspect of - Vitamin B12 supplements
the thigh - Alcohol or phenol injections
- Muscle weakness or paralysis
PT ASSESSMENT
- Hyporeflexia
- History taking: Onset of symptoms,
- Hypotonia
determine presence of metabolic disorders,
- Atrophy
pt’s lifestyle
- Sensory loss
- Skin inspection & palpation
- Autonomic dysfunction
- ROM
- Hyperexcitability of the remaining nerve
- MMT
fibers
- MBT
- (+) Fasciculations
- Neurologic assessment
- (+) Fyalgia
- Sensory & DTRs
PROGNOSIS - Posture assessment
- lLcation of the injury - Gait assessment
• The more proximal the injury, the less - Functional assessment
likelihood of nerve reinnervation
- Is also dependent on the: PT GOALS
- Reduce pain
• Age & overall condition of the pt
- Improve muscle strength
- Integrity of the supporting structures
- Increase ROM
• With an intact endoneurial tube,
- Promote pt education
prognosis is good
- Such as skin inspection
COMPLICATIONS - Promote independence in ADLs
- Skin ulcers - Assess if pt needs an assistive or orthotic
- Contractures device
- Decreased ROM - Improve muscular endurance
- Postural deformities
- Gait deviations PT MANAGEMENT
- Fatigue I. MODALITY:
- Pain management
- Decreased muscular endurance
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 • HMP; cold packs
• TENS
• IFC
• US
• ES
• Diadynamics
- Muscle weakness
- Contractures
• ES
• FES
• HMP
• IFC
• US
II. NON MODALITY:
- Decreased ROM
• Stretching Exercises
• Use of splints; proper positioning
- Muscle Weakness and Fatigue
• FIIT Principle
- Decreased cardiorespiratory endurance and
generalized fatigue
• Conditioning Exercises

MOTOR NEURON DISEASE

UMNL
Primary Lateral Sclerosis
Tropical Spastic Paraparesis
Lathyrism
Epidemic Spastic Paraparesis
Familial (hereditary) spastic paraplegia
LMNL
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 Acute Infantile Muscular Atrophy 3. Lathyrism
Chronic Infantile SMA - A disorder due to excessive consumption of
Juvenile SMA or BSMA chickling pea (lathyrus sativus)
Type IV - Prevalent among males
Type V - Endemic in the Indian subcontinent
Distal SMA 4. Epidemic Spastic Paraparesis
Charcot-Marie-Tooth Disease - Similar to tropical spastic paraparesis
CMTD I - Cause is known
CMTD II - Related to a viral or bacterial infection &
CMTD III nutritional problem
CMTD IV - Children are also affected
CMTD V 5. Familial (Hereditary) Spastic Paraplegia
CMTD VI - Usually transmitted as an AD disease
CMTD VII - Occasionally as AR
Bulbar Diseases of Childhood - Rarely as an X – linked recessive disease
Brown Violetto Van Laere syndrome - most of the cases: children are affected &
Fazio Londe disease early adulthood
Adult Forms of SMA or BSMA - Clinical Features:
Scapuloperoneal SMA A. Stiffness
Chronic BSMA of late onset B. Unsteadiness of the legs
Monomelic SMA C. Muscular atrophy
Poliomyelitis
Polio Virus b. TYPES OF LMNL
Paralytic Polio 1. Infantile Forms of Spinal or Bulbospinal Muscular
Guillain Barre Syndrome Atrophies
- Aka hereditary motor neuropathy
I.GENERAL MEDICAL BACKGROUND - Leads to degeneration of the anterior horn cells
A. DEFINITION
- Conditions that affect either the upper motor • Acute Infantile Muscular Atrophy
neurons (motor cortex, posterior limb of the - Aka Werdnig Hoffman disease
internal capsule, corticobulbar or - Type I SMA
corticospinal tracts) or lower motor neurons - ACUTE PROXIMAL HEREDITARY MOTOR
(bulbar nuclei, anterior horn cells of the NEUROPATHY (HMN)
spinal cord) or both resulting in motor - Most severe & most progressive type
dysfunction. - An AR disorder
- Pathognomonic Sign: open mouth & tongue
B .CLASSIFICATION fasciculation
A. UMNL - Age of Onset: in utero – 6 mo
B. LMNL - Age of Diagnosis: 3 mo
C. Combined - Certain or definite: 6 mo
- Lifespan: 6 – 9 mo, does not exceed 3 y/o
a. TYPES OF UMNL - Most common cause of death: respiratory
1. Primary Lateral Sclerosis failure
- A rare, non-familial slowly progressive - Developmental delays: inability to sit, stand
corticobulbar & corticospinal tract disease & walk
- Cause is unknown - Clinical Features:
- Equal distribution between males & females A. Hypotonia
- As to age: 20 – 60 y/o B. Areflexia
- Clinical Features: C. Intercostal & oropharyngeal mm
A. Spastic extremities, initially LE then UE paralysis
B. (+) urinary incontinence D. Impaired facial mm movements
C. Spastic dysphagia - Distribution of Weakness: LE
D. (-) EMG findings of denervation - Legs are abducted
E. (-) fasciculation - Pathogenesis is unknown
- Lifespan: 2 – 3 decades - Pathological Finding: severe loss of motor
- Important Findings: decreased Betz’s cells in neurons in the brainstem & spinal cord
area 4 & degeneration of CST
2. Tropical Spastic Paraparesis • Chronic Infantile SMA
- A rare disorder - Aka Chronic Werdnig Hoffman Disease
- Equal distribution between males & females - Type II SMA
- As to race, prevalent among blacks - Chronic Proximal HMN
- As to age: adulthood - Transmitted as an AR disorder
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 - (+) problem in chromosome 5q • Affects 150, 000 people in US
- Age of Onset: 3 y/o • Worldwide – 1:2500
- Age of diagnosis & definite: 3 y/o - -Etiology: mutations that cause defects in
- Lifespan: up to 3rd decade, median age of 12 neuronal proteins
y/o
- Developmental Delays: inability to walk A. CMTD I
- Most common cause of death: respiratory - Aka HSMN I
failure - AD
- Clinical Features: - Spinal form of CMTD
A. Proximal mm weakness, initially LE - Hypertrophic type
B. Mm atrophy - Characterized by segmental demyelination
C. Hyporeflexia or areflexia - Decreased NCV
- Complications: - (+) enlarged peripheral nerves known as
A. Scoliosis ‘onion bulbs’
B. Equinus deformities
- Pathogenesis: unknown B. CMTD II
- Pathologic Finding: severe loss of motor - Aka HSMN II
neurons in the brainstem & spinal cord - AD
- Axonal form of CMTD
2. Juvenile SMA or BSMA - Neuronal type of peroneal muscular atrophy
• Kugelberg Welander disease - Characterized by near normal or normal NCV
- Aka type III SMA - (+) Wallerian degeneration
- Aka Recessive proximal HMN
- AR C. CMTD III
- Etiology: unknown - Aka HSMN III
- Age of Onset: juvenile - Aka Dejerine Sottas
- Males > females - AR
- Lifespan: normal - Progressive hypertrophic neuropathy
- Clinical Features:
A. Symmetrical weakness & atrophy D. CMTD IV
of the pelvic girdle & proximal LE - Aka HSMN IV
B. Symmetrical weakness & atrophy - Aka Refsum’s disease
of the shoulder girdle & upper arms - AR
C. (+) Gower’s sign - Associated with abnormal phytamic acid
D. (+) waddling gait metabolism
E. Dysphagia & dysarthria
F. Fasciculations E. CMTD V
- aka HSMN V
• Type IV - AD
- Aka Dominant proximal HMN - associated with spinocerebellar
- AD degeneration
- Same as above
F. CMTD VI
• Type V - aka HSMN VI
- AD - associated with optic neuritis
- Age of onset: adulthood
- Same as above G. CMTD VII
- aka HSMN VII, associated with retinitis
• Distal SMA pigmentosa, loss of rods, degeneration of
- Aka Hereditary Sensory & Motor Neuropathy cones
- Aka Spinal form of Charcot Marie Tooth
Disease CLINICAL FEATURES OF CMTD
- Aka Distal HMN A. Peroneal muscular atrophy
- Age of onset: childhood to middle age B. Atrophy of intrinsic foot mm
- Progression of disease: slow with periods of C. Pes cavus
stability D. Foot drop/foot slap
E. Steppage gait
3. Charcot-Marie-Tooth Disease F. Mild sensory impairment
- A group of progressive disorders that affect G. Later stages: distal UE mm are involved
the peripheral nerves and result in problems
with movement and sensation. DIAGNOSIS of CMTD
- Epidemiology: - Standard medical history
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 - Family history C. Dysphagia
- Neurological examination. D. Tongue atrophy
- Suspected CMTD: Nerve Conduction Studies E. Intact bowel & bladder function
(electrodes placed on skin over a motor or
sensory nerve) and electromyography C. Monomelic SMA
(inserting a needle electrode through the - Aka segmental SMA
skin to measure the bioelectrical activity of - Non hereditary
muscles) - Focal or localized
- Unknown cause & pathogenesis
PROGNOSIS OF CMTD - Males > females
- Not considered a fatal disease and people - Clinical features:
with most forms of CMT have a normal life A. Weakness & atrophy in the legs, thigh,
expectancy. pelvis, shoulder, arm, neck & face mm
B. Spared cranial nerves, bowel & bladder
4. Bulbar Diseases of Childhood functions
A. Brown Violetto Van Laere syndrome
- Aka type I bulbar disease Diagnosis:
- AR • Genetic testing
- Unknown cause & pathogenesis • A physical examination
- Onset: 12 y/o • Personal medical history
- Lifespan: 2 decades after onset
• Family medical history
- Clinical features:
A. Initially, bilateral deafness • Laboratory tests, including genetic testing
B. Cranial nerve affectation (VII – XII), http://ghr.nlm.nih.gov/handbook/consult/diagnosis
occasionally (III, V & VI)
POLIOMYELITIS
B. Fazio Londe disease - Aka acute anterior poliomyelitis
- Aka type II bulbar disease - Aka infantile paralysis
- AR - Aka Heine Medin disease
- Unknown cause & pathogenesis - Highly communicable acute infection caused
- Age of onset: 2 y/o by a group of enteroviruses
- Lifespan: 8 – 9 y/o - The virus attacks primarily the GIT, then the
- Clinical features: nervous system
A. (-) deafness - The anterior horn cells of the gray matter
B. Affectation of all bulbar neurons (spinal cord & brain) are affected
- High risk individuals:
5. Adult Forms of SMA or BSMA A. Severely immunocompromised
A. Scapuloperoneal SMA B. Without vaccination
- Aka fascioscapulohumeral SMA - Prevalent among countries with poor health
- AD care systems
- Unknown cause & pathology - Average age of onset: 5 – 10 y/o
- Age of onset: 30 – 50 y/o - Children > adults
- Lifespan: normal - Males > females
- Clinical features:
A. Weakness & atrophy in the legs POLIO VIRUS
B. Spared intrinsic mm of the foot - Aka legio debilitans
C. Late stages: weakness & atrophy in the - A single stranded RNA
shoulder girdle mm, pelvic girdle, thigh, - Belongs to the enterovirus group of the
upper arm, neck & facial mm picornavirus family
D. (+) fibrillation & fasciculation - Has an affinity for motor neurons
- Similar to fascioscapuloperoneal muscular - Has 3 types:
dystrophy A. type I – aka Brunhilde
- Most frequent & most severe
B. Chronic BSMA of late onset B. type II – aka Lansing
- Aka Kennedy’s disease - Next most frequent
- X – linked recessive C. type III – aka Leon
- Unknown cause & pathology - Least frequent & severe
- Age of onset: 3rd – 6th decade
- Clinical features: PATHOPHYSIOLOGY
A. Weakness & atrophy initially in the - Oropharyngeal secretions/stools
shoulder & pelvic girdle mm - Ingestion (oral)
B. Dysarthria
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 - Viral multiplication in lymphoid - Cause of death: respiratory
tissue of pharynx & intestine involvement
- Viremia
- Nervous system affectation IMMUNITY
a. Salk’s vaccine
a. Sources of the virus o By Dr. Jonas Salk
1. Stools o Active immunization
2. Oropharyngeal secretions o Contains prototype strains of all
3. Contaminated water supplies virus types
4. Infected milk o For individuals with
immunodeficient diseases,
b. Mode of transmission lymphoma, leukemia, under
1. Fecal – oral corticosteroids or radiation
2. Oral – oral treatments
3. Mother – newborn b. Sabin vaccine
c. Incubation period: 7 – 14 days o Oral vaccination
o Contains live but weakened virus
CLINICAL TYPES o For infants, pregnant women
a. Inapparent
- Aka subclinical infection DIAGNOSIS
- Aka asymptomatic carrier type A. Oropharyngeal secretions
B. Stool
b. Abortive C. Blood samples
- Minor illness
- Nonspecific febrile illness MEDICAL SURGICAL MANAGEMENT
- Does not involve the CNS A. Correction of deformities
B. Surgery for contractures
c. Major poliomyelitis
1. Non paralytic POST POLIO SYNDROME
- Presents with tight neck, back & - Occurrence of new health problems several years
hamstring mm after acute poliomyelitis
- Transient paresis - New health problems:
- (+) meningeal irritation A. fatigue
- Lab findings: increase protein in CSF B. mm pain
C. joint pain
2. Paralytic polio D. weakness of previously affected &
- Involves the CNS unaffected mm
- Presents with asymmetrical weakness E. difficulty with walking, stair climbing &
- Urinary retention dressing
- Constipation - Fatigue is described as ‘hitting the wall’
- Cardiac arrythmias phenomenon
- Muscle soreness - Fatigue happens in mid late pm & improves with
- Headache rest
- Paresthesias - Significant risk factors:
- (+) meningeal irritation A. prolonged hospitalization
- Has 4 types: B. respiratory involvement
a. Spinal C. onset after 10y/o
- Most frequent D. severe & extensive poliomyelitis
- Cervical, thoracic & lumbar - Cause is unknown
segments are involved
b. Bulbar CLINICAL CRITERIA OF POLIOMYELITIS
- Most severe - by Halstead & Rossi
- Presents with facial weakness a. Confirmed history of paralytic polio
- Dysphagia b. Partial to fairly complete neurologic
- Dyspnea & functional recovery
c. Bulbospinal c. Neurologic & functional stability for
- Mixed type at least 15 years
d. Cerebral d. Onset of 2/more of the following
- Aka polioencephalitis health problems since achieving a
- Rare period of stability such as:
- unaccustomed fatigue
PARALYTIC POLIO - mm or joint pain
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 - new weakness in mm previously i. extraocular mm & sphincters are rarely
affected & unaffected affected
- functional loss
- cold intolerance COMBINED UMNL & LMNL
- new atrophy Amyotrophic Lateral Sclerosis (ALS)
e. No other medical diagnosis to - Aka Lou Gehrig’s disease
explain these health problems - A chronic progressive degenerative disease
- The benchmark of motor neuron disorders
DIFFERENTIAL DIAGNOSIS - is characterized by rapid degeneration &
Criteria GBS Polio demyelination of the giant pyramidal cells of
the cerebral cortex, CST, cell bodies of the
lower motor neurons in the gray matter,
location PNS PNS
anterior horn cells, precentral gyrus of the
cortex which results in degeneration,
structures myelin sheath anterior horn denervation of muscle fibers, muscle atrophy
involved cells & weakness
- Cause is unknown
cause idiopathic virus - Suspected causes: hereditary, virus,
metabolic
distribution symmetrical asymmetrical - Age of onset: 40 – 70 y/o
- Lifespan: 2.5 years
pattern distal – proximal – - Has several types:
proximal distal A. classic ALS
• most prevalent
pain common not common
B. familial ALS
• AD trait
sensory common (mild) rare
• age of onset: 46 y/o
symptoms
• lifespan: 2 – 12 years
C. Western pacific ALS – Parkinsonism
GUILLAIN BARRÉ SYNDROME dementia complex
 Aka acute inflammatory demyelinating • a combination of ALS, parkinsonism
polyradiculopathy & dementia
 Aka polyneuropathy or acute polyradiculitis D. postencephalitic ALS (encephalitis
 An acquired symmetrical polyneuropathy lethargica)
 Characterized by temporary inflammation & E. juvenile inclusion body ALS
demyelination of the peripheral nerves • rare
resulting in axonal degeneration that leads to
motor weakness & sensory impairments CLINICAL MANIFESTATIONS
 Cause is unknown, suspected cause is viral or A. asymmetric muscle weakness
bacterial infection - distal to proximal pattern
 Prevalent among young male adults B. mm cramps
 Age of onset: 5th – 6th decades C. mm atrophy usually involving the hands
 Whites > blacks D. fasciculations
 cause of death: respiratory mm involvement E. dysarthria
 prognosis: recovery is slow F. dysphagia
 has variants: G. emotional lability
a. Miller – Fisher H. fatigue
- triad of ataxia, opthalmoplegia, depressed I. respiratory involvement
DTRs J. incoordination
b. Landry’s paralysis K. hyperreflexia
- rapid progressive ascending paralysis L. spared bowel, bladder functions, intellect,
sensation & eye mm (voluntary)
CLINICAL MANIFESTATIONS - cause of death: respiratory failure
a. distal & symmetrical motor weakness
b. areflexia COMPLICATIONS:
c. bilateral facial weakness A. Contractures
d. respiratory mm paralysis B. Pressure ulcers
e. mild sensory impairments C. Pulmonary infection
f. transient paresthesias
g. cardiac arrhythmias DIAGNOSIS
h. cranial nerve affectation (VII, IX, X, XI) A. EMG

240 | P a g e
 B. muscle biopsy
C. spinal tap
D. CT scan
PT MANAGEMENT
Has 3 phases:
A. Phase I (indep)
1st stage:
- Ambulatory, indep in ADL, mild weakness
- Mgmt: ROM, strengthening, patient
education
2nd stage:
- Ambulatory with moderate selective
weakness & slightly decreased independence
- Mgmt: selective strengthening, stretching,
consider adaptive & assistive devices
rd
3 stage:
- Ambulatory but fatigues easily
- Mgmt: keep as indep as possible, DBEs,
consider continued use of adaptive or
assistive devices
B. Phase II (partially indep)
4th stage:
- Wheelchair bound with severe weakness in
the LE, with or without spasticity, with
moderate UE weakness, needs partial
assistance with ADLs, may have shoulder pain
& edema of the hand
- Mgmt: address pain, PROM, stretching ex,
isometric ex to intact mm
5th stage:
- Severe UE/LE weakness, strength continues
to decline, needs more assistance with ADLs,
complications may occur
- Mgmt: ROM, strengthening ex, patient &
family education regarding transfers &
positioning, consider environmental
modification
C. Phase III (totally dependent)
- Bedridden, completely dependent in ADL
- Mgmt: ROM, stretching ex, soft diet,
suctioning of the saliva, postural drainage
a. Spasticity and muscle cramps -
diazepam,baclofen, tizanidine, phenytoin and quinin
e
b. Respiratory distress – opioid medication
c. Depression – antidepressants
d. Pain – NSAIDs and opioids
e. Drooling – anticholinergic
APPLICABLE TO ALL
COMPLICATIONS
• Respiratory failure and death.
• Pneumonia due to infection or aspiration.
• Urinary tract infections.
• Constipation.
• Spasticity and cramping of muscles.
• Depression
• Loss of speech as a means of communication.
• Immobility and attendant disability.
• Complications of immobility such as skin
infections/bedsores and ulcers.
Cognitive deterioration is rare but is seen occasionally
PT EXAMINATION:
a. ROM
b. MMT
c. Mm tone
d. DTR’s
e. Cardiorespiratory endurance
f. Anthropometric characterisitics
g. Posture and Gait
h. Functional assessment
General Principles of Rehabilitation:
a. energy conservation techniques
b. activity pacing
c. splinting to prevent contractures
d. ROM exercise- utilization of PNF patterns &
techniques
e. Stretching exercises
f. Strengthening exercises
g. Pool therapy
h. Breathing exercises

ALS SMA Assistive Devices:

- Beginning: straight or quad canes
asymmetrical symmetrical - Progress to walker; rolling walkers are
beneficial to those with upper limb weakness
ascending descending - Wheelchair is considered for patients who
pattern of pattern can ambulate for only a short distance
weakness
UE affected LE affected Orthoses:
1st 1st - Cervical collar for neck extensor weakness
- AFO can allow safer ambulation for patients
with lower limb weakness and to stretch the
PROGNOSIS ankle plantar flexors
-About 30% of patients survive beyond five years
-Rapidly progressive and fatal

PHARMACOLOGIC TREATMENT:

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 - Balanced forearm orthosis – proximal upper
extremity weaknes

Problem List Plan of Care Intervention

Pain Hot packs
TENS
Muscle weakness Increase strength of muscles to Strengthening exercises
provide adequate strength for ADLs
LOM Increase range of motion AROM and PROM exercises
Contractures Increase flexibility Stretching exercises
splinting
Spasticity Decrease spasticity to provide Inhibitory techniques
adequate rom for ADLs
Impaired gait improve gait pattern to prevent falls Gait training
pattern and for better ambulation
Impaired respiration Improve respiration Breathing exercises
Postural drainage
Swallowing problem Improve swallowing for better food Adjustment of head position and
intake and decrease frustration, diet modification
anxiety and depression
Speech problem Improve speech for better Energy conservation techniques
communication and decrease Consult speech pathologist
frustration, anxiety and depression
Easily fatigues Energy conservation techniques
Activity pacing

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 NEUROMUSCULAR JUNCTION DISORDERS
Myasthenia Gravis
Myasthenic Syndrome
GENERAL MEDICAL BACKGROUND
Nerves connect with muscles at the
neuromuscular junction. There, the ends of
nerve fibers connect to special sites on the
muscle's membrane called motor end plates.
These plates contain receptors that enable the
muscle to respond to acetylcholine, a chemical
messenger (neurotransmitter) released by the
nerve to transmit a nerve impulse across the
neuromuscular junction. After a nerve
stimulates a muscle at this junction, an electrical
impulse flows through the muscle, causing it to
contract
Definition
- Abnormalities that occurs in the
connection between a nerve cell & the
mm fiber that it supplies due to
autoimmune reactions that result in mm
weakness
A. Myasthenia Gravis
Definition
- A chronic autoimmune disease
characterized by weakness & fatiguing
of some or all mm groups
- Weakness worsens as a result of
sustained or repeated exertion or
towards the end of the day & is relieved
by rest
- Often associated with thymoma (tumor
originating from the epithelial cells of
the thymus. Thymoma is an uncommon
tumor, best known for its association
with the neuromuscular disorder
myasthenia gravis)
- Common among females
- Increase predilection with young adults
- Due to autoimmune destruction of
nicotinic postsynaptic receptors for Ach
- An autoimmune disorder, in which
weakness is caused by circulating
antibodies that block acetylcholine
receptors at the postsynaptic
neuromuscular junction, inhibiting the
excitatory effects of the
neurotransmitter acetylcholine on
nicotinic receptors throughout
neuromuscular junctions (Wikipedia)
Classification
- Type I
• Ocular myasthenia
• With slow progression
• With very good prognosis
- Type IIA
• Mild, generalized weakness
• With slow progression
• With good reaction to drugs
- Type IIB
• Moderate generalized weakness
• With bulbar involvement
• (+) Diplopia & ptosis
• (+) Respiratory involvement
• Poor prognosis
- Type III
• Acute fulminating
• Rapid progression
• With respiratory involvement
• With poor response to drugs
- Type IV
• Same as type III
• Also with respiratory involvement
• Progresses to type I – II in 2 years
Epidemiology
- Occurs in all ethnic groups and both
sexes
- Commonly affects women under 40
and people from 50 to 70 years old of
either sex
- Three types of myasthenic symptoms in
children can be distinguished:
• Neonatal (mother’s antibodies
with MG)
• Congenital
• Juvenile myasthenia gravis
(occurring in childhood, but after
the peripartum period)
Etiology
- In adults with myasthenia gravis, the
thymus gland remains large and
abnormal –indicative of thymoma
- Contains clusters of antibodies which
are indicative of lymphoid hyperplasia-
indicative of immune response
- Antibodies block, alter, or destroy the
receptors for acetylcholine at the NMJ
- Preventing the muscle contraction from
occurring
- No causative pathogen that could
account for myasthenia
Pathophysiology
Autoimmune channelopathy
Antibodies from the thymoma act against the
nicotinic acetylcholine receptor by blocking the
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 channels, the receptor in the motor end plate
that stimulates muscle contraction
Impair the ability to bind with sodium ions or
destruction of the receptors
Decrease number of functioning receptors limits
the depolarization of the muscle
Impairment of muscle contraction
Clinical Manifestations
- Muscle weakness or fatigability – mm
progressively weakens during activity
and improve after rest
- Slurred speech with nasal twang
- Possible dysphagia and facial mm
paresis involvement (myasthenic snarl)
- Most cases, first noticeable symptom is
weakness of the eye muscles (Ocular
Myasthenia)
- Affected: eye control, talking,
swallowing, breathing, neck, and limb
muscles
- Hallmark: post exertional mm weakness
- Post exertional mm weakness:
• Muscle weakness due to repetitive
movements
• Prolonged static muscle tension
• Forceful gross
movements
Complications (Secondary to Clinical
Manifestation)
- Ocular Myasthenia:
• Asymmetrical ptosis (drooping of
one or both eyelids)
• Diplopia (double vision)
- Others:
• Waddling gait
• Weakness in arms, hands fingers,
legs, and neck
• Change in facial expression
• Dysphagia (difficulty in swallowing)
• Shortness of breath
• Dysarthria (impaired speech, often
nasal due to weakness of the velar
muscles)
Complications
Complications of myasthenia gravis are
treatable, but some can be life-threatening.
- Myasthenic crisis - a life-threatening
condition, which occurs when the
muscles that control breathing become
too weak to do their jobs.
- Thymus tumors – mostly noncancerous
- Underactive or overactive thyroid
- Lupus - a disease in which your immune
system attacks certain parts of your
body. Common symptoms include
painful or swollen joints, hair loss,
extreme fatigue and a red rash on the
face.
- Rheumatoid arthritis - a type of arthritis
is caused by problems with your
immune system. It is most conspicuous
in the wrists and fingers, and can result
in joint deformities that make it difficult
to use your hands
Diagnosis
- Physical Examination
• Looking upward and sideward for 30
seconds: ptosis and diplopia
• Looking at the feet while lying on
the back for 60 sec
• Hold arms stretched forward for 60
sec
• Ten deep knee bends
- Blood Test
• test for antibodies against the
acetylcholine receptor
- Electro diagnostics
• Stimulation of nerve-muscle motor
unit with short sequences of rapid,
regular, electrical impulses, before
and after exercising the motor unit,
the fatigability of the muscle can be
measured.
- Ice Test
• Application of ice to weak muscle
groups leads to improvement in
strength in normal muscles
- Edrophonium Chloride Test
• Uncommon and is the last resort for
diagnosis
• Requires intravenous administration
of edrophonium chloride or
neostigmine which block the
breakdown of acetylcholine by
cholinesterase and temporarily
increases the levels of acetylcholine
at the NMJ
• (+) improvement of strength during
fatigue
Differential Diagnosis
Myasthenia Gravis Myasthenic
syndrome
Postsynaptic Presynaptic
Associated with Associated with lung
thymoma carcinoma
Females > males Mates > Females
Decrementing Incrementing
response to RNS response to RNS
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 (+) with tensilon or - MMT
mestinon test - Posture
- Fatigue – Modified Fatigue Impact Scale
Prognosis (MFIS)
- With treatment, pt have normal life - Gait, Locomotion, balance – wheelchair
expectancy skills, orthotic and assistive devices
- Malignant thymoma – itself lessens life - Aerobic capacity and endurance
expectancy - Functional Assessment – FIM
- Drugs used to control MG either
diminish in effectiveness over time or Problem List
can cause side effects. - Breathing difficulty
- Thymectomy – effective treatment with - Weakness of limb and other muscles
long-term remission. and fatigability
- Visual changes: Double vision, difficulty
Medical / Surgical / Pharmacologic Management maintaining gaze, and drooping eyelids
- Medication: - Gait changes
• Acetylcholinesterase inhibitors: - Speech and feeding problems
neostigmine and pyridostigmine - Psychosocial issues
 Improve muscle function by
slowing the natural enzyme Physical Therapy Diagnosis
cholinesterase that degrades - Difficulty breathing. Impaired muscle
acetylcholine in the motor end function, vision, gait, communication,
plate; the neurotransmitter is and feeding
therefore around longer to
stimulate its receptor. Plan of Care & Intervention
• Immunosuppressive drugs: Problem Plan of Intervention Rationale
prednisone, cyclosporine, List Care
mycophenolate mofetil and Breathing Relieve Home Improve
azathioprine difficulty difficulty program respiratory
 Treated with a combination of in training in muscle strength,
these drugs with an breathing diaphragmatic chest wall
acetylcholinesterase inhibitor breathing, mobility,
- Surgical: pursed lip respiratory
• Thymectomy breathing pattern, and
 Surgical removal of the thymus, respiratory
essential in cases of thymoma in endurance.
view of effects of the tumor. Weakness Strengthe Free weight Emphasizing
of limb n the strengthening more on
Other Rehabilitative / Supportive and other muscles of muscles repetition than
- Patient & family education muscles and emphasizing intensity will
- Consider use of adaptive equipment or and prevent more on develop muscle
Assistive devices fatigability fatigue repetition endurance thus
- Point out submaximal exercises or than intensity reduce if not
activities prevent
- Emphasize rest occurrence of
- Inspiratory muscle therapy: fatigability
diaphragmatic breathing, pursed lip Visual Correct Strengthen Develop eye
breathing Changes visual ocular and control and visual
changes extra ocular functions
Points of Emphasis in Examination muscles: eye
- Cognitive gazing and
- Affective and psychosocial tracking
- Sensory integrity exercises,
- Visual stimulation of
- Pain –McGill Pain Questionnaire and extra ocular
VAS muscles with
- CN integrity ES
- ROM

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Gait Correct Ambulation Develop proper - Weakness of proximal LE mm 1st then
changes gait exercise: gait and UE
changes crutch, walker, ambulation - Fatigue
or wheelchair; performance - Dry mouth
use of orthosis - Sexual dysfunction
can be - Areflexia
necessary - Improvement in mm power after brief
Speech, Improve Correct Integrate exercise
feeding communic posture to socializing and - Occasional bulbar signs (ocular mm)
problems, ation and improve the communication
and nutrition feeding which would Complications
psychosoc process. prevent - Cancer is found in 40% of patients
ial issues Stimulation depression and (usually small-cell carcinoma of the
techniques promote lungs
such as icing nutrition by Also associated with:
on the functioning of the • Lymphosarcoma
muscles muscles e.g. • Carcinoma
affected for pharynx of breast, stomach, colon, prost
speech or ate, bladder, kidney or
feeding. gallbladder

B. Myasthenic Syndrome Diagnosis

GENERAL MEDICAL BACKGROUND
Definition
- It is an autoimmune disorder
characterized by failure of release of
Ach on the neuromuscular junction. It is
also known as Eaton Lambert Syndrome
and it is associated with malignancy of
the lungs (bronchial carcinoma).
Epidemiology
- Common among males
- Increase predilection with middle age
Etiology
- Pre synaptic disorder of neuromuscular
transmission in which insufficient
release of acetylcholine (ACh)
- Autoimmune disease
- Known patients without history of
malignancy frequently have elevated
serum levels of organ-specific
autoantibodies
Pathophysiology
- Autoantibodies attacking Ca2+ gated
channels of presynaptic terminal
- Ca2+ is needed for the release of Ach
from the vesicles inside the presynaptic
terminal
- This will therefore lead to reduce in the
release of Ach without any impact on
the number of Ach receptors
Clinical Manifestations
- Incrementing response with repetitive
supramaximal nerve stimulation (RNS)
- Second wind phenomenon
Differential Diagnosis
- Myasthenia gravis.
- Acute or chronic inflammatory
demyelinating polyradiculopathy.
- Dermatomyositis/polymyositis
- Inclusion body myositis.
- Spinal muscular atrophy
Prognosis
- This depends mainly on the presence
and nature of any underlying
malignancy, or the severity of any
associated autoimmune disease
- Maximum severity is usually established
within months of first symptoms
appearing. Exacerbations may occur
secondary to intercurrent illness and
drugs that affect neuromuscular
transmission, e.g. anesthetic.
- Most patients find therapy may help to
relieve symptoms partially; however,
usually symptoms progress over time.
Medical / Surgical / Pharmacologic Management
- Removal of neoplasm
- Plasma exchange
- Steroids
- Medications that enhance the release of
Ach
Points of emphasis in Examination
- ROM

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 - MMT
- Sensory integrity
- Reflexes
- Visual Function
- Balance
- Gait Pattern
- Posture

Problem List
- Muscle weakness
- LOM
- Impaired balance
- Diminished visual functions
- Gait changes

Physical Therapy Diagnosis

- Muscle weakness, decreased ROM,
areflexia, decreased visual function,
disturbed balance, gait and posture 2°
Myasthenic Syndrome.

Plan of Care & Intervention

PROBLEM PLAN OF CARE INTERVENTION

LIST
Muscle Increase strength Facilitatory Techniques
weakness (Roods, PREs,
strengthening exercises)
LOM Increase ROM to PROM progress to AAROM
maintain joint then AROM
mobility
Impaired Improve balance Balance exercises
balance in standing, sitting (perturbations, static and
and other dynamic positions in even
functional and uneven surfaces,
positions reaching activities, etc.)
Diminished Correct visual Strengthen ocular and
visual changes extra ocular muscles: eye
functions gazing and tracking
exercises, stimulation of
extra ocular muscles
Gait Correct gait Ambulation exercise:
changes deviations crutch, walker, or
wheelchair; use of orthosis
can be necessary

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