NEUROMUSCULAR CONDITIONS REVA COMPILATION

VELEZ COLLEGE PHYSICAL THERAPY BATCH 2022

CEREBROVASCULAR ACCIDENT neurological deficit after

admission to hospital and a
deteriorating stroke
WHAT’S INSIDE o Completed Stroke
▪ Has stable signs and present
with the all total neurological
1. Vertebrobasilar Artery Syndrome deficits at the onset
2. Brainstem Strokes ◊ Management Category:
3. Ischemic Stroke o Major stroke
4. Hemorrhagic Stroke ▪ Presence of stable, usually
5. Internal Carotid Artery Syndrome severe, impairments.
6. Anterior Cerebral Artery Syndrome o Deteriorating stroke
7. Middle Cerebral Artery Syndrome ▪ Used to refer to the patient
8. Posterior Cerebral Artery Syndrome whose neurological status
deteriorates after admission to
the hospital.
o Young stroke
VERTEBROBASILAR ARTERY SYNDROME ▪ Used to describe a stroke
affecting persons younger than
GENERAL MEDICAL BACKGROUND age 45.

DEFINITION RISK FACTORS

◊ The vertebral arteries arise from the subclavian
◊ Non-Modifiable
arteries and travel into the brain along the
medulla where they merge at the inferior border o Previous hx. of stroke (especially TIA, is
of the pons to form the basilar artery a warning for a certain type of stroke)
◊ Vertebrobasilar insufficiency is a condition o Race
characterized by poor blood flow to the posterior o Age (most common and most
(back) portion of the brain, which is fed by two importance): 73% of CVA patients are
vertebral arteries that join to become the basilar >65 y/o
artery o Gender
o Genetic predisposition
EPIDEMIOLOGY o Transient ischemic attack
◊ Modifiable
◊ 3rd leading cause of death (after heart dse. & o Diabetes Mellitus & Metabolic Syndrome
cancer) o Obesity
◊ Leading cause of long-term disability among o Smoking
adults in the US o Hyperlipidemia
◊ If over 85 y/o, F > M o HTN (most common risk factor for all;
◊ African Americans > Whites common in hemorrhagic stroke)
◊ Rates are high in Mexican-Americans, o Heart disease (Rheumatic vulvar dse.,
American-Indians, & Alaska Natives Endocarditis, Arrhythmias, Post-op
◊ Old > young cardiac surgeries)
◊ Occurs more in evenings because of sluggish ◊ Primary
blood flow at night o HTN
◊ 5% for women & 14% for men recurrence within o Cardiac dse. or arrhythmias
1 yr o DM
o Cigarette smoking
ETIOLOGY o TIA
◊ Atherosclerosis ◊ Secondary
o Obesity
◊ Cerebral thrombosis
o High cholesterol
◊ Cerebral embolus
o Behaviors related to HTM (stress,
◊ Low systematic perfusion
excessive salt intake)
◊ Significant blood loss with resulting hypotension
o Physical inactivity
◊ Hemorrhage
o Increased alcohol consumption
◊ Arteriovenous malformation (AVM)
◊ Temporal Types:
o Transient Ischemic Attack:
▪ Transient ischemic attack (TIA)
refers to the temporary
interruption of blood supply to
the brain.
o Reversible Ischemic Neurologic Deficit
(RIND)
▪ Secondary to brain swelling and
reversed within 3 weeks
o Stroke in Evolution
▪ Caused by thrombus that
gradually progresses and total
neurological deficits are not yet
seen for 1 or 2 days,progressive
 affectation of bulbar
nuclei
● Classic presentation of
PATHOMECHANICS / PATHOPHYSIOLOGY crossed anesthesia
◊ The most common vascular condition affecting ● Ocular tilt reactions
the vertebrobasilar system is atherosclerosis
o The pathology of small vessel (affecting Medial Superior Pontine Syndrome - occlusion of
arteries 50-200 µm in diameter) is paramedian branches of upper basilar artery
different from that of atherosclerosis, S/sx. Structures Involved
because the small vessels become Cerebellar ataxia Superior or middle
occluded by a process called cerebellar peduncle
lipohyalinosis, which frequently occurs Internuclear Medial longitudinal
in association with hypertension opthalmoplegia fasciculus
o Occlusions of these small vessels lead C/L paralysis of face, UE, Corticobulbar tract &
to small, round infarctions called & LE Corticospinal tract
lacunes, which may appear as single
lesions or may be distributed as multiple Lateral Superior Pontine Syndrome - occlusion of
lesions scattered widely throughout the paramedian branches of upper basilar artery
subcortex & brainstem S/sx. Structures Involved
◊ Lipohyalinosis weakens the vessel wall, and in
Ipsilateral cerebellar Middle and superior
hypertensive individuals, rupture of the artery
ataxia of limbs & gait, cerebellar peduncles,
may occur, resulting in a focal hemorrhage
falling to side of lesion superior surface of
o Almost all intracerebral hemorrhages
cerebellum, dentate
originate from the rupture of these small,
nucleus
penetrating vessels
Dizziness, nausea, Vestibular nuclei
◊ Because of the close anatomical relationship
vomiting
between the vertebral arteries and the cervical
spine, chiropractic manipulation or neck rotation Horizontal nystagmus
may traumatize the vertebral arteries in the neck Ipsilateral paresis of Uncertain
o The damaged arteries may occlude with conjugate gaze
thrombus or undergo dissection Loss of optokinetic
◊ Embolic occlusion of the vertebrobasilar system nystagmus
is not common and usually is artery-to-artery Homer’s syndrome: Descending fiber tracts
with occlusion of the basilar artery miosis, ptosis, decreased
o Donor sites for the emboli typically are sweating on opposite side
the aortic arch, the subclavian artery, face
and the origin of the vertebral arteries C/L to lesion: Spinothalamic tract
Impaired pain & thermal
CLASSIFICATION sense of face, limbs, &
trunk
Vertebrobasilar Artery Syndrome Impaired touch, vibration, Medial lemniscus (lateral
SICA & position sense more on portion)
S/sx. Structures Involved LE than UE (tendency to
● Ipsilateral ptosis ● Midbrain affectation incongruity of pain & touch
● Ataxia ● CN III-IV deficits)
● VertigoNystagmus
● C/L sensory loss of Medial Midpontine Syndrome (Foville) - occlusion of
face and body paramedian branch of midbasilar artery
● Transient chorea S/sx. Structures Involved
● Loss of pain and temp Ipsilateral ataxia of limbs Middle cerebellar
● C/L supranuclear facial & gait (more prominent in peduncle
palsy bilat. movement)
C/L paralysis of UE & LE CBT & CST
AICA Deviation of eyes CN VI, medial longitudinal
S/sx. Structures Involved fasciculus
● Vertigo ● Pons
● Nystagmus ● CN V-VIII Lateral Midpontine Syndrome (Marie Foix) - occlusion of
● Internal strabismus short circumferential artery
● Ipsilateral facial S/sx. Structures Involved
anesthesia & palsy Ipsilateral ataxia of limbs Middle cerebellar
● Hyperacusis peduncle
● C/L hemiparesis Paralysis of muscles of Motor fibers or nucleus of
mastication CN V
PICA note: motor function of CN
S/sx. Structures Involved V is the innervation of
● Vertigo ● Medulla oblongata TIME muscles (muscles of
● Nystagmus ● CN V, VIII-XII mastication)
● Dysphonia & Impaired sensation ver Sensory fibers or nucleus
dysphagia d/t side of face of CN V

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Medial Inferior Pontine Syndrome - occlusion of the C/L chorea, incoordination Red Nucleus
paramedian branch of basilar artery C/L Ataxia Superior Cerebellar
S/sx. Structures Involved Peduncle
Ipsilateral paralysis of Pontine center for lateral
conjugate gaze to side of gaze parapontine reticular MEDULLA:
lesion (preservation of formation (PPRF) - Medial Medullary Syndrome (Dejerine) -occlusion of
congruence) horizontal gaze center vertebral artery, medullary branch
Nystagmus Vestibular nuclei & S/sx. Structures Involved
connections Ipsilateral paralysis with CN XII
Ataxia of limbs & gait Middle cerebellar atrophy of half of the
peduncle tongue with deviation to
Diplopia on lateral gaze CN VI (innervates the the paralyzed side when
lateral rectus) tongue is protruded
note: if the affectation was C/L paralysis of UE & LE CST
the CN IV, the diplopia C/L hemisensory loss Medial Lemniscus
vertical (vertical
diplopia); because CN IV Lateral Medullary (Wallenburg’s) Syndrome- occlusion of
innervates the superior posterior inferior cerebellar artery or vertebral artery
oblique muscle S/sx. Structures Involved
C/L paresis of face, UE, & CBT & CST in lower pons Decreased pain & Descending tract &
LE temperature sensation on nucleus of CN V
Impaired tactile & Medial lemniscus the ipsilateral face
proprioceptive sense over Cerebellar ataxia: gait & Cerebellum or inferior
50% of the body limb ataxia cerebellar peduncle
Vertigo, nausea, vomiting Vestibular nuclei &
Lateral Inferior Pontine Syndrome (Millard Gubler) - Nystagmus connections
occlusion of AICA, a branch of basilar artery Horner’s Syndrome: Descending sympathetic
S/sx. Structures Involved miosis, ptosis, decreased tract
Ipsilateral horizontal & CN VIII sweating of face
vertical nystagmus, Dysphagia & dysphonia: CN XI & CN X
vertigo, nausea, vomiting paralysis of palatal &
Facial paralysis CN VII laryngeal muscles,
Paralysis of conjugate Pontine center for lateral diminished gag reflex
gaze to side of lesion gaze (PPRF) (nucleus ambiguus)
Deafness, tinnitus CN VIII Ipsilateral CN XI & XII CN XI & XII
Ataxia Middle cerebellar palsy (Uvula deviation
peduncle & cerebellar towards good side)
hemisphere Sensory impairment of Cuneate & gracile nuclei
Impaired sensation over Main sensory nucleus & ipsilateral UE, trunk or LE
face descending tract of CN V C/L impaired pain & Spinal lemniscus- STT
C/L impaired pain & STT (spinothalamic tract) thermal sense over 50%
thermal sense over half of body, sometimes face
the body (may include
face) BRAINSTEM STROKES:
BENEDIKT- tegmentum of the midbrain
Complete Basilar Artery Syndrome (Locked-In S/sx. Structures Involved
Syndrome) - basilar artery, ventral pons Ipsilateral CN III palsy, CN III
S/sx. Structures Involved ptosis
Tetraplegia (quadriplegia) CSTs bilaterally C/L loss of pain, Medial Lemniscus
Bilat. cranial nerve palsy: Long tracts to CN nuclei temperature, joint &
upward gaze is spared bilaterally position sense
Coma Reticular activating C/L chorea, incoordination Red Nucleus
system C/L Ataxia Superior Cerebellar
Cognition is spared Peduncle

MIDBRAIN: LOCKED IN- Bilateral Basal Pons

WEBER Syndrome- occlusion of the medial basal S/sx. Structures Involved
midbrain Bilateral hemiplegia CST
S/sx. Structures Involved Bilateral CN palsy CST
Ipsilateral CN III palsy CN III Spared Upward Gaze
C/L hemiplegia CST
MILLARD-GUBLER- lateral pons
BENEDIKT- occlusions at the tegmentum of the midbrain S/sx. Structures Involved
S/sx. Structures Involved Ipsilateral CN VI palsy CN VI
Ipsilateral CN III palsy, CN III Ipsilateral facial weakness CN VII
ptosis C/L hemiplegia CST
C/L loss of pain, Medial Lemniscus
temperature, joint & MARIE FOIX- lateral pons
position sense S/sx. Structures Involved
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C/L hemiplegia CST ◊ Osteoporosis, fall & fx. risk
Ipsilateral Ataxia ◊ Musculoskeletal
o Contractures
OTHER BRAINSTEM STROKES: o Heterotrophic ossification
Syndrome Location S/sx o Shoulder-Hand Syndrome (occurs
Raymond Ventral Pons Incoordination 2nd-4th mo. after stroke)
Ipsilateral Ataxia o Associated reactions
C/L hemiparesis
Foville’s Inferior medial Ipsilateral facial MEDICAL DIAGNOSIS
pons palsy ◊ Cerebrovascular Imaging
C/L hemiplegia o Main tool to establish the diagnosis of
Loss of suspected ischemic stroke and to rule
conjugate gaze out hemorrhagic stroke and other types
Dejerine Medial Medulla Ipsilateral of central nervous system (CNS) lesions
hypoglossal (e.g., tumor or abscess)
palsy ◊ Computed Tomography (CT Scan)
C/L hemiparesis o Most commonly used and readily
C/L lemniscal available neuroimaging technique. CT
sensory loss resolution allows identification of large
Wallenburg Lateral Medulla OTR (triad: arteries and veins and venous sinuses.
ocular torsion, o In the subacute phase, CT scans can
head tilt to the delineate the development of cerebral
R, skew edema (within 3 days), which then fades
deviation) over the next 2 to 3 weeks. Cerebral
Uvula deviation infarction (within 3 to 5 days) is visible
towards good with the addition of contrast material by
side showing areas of decreased density.
Dysphagia, ◊ Magnetic Resonance Imaging (MRI)
dysphonia o More sensitive in the diagnosis of acute
Ipsilateral Ataxia strokes, allowing detection of cerebral
Ipsilateral facial ischemia as early as 30 minutes after
anesthesia vascular occlusion and infarction within
C/L loss of pain, 2 to 6 hours.
temperature, o It is also able to detail the extent of
light touch of the infarction or hemorrhage and can detect
body- crossed smaller lesions than a CT scan.
anesthesia o Use of contrast enhancement allows
Ipsilateral documentation of changes in an infarct
Horner’s over the first 2 to 3 weeks.
syndrome- facial ◊ Magnetic Resonance Angiography
anhidrosis, o Used to identify vascular abnormalities
enophthalmos, (e.g., stenosis), and alterations in blood
ptosis, miosis flow as a result of embolus or
thrombosis.
◊ Doppler Ultrasound
CLINICAL PRESENTATION o Used to examine the carotid arteries
◊ Visual impairments and typically precedes carotid
◊ Ipsilateral ptosis endarterectomy.
◊ Ataxia ◊ Arteriography
◊ Vertigo o An x-ray of the carotid artery with a
◊ Nystagmus special dye injected into an artery in the
◊ C/L sensory loss of face and body leg or arm.
◊ Transient chorea ◊ Digital Subtraction Angiography
◊ Loss of pain and temp o An x-ray of the carotid artery with less
◊ C/L supranuclear facial palsy dye used. These procedures are
considered invasive and carry a small
COMPLICATIONS risk of causing a stroke
◊ Altered consciousness (coma, decreased
DIFFERENTIAL DIAGNOSIS
arousal levels)
◊ Aphasia
CVA TBI
o Fluent aphasia (Wernicke’s)
o Non-Fluent aphasia (Broca’s) Sudden trauma
Vascular
o Global aphasia Etiology from external
complication
o Conduction aphasia force
◊ Verbal apraxia Sudden, Acquired,
Onset
◊ Dysarthria progressive non-progressive
◊ Seizures Age 40 y/o onwards 15-25 y/o
◊ Bladder & bowel dysfunction Blood Concussion
◊ Cardiovascular & pulmonary dysfunction Pathophysiology turbulence assoc. c DAI
◊ DVT & pulmonary embolism leading to (diffused axonal
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 intimal wall injury), focal
damage injury & coup &
counter coup; Cerebellum Spinal Cord
hemorrhage Diagnosis/ Tumor, stroke Trauma, tumor,
Vomiting, LOC, Pathology vascular insult:
Loss of motor aggression, complete,
function, behavioral incomplete SCI
Sensation Not affected Impaired or
sensation, changes,
Clinical absent below level
weakness, CN seizures, battle’s of lesion
Manifestation
involvement, sign, raccoon’s Tone Normal, may be Hypertonia/
seizures, eyes, PTA decreased spasticity below
neglect (post-traumatic the level of lesion
amnesia) Initial flaccidity:
Unilateral or spinal shock
Involvement Bilateral Reflexes Normal, may be Hyperreflexia
bilateral
Usually not decreased
Cognition impaired, (-) May be impaired Strength Normal or weak; Impaired or
asthenia absent below level
gestures
of lesion;
Loss of paraplegia or
N°, may be
conjugate eye paraparesis;
Visual accompanied c
movement, tetraplegia or
visual neglect
nystagmus tetraparesis
Speech & Aphasia may be Muscle Bulk Normal Disuse atrophy
N°, slurred
Hearing present Involuntary None Spasms
Recover Movements
Depending on
Prognosis depending on Voluntary Ataxia: intention Normal above
GCS & RLA tremor, dysdiadoc- level of lesion
severity of CVA Movements
hokinesia, Impaired or
dysmetria, absent below level
Comparison of Major Types of CNS Disorder
dyssynergia, of lesion
Cerebral Basal Ganglia nystagmus
Cortex Postural Truncal ataxia Impaired or
Corticospinal Control Impaired balance absent below level
Tracts of lesion
Diagnosis/ Stroke Parkinson’s Impaired balance
Pathology disease Gatit Ataxic gait deficits. Impaired or
Sensation Impaired or Not affected wide-based, absent: depends
absent; depends unsteady on level of lesion
on lesion location;
C/L sensory loss
Tone Hypertonia/spastic Lead-pipe rigidity: PROGNOSIS
ity increased, uniform
velocity-dependen resistance ◊ Typically, the first 3 months of recovery is the
t; clasp-knife initial Cogwheel rigidity: most important time – it’s the Golden Period for
flaccidity; cerebral increased, treatment of CVA pt.
schock ratchet-like ◊ Pt. has poor prognosis of neurologi activity if pt.
resistance has:
Reflexes Hyperreflexia Normal or may be o Previous hx. of stroke
decreased
o Old age
Strength C/L weakness or Disuse weakness
paralysis; in chronic stage o Visuospatial defect
hemiplegia or o Urinary incontinence
hemiparesis; ◊ Pt. has poor prognosis of functional recovery if
disuse weakness pt. has:
in chronic stage o Prolonged flaccidity
Muscle Bulk Normal during Normal or disuse o Late onset of rigidity and DTR around
acute stage; atrophy 2-4 weeks following stroke
disuse atrophy in o No voluntary hand movement by 4-6
chronic stage after stroke
Involuntary Spasms Resting tremor o Severe proximal spasticity
Movements
Voluntary Dyssynergic: abn. Bradykinesia or GENERAL HEALTHCARE MANAGEMENT
Movements timing, akinesia
co-activation,
fatigability MEDICAL MANAGEMENT
Postural Impaired or Impaired: stooped ◊ Diet restriction/lifestyle modifications
Control absent, depends (flexed)
◊ Fluid & electrolyte balance
on lesion location; Impaired balance
impaired balance ◊ Oxygenations (to improve perfusion)
Gatit Impaired; gait Shuffling, ◊ Blood pressure management
deficits d/t abn. festinating gait ◊ Glucose level management
weakness, ◊ Control seizures & infection
synergies,
spasticity, timing SURGICAL MANAGEMENT
deficits
5
 ◊ CABG
POINTS OF EMPHASIS ON EXAMINATION
◊ Embolectomy
◊ Endarterectomy
◊ Craniotomy General Points of Examination
◊ Craniectomy ◊ Subjective
◊ Ventriculostomy ◊ Pain
◊ Cognition
PHARMACOLOGICAL MANAGEMENT ◊ Perception
◊ Behavior
◊ Signs of increased intracranial pressure
Medication Function
◊ Level of consciousness
◊ Emotional status & behavior
Hyperosmolar agents to reduce edema d/t
◊ Cognition
● Mannitol, Glycerol severe ischemia &
◊ Communication & language
hemorrhage
◊ Integumentary integrity
◊ Vital signs
Thrombolytic agents achieve
◊ Aerobic capacity/endurance
● Streptokinase, RTPA recanalization of
◊ Sensory examination
occluded cranial
◊ Cranial & peripheral nerve integrity
artery
◊ Neuromuscular & reflexes
◊ Musculoskeletal
Hyperosmolar Agents To reduce edema
o ROM
● Mannitol, Glycerol due to severe
o MMT
ischemia &
o MBT
hemorrhage
◊ Balance & tolerance
◊ Coordination
Anti-coagulants
◊ Gait & locomotion
● Heparin (intravenous,
◊ Functional Assessment
quick-acting), warfarin
(oral)
● Heparin first for the PT PROBLEM LIST
first few days, then
warfarin for long-term General Problem List
◊ LOM (due to hemiplegia or hemiparesis)
Anti-platelet agents for potential ◊ Muscle weakness (due to hemiplegia or
● Aspirin, salicylic acid long-term use to hemiparesis)
prevent stroke ◊ Increased/decreased muscle tone (depends on
recurrence age of recovery)
◊ Impaired perception and perceptual deficit
Anti-spasticity for increased tone, (depend on severity and location of affectation)
● Baclofen, diazepam usually seen in CVA, ◊ Impaired cardiorespiratory
(valium), dantrolene SCI, & MS ◊ Impaired balance and tolerance
(sodium) ◊ Impaired posture and gait
Side effects: ◊ Dependent in ADLs
drowsiness, ◊ Risk for developing DVT, edema, pressure
confusion, sores, contractures, and other complications
headache,
dizziness, PT DIAGNOSIS
generalized muscle ◊ Neuromuscular Practice Pattern D: Impaired
weakness, Motor Function & Sensory Integrity Associated
hepatotoxicity With Non-Progressive Disorders of the Central
potential with Nervous System - Acquired in Adolescence or
dantrium sodium, Adulthood
tolerance, &
dependence
PT PROGNOSIS
Antihypertensives ◊ Impairments may resolve spontaneously as
● Thiazide diuretics brain swelling subsides (reversible ischemic
neurological deficit), within 3 weeks. Residual
neurological impairments are those that persist
OTHER HEALTHCARE MANAGEMENT
longer than 3 weeks & may lead to lasting
◊ Speech-Language Pathologist disability
o Language and speech disorder ◊ DTR usually return within 24-28 hrs. Motor
o Swallowing problems paralysis resolves through synergy patterns to
voluntary segmental movements.
◊ Occupation Therapists
◊ The first three months of recovery is the MOST
o Fine movement impairments
important month - golden period percent for
◊ Nutritionist treating cva patients as it reveals most
measurable neurologic recovery and the
PHYSICAL THERAPY, EXAMINATION, EVALUATION, potential for plasticity of the nervous system
AND DIAGNOSIS ◊ Brunnstrom’s Stages of Motor Recovery
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 ◊ Poor Prognosis for Neurologic Activity
o Previous history of stroke
o Old age
o Visuospatial defect
o Urinary incontinence
◊ Poor Prognosis for Functional Recovery
o Prolonged flaccidity
o Late onset of rigidity & DTR
o No voluntary hand movement
o Severe proximal spasticity
PHYSICAL THERAPY PLAN OF CARE
PT LONG AND SHORT TERM GOALS
◊ LTG:
o Pt. will exhibit an improvement in
sensatiom, range of movement, muscle
strength,,postural control, balance and
tolerance, and correct his/her gait p 20
PTR sessions to be able to achieve
functional ADLs and improve his quality
of life.
◊ STG:
o Pt. will demonstrate an ↑ in sensation
from a score of 0 to 1 in sensory
assessment p 9 PTR session to improve
functional performance.
o Pt. will manifest an increase in range of
motion p 10 PTR sessions to improve
functional independence
o Pt. will manifest an ↑ of 1 grade in
muscle strength within 10 PTR sessions
to improve muscle performance. and
increase functional performance
o Pt. will exhibit decreased mm tone from
a grade 1 to grade 0 p 10 PTR sessions
to increase functional performance
o Pt. will manifest an improvmeent in
cardiorespiratory p 10 PTR sessions to
improve aerobic capacity
o Pt. will exhibity improvements in
perception p 15 PTR sessions to
improve functional performance
o Pt. will exhibit improvements in balance
and tolerance p 15 PTR sessions to
improve functional independence
o Pt. will exhibit improvements in
coordination p 15 PTR sessions to
improve functional independence
o Pt. will show an improved gait within 15
PTR sessions to ↑ safety and achieve
better mobility independence
o Pt. will exhibit an improved posture in 12
PTR sessions to ↑ safety & functional
independence
o Pt will manifest ↑ independence as to
self-care & mobility within 20 PTR
sessions to ↑ functional independence
PT INTERVENTIONS
◊ Mirror therapy x 10 ins to improve detection of
light touch, pressure and temperature pain and
improve perception
◊ Thermal stimulation x 10 mins to improve rate of
recovery of sensation
◊ Neuromuscular electrical stimulation (NMES) x
10 mins to reduce spasticity, improve sensory
awareness, prevent or reduce shoulder
subluxation, and stimulate volitional movements
◊ Intermittent pneumatic compression x 10 mins
for improving tactile and kinesthetic sensation
◊ PROM exercises x 2 sets x 8 reps to improve
range of motion and improve functional
independence
◊ AROM exercises x 2 sets x 8 reps to improve
range of motion and improve functional
independence
◊ Self-ROM Activitiesx 2 sets x 8 reps to improve
range of motion and improve functional
independence
o Arm cradling:
o Table-top polishing
o Sitting, the patient leans forward and
reaches both hands down to the floor to
encourage forward flexion of the
humerus with scapular protraction, and
extension of the elbow, wrist, and
fingers
o Supine, hands are clasped together and
placed behind the head, the elbows fall
flat to the mat.
◊ Progressive resistive strength training x 2 sets x
8 repss x 10 SH to improve muscle strength and
increase functional independence
◊ Strengthening exercises with modalities such as
free weights, elastic bands or tubing x 2 sets x 8
reps to improve muscle performance and
increase functional independence
◊ Gravity-resisted active movements such as arm
lifts and leg lifts x 2 sets x 8 reps to improve
graded 3/5 muscle strength and increase
functional independence
◊ Bridging x 2 setx x 8 reps to promote muscle
improvements in knee flexors and hip extensors
◊ Lower trunk rotation (LTR) activities such as n
side-lying; supine, modified hook-lying; kneeling;
or standing x 2 sets x 8 reps to improve pelvic
control
◊ Rhythmic rotation incorporates with slow gentle
rotations of the limb while progressively moving
the limb into its lengthening range x 2 sets x 8
reps to decrease spasticity
◊ Roods technique (inhibitory techniques) x 10
mins to decrease spasticity
◊ Electromyographic biofeedback (EMG-BFB) x
10 mins to improve motor function in patients
and decrease spasticity
◊ Rood’s facilitatory technique such - A-icing x 10
mins to decrease flaccidity
◊ Rood’s facilitatory technique - Tapping x 10 mins
to decrease flaccidity
◊ Rood’s facilitatory technique - VIbration x 10
mins to decrease flaccidity
◊ Upper and lower body ergometer x 15 mins to
improve aerobic capacity
◊ Seated stepper.x 15 mins to improve aerobic
capacity
◊ Standing on a half-foam roller or wobble board x
15 mins to promote ankle strategies
◊ Anterior posterior shifts or stronger perturbations
x 10 mins to promote hip strategies
7
◊ Tandem stance on floor or foam roller x 10 mins step-ups, stair climbing while the patient is
wearing weighted cuffs)
to promote medial-lateral hip strategies.
◊ Forward, backward, or sideward leans x 10 mins REFERENCES
to promote stepping strategies.
◊ Tandem walking on a lime x 10 mins to improve Books:
balance ◊ O’Sullivan, S.B., Schmitz, T.J., & Fulk, G.D.
◊ Walking on/off foams x 10 mins to improve (2014). Physical Rehabilitation (6th ed.).
balance ◊ Goodman, C. C., & Fuller, K. S. (2009).
◊ Reaching and manipulation techniques x 10mins Pathology: Implications for the physical
to improve upper extremity function and therapist. St. Louis, Mo: Saunders/Elsevier. (4th
coordination ed.)
◊ PNF LE D1 extension pattern; holding against
elastic band resistance around the upper thighs Websites:
in supine or standing positions x 2 sets x 8 reps ◊ Kaye V. (2020). Vertebrobasilar Stroke.
to improve lower extremity functions and
MedSpace. Retrieved May 27, 2021.
coordination
https://emedicine.medscape.com/article/323409-
◊ Lateral side-steps x 2 sets x 8 reps to improve
overview#a1
lower extremity functions and coordination
◊ Standing step-ups x 2 sets x 8 reps to improve ◊ UC Davis. (nd.) Vertebrobasilar Insufficiency.
lower extremity function to improve coordination Retrieved May 27, 2021.
◊ Frenkel’s Exercises x 2 sets x8 reps to improve https://health.ucdavis.edu/vascular/diseases/vert
coordination and proprioception ebrobasilar.html#:~:text=Vertebrobasilar%20insu
◊ Task-specific overground locomotor training (LT) fficiency%20is%20a%20condition,the%20build%
2Dup%20of%20plaque.
x 15 mins focuses on practicing a variety of
activities and on improving the quality of walking
and walking endurance.
◊ Gait Training x15 mins c gait belt and CGA to
improve gait and functional performance :
o Walking forward
o Walking backward
o Side stepping
o Crossed stepping
o Step-up/step-down activities; lateral
set=ups
o Stair climbing; step-over-step
o Walking in a simulated home
environment:
o Walking in a community environment:
o Activities that involve coincident timing:
Crossing at a streetlight; stepping on
and off elevators or escalators; walking
through automatic doors
o Dual-task activities: Walking while
holding a ball, bouncing a ball, carrying
a tray, carrying on a conversation
◊ Lifting free weights or using elastic bands x 2
sets x 8 reps to improve postural stability in
sitting and standing
◊ Postural correction exercises done in front of a
mirror x 10-15 min to improve body image while
providing tactile, verbal cues, feedback, head
straps
◊ Functional Training Exercises to improve
functional perofrmance
o PNF D1 flexion of the LE x 2 sets x 8
reps to improve bed mobility
o Sitting on a therapy ball x 10 mins to
promote pelvic alignment and mobility
o Sit-to-stand and sit-down transfers x 2
sets 8 repts to improve functional
independence
o Transfers activitng x 2 sets x 8 reps to
improve functional performance
◊ Combining resistance training with task-oriented
functional activities x 2 sets x 8 reps to enhance
carryover in terms of improving function (e.g.,
sit-to-stand transfers, partial wall squats],

8
PHARMACOLOGICAL MANAGEMENT SUMMARY

Medications Functions Side Effects PT Implications

Thrombolytics Converts plasminogen to plasmin, Blunted HR, Dizziness, OH Pt. is at risk in severe high blood pressure and active bleeding
degrades fibrin present in clots, or severe blood loss
dissolves clots and reestablishes
blood flow

Hyperosmolar To reduce edema due to severe Nausea, vomiting, headache, increased thirst, chills, fever, confusion PT should be alert because pt. is at risk of low blood volume
Agents (Mannitol, ischemia & hemorrhage or disorientation, electrolyte imbalances, urinary retention or hypovolemia, headache and excessive thirst
Glycerol)
Tissue Only stroke drug that actually Other important side effects include: The most common and serious side effect of alteplase is
plasminogen breaks up a blood clot. It’s used as ● Nausea bleeding. Minor bleeding is more common, but significant
activator (tPA) a common emergency treatment ● Vomiting bleeding such as into the brain (intracranial hemorrhage) or
during a st Other possible serious side effects include: fatal bleeding also occurs.
● Pulmonary embolism
● Cholesterol embolism
● Abnormal heartbeats
● Allergic reactions
● Re-embolization of deep DVT venous thrombi during
treatment of acute massive pulmonary embolism
● Angioedema
● Bleeding
Antiplatelets Prevent excessive clotting caused Increased risk of bleeding Patients taking these agents should be especially alert for any
(clopidogrel and by increased platelet activity Hypotension unexplained or heavy bleeding or any other symptoms that
plavix) might indicate hemorrhage (sudden increases in joint or back
pain, severe headaches, etc.)
Hyperosmolar To reduce edema due to severe Nausea, vomiting, headache, increased thirst, chills, fever, confusion PT should be alert because pt. is at risk of low blood volume
Agents (Mannitol, ischemia & hemorrhage or disorientation, electrolyte imbalances, urinary retention or hypovolemia, headache and excessive thirst
Glycerol)

PT PLAN OF CARE SUMMARY

PROBLEM GOAL INTERVENTION

Impaired sensation ◊ Mirror therapy x 10 ins to improve detection of light touch, pressure and temperature
pain and improve perception
Pt. will demonstrate an ↑ in sensation from a score of 0 to 1 in ◊ Thermal stimulation x 10 mins to improve rate of recovery of sensation
sensory assessment p 9 PTR session to improve functional ◊ Neuromuscular electrical stimulation (NMES) x 10 mins to reduce spasticity, improve
performance. sensory awareness, prevent or reduce shoulder subluxation, and stimulate volitional
movements
◊ Intermittent pneumatic compression x 10 mins for improving tactile and kinesthetic
sensation
9
LOM on one side of the ◊ PROM exercises x 2 sets x 8 reps to improve range of motion and improve functional
body (due to hemiplegia or independence
hemiparesis) ◊ AROM exercises x 2 sets x 8 reps to improve range of motion and improve functional
independence
◊ Self-ROM Activitiesx 2 sets x 8 reps to improve range of motion and improve
functional independence
Pt. will manifest an increase in range of motion p 10 PTR sessions o Arm cradling:
to improve functional independence o Table-top polishing
o Sitting, the patient leans forward and reaches both hands down to the floor to
encourage forward flexion of the humerus with scapular protraction, and
extension of the elbow, wrist, and fingers
o Supine, hands are clasped together and placed behind the head, the elbows
fall flat to the mat.

Muscle weakness on one ◊ Progressive resistive strength training x 2 sets x 8 repss x 10 SH to improve muscle
side of the body (due to
strength and increase functional independence
hemiplegia or hemiparesis)
◊ Strengthening exercises with modalities such as free weights, elastic bands or tubing
x 2 sets x 8 reps to improve muscle performance and increase functional
Pt. will manifest an ↑ of 1 grade in muscle strength within 10 PTR independence
sessions to improve muscle performance. and increase functional ◊ Gravity-resisted active movements such as arm lifts and leg lifts x 2 sets x 8 reps to
performance improve graded 3/5 muscle strength and increase functional independence
◊ Bridging x 2 setx x 8 reps to promote muscle improvements in knee flexors and hip
extensors
◊ Lower trunk rotation (LTR) activities such as n side-lying; supine, modified hook-lying;
kneeling; or standing x 2 sets x 8 reps to improve pelvic control.
Increased/decreased ◊ Rhythmic rotation incorporates with slow gentle rotations of the limb while
muscle tone or spasticity progressively moving the limb into its lengthening range x 2 sets x 8 reps to decrease
(depends on ·Brunnstrom’s spasticity
Stages of Motor Recovery) ◊ Roods technique (inhibitory techniques) x 10 mins to decrease spasticity
Pt. will exhibit decreased mm tone from a grade 1 to grade 0 p 10
PTR sessions to increase functional performance ◊ Electromyographic biofeedback (EMG-BFB) x 10 mins to improve motor function in
patients and decrease spasticity
◊ Neuromuscular electrical stimulation (NMES) x 10 mins to reduce spasticity, improve
sensory awareness,

1. Flaccidity
(depends on ◊ Rood’s facilitatory technique such - A-icing x 10 mins to decrease flaccidity
Pt. will manifest an ↑ in muscle tone within 10 PTR sessions to
·Brunnstrom’s ◊ Rood’s facilitatory technique - Tapping x 10 mins to decrease flaccidity
improve muscle performance
Stages of Motor ◊ Rood’s facilitatory technique - VIbration x 10 mins to decrease flaccidity
Recovery)

10
ISCHEMIC STROKE
GENERAL MEDICAL BACKGROUND
DEFINITION
◊ Most common type
◊ Occurs when a clot blocks or impairs blood flow,
depriving the brain of essential oxygen and
nutrients
EPIDEMIOLOGY
◊ Affects 80% of individuals with stroke
◊ Have a mortality rate of only 8% to 12% at 1
month
◊ Ischemic stroke survivors 65 or older, incidences
of disabilities observed at 6 months include
hemiparesis (50%), unable to walk without
assistance (30%), dependent in activities of daily
living (ADL) (26%), aphasia (19%), and
depression (35%).
ETIOLOGY
◊ Result of a thrombus, embolism, or conditions
that produce low systemic perfusion pressures.
◊ Resulting lack of cerebral blood flow (CBF)
deprives the brain of needed oxygen and
glucose, disrupts cellular metabolism, and leads
to injury and death of tissues.
◊ Thrombus
o Results from platelet adhesion and
aggregation on plaques.
o Cerebral thrombosis
o Refers to the formation or development
of a blood clot within the cerebral
arteries or their branches.
o It should be noted that lesions of
extracranial vessels (carotid or vertebral
arteries) can also produce symptoms of
stroke.
o Thrombi lead to ischemia, or occlusion
of an artery with resulting cerebral
infarction or tissue death
(atherothrombotic brain infarction [ABI]).
o Thrombi can also become dislodged
and travel to a more distal site in the
form of an intra-artery embolus.
● Cerebral Embolus (CE)
○ Composed of bits of matter (blood clot,
plaque) formed elsewhere and released
into the bloodstream, traveling to the
cerebral arteries where they lodge in a
vessel, producing occlusion and
infarction.
○ The most common source of CE is
disease of the cardiovascular system.
○ Occasionally systemic disorders may
produce septic, fat, or air emboli that
affect the cerebral circulation.
◊ Ischemic strokes may also result from low
systemic perfusion, the result of cardiac failure
or significant blood loss with resulting systemic
hypotension.
◊ The neurological deficits produced with systemic
failure are global in nature with bilateral
neurological deficits.
RISK FACTORS
◊ Women with early menopause (before 42 years
of age)
o Twice the risk of ischemic stroke as
women with later menopause.
◊ The use of estrogen alone or estrogen plus
progestin
o Increases the risk of ischemic stroke (up
to 44% to 55% or higher).
◊ Pregnancy, birth, and the first 6 weeks
postpartum
o Increase risk of stroke, especially in
older women and African Americans.
◊ Preeclampsia
o Independent risk factor for stroke.
PATHOMECHANICS / PATHOPHYSIOLOGY
◊ Produce cerebral edema, an accumulation of
fluids within the brain that begins within minutes
of the insult and reaches a maximum by 3 to 4
days.
◊ It is the result of tissue necrosis and widespread
rupture of cell membranes with movement of
fluid from the blood into brain tissues.
◊ The swelling gradually subsides and generally
disappears by 2 to 3 weeks.
◊ Significant edema can elevate intracranial
pressures
o Leading to intracranial hypertension and
neurological deterioration associated
with contralateral and caudal shifts of
brain structures (brainstem herniation).
◊ Clinical signs of elevating intracranial pressure
(ICP) include:
o Decreasing level of consciousness
(stupor and coma)
o Widened pulse pressure
o Increased heart rate
o Irregular respirations (Cheyne-Stokes
respirations)
o Vomiting
o Unreacting pupils (cranial nerve [CN] III
signs)
o Papilledema.
◊ Cerebral edema is the most frequent cause of
death in acute stroke and is characteristic of
large infarcts involving the middle cerebral artery
and the internal carotid artery
CLASSIFICATION
◊ Four main types of ischemic stroke
o Large vessel atherosclerosis,
o Small vessel diseases (lacunar infarcts)
o Cardioembolic strokes
o Cryptogenic strokes
CLINICAL PRESENTATION
◊ Sudden numbness or weakness of your face,
arm, or leg, often on one side of the body
11
◊ Confusion
◊ Problems speaking or understanding others
◊ Dizziness, loss of balance or coordination, or
trouble walking
◊ Vision loss or double vision
COMPLICATIONS
◊ Fluid buildup, swelling, and bleeding in your
brain
◊ Seizures
◊ Problems with memory and understanding
MEDICAL DIAGNOSIS
◊ Cerebrovascular Imaging
o Main tool to establish the diagnosis of
suspected ischemic stroke and to rule
out hemorrhagic stroke and other types
of central nervous system (CNS) lesions
(e.g., tumor or abscess)
◊ Computed Tomography (CT Scan)
o Most commonly used and readily
available neuroimaging technique. CT
resolution allows identification of large
arteries and veins and venous sinuses.
o In the subacute phase, CT scans can
delineate the development of cerebral
edema (within 3 days), which then fades
over the next 2 to 3 weeks. Cerebral
infarction (within 3 to 5 days) is visible
with the addition of contrast material by
showing areas of decreased density.
◊ Magnetic Resonance Imaging (MRI)
o More sensitive in the diagnosis of acute
strokes, allowing detection of cerebral
ischemia as early as 30 minutes after
vascular occlusion and infarction within
2 to 6 hours.
o It is also able to detail the extent of
infarction or hemorrhage and can detect
smaller lesions than a CT scan.
o Use of contrast enhancement allows
documentation of changes in an infarct
over the first 2 to 3 weeks.
◊ Magnetic Resonance Angiography
o Used to identify vascular abnormalities
(e.g., stenosis), and alterations in blood
flow as a result of embolus or
thrombosis.
◊ Doppler Ultrasound
o Used to examine the carotid arteries
and typically precedes carotid
endarterectomy.
◊ Arteriography
o An x-ray of the carotid artery with a
special dye injected into an artery in the
leg or arm.
◊ Digital Subtraction Angiography
o An x-ray of the carotid artery with less
dye used. These procedures are
considered invasive and carry a small
risk of causing a stroke
DIFFERENTIAL DIAGNOSIS
Ischemic Stroke Caused by a
blockage cutting off
the blood supply to
the brain
Most commonly type
Hemorrhagic Stroke Caused by a bleeding
in our around the
brain
Transient Ischemic Same as stroke
Attack except that the
symptoms only last
for a short amount of
time because the
blockage that stops
the blood getting to
your brain is
temporary
PROGNOSIS
o The mortality risk is higher than the
general population, the risk of recurrent
vascular events is considerable, and
only about 50% of patients recover fully
(without significant disability) and return
to work after first-ever ischemic stroke.
GENERAL HEALTHCARE MANAGEMENT
MEDICAL MANAGEMENT
◊ Endovascular therapy
o Has been shown to significantly improve
outcomes and reduce long-term
disability after ischemic stroke
◊
SURGICAL MANAGEMENT
◊ Carotid Endarterectomy
o Used to remove fatty deposits from the
carotid artery. It is a useful procedure to
prevent recurrent strokes or the
development of stroke in individuals with
TIAs
PHARMACOLOGICAL MANAGEMENT
◊ Thrombolytics
o Converts plasminogen to plasmin,
degrades fibrin present in clots,
dissolves clots and reestablishes blood
flow
o E.g., lysis of thrombi causing ischemic
stroke; also to dissolve clots in coronary
arteries, pulmonary emboli, deep vein
thrombosis
◊ Hyperosmolar Agents (Mannitol, Glycerol)
o To reduce edema due to severe
ischemia & hemorrhage
◊ Tissue plasminogen activator (tPA)
o Only stroke drug that actually breaks up
a blood clot. It’s used as a common
emergency treatment during a stroke..
OTHER HEALTHCARE MANAGEMENT
◊ Speech-Language Pathologist
o Language and speech disorder
o Swallowing problems
◊ Occupation Therapists
o Fine movement impairments
◊ Nutritionist
12
PHYSICAL THERAPY, EXAMINATION, EVALUATION,
AND DIAGNOSIS
POINTS OF EMPHASIS ON EXAMINATION
General Points of Examination
◊ Subjective
◊ Pain
◊ Signs of increased intracranial pressure
◊ Level of consciousness
◊ Emotional status & behavior
◊ Cognition
◊ Communication & language
◊ Integumentary integrity
◊ Vital signs
◊ Aerobic capacity/endurance
◊ Sensory examination
◊ Cranial & peripheral nerve integrity
◊ Neuromuscular & reflexes
◊ Musculoskeletal
o ROM
o MMT
o MBT
◊ Balance & tolerance
◊ Coordination
◊ Gait & locomotion
◊ Functional Assessment
PT PROBLEM LIST
◊ Impaired sensation
◊ LOM on one side of the body (due to hemiplegia
or hemiparesis)
◊ Muscle weakness on one side of the body (due
to hemiplegia or hemiparesis)
◊ Increased/decreased muscle tone or spasticity
(depends on ·Brunnstrom’s Stages of Motor
Recovery)
◊ Flaccidity (depends on ·Brunnstrom’s Stages of
Motor Recovery)
◊ Impaired cardiorespiratory
◊ Impaired perception and perceptual deficit
(depend on severity and location of affectation)
◊ Impaired balance and tolerance
◊ Impaired coordination
◊ Impaired gait
◊ Impaired posture
◊ Dependent in ADLs
PT DIAGNOSIS
◊ Neuromuscular Practice Pattern D: Impaired
Motor Function & Sensory Integrity Associated
With Non-Progressive Disorders of the Central
Nervous System - Acquired in Adolescence or
Adulthood
PT PROGNOSIS
◊ Impairments may resolve spontaneously as
brain swelling subsides (reversible ischemic
neurological deficit), within 3 weeks. Residual
neurological impairments are those that persist
longer than 3 weeks & may lead to lasting
disability
◊ DTR usually return within 24-28 hrs. Motor
paralysis resolves through synergy patterns to
voluntary segmental movements.
◊ The first three months of recovery is the MOST
important month - golden period percent for
treating cva patients as it reveals most
measurable neurologic recovery and the
potential for plasticity of the nervous system
◊ Brunnstrom’s Stages of Motor Recovery
◊ Poor Prognosis for Neurologic Activity
o Previous history of stroke
o Old age
o Visuospatial defect
o Urinary incontinence
◊ Poor Prognosis for Functional Recovery
o Prolonged flaccidity
o Late onset of rigidity & DTR
o No voluntary hand movement
o Severe proximal spasticity
PHYSICAL THERAPY PLAN OF CARE
PT LONG AND SHORT TERM GOALS
◊ LTG:
o Pt. will exhibit an improvement in
sensation, range of movement, muscle
strength,,postural control, balance and
tolerance, and correct his/her gait p 20
PTR sessions to be able to achieve
functional ADLs and improve his quality
of life.
o
◊ STG:
o Pt. will demonstrate an ↑ in sensation
from a score of 0 to 1 in sensory
assessment p 9 PTR session to improve
functional performance.
o Pt. will manifest an increase in range of
motion p 10 PTR sessions to improve
functional independence
o Pt. will manifest an ↑ of 1 grade in
muscle strength within 10 PTR sessions
to improve muscle performance. and
increase functional performance
o Pt. will exhibit decreased mm tone from
a grade 1 to grade 0 p 10 PTR sessions
to increase functional performance
o Pt. will manifest an improvmeent in
cardiorespiratory p 10 PTR sessions to
improve aerobic capacity
o Pt. will exhibity improvements in
perception p 15 PTR sessions to
improve functional performance
o Pt. will exhibit improvements in balance
and tolerance p 15 PTR sessions to
improve functional independence
o Pt. will exhibit improvements in
coordination p 15 PTR sessions to
improve functional independence
o Pt. will show an improved gait within 15
PTR sessions to ↑ safety and achieve
better mobility independence
o Pt. will exhibit an improved posture in 12
PTR sessions to ↑ safety & functional
independence
o Pt will manifest ↑ independence as to
self-care & mobility within 20 PTR
sessions to ↑ functional independence
PT INTERVENTIONS
◊ Mirror therapy x 10 ins to improve detection of
light touch, pressure and temperature pain and
improve perception
13
◊ Thermal stimulation x 10 mins to improve rate of
recovery of sensation
◊ Neuromuscular electrical stimulation (NMES) x
10 mins to reduce spasticity, improve sensory
awareness, prevent or reduce shoulder
subluxation, and stimulate volitional movements
◊ Intermittent pneumatic compression x 10 mins
for improving tactile and kinesthetic sensation
◊ PROM exercises x 2 sets x 8 reps to improve
range of motion and improve functional
independence
◊ AROM exercises x 2 sets x 8 reps to improve
range of motion and improve functional
independence
◊ Self-ROM Activitiesx 2 sets x 8 reps to improve
range of motion and improve functional
independence
o Arm cradling:
o Table-top polishing
o Sitting, the patient leans forward and
reaches both hands down to the floor to
encourage forward flexion of the
humerus with scapular protraction, and
extension of the elbow, wrist, and
fingers
o Supine, hands are clasped together and
placed behind the head, the elbows fall
flat to the mat.
◊ Progressive resistive strength training x 2 sets x
8 repss x 10 SH to improve muscle strength and
increase functional independence
◊ Strengthening exercises with modalities such as
free weights, elastic bands or tubing x 2 sets x 8
reps to improve muscle performance and
increase functional independence
◊ Gravity-resisted active movements such as arm
lifts and leg lifts x 2 sets x 8 reps to improve
grade 3/5 muscle strength and increase
functional independence
◊ Bridging x 2 setx x 8 reps to promote muscle
improvements in knee flexors and hip extensors
◊ Lower trunk rotation (LTR) activities such as n
side-lying; supine, modified hook-lying; kneeling;
or standing x 2 sets x 8 reps to improve pelvic
control
◊ Rhythmic rotation incorporates with slow gentle
rotations of the limb while progressively moving
the limb into its lengthening range x 2 sets x 8
reps to decrease spasticity
◊ Roods technique (inhibitory techniques) x 10
mins to decrease spasticity
◊ Electromyographic biofeedback (EMG-BFB) x
10 mins to improve motor function in patients
and decrease spasticity
◊ Rood’s facilitatory technique such - A-icing x 10
mins to decrease flaccidity
◊ Rood’s facilitatory technique - Tapping x 10 mins
to decrease flaccidity
◊ Rood’s facilitatory technique - VIbration x 10
mins to decrease flaccidity
◊ Upper and lower body ergometer x 15 mins to
improve aerobic capacity
◊ Seated stepper.x 15 mins to improve aerobic
capacity
◊ Standing on a half-foam roller or wobble board x
15 mins to promote ankle strategies
◊ Anteriorposterior shifts or stronger perturbations
x 10 mins to promote hip strategies
◊ Tandem stance on floor or foam roller x 10 mins
to promote medial-lateral hip strategies.
◊ Forward, backward, or sideward leans x 10 mins
to promote stepping strategies.
◊ Tandem walking on a lime x 10 mins to improve
balance
◊ Walking on/off foams x 10 mins to improve
balance
◊ Reaching and manipulation techniques x 10mins
to improve upper extremity function and
coordination
◊ PNF LE D1 extension pattern; holding against
elastic band resistance around the upper thighs
in supine or standing positions x 2 sets x 8 reps
to improve lower extremity functions and
coordination
◊ Lateral side-steps x 2 sets x 8 reps to improve
lower extremity functions and coordination
◊ Standing step-ups x 2 sets x 8 reps to improve
lower extremity function to improve coordination
◊ Frenkel’s Exercises x 2 sets x8 reps to improve
coordination and proprioception
◊ Task-specific overground locomotor training (LT)
x 15 mins focuses on practicing a variety of
activities and on improving the quality of walking
and walking endurance.
◊ Gait Training x15 mins c gait belt and CGA to
improve gait and functional performance :
o Walking forward
o Walking backward
o Side stepping
o Crossed stepping
o Step-up/step-down activities; lateral
set=ups
o Stair climbing; step-over-step
o Walking in a simulated home
environment:
o Walking in a community environment:
o Activities that involve coincident timing:
Crossing at a streetlight; stepping on
and off elevators or escalators; walking
through automatic doors
o Dual-task activities: Walking while
holding a ball, bouncing a ball, carrying
a tray, carrying on a conversation
◊ Lifting free weights or using elastic bands x 2
sets x 8 reps to improve postural stability in
sitting and standing
◊ Postural correction exercises done in front of a
mirror x 10-15 min to improve body image while
providing tactile, verbal cues, feedback, head
straps
◊ Functional Training Exercises to improve
functional performance
o PNF D1 flexion of the LE x 2 sets x 8
reps to improve bed mobility
o Sitting on a therapy ball x 10 mins to
promote pelvic alignment and mobility
o Sit-to-stand and sit-down transfers x 2
sets 8 reps to improve functional
independence
o Transfers activities x 2 sets x 8 reps to
improve functional performance
◊ Combining resistance training with task-oriented
functional activities x 2 sets x 8 reps to enhance
carryover in terms of improving function (e.g.,
14
 sit-to-stand transfers, partial wall squats],
step-ups, stair climbing while the patient is
wearing weighted cuffs)

REFERENCES
Books:
◊ O’Sullivan, S.B., Schmitz, T.J., & Fulk, G.D.
(2014). Physical Rehabilitation (6th ed.).
Websites:
◊ Stroke. (n.d.). Retrieved May 08, 2021, from
https://www.physio-pedia.com/Stroke
◊ Types of Stroke: Ischemic, Hemorrhagic, and
TIA. WebMD.
https://www.webmd.com/stroke/guide/types-stro
ke. Accessed May 8, 2021.
◊ Stroke. Mayo Clinic.
https://www.mayoclinic.org/diseases-conditions/
stroke/care-at-mayo-clinic/mac-20350122.
Published February 9, 2021. Accessed May 8,
2021.
◊ Types of stroke. Stroke Association.
https://www.stroke.org.uk/what-is-stroke/types-of
-stroke#:~:text=An%20ischaemic%20stroke%20i
s%20caused,known%20as%20a%20mini%2Dst
roke. Published April 7, 2021. Accessed May 8,
2021.
◊ Varona JF. Long-term prognosis of ischemic
stroke in young adults. Stroke Res Treat.
2010;2011:879817. Published 2010 Dec 20.
doi:10.4061/2011/879817
◊ Omudhome Ogbru, P. D. (2019, July 5).
alteplase (TPA, Cathflo Activase): Uses, Side
Effects, and Dosage. MedicineNet.
https://www.medicinenet.com/alteplase/article.ht
m.
◊ RxList. (2020, September 22). Activase
(Alteplase): Uses, Dosage, Side Effects,
Interactions, Warning. RxList.
https://www.rxlist.com/activase-drug.htm.
◊ WebMD. (n.d.). Thrombolysis: Definition, Types,
Uses, Effects, and More. WebMD.
https://www.webmd.com/stroke/thrombolysis-def
inition-and-facts.
◊ RxList. (2017, September 6). Mannitol: Side
Effects, Dosages, Treatment, Interactions,
Warnings. RxList.
https://www.rxlist.com/consumer_mannitol_osmit
rol/drugs-condition.htm.

15
PHARMACOLOGICAL MANAGEMENT SUMMARY

Medications Functions Side Effects PT Implications

Thrombolytics Converts plasminogen to plasmin, degrades fibrin Blunted HR, Dizziness, OH Pt. is at risk in severe high blood pressure and
present in clots, dissolves clots and reestablishes active bleeding or severe blood loss
blood flow

Hyperosmolar To reduce edema due to severe ischemia & ● Nausea PT should be alert because pt. is at risk of low
Agents (Mannitol, hemorrhage ● Vomiting blood volume or hypovolemia, headache and
Glycerol) ● Headache excessive thirst
● Increased thirst
● Chills, fever
● Confusion or disorientation,
● Electrolyte imbalances
● Urinary retention
Tissue plasminogen Only stroke drug that actually breaks up a blood Other important side effects include: The most common and serious side effect of
activator (tPA) clot. It’s used as a common emergency treatment ● Nausea alteplase is bleeding. Minor bleeding is more
during a st ● Vomiting common, but significant bleeding such as into
Other possible serious side effects include: the brain (intracranial hemorrhage) or fatal
● Pulmonary embolism bleeding also occurs.
● Cholesterol embolism
● Abnormal heartbeats
● Allergic reactions
● Re-embolization of deep DVT venous thrombi during
treatment of acute massive pulmonary embolism
● Angioedema
● Bleeding

PT PLAN OF CARE SUMMARY

PROBLEM GOAL INTERVENTION

Impaired sensation Pt. will demonstrate an ↑ in sensation from a score of 0 to 1 in sensory
assessment p 9 PTR session to improve functional performance.
◊ Mirror therapy x 10 ins to improve detection of light
touch, pressure and temperature pain and improve
perception
◊ Thermal stimulation x 10 mins to improve rate of
recovery of sensation
◊ Neuromuscular electrical stimulation (NMES) x 10 mins
to reduce spasticity, improve sensory awareness,
prevent or reduce shoulder subluxation, and stimulate
volitional movements
◊ Intermittent pneumatic compression x 10 mins for
improving tactile and kinesthetic sensation
16
LOM on one side of the body (due to
hemiplegia or hemiparesis)
Muscle weakness on one side of the body (due
to hemiplegia or hemiparesis)
Increased/decreased muscle tone or spasticity
(depends on ·Brunnstrom’s Stages of Motor
Recovery)
Pt. will manifest an increase in range of motion p 10 PTR sessions to
improve functional independence
Pt. will manifest an ↑ of 1 grade in muscle strength within 10 PTR sessions
to improve muscle performance. and increase functional performance
Pt. will exhibit decreased mm tone from a grade 1 to grade 0 p 10 PTR
sessions to increase functional performance
◊ PROM exercises x 2 sets x 8 reps to improve range of
motion and improve functional independence
◊ AROM exercises x 2 sets x 8 reps to improve range of
motion and improve functional independence
◊ Self-ROM Activities x 2 sets x 8 reps to improve range of
motion and improve functional independence
o Arm cradling:
o Table-top polishing
o Sitting, the patient leans forward and reaches
both hands down to the floor to encourage
forward flexion of the humerus with scapular
protraction, and extension of the elbow, wrist,
and fingers
o Supine, hands are clasped together and placed
behind the head, the elbows fall flat to the mat.
◊ Progressive resistive strength training x 2 sets x 8 repss
x 10 SH to improve muscle strength and increase
functional independence
◊ Strengthening exercises with modalities such as free
weights, elastic bands or tubing x 2 sets x 8 reps to
improve muscle performance and increase functional
independence
◊ Gravity-resisted active movements such as arm lifts and
leg lifts x 2 sets x 8 reps to improve grade 3/5 muscle
strength and increase functional independence
◊ Bridging x 2 setx x 8 reps to promote muscle
improvements in knee flexors and hip extensors
◊ Lower trunk rotation (LTR) activities such as n side-lying;
supine, modified hook-lying; kneeling; or standing x 2
sets x 8 reps to improve pelvic control.
◊ Rhythmic rotation incorporates with slow gentle rotations
of the limb while progressively moving the limb into its
lengthening range x 2 sets x 8 reps to decrease
spasticity
◊ Roods technique (inhibitory techniques) x 10 mins to
decrease spasticity
◊ Electromyographic biofeedback (EMG-BFB) x 10 mins to
improve motor function in patients and decrease
spasticity
17

Flaccidity (depends on ·Brunnstrom’s Stages of
Motor Recovery)
Impaired cardiorespiratory
Impaired perception and perceptual deficit
(depend on severity and location of affectation)
Impaired balance and tolerance
Impaired coordination
Pt. will manifest an ↑ in muscle tone within 10 PTR sessions to improve
muscle performance
Pt. will manifest an improvmeent in cardiorespiratory p 10 PTR sessions to
improve aerobic capacity
Pt. will exhibity improvements in perception p 15 PTR sessions to improve
functional performance
Pt. will exhibit improvements in balance and tolerance p 15 PTR sessions
to improve functional independence
Pt. will exhibit improvements in coordination p 15 PTR sessions to improve
functional independence
◊ Neuromuscular electrical stimulation (NMES) x 10 mins
to reduce spasticity, improve sensory awareness,
◊ Rood’s facilitatory technique such - A-icing x 10 mins to
decrease flaccidity
◊ Rood’s facilitatory technique - Tapping x 10 mins to
decrease flaccidity
◊ Rood’s facilitatory technique - VIbration x 10 mins to
decrease flaccidity
◊ Upper and lower body ergometer x 15 mins to improve
aerobic capacity
◊ Seated stepper.x 15 mins to improve aerobic capacity
◊ Mirror therapy x 10 mins to improve detection of light
touch, pressure and temperature pain and improve
perception
◊ Intermittent pneumatic compression x 10 mins for
improving tactile and kinesthetic sensation and
perception
◊ Neuromuscular electrical stimulation (NMES) x 10 mins
to reduce spasticity, improve sensory awareness and
perception, prevent or reduce shoulder subluxation, and
stimulate volitional movements
◊ Frenkel’s Exercises x 2 sets x 8 reps to improve
coordination and proprioception
◊ Standing on a half-foam roller or wobble board x 15 mins
to promote ankle strategies
◊ Anterior posterior shifts or stronger perturbations x 10
mins to promote hip strategies
◊ Tandem stance on floor or foam roller x 10 mins to
promote medial-lateral hip strategies.
◊ Forward, backward, or sideward leans x 10 mins to
promote stepping strategies.
◊ Tandem walking on a lime x 10 mins to improve balance
◊ Walking on/off foams x 10 mins to improve balance
18
 ◊ Reaching and manipulation techniques x 10mins to
improve upper extremity function and coordination
◊ PNF LE D1 extension pattern; holding against elastic
band resistance around the upper thighs in supine or
standing positions x 2 sets x 8 reps to improve lower
extremity functions and coordination
◊ Lateral side-steps x 2 sets x 8 reps to improve lower
extremity functions and coordination
◊ Standing step-ups x 2 sets x 8 reps to improve lower
extremity function to improve coordination
◊ Frenkel’s Exercises x 2 sets x 8 reps to improve
coordination and proprioception

Impaired gait Pt. will show an improved gait within 15 PTR sessions to ↑ safety and ◊ Task-specific overground locomotor training (LT) x 15
achieve better mobility independence mins focuses on practicing a variety of activities and on
improving the quality of walking and walking endurance.
◊ Gait Training x15 mins c gait belt and CGA to improve
gait and functional performance :
o Walking forward
o Walking backward
o Side stepping
o Crossed stepping
o Step-up/step-down activities; lateral set=ups
o Stair climbing; step-over-step
o Walking in a simulated home environment:
o Walking in a community environment:
o Activities that involve coincident timing: Crossing
at a streetlight; stepping on and off elevators or
escalators; walking through automatic doors
o Dual-task activities: Walking while holding a ball,
bouncing a ball, carrying a tray, carrying on a
conversation
Impaired posture Pt. will exhibit an improved posture in 12 PTR sessions to ↑ safety & ◊ Lifting free weights or using elastic bands x 2 sets x 8
functional independence reps to improve postural stability in sitting and standing
◊ Postural correction exercises done in front of a mirror x
10-15 min to improve body image while providing tactile,
verbal cues, feedback, head straps

Dependent in ADLs Pt will manifest ↑ independence as to self-care & mobility within 20 PTR ◊ Functional Training Exercises to improve functional
sessions to ↑ functional independence performance
o PNF D1 flexion of the LE x 2 sets x 8 reps to
improve bed mobility
19
 o Sitting on a therapy ball x 10 mins to promote
pelvic alignment and mobility
o Sit-to-stand and sit-down transfers x 2 sets 8
repts to improve functional independence
o Transfers activitng x 2 sets x 8 reps to improve
functional performance
◊ Combining resistance training with task-oriented
functional activities x 2 sets x 8 reps to enhance
carryover in terms of improving function (e.g.,
sit-to-stand transfers, partial wall squats], step-ups, stair
climbing while the patient is wearing weighted cuffs).

HOME EXERCISE PROGRAM PRECAUTIONS

1. 1.Mirror therapy using mirrors at home x 10 mins to improve detection of
light touch, pressure and temperature pain and improve perception 1. Fall risk
2. Self-ROM Activities x 2 sets x 8 reps to improve range of motion and 2. Always monitor vital signs before and after performing exercises.
improve functional independence 3. Avoid valsalva maneuver to prevent increase in blood pressure.
a. Arm cradling: 4. Pt. must be encouraged to rest intervals between exercises or activities in order to avoid fatigue.
b. Table-top polishing 5. Maintain proper posture during exercises.
c. Sitting, the patient leans forward and reaches both hands down 6. Avoid activities that worsen the condition.
to the floor to encourage forward flexion of the humerus with 7. Take precautions to avoid falls by adding environmental modifications such as handrails, non slip mat
scapular protraction, and extension of the elbow, wrist, and etc.
fingers 8. Risk for developing DVT, edema, pressure sores, contractures, and other complications
d. Supine, hands are clasped together and placed behind the
head, the elbows fall flat to the mat.
3. Progressive resistive strength training x 2 sets x 8 repss x 10 SH to
improve muscle strength and increase functional independence
4. Strengthening exercises with modalities such as free weights, elastic
bands or tubing x 2 sets x 8 reps to improve muscle performance and
increase functional independence
5. Rhythmic rotation incorporates with slow gentle rotations of the limb
while progressively moving the limb into its lengthening range x 2 sets x
8 reps to decrease spasticity
6. Tandem walking on a lime x 10 mins to improve balance
7. Walking on/off foams x 10 mins to improve balance
8. Lateral side-steps x 2 sets x 8 reps to improve lower extremity functions
and coordination
9. Standing step-ups x 2 sets x 8 reps to improve lower extremity function
to improve coordination
10. Gait Training x15 mins c gait belt and CGA to improve gait and
functional performance :
20
 a. Walking forward
b. Walking backward
11. Postural correction exercises done in front of a mirror x 10-15 min to
improve body image while providing tactile, verbal cues, feedback, head
straps
12. Functional Training Exercises to improve functional performance
a. PNF D1 flexion of the LE x 2 sets x 8 reps to improve bed
mobility
b. Sitting on a therapy ball x 10 mins to promote pelvic alignment
and mobility
c. Sit-to-stand and sit-down transfers x 2 sets 8 reps to improve
functional independence
d. Transfers activity x 2 sets x 8 reps to improve functional
performance

21
HEMORRHAGIC STROKE
GENERAL MEDICAL BACKGROUND
DEFINITION
◊ Occurs when blood vessels rupture, causing
leakage of blood in or around the brain
EPIDEMIOLOGY
◊ Largest number of deaths
◊ With mortality rates of 37% to 38% at 1 month
◊ 50% of deaths of hemorrhagic strokes actually
occur within the 1st 48 hours
ETIOLOGY
◊ Abnormal bleeding into the extravascular areas
of the brain, are the result of rupture of a
cerebral vessel or trauma.
◊ Results in increased intracranial pressures with
injury to brain tissues and restriction of distal
blood flow.
◊ Intracerebral hemorrhage (IH)
o Caused by rupture of a cerebral vessel
with subsequent bleeding into the brain.
◊ Primary cerebral hemorrhage (nontraumatic
spontaneous hemorrhage)
o Typically occurs in small blood vessels
weakened by atherosclerosis producing
an aneurysm.
◊ Subarachnoid hemorrhage (SH)
o Occurs from bleeding into the
subarachnoid space typically from a
saccular or berry aneurysm affecting
primarily large blood vessels.
◊ Congenital defects that produce weakness in the
blood vessel wall
o Major contributing factors to the
formation of an aneurysm.
◊ Hemorrhage is closely linked to chronic
hypertension.
◊ Arteriovenous malformation (AVM)
o Another congenital defect that can result
in stroke.
o Characterized by a tortuous tangle of
arteries and veins with agenesis of an
interposing capillary system.
o The abnormal vessels undergo
progressive dilation with age and
eventually bleed in about 50% of cases.
◊ Sudden and severe cerebral bleeding can result
in death within hours, because intracranial
pressures rise rapidly and adjacent cortical
tissues are compressed or displaced as in
brainstem herniation.
RISK FACTORS
◊ Women with early menopause (before 42 years
of age)
o Twice the risk of ischemic stroke as
women with later menopause.
◊ The use of estrogen alone or estrogen plus
progestin
o Increases the risk of ischemic stroke (up
to 44% to 55% or higher).
◊ Pregnancy, birth, and the first 6 weeks
postpartum
o Increase risk of stroke, especially in
older women and African Americans.
◊ Preeclampsia
o Independent risk factor for stroke.
PATHOMECHANICS / PATHOPHYSIOLOGY
◊ In intracerebral hemorrhage, bleeding occurs
directly into the brain parenchyma.
◊ The usual mechanism is thought to be leakage
from small intracerebral arteries damaged by
chronic hypertension.
◊ Other mechanisms include bleeding diatheses,
iatrogenic anticoagulation, cerebral amyloidosis,
and cocaine abuse.
◊ Intracerebral hemorrhage has a predilection for
certain sites in the brain, including the thalamus,
putamen, cerebellum, and brainstem.
◊ In addition to the area of the brain injured by the
hemorrhage, the surrounding brain can be
damaged by pressure produced by the mass
effect of the hematoma. A general increase in
intracranial pressure may occur.
CLASSIFICATION
◊ Intracerebral Hemorrhagic Stroke
o Primary cerebral hemorrhage
o Bleeding from blood vessel within the
brain
o High blood pressure is the main cause
of intracerebral hemorrhagic stroke
◊ Subarachnoid Hemorrhagic Stroke
o Bleeding from a blood vessel between
the surface of the brain and the
arachnoid tissues that cover the brain
o Arteriovenous Malformation
▪ Tangles of arteries and veins
and interimposing agenesis of
capillary system and usually
occurs in 2nd and 3rd decade
with triad of hemorrhage,
seizure and migraine
o Saccular/Berry Aneurysm
▪ Congenital defect of cerebral
wall with progressive
degeneration of tunica
adventitia which lead to
ballooning of the blood vessel
up to 10 mm
CLINICAL PRESENTATION
◊ Intense headache - some people describe it as
the worst headache they’ve ever had
◊ Confusion
◊ Nausea or throwing up
◊ Sensitivity to light
◊ Problems with vision
◊ Passing out
COMPLICATIONS
◊ Seizures
◊ Memory and thinking problems
◊ Heart problems
22
◊ Swallowing problems and trouble eating and
drinking
◊ Permanent neurologic disability
MEDICAL DIAGNOSIS
◊ Computed Tomography (CT Scan)
o Many times CT scans during the acute
phase are negative with no clear
evidence of abnormalities. However,
acute bleeding and hemorrhagic
transformation are visible on CT
scanning
◊ Magnetic Resonance Imaging
◊ Able to detail the extent of infarction or
hemorrhage and can detect smaller lesions than
a CT scan. scanning
DIFFERENTIAL DIAGNOSIS
Ischemic Stroke Caused by a
blockage cutting off
the blood supply to
the brain
Most commonly type
Hemorrhagic Stroke Caused by a bleeding
in our around the
brain
Transient Ischemic Same as stroke
Attack except that the
symptoms only last
for a short amount of
time because the
blockage that stops
the blood getting to
your brain is
temporary
PROGNOSIS
◊ About 30% to 60% of people with an
intracerebral hemorrhage die. In those who
survive long enough to reach an emergency
room, bleeding usually has stopped by the time
they are seen by a doctor. Many people with
ruptured aneurysms or subarachnoid
hemorrhages also do not survive long enough to
reach a hospital. Of those who do, about 50%
die within the first month of treatment. However,
in people with subarachnoid hemorrhages
resulting from arteriovenous malformations, the
risk of death is only about 15%.
◊ Among the 25% of people who survive an
intracerebral hemorrhage, many experience a
major improvement in their symptoms as their
bodies naturally and gradually reabsorb the
clotted blood within the brain
◊ Among the 25% of people who survive an
intracerebral hemorrhage, many experience a
major improvement in their symptoms as their
bodies naturally and gradually reabsorb the
clotted blood within the brain.
◊ Among those who survive a bleeding aneurysm,
about 50% suffer long-term neurological
problems.
◊ People who bleed from an aneurysm or AVM
and do not have this problem treated are at risk
for having a repeat bleeding event.
◊ If the blood vessel is not repaired or removed,
one out of 5 survivors of subarachnoid
hemorrhage have bleeding again within 14 days
if the abnormal blood vessel was not repaired or
removed. 50% who do not have surgical
treatment have a repeat bleed within 6 months.
◊ When surgery is used to clip a bleeding
aneurysm, there is a good chance of success.
GENERAL HEALTHCARE MANAGEMENT
MEDICAL MANAGEMENT
◊ Immediate emergency care is crucial for a
hemorrhagic stroke. This treatment focuses on
controlling the bleeding in your brain and
reducing the pressure caused by the bleeding.
SURGICAL MANAGEMENT
◊ Surgery may be indicated to repair a superficial
ruptured aneurysm or AVM, prevent rebleeding,
and evacuate a clot (hematoma).
◊ Larger, deeper intracranial or brainstem vascular
lesions are generally not amenable to surgery.
◊ Surgery may also be indicated for resection of a
superficial unruptured AVM when there is high
risk of rupture and stroke.
PHARMACOLOGICAL MANAGEMENT
◊ Antiplatelets (clopidogrel and plavix)
o Can be used to help prevent blood clots.
They work by making it more difficult for
the platelets in your blood to stick
together, which is the first step in the
formation of blood clots
◊ Hyperosmolar Agents (Mannitol, Glycerol)
o To reduce edema due to severe
ischemia & hemorrhage
◊ Tissue plasminogen activator (tPA)
o Only stroke drug that actually breaks up
a blood clot. It’s used as a common
emergency treatment during a stroke..
OTHER HEALTHCARE MANAGEMENT
◊ Occupational Therapy
◊ Speech Therapy
◊ Nutritionist
PHYSICAL THERAPY, EXAMINATION, EVALUATION,
AND DIAGNOSIS
POINTS OF EMPHASIS ON EXAMINATION
General Points of Examination
◊ Subjective
◊ Pain
◊ Signs of increased intracranial pressure
◊ Level of consciousness
◊ Emotional status & behavior
◊ Cognition
◊ Communication & language
◊ Integumentary integrity
◊ Vital signs
◊ Aerobic capacity/endurance
◊ Sensory examination
◊ Cranial & peripheral nerve integrity
◊ Neuromuscular & reflexes
◊ Musculoskeletal
23
 o ROM
o MMT
o MBT
◊ Balance & tolerance
◊ Coordination
◊ Gait & locomotion
◊ Functional Assessment
PT PROBLEM LIST
◊ Impaired sensation
◊ LOM on one side of the body (due to hemiplegia
or hemiparesis)
◊ Muscle weakness on one side of the body (due
to hemiplegia or hemiparesis)
◊ Increased/decreased muscle tone or spasticity
(depends on ·Brunnstrom’s Stages of Motor
Recovery)
◊ Flaccidity (depends on ·Brunnstrom’s Stages of
Motor Recovery)
◊ Impaired cardiorespiratory
◊ Impaired perception and perceptual deficit
(depend on severity and location of affectation)
◊ Impaired balance and tolerance
◊ Impaired coordination
◊ Impaired gait
◊ Impaired posture
◊ Dependent in ADLs
PT DIAGNOSIS
◊ Neuromuscular Practice Pattern D: Impaired
Motor Function & Sensory Integrity Associated
With Non-Progressive Disorders of the Central
Nervous System - Acquired in Adolescence or
Adulthood
PT PROGNOSIS
◊ Impairments may resolve spontaneously as
brain swelling subsides (reversible ischemic
neurological deficit), within 3 weeks. Residual
neurological impairments are those that persist
longer than 3 weeks & may lead to lasting
disability
◊ DTR usually return within 24-28 hrs. Motor
paralysis resolves through synergy patterns to
voluntary segmental movements.
◊ The first three months of recovery is the MOST
important month - golden period percent for
treating cva patients as it reveals most
measurable neurologic recovery and the
potential for plasticity of the nervous system
◊ Brunnstrom’s Stages of Motor Recovery
◊ Poor Prognosis for Neurologic Activity
o Previous history of stroke
o Old age
o Visuospatial defect
o Urinary incontinence
◊ Poor Prognosis for Functional Recovery
o Prolonged flaccidity
o Late onset of rigidity & DTR
o No voluntary hand movement
o Severe proximal spasticity
PHYSICAL THERAPY PLAN OF CARE
PT LONG AND SHORT TERM GOALS
◊ Pt. will demonstrate an ↑ in sensation from a
score of 0 to 1 in sensory assessment p 9 PTR
session to improve functional performance.
◊ Pt. will manifest an increase in range of motion p
10 PTR sessions to improve functional
independence
◊ Pt. will manifest an ↑ of 1 grade in muscle
strength within 10 PTR sessions to improve
muscle performance. and increase functional
performance
◊ Pt. will exhibit decreased mm tone from a grade
1 to grade 0 p 10 PTR sessions to increase
functional performance
◊ Pt. will manifest an improvmeent in
cardiorespiratory p 10 PTR sessions to improve
aerobic capacity
◊ Pt. will exhibity improvements in perception p 15
PTR sessions to improve functional performance
◊ Pt. will exhibit improvements in balance and
tolerance p 15 PTR sessions to improve
functional independence
◊ Pt. will exhibit improvements in coordination p
15 PTR sessions to improve functional
independence
◊ Pt. will show an improved gait within 15 PTR
sessions to ↑ safety and achieve better mobility
independence
◊ Pt. will exhibit an improved posture in 12 PTR
sessions to ↑ safety & functional independence
◊ Pt will manifest ↑ independence as to self-care &
mobility within 20 PTR sessions to ↑ functional
independence
PT INTERVENTIONS
◊ Mirror therapy x 10 ins to improve detection of
light touch, pressure and temperature pain and
improve perception
◊ Thermal stimulation x 10 mins to improve rate of
recovery of sensation
◊ Neuromuscular electrical stimulation (NMES) x
10 mins to reduce spasticity, improve sensory
awareness, prevent or reduce shoulder
subluxation, and stimulate volitional movements
◊ Intermittent pneumatic compression x 10 mins
for improving tactile and kinesthetic sensation
◊ PROM exercises x 2 sets x 8 reps to improve
range of motion and improve functional
independence
◊ AROM exercises x 2 sets x 8 reps to improve
range of motion and improve functional
independence
◊ Self-ROM Activitiesx 2 sets x 8 reps to improve
range of motion and improve functional
independence
o Arm cradling:
o Table-top polishing
o Sitting, the patient leans forward and
reaches both hands down to the floor to
encourage forward flexion of the
humerus with scapular protraction, and
extension of the elbow, wrist, and
fingers
o Supine, hands are clasped together and
placed behind the head, the elbows fall
flat to the mat.
◊ Progressive resistive strength training x 2 sets x
8 repss x 10 SH to improve muscle strength and
increase functional independence
24
◊ Strengthening exercises with modalities such as
free weights, elastic bands or tubing x 2 sets x 8
reps to improve muscle performance and
increase functional independence
◊ Gravity-resisted active movements such as arm
lifts and leg lifts x 2 sets x 8 reps to improve
graded 3/5 muscle strength and increase
functional independence
◊ Bridging x 2 setx x 8 reps to promote muscle
improvements in knee flexors and hip extensors
◊ Lower trunk rotation (LTR) activities such as n
side-lying; supine, modified hook-lying; kneeling;
or standing x 2 sets x 8 reps to improve pelvic
control
◊ Rhythmic rotation incorporates with slow gentle
rotations of the limb while progressively moving
the limb into its lengthening range x 2 sets x 8
reps to decrease spasticity
◊ Roods technique (inhibitory techniques) x 10
mins to decrease spasticity
◊ Electromyographic biofeedback (EMG-BFB) x
10 mins to improve motor function in patients
and decrease spasticity
◊ Rood’s facilitatory technique such - A-icing x 10
mins to decrease flaccidity
◊ Rood’s facilitatory technique - Tapping x 10 mins
to decrease flaccidity
◊ Rood’s facilitatory technique - VIbration x 10
mins to decrease flaccidity
◊ Upper and lower body ergometer x 15 minsto
improve aerobic capacity
◊ Seated stepper.x 15 mins to improve aerobic
capacity
◊ Standing on a half-foam roller or wobble board x
15 mins to promote ankle strategies
◊ Anteriorposterior shifts or stronger perturbations
x 10 mins to promote hip strategies
◊ Tandem stance on floor or foam roller x 10 mins
to promote medial-lateral hip strategies.
◊ Forward, backward, or sideward leans x 10 mins
to promote stepping strategies.
◊ Tandem walking on a lime x 10 mins to improve
balance
◊ Walking on/off foams x 10 mins to improve
balance
◊ Reaching and manipulation techniques x 10mins
to improve upper extremity function and
coordination
◊ PNF LE D1 extension pattern; holding against
elastic band resistance around the upper thighs
in supine or standing positions x 2 sets x 8 reps
to improve lower extremity functions and
coordination
◊ Lateral side-steps x 2 sets x 8 reps to improve
lower extremity functions and coordination
◊ Standing step-ups x 2 sets x 8 reps to improve
lower extremity function to improve coordination
◊ Frenkel’s Exercises x 2 sets x8 reps to improve
coordination and proprioception
◊ Task-specific overground locomotor training (LT)
x 15 mins focuses on practicing a variety of
activities and on improving the quality of walking
and walking endurance.
◊ Gait Training x15 mins c gait belt and CGA to
improve gait and functional performance :
o Walking forward
o Walking backward
o Side stepping
o Crossed stepping
o Step-up/step-down activities; lateral
set=ups
o Stair climbing; step-over-step
o Walking in a simulated home
environment:
o Walking in a community environment:
o Activities that involve coincident timing:
Crossing at a streetlight; stepping on
and off elevators or escalators; walking
through automatic doors
o Dual-task activities: Walking while
holding a ball, bouncing a ball, carrying
a tray, carrying on a conversation
◊ Lifting free weights or using elastic bands x 2
sets x 8 reps to improve postural stability in
sitting and standing
◊ Postural correction exercises done in front of a
mirror x 10-15 min to improve body image while
providing tactile, verbal cues, feedback, head
straps
◊ Functional Training Exercises to improve
functional perofrmance
o PNF D1 flexion of the LE x 2 sets x 8
reps to improve bed mobility
o Sitting on a therapy ball x 10 mins to
promote pelvic alignment and mobility
o Sit-to-stand and sit-down transfers x 2
sets 8 repts to improve functional
independence
o Transfers activitng x 2 sets x 8 reps to
improve functional performance
◊ Combining resistance training with task-oriented
functional activities x 2 sets x 8 reps to enhance
carryover in terms of improving function (e.g.,
sit-to-stand transfers, partial wall squats],
step-ups, stair climbing while the patient is
wearing weighted cuffs)
REFERENCES
◊ Please cite accordingly.
Books:
◊ O’Sullivan, S.B., Schmitz, T.J., & Fulk, G.D.
(2014). Physical Rehabilitation (6th ed.).
◊ CICCONE, C. D. (2021). PHARMACOLOGY IN
REHABILITATION. S.l.: F A DAVIS.
Websites:
◊ Stroke. (n.d.). Retrieved May 08, 2021, from
https://www.physio-pedia.com/Stroke
◊ Types of Stroke: Ischemic, Hemorrhagic, and
TIA. WebMD.
https://www.webmd.com/stroke/guide/types-stro
ke. Accessed May 8, 2021.
◊ Types of stroke. Stroke Association.
https://www.stroke.org.uk/what-is-stroke/types-of
-stroke#:~:text=An%20ischaemic%20stroke%20i
s%20caused,known%20as%20a%20mini%2Dst
roke. Published April 7, 2021. Accessed May 8,
2021.
◊ Ellis ME. Hemorrhagic Stroke: Symptoms,
Treatment, and Long-Term Outlook. Healthline.
https://www.healthline.com/health/hemorrhagic-s
troke#recovery. Published September 18, 2018.
Accessed May 8, 2021.
25
◊ Team the HE. Stroke Medication:
Anticoagulants, tPA, Statins, and More.
Healthline.
https://www.healthline.com/health/stroke/drugs#t
akeaway. Published June 7, 2019. Accessed
May 8, 2021.

◊ Publishing HH. Hemorrhagic Stroke. Harvard

Health.
https://www.health.harvard.edu/a_to_z/hemorrha
gic-stroke-a-to-z#:~:text=About%2030%25%20t
o%2060%25%20of,enough%20to%20reach%20
a%20hospital. Accessed May 8, 2021.

◊ Hemorrhagic Strokes (Bleeds). www.stroke.org.

https://www.stroke.org/en/about-stroke/types-of-
stroke/hemorrhagic-strokes-bleeds. Accessed
May 8, 2021.

◊ What is the pathophysiology of hemorrhagic

stroke? Latest Medical News, Clinical Trials,
Guidelines - Today on Medscape.
https://www.medscape.com/answers/1916662-5
3869/what-is-the-pathophysiology-of-hemorrhagi
c-stroke. Published November 10, 2019.
Accessed May 8, 2021.

◊ Matos Casano HA, Tadi P, Ciofoaia GA. Anterior

Cerebral Artery Stroke. [Updated 2021 Jan 31].
In: StatPearls [Internet]. Treasure Island (FL):
StatPearls Publishing; 2021 Jan-. Available
from:
https://www.ncbi.nlm.nih.gov/books/NBK537333/
◊ Omudhome Ogbru, P. D. (2019, July 5).
alteplase (TPA, Cathflo Activase): Uses, Side
Effects, and Dosage. MedicineNet.
https://www.medicinenet.com/alteplase/article.ht
m.
◊ RxList. (2017, September 6). Mannitol: Side
Effects, Dosages, Treatment, Interactions,
Warnings. RxList.
https://www.rxlist.com/consumer_mannitol_osmit
rol/drugs-condition.htm

26
PHARMACOLOGICAL MANAGEMENT SUMMARY

Medications Functions Side Effects PT Implications

Antiplatelets Prevent excessive clotting caused by increased Increased risk of bleeding Patients taking these agents should be especially alert for any unexplained or
(clopidogrel and platelet activity Hypotension heavy bleeding or any other symptoms that might indicate hemorrhage
plavix) (sudden increases in joint or back pain, severe headaches, etc.)

Hyperosmolar To reduce edema due to severe ischemia & ● Nausea PT should be alert because pt. is at risk of low blood volume or hypovolemia,
Agents (Mannitol, hemorrhage ● Vomiting headache and excessive thirst
Glycerol) ● Headache
● Increased thirst
● Chills, fever
● Confusion or disorientation,
● Electrolyte imbalances
● Urinary retention
Tissue plasminogen Only stroke drug that actually breaks up a blood Other important side effects include: PT should be alert because the most common and serious side effect of
activator (tPA) clot. It’s used as a common emergency ● Nausea alteplase is bleeding. Minor bleeding is more common, but significant bleeding
treatment during a st ● Vomiting such as into the brain (intracranial hemorrhage) or fatal bleeding also occurs.
Other possible serious side effects
include:
● Pulmonary embolism
● Cholesterol embolism
● Abnormal heartbeats
● Allergic reactions
● Re-embolization of deep
DVT venous thrombi during
treatment of acute massive
pulmonary embolism
● Angioedema
● Bleeding

PT PLAN OF CARE SUMMARY

PROBLEM GOAL INTERVENTION

Impaired sensation
Pt. will demonstrate an ↑ in sensation from a score of 0 to 1 in
sensory assessment p 9 PTR session to improve functional
performance.
◊ Mirror therapy x 10 ins to improve detection of light touch, pressure and temperature pain
and improve perception
◊ Thermal stimulation x 10 mins to improve rate of recovery of sensation
◊ Neuromuscular electrical stimulation (NMES) x 10 mins to reduce spasticity, improve
sensory awareness, prevent or reduce shoulder subluxation, and stimulate volitional
movements
◊ Intermittent pneumatic compression x 10 mins for improving tactile and kinesthetic
sensation
27
LOM on one side of the body
(due to hemiplegia or
hemiparesis)
Muscle weakness on one
side of the body (due to
hemiplegia or hemiparesis)
Increased/decreased muscle
tone or spasticity (depends
on ·Brunnstrom’s Stages of
Motor Recovery)
Flaccidity (depends on
·Brunnstrom’s Stages of
Motor Recovery)
Impaired cardiorespiratory
Pt. will manifest an increase in range of motion p 10 PTR
sessions to improve functional independence
Pt. will manifest an ↑ of 1 grade in muscle strength within 10
PTR sessions to improve muscle performance. and increase
functional performance
Pt. will exhibit decreased mm tone from a grade 1 to grade 0
p 10 PTR sessions to increase functional performance
Pt. will manifest an ↑ in muscle tone within 10 PTR sessions
to improve muscle performance
Pt. will manifest an improvement in cardiorespiratory p 10
PTR sessions to improve aerobic capacity
◊ PROM exercises x 2 sets x 8 reps to improve range of motion and improve functional
independence
◊ AROM exercises x 2 sets x 8 reps to improve range of motion and improve functional
independence
◊ Self-ROM Activitiesx 2 sets x 8 reps to improve range of motion and improve functional
independence
o Arm cradling:
o Table-top polishing
o Sitting, the patient leans forward and reaches both hands down to the floor to
encourage forward flexion of the humerus with scapular protraction, and extension
of the elbow, wrist, and fingers
o Supine, hands are clasped together and placed behind the head, the elbows fall
flat to the mat.
◊ Progressive resistive strength training x 2 sets x 8 repss x 10 SH to improve muscle
strength and increase functional independence
◊ Strengthening exercises with modalities such as free weights, elastic bands or tubing x 2
sets x 8 reps to improve muscle performance and increase functional independence
◊ Gravity-resisted active movements such as arm lifts and leg lifts x 2 sets x 8 reps to
improve graded 3/5 muscle strength and increase functional independence
◊ Bridging x 2 setx x 8 reps to promote muscle improvements in knee flexors and hip
extensors
◊ Lower trunk rotation (LTR) activities such as n side-lying; supine, modified hook-lying;
kneeling; or standing x 2 sets x 8 reps to improve pelvic control.
◊ Rhythmic rotation incorporates with slow gentle rotations of the limb while progressively
moving the limb into its lengthening range x 2 sets x 8 reps to decrease spasticity
◊ Roods technique (inhibitory techniques) x 10 mins to decrease spasticity
◊ Electromyographic biofeedback (EMG-BFB) x 10 mins to improve motor function in
patients and decrease spasticity
◊ Neuromuscular electrical stimulation (NMES) x 10 mins to reduce spasticity, improve
sensory awareness,
◊ Rood’s facilitatory technique such - A-icing x 10 mins to decrease flaccidity
◊ Rood’s facilitatory technique - Tapping x 10 mins to decrease flaccidity
◊ Rood’s facilitatory technique - VIbration x 10 mins to decrease flaccidity
◊ Upper and lower body ergometer x 15 mins to improve aerobic capacity
◊ Seated stepper.x 15 mins to improve aerobic capacity
28
Impaired perception and
perceptual deficit (depend on
severity and location of
affectation)
Pt. will exhibit improvements in perception p 15 PTR sessions ◊ Mirror therapy x 10 mins to improve detection of light touch, pressure and temperature
to improve functional performance
pain and improve perception
◊ Intermittent pneumatic compression x 10 mins for improving tactile and kinesthetic
sensation and perception
◊ Neuromuscular electrical stimulation (NMES) x 10 mins to reduce spasticity, improve
sensory awareness and perception, prevent or reduce shoulder subluxation, and stimulate
volitional movements
◊ Frenkel’s Exercises x 2 sets x 8 reps to improve coordination and proprioception

Impaired balance and Pt. will exhibit improvements in balance and tolerance p 15 ◊ Standing on a half-foam roller or wobble board x 15 mins to promote ankle strategies
tolerance PTR sessions to improve functional independence
◊ Anterior posterior shifts or stronger perturbations x 10 mins to promote hip strategies
◊ Tandem stance on floor or foam roller x 10 mins to promote medial-lateral hip strategies.
◊ Forward, backward, or sideward leans x 10 mins to promote stepping strategies.
◊ Tandem walking on a lime x 10 mins to improve balance
◊ Walking on/off foams x 10 mins to improve balance

Impaired coordination Pt. will exhibit improvements in coordination p 15 PTR

sessions to improve functional independence
◊ Reaching and manipulation techniques x 10mins to improve upper extremity function and
coordination
◊ PNF LE D1 extension pattern; holding against elastic band resistance around the upper
thighs in supine or standing positions x 2 sets x 8 reps to improve lower extremity
functions and coordination
◊ Lateral side-steps x 2 sets x 8 reps to improve lower extremity functions and coordination
◊ Standing step-ups x 2 sets x 8 reps to improve lower extremity function to improve
coordination
◊ Frenkel’s Exercises x 2 sets x 8 reps to improve coordination and proprioception

Impaired gait Pt. will show an improved gait within 15 PTR sessions to ↑
safety and achieve better mobility independence
◊ Task-specific overground locomotor training (LT) x 15 mins focuses on practicing a variety
of activities and on improving the quality of walking and walking endurance.
◊ Gait Training x15 mins c gait belt and CGA to improve gait and functional performance :
o Walking forward
o Walking backward
o Side stepping
o Crossed stepping
o Step-up/step-down activities; lateral set=ups
o Stair climbing; step-over-step
o Walking in a simulated home environment:
o Walking in a community environment:

29

Impaired posture Pt. will exhibit an improved posture in 12 PTR sessions to ↑
safety & functional independence
Dependent in ADLs Pt will manifest ↑ independence as to self-care & mobility
within 20 PTR sessions to ↑ functional independence
HOME EXERCISE PROGRAM
13. Mirror therapy using mirrors at home x 10 mins to improve detection of light touch,
pressure and temperature pain and improve perception
14. Self-ROM Activities x 2 sets x 8 reps to improve range of motion and improve
functional independence
a. Arm cradling:
b. Table-top polishing
c. Sitting, the patient leans forward and reaches both hands down to the floor
to encourage forward flexion of the humerus with scapular protraction, and
extension of the elbow, wrist, and fingers
d. Supine, hands are clasped together and placed behind the head, the elbows
fall flat to the mat.
15. Progressive resistive strength training x 2 sets x 8 repss x 10 SH to improve muscle
strength and increase functional independence
16. Strengthening exercises with modalities such as free weights, elastic bands or
tubing x 2 sets x 8 reps to improve muscle performance and increase functional
independence
17. Rhythmic rotation incorporates with slow gentle rotations of the limb while
progressively moving the limb into its lengthening range x 2 sets x 8 reps to
decrease spasticity
18. Tandem walking on a lime x 10 mins to improve balance
o Activities that involve coincident timing: Crossing at a streetlight; stepping on and
off elevators or escalators; walking through automatic doors
o Dual-task activities: Walking while holding a ball, bouncing a ball, carrying a tray,
carrying on a conversation
◊ Lifting free weights or using elastic bands x 2 sets x 8 reps to improve postural stability in
sitting and standing
◊ Postural correction exercises done in front of a mirror x 10-15 min to improve body image
while providing tactile, verbal cues, feedback, head straps
◊ Functional Training Exercises to improve functional performance
o PNF D1 flexion of the LE x 2 sets x 8 reps to improve bed mobility
o Sitting on a therapy ball x 10 mins to promote pelvic alignment and mobility
o Sit-to-stand and sit-down transfers x 2 sets 8 reps to improve functional
independence
o Transfers activitng x 2 sets x 8 reps to improve functional performance
◊ Combining resistance training with task-oriented functional activities x 2 sets x 8 reps to
enhance carryover in terms of improving function (e.g., sit-to-stand transfers, partial wall
squats], step-ups, stair climbing while the patient is wearing weighted cuffs).
PRECAUTIONS
9. Fall risk
10. Always monitor vital signs before and after performing exercises.
11. Avoid valsalva maneuver to prevent increase in blood pressure.
12. Pt. must be encouraged to rest intervals between exercises or activities in order to avoid
fatigue.
13. Maintain proper posture during exercises.
14. Avoid activities that worsen the condition.
15. Take precautions to avoid falls by adding environmental modifications such as handrails,
non slip mat etc.
16. Risk for developing DVT, edema, pressure sores, contractures, and other complications
30
19. Walking on/off foams x 10 mins to improve balance
20. Lateral side-steps x 2 sets x 8 reps to improve lower extremity functions and
coordination
21. Standing step-ups x 2 sets x 8 reps to improve lower extremity function to improve
coordination
22. Gait Training x15 mins c gait belt and CGA to improve gait and functional
performance :
a. Walking forward
b. Walking backward
23. Postural correction exercises done in front of a mirror x 10-15 min to improve body
image while providing tactile, verbal cues, feedback, head straps
24. Functional Training Exercises to improve functional performance
a. PNF D1 flexion of the LE x 2 sets x 8 reps to improve bed mobility
b. Sitting on a therapy ball x 10 mins to promote pelvic alignment and mobility
c. Sit-to-stand and sit-down transfers x 2 sets 8 reps to improve functional
independence
d. Transfers activitng x 2 sets x 8 reps to improve functional performance

31

INTERNAL CAROTID ARTERY SYNDROME
GENERAL MEDICAL BACKGROUND
DEFINITION
◊ Occlusion of the internal carotid artery (ICA) due
to atherosclerosis produces massive infarction in
the region of the brain supplied by the middle
cerebral artery.
◊ The clinical spectrum of ICA occlusion ranges
from being a completely asymptomatic occlusion
to a devastating stroke or death.
EPIDEMIOLOGY
◊ The accurate prevalence and incidence rates of
internal carotid artery (ICA) occlusion are difficult
to ascertain as ICA occlusion can remain
asymptomatic.
◊ Symptomatic internal carotid artery occlusion
has an incidence of six per 100,000, though the
rate of asymptomatic chronic occlusion is
unknown and may be higher.
◊ Internal carotid artery occlusion is a known risk
factor for stroke in the United States.
◊ One-third of all the strokes are related to carotid
occlusive disease. Stroke ranks third among all
causes of death in the United States, behind
heart disease and cancer.
◊ Annually about 55,000 more women are affected
compared with men, and approximately 60% of
all stroke deaths occur in females.
◊ African Americans and Mexican Americans have
a higher risk of stroke compared with
Caucasians.
ETIOLOGY
◊ Most cases of ischemic strokes are due to
stenosis, clot and embolism and carotid artery
stenosis (CAS) accounts for 20 to 30% of all
ischemic strokes cases caused by extracranial
CAS and around 5 to while intracranial CAS
accounts for 5 to 10% of strokes.
◊ CAS is due to atherosclerosis. As the
atherosclerosis progresses the atherosclerotic
plaques rupture resulting in the formation of
thrombus and arterial occlusion or dislodged
materials from the plaques blocking the smaller
branches of the carotid artery.
◊ Transient ischemic attacks (TIA) are a brief
period of symptoms similar to stroke due to
temporary blockage of blood supply to a section
of the brain and often lasts less than 24 hours.
RISK FACTORS
◊ Risk of developing stroke after TIAs is as high
as 20% within the 1st month. If untreated, TIAs
result in development of stroke within 2 years.
Risk of stroke events remains high for 10 to 15
years after TIAs.
◊ Risk factors for development of CAS are similar
to those for CAD and other peripheral vascular
disease. These risk factors include:
dyslipidemia, hypertension, diabetes, advanced
glycation end products (AGEs) and its receptors,
obesity, cigarette smoking, lack of exercise, age,
and C-reactive protein.
PATHOMECHANICS / PATHOPHYSIOLOGY
◊ Total internal carotid artery occlusion results
from thrombosis in the setting of chronic
stenosis.
◊ Cardiogenic embolization to a normal carotid
bifurcation of carotid dissection may also cause
total occlusion of the internal carotid artery
occlusion. Acute occlusion may result in a
carotid territory stroke.
◊ A previously asymptomatic chronic internal
carotid artery occlusion may become
symptomatic if related to embolic or
hemodynamic issues.
◊ Embolism may occur from the ipsilateral external
carotid artery via collaterals to the cerebral
circulation. It may also happen when there is
occult patency of the occluded internal carotid
artery occlusion, which then serves as the
source of embolic material.
◊ Hemodynamic insufficiency may occur when any
condition that interferes with cerebral perfusions
such as orthostasis, hypotension, volume
depletion, or cardiac failure is superimposed on
the carotid occlusion, especially when the
contralateral carotid disease is significant.
CLINICAL PRESENTATION
◊ ICA occlusion ranges from being a completely
asymptomatic occlusion (for adequate collateral
flow) to a devastating stroke or death.
◊ Similar clinical features of transient ischemic
attack or stroke (MCA or mixed of MCA and
ACA syndrome)
◊ Transient monocular blindness or (amaurosis
fugax) is highly suggestive of ICA disease
proximal to the ophthalmic branch.
o retinal ischemia in rare cases
o Venous stasis retinopathy occurs in
about one third of the patients with
symptomatic ICA occlusion but clinical
manifestations are rare.
◊ With limited or decreased blood flow to the
brain, cerebral perfusion decreases.
◊ Unaccustomed headaches in chronic ICA
occlusion
◊ ABC pulsations of Fisher is the ipsilateral brisk
pulsations at the angle of the jaw, brow and
cheek
o caused by the collateral flow from the
branches of external carotid artery
(ECA)
◊ Syncopal episodes
◊ Chronic cerebral ischemia is caused by ICA
occlusion could cause dementia.
COMPLICATIONS
◊ Limb shaking as a hemodynamic compromise
in ICA occlusion.
o complain of repetitive involuntary
movements of one or both limbs on one
side.
o misdiagnosed as partial seizures
◊ Retinal claudication resulting from an increase in
metabolic demand in the retina on the
background of an already reduced perfusion.
◊ Chronic ocular ischemia occurs when severe
occlusion develops and the patient complains of
progressive loss of visual acuity.
MEDICAL DIAGNOSIS
32
 ◊ Ultrasonography is usually the initial imaging
modality for the evaluation of symptomatic ICA
disease.
o B‐mode (brightness modulation)
ultrasonography is quite accurate for
assessing luminal narrowing and for
differentiating normal artery or artery
with non‐significant plaque disease from
a severely stenotic lesion
o The use of a contrast agent with duplex
ultrasound imaging techniques has
improved reliability in distinguishing total
occlusions from near‐total occlusions
◊ Magnetic resonance angiography (MRA)
o with or without gadolinium
enhancement, is increasingly used in
the evaluation of stroke
o does not show the vessel anatomy but
creates an image of flow in the vessels
◊ Computed tomography–angiography (CTA)
◊ Digital subtraction angiography is the “gold
standard” imaging modality for the evaluation of
carotid occlusive disease.
DIFFERENTIAL DIAGNOSIS
Caused by a blockage cutting off the
Ischemic
blood supply to the brain
Stroke
Most commonly type
Hemorrhagic Caused by a bleeding in our around the
Stroke brain
Same as stroke except that the
Transient symptoms only last for a short amount
Ischemic of time because the blockage that stops
Attack the blood getting to your brain is
temporary
caused by the restriction of blood
supply on the medial aspect of the
cerebral hemisphere (frontal and
Anterior parietal lobes) and subcortical
Cerebral structures; problems with imitation &
Artery bimanual tasks, apraxia,
unresponsiveness, slowness, delay,
lack of spontaneity, motor inaction
condition involving the restriction of
blood flow which supplies the parts of
the frontal, tempora, and parietal lobes
Middle of the brain including its deeper
Cerebral structures; problem with perceptual
Palsy deficits, fluent aphasia, global aphasia,
aprosody, affective agnosia, apraxia,
frontal gaze palsy, premotor
hemiplegia, Gerstmann syndrome
PROGNOSIS
◊ The subject of future risk of stroke or TIA in
patients with ICA occlusion is complex. A
never‐symptomatic ICA occlusion is considered
to have a benign course. However, symptomatic
ICA occlusion increases the risk of future
cerebrovascular events.
GENERAL HEALTHCARE MANAGEMENT
MEDICAL MANAGEMENT
◊ Prescription, operative techniques and patient
education of neurologists with collaboration with
other healthcare professionals to treat internal
carotid occlusion which lead to complication of
the MCA or MCA & ACA stroke.
SURGICAL MANAGEMENT
◊ External carotid–internal carotid bypass surgery:
the superficial temporal artery to middle cerebral
artery bypass can improve CBF in patients with
symptomatic unilateral carotid occlusion.
◊ Endarterectomy or angioplasty stenting of a
hemodynamically relevant stenosis of the
contralateral ICA.
o In patients with ICA occlusion resulted in
a long‐term cerebral haemodynamic
improvement not only on the side of
surgery but also on the side of the ICA
occlusion.
PHARMACOLOGICAL MANAGEMENT
◊ Antiplatelets (clopidogrel and plavix)
o Can be used to help prevent blood clots.
They work by making it more difficult for
the platelets in your blood to stick
together, which is the first step in the
formation of blood clots
◊ Aspirin has shown to reduce risk of future
cardiovascular events in patients with TIAs or
non‐disabling ischaemic stroke from any cause.
OTHER HEALTHCARE MANAGEMENT
◊ Modification of risk factors such as modifying a
patient's diet, lifestyle and other factors to
address cardiovascular diseases hypertension,
diabetes, hyperlipidaemia and smoking—are
vital secondary prevention measures.
PHYSICAL THERAPY, EXAMINATION, EVALUATION,
AND DIAGNOSIS
◊ Refer to Middle Cerebral Artery Syndrome or
Anterior Cerebral Artery Syndrome Subjective
REFERENCES
Books:
◊ O’Sullivan, S.B., Schmitz, T.J., & Fulk, G.D.
(2014). Physical Rehabilitation (6th ed.).
◊ CICCONE, C. D. (2021). Pharmacology In
Rehabilitation. S.L.: F A Davis.
Websites:
◊ What is cerebral perfusion pressure? (2018,
October 10). University of Iowa Hospitals &
Clinics.
https://uihc.org/health-topics/what-cerebral-perfu
sion-pressure
◊ Prasad K. (2015). Pathophysiology and Medical
Treatment of Carotid Artery Stenosis. The
International journal of angiology : official
publication of the International College of
Angiology, Inc, 24(3), 158–172.
https://doi.org/10.1055/s-0035-1554911
◊ Tsiskaridze, A. (2001, April 1). Stroke With
Internal Carotid Artery Stenosis.
33
 Cerebrovascular Disease | JAMA Neurology |
JAMA Network.
◊ https://jamanetwork.com/journals/jamaneurology
/fullarticle/779136
◊ Thanvi, B., & Robinson, T. (2007). Complete
occlusion of extracranial internal carotid artery:
clinical features, pathophysiology, diagnosis and
management. Postgraduate medical journal,
83(976), 95–99.
https://doi.org/10.1136/pgmj.2006.048041
◊ StatPearls. (2021, February 17). Carotid Artery
Stenosis.
https://www.statpearls.com/ArticleLibrary/viewart
icle/18961
◊ Zohrabian, D. (2021, April 29). Carotid Artery
Dissection Clinical Presentation: History,
Physical Examination. StatPearls.
https://emedicine.medscape.com/article/757906-
clinical#b1
◊ Padalino, D. J. (2014, January 22). Management
of Atherosclerotic Carotid Artery Stenosis.
IntechOpen.
https://www.intechopen.com/books/carotid-artery
-disease-from-bench-to-bedside-and-beyond/ma
nagement-of-atherosclerotic-carotid-artery-steno
sis
◊ Lanzino, G., Rabinstein, A. A., & Brown, R. D.,
Jr (2009). Treatment of carotid artery stenosis:
medical therapy, surgery, or stenting?. Mayo
Clinic proceedings, 84(4), 362–368.
https://doi.org/10.1016/S0025-6196(11)60546-6

34
ANTERIOR CEREBRAL ARTERY SYNDROME
Urinary incontinence Posteromedial aspect of
superior frontal gyrus
GENERAL MEDICAL BACKGROUND
Problems with imitation & Corpus callosum
DEFINITION
bimanual tasks, apraxia
A condition caused by the restriction of blood supply on Aulia (total Uncertain location
the medial aspect of the cerebral hemisphere (frontal unresponsiveness),
and parietal lobes) and subcortical structures. akinetic mutism (partial
unresponsiveness),
EPIDEMIOLOGY slowness, delay, lack of
ACA accounts for 0.3-4.4% of stroke cases in series spontaneity, motor inaction
reports and is considered one of the rare causes of
ischemic infarctions. C/L grasp reflex, sucking
Men > Women reflex
Mean age: 59 - 74.4 years old. Prevalent among > 85
y.o. Paratonia/Gegenhalten -
Left-sided ACA infarcts are more frequent ipsilateral/bilateral rigidity
or hypertonia with
ETIOLOGY involuntary variable
Atherosclerosis is a primary cause of ischemic stroke. resistance to PROM
Artherosclerotic large vessel disease is oftenly caused in
stroke 2° to either local branch occlusion by plaque, Possible frontal
artery to artery embolism, and in situ thrombosis. This is (horizontal) gaze palsy
the most frequently reported etiology among patients of
Asian origin.
COMPLICATIONS
RISK FACTORS
Cardiac embolism from different sources, including atrial
Most Common: Hypertension, diabetes mellitus,
fibrillation, intracardiac thrombus, valve disease, and
hypercholesterolemia, and smoking. Found in stroke
tumors are other significant causes of ACA infarction.
patients.
Some reports suggest that cardiac emboli are more
Eating fatty and sweet meals and continuous use of
frequently the cause of ACA as compared to MCA and
cigarettes and unhealthy lifestyle may increase the risk
PCA infarcts.
of the patient having these conditions.
Patients with large infarctions are at high risk of
developing brain edema.
Early transfer of patients at risk to an institution with MEDICAL DIAGNOSIS
neurosurgical expertise should be considered.
CLASSIFICATION Test Result Healthy
Left ACA - Right leg upper-motor neuron weakness due
to damage to the motor cortex and right leg cortical National Severity of stroke A patient
sensory loss due to damage to the sensory cortex. Institutes of based on scoring: has a score
Grasp reflex, frontal lobe behavioral abnormalities, and Health Stroke 1-4: Mild stroke of 0.
transcortical aphasia can also be seen if the prefrontal Scale (NIHSS) - 5-15: Moderate
cortex and supplementary motor areas are involved. a standardized stroke
Right ACA - Left leg upper-motor neuron weakness due method for 16-20: Moderate to
to damage to the motor cortex and left leg cortical type quantifiable severe stroke
sensory loss due to damage to the sensory cortex. assessment of 21-42: Severe
Grasp reflex, frontal lobe behavioural abnormalities and stroke stroke
left hemineglect can also be seen if the prefrontal cortex symptoms. It is
and non-dominant association cortex are involved. the preferred
PATHOMECHANICS / PATHOPHYSIOLOGY scoring system,
The size of the infarct will also influence the clinical and scores range
presentation. Most commonly, patients will present with from 0 to 42
motor deficits characteristically involving the lower
extremity contralateral to the infarct site. This finding is CT scan - a Ischemic changes No ischemic
present in 86.3 to 90% of patients. non-contrast CT may classify as changes
of the head is the acute, subacute, detected
CLINICAL PRESENTATION imaging modality and chronic,
of choice depending on the
time in which they
S/Sx Structure Involved present after the
onset of stroke. CT
C/L hemiparesis of LE Primary motor are (Area scan can also rule
4 & 6), medial aspect of out intracranial
cortex, IC hemorrhage.
C/L hemisensory loss of Primary sensory area MRI with There is a No
LE (Area 3, 1, 2), medial diffusion-weight demarcation of demarcation
aspect of cortex ed imaging - a ischemic detected

35
 o ROM
highly useful boundaries in the
o MMT
modality which territory of the ACA
o MBT
can detect the
◊ Balance & tolerance
boundaries of the
◊ Coordination
ACA.
◊ Gait & locomotion
◊ Functional Assessment
DIFFERENTIAL DIAGNOSIS
The differential of stroke in general, as well as one that PT PROBLEM LIST
involves the anterior cerebral artery, include metabolic,
hypoglycemia, infectious (fever, sepsis), cardiovascular ◊ Spasticity
(e.g., syncope), migraines, tumors, abscess, ◊ LOM on C/L LE
neuromuscular and varied neuropsychiatric conditions. ◊ Weakness at the C/L LE
◊ Loss of Sensation at the C/L LE
PROGNOSIS ◊ Impaired standing and balance tolerance
In-hospital mortality of ACA Pt. can range between 0 and ◊ Incoordination
7.8%. ◊ Impaired posture
In terms of specific deficits, aphasias from ACA tend to ◊ Impaired Gait
improve within a short period as compared to MCA ◊ Impaired performance of ADLs
lesions. Infarct size has a poor correlation with functional
recovery, PT DIAGNOSIS
Patients with major neurological deficits have a high risk ◊ Neuromuscular Practice Pattern D: Impaired
of poor outcome as compared to with minor deficits.
Motor Function & Sensory Integrity Associated
PT intervention can improve a patient's recovery of
With Non-Progressive Disorders of the Central
function and mobility after a case of stroke.
Nervous System - Acquired in Adolescence or
Adulthood
GENERAL HEALTHCARE MANAGEMENT
PT PROGNOSIS
MEDICAL MANAGEMENT
Endovascular treatment with mechanical thrombectomy ◊ Brunnstrom’s Stages of Motor Recovery
(MT) is another proven treatment modality in the ◊ Impairment may begin to subside once brain
management of patients with acute stroke suffering a swelling subsides within 3 weeks. Residual
large vessel occlusion, although treatment efficacy is neurological impairments are those that persist
highly time-dependent. longer than 3 weeks & may lead to lasting
disability
SURGICAL MANAGEMENT ◊ The first three months of recovery is the MOST
Intracranial aneurysm surgery is done to preserve
important month - golden period percent for
perforating arteries. It has shown to have good recovery
treating cva patients as it reveals most
in 15 (75%) patients, moderate disability in 2 (10%)
measurable neurologic recovery and the
patients, severe disability in 2 (10%) patients, and death
potential for plasticity of the nervous system
in 1 (5%) patient.
PHYSICAL THERAPY PLAN OF CARE
PHARMACOLOGICAL MANAGEMENT
Antihypertensives, dual antiplatelet therapy, PT LONG AND SHORT TERM GOALS
anticoagulants, carotid endarterectomy - used to
prevent recurrent events. ◊ LTG: Pt will present an improvement of function
Dual antiplatelet therapy (aspirin and clopidogrel) - are in the affected LE extremities in ROM, strength,
recommended to start within 24 hours for 21 days in fine motor skills, posture, and gait in order to
patients with minor stroke for early secondary stroke functionally perform basic ADLs and improve
prevention. quality of life.
PHYSICAL THERAPY, EXAMINATION, EVALUATION, ◊ Pt. will present a decrease in spasticity from
AND DIAGNOSIS
grade 3 to 1 p 10 PTR to be able to perform
ROM exercises and functional activities.
POINTS OF EMPHASIS ON EXAMINATION
General Points of Examination ◊ Pt. will manifest an increase in range of motion
Subjective in LE p 10 PTR sessions to improve functional
Pain independence
Signs of increased intracranial pressure ◊ Pt. will manifest an ↑ of 1 grade in muscle
◊ Level of consciousness strength in LE within 10 PTR sessions to
◊ Emotional status & behavior improve muscle performance. and increase
◊ Cognition functional performance
◊ Communication & language ◊ Pt. will demonstrate an ↑ in sensation from a
◊ Integumentary integrity
score of 0 to 1 in sensory assessment p 10 PTR
◊ Vital signs
session to improve functional performance.
◊ Aerobic capacity/endurance
◊ Pt. will exhibit improvements in balance and
◊ Sensory examination
tolerance p 13 PTR sessions to improve
◊ Cranial & peripheral nerve integrity
functional independence
◊ Neuromuscular & reflexes
◊ Pt. will exhibit improvements in coordination p
◊ Fine Motor Skills
15 PTR sessions to improve functional
◊ Musculoskeletal
independence
36
 ◊ Pt. will exhibit an improved posture in 10 PTR
stimulation by
sessions to ↑ safety & functional independence
stroking material
◊ Pt. will show an improved gait within 15 PTR
over the patient
sessions to ↑ safety and achieve better mobility
X 10 mins.
independence
◊ Pt will manifest ↑ independence as to self-care &
Pin-prick
mobility within 25 PTR sessions to ↑ functional
sensation X 10
independence
times while Pt
has eyes
PT INTERVENTIONS
opened and
closed.
Problem POC Intervention
Thermal
Spasticity To improve Roods sensation
motor function (inhibitory desensitization
and decrease techniques) by application of
spasticity through gentle warm and cold
rocking x 10 temperature on
mins Pt X 10 times
while Pt has
Electromyograp eyes opened
hic biofeedback and closed.
(EMG-BFB) x
10 mins Impaired To improve
standing coordination in Equilibrium
Gentle Passive balance and performing exercises (e.g.
Stretching on tolerance, and functional tandem walking)
affected LE coordination activities and
extremity x 10 nonequilibrium
reps x 2 sets x 5 exercises (e.g.
SH finger to nose) x
15 minutes
LOM on C/L LE To improve Progression to
range of motion PROM -> Static ->
and improve AAROM -> dynamic
functional AROM balance training
independence exercises x 2 in sitting and
sets x 8 reps standing and
Color match
stepping
Weakness at To improve Strengthening
the C/L LE muscle exercises with
performance progressive use Progress
and increase of theraband activities by
functional colors x 2 sets x working on soft
independence 10 reps surfaces (foam,
grass, sand),
Isometric narrowing base
exercise on of support,
affected moving arms or
muscles x 3 6 closing the
secs hold x 10 eyes.
reps x 2 sets

Progressive Impaired To correct Postural

resistive Posture postural correction
strength training deviations and exercises done
x 10 reps x 2 improve body in front of a
sets x 10 SH image while mirror x 10-15
providing tactile, min
verbal cues,
feedback, head Progress to
straps perturbation
Loss of To improve Desensitization exercises as
Sensation at the sensory through tolerated
C/L LE awareness and application of
prevent multiple types of Stretching of
secondary texture that can tight muscles 10
complications promote reps x 2 sets
sensory

37
 One-Year Outcomes. Stroke, 51(7), 2087–2094.
Impaired Gait To improve gait Progression of
https://doi.org/10.1161/STROKEAHA.119.028418
cycle and gait training
increase from parallel
endurance. bars to even
and uneven MIDDLE CEREBRAL ARTERY SYNDROME
surfaces,
ascending and GENERAL MEDICAL BACKGROUND
descending
stairs DEFINITION
Gait training c
gait belt and ◊ A condition involving the restriction of blood flow
close contact which supplies the parts of the frontal, tempora,
guard from PT and parietal lobes of the brain including its
performing X 10 deeper structures. The MCA is the most
mins common artery that is involved in acute stroke.

Dual-performan EPIDEMIOLOGY
ce of activities ◊ Approximately 85% of stroke cases are ischemic
through walking strokes, and over half of all ischemic strokes
while engaging occur in MCA territory.
in conversation ◊ Men > Women: Young and Middle-aged
with a therapist ◊ Women have a higher risk of stroke than men
x 10 mins. over the course of a lifetime, with the risk for
women being 20% to 21% versus 14% to 17% in
Impaired To promote Transfer men.
performance of independence activities x 10 ◊ Risk of stroke is higher in Blacks and Hispanics
ADLs and improve reps x 2 sets than Whites.
functional from chair to
performance of bed, bed to car,
patients. chair to toilet ETIOLOGY
seat, etc. ◊ Hypertension - MCA stroke is most frequent in
this case.
Stair ambulation
exercises c ◊ Atherosclerosis - Occurs at the origin of the
railings and common carotid artery or at its transition from
assistive device the common carotid artery to the middle cerebral
(e.g. cane) x 5 artery. It can also occur at the main bifurcation of
reps x 2 sets the middle cerebral artery as well as the junction
of the vertebral arteries with the basal artery.
◊ Angiopathies - Less frequent type of stroke.

REFERENCES
Books:
O’Sullivan, S.B., Schmitz, T.J., & Fulk, G.D. (2014).
Physical Rehabilitation (6th ed.).
Websites:
Casano, M. HA, Ciofoaia, T. GA. (2021). Anterior
Cerebral Artery Stroke. In: StatPearls [Internet].
Treasure Island (FL): StatPearls Publishing; 2021 Jan-.
Retrieved from:
https://www.ncbi.nlm.nih.gov/books/NBK537333/
Arboix, A., García-Eroles, L., Comes, E., Oliveres, M.,
Balcells, M., Pacheco, G., & Targa, C. (2003). Predicting
spontaneous early neurological recovery after acute
ischemic stroke. European journal of neurology, 10(4),
429–435.
https://doi.org/10.1046/j.1468-1331.2003.00630.x
Zaidat, O. O., Hanel, R. A., Sauvageau, E. A.,
Aghaebrahim, A., Lin, E., Jadhav, A. P., Jovin, T. G.,
Khaldi, A., Gupta, R. G., Johnson, A., Frei, D., Loy, D.,
Malek, A., Toth, G., Siddiqui, A., Reavey-Cantwell, J.,
Thomas, A., Hetts, S. W., Jankowitz, B. T., & ATLAS
Investigators (2020). Pivotal Trial of the Neuroform Atlas
Stent for Treatment of Anterior Circulation Aneurysms:
RISK FACTORS
◊ Nonmodifiable risk factors of each include age,
sex, race, and genetics. RIsk increases as you
get older. The risk is higher in younger adult
men, but the risk of death is higher overall in
women. Risk is greater in African Americans,
slightly higher in Hispanics and Native
Americans.
◊ Modifiable risk factors, including hypertension,
smoking, obesity, alcohol consumption, and diet
all contribute to both ischemic and hemorrhagic
stroke.
PATHOMECHANICS / PATHOPHYSIOLOGY
◊ MCA stroke occurs when there is an occlusion
of blood supply at the middle cerebral artery
which is responsible for supplying the frontal
lobe and lateral surface of the temporal and
parietal lobes with blood this causes a malignant
MCA infarction manifesting a severe
hemispheric syndrome.
CLINICAL PRESENTATION
S/sx Structures involved
C/L hemiparesis involving Primary motor cortex & IC

38
mainly the UE & face
(*recall the homunculus.
The UE and the face are
at the lateral side.)
C/L hemisensory loss
involving mainly the UE &
face
Motor speech
impairment: Broca’s or
nonfluent aphasia with
limited vocabulary & slow,
hesitant speech (*but the
auditory comprehension
is intact)
Receptive speech
impairment: Wernicke’s or
fluent aphasia with
impaired auditory
comprehension but fluent
speech with normal rate
& melody
Global aphasia: nonfluent
speech with poor
comprehension
Aprosody = *absence of
normal variation, stress,
rhythm, and pitch of
speech resulting in
monotonous speech
Affective agnosia
(*Auditory Affective
Agnosia. It’s like a mix
between auditory and
aprody anopsia. The
inability to recognise
different tone or emotion
behind speech heard.
E.g., If you shout at the
person because you are
angry at him, he won’t
recognize that you are
mad.)
Perceptual deficits:
unilateral neglect, depth
perception, spatial
relations, agnosia (*etc)
Apraxia (inability to
perform previously
learned tasks) (*difficulty
to create a motor plan
when asked to do an
action, provided that
these task are common
and are already known.)
- Ideomotor
(*cannot do upon
command, but
can
spontaneously do
it)
- Ideational
(*cannot do even
upon command
or spontaneously)
C/L homonymous Optic radiation in IC
Primary sensory cortex & hemianopsia
IC
Frontal gaze palsy (loss Frontal eye fields (Area 8)
of conjugate gaze to the or their descending tracts
Broca’s cortical area opposite side) (*like in
(Area 44 & 45; inferior ACA) (*e.g., R frontal eye
frontal gyrus) in the field affected = can look
dominant hemisphere to R but cannot look to
(usually L) the L with both eyes)
C/L ataxia of the limbs Parietal lobe
(sensory ataxia)
Wernicke’s cortical area
(Area 22; superior Premotor hemiplegia Upper portion of posterior
temporal gyrus) in the (lacunar stroke) (*if it only limb of IC
dominant hemisphere affects the upper portion
(usually L) of the posterior limb of
the internal capsule)
Gerstmann syndrome = L Angular gyrus (Area 39)
Both Broca’s & *the R & L discrimination
Wernicke’s cortical area problems, finger agnosia,
agraphia, acalculia
R Area 44 & 45 - *R&L
discrimination =
inability to identify
which is R and
which is L
- *Finger agnosia =
R Area 22 inability to
recognize the
fingers (patient’s
fingers, others’
fingers, or images
of fingers)
- *Agraphia
=inability to write
- *Acalculia =
inability to
perform simple
mathematical
calculations
(*tune: I Have 2 Hands. “I
Parietal sensory have Gerstmann the L &
association cortex in the the R. finger agnosia,
non dominant agraphia, acalculia, 1, 2,
hemisphere (usually R) 3, Area 39 Left angular)
Premotor or parietal Dressing Apraxia = *L R Angular gyrus (Area
cortex neglect when dressing 39)
Constructional Apraxia =
*inability to build,
assemble, or draw
objects
COMPLICATIONS
◊ The most common complications to occur in
stroke patients while they are still hospitalized
include infections, particularly pneumonia or
urinary tract infections; falls; and pain. Falls
have to do with the functions that MCA strokes
impact most. Mobility is affected, particularly in
39
 the setting of decreased sensation and strength, the process of recovery varies so drastically
which makes falls more likely to occur. between individuals.
◊ Less common complications include pressure ◊ Severe MCA strokes, in which patients often
sores, seizures, recurrent stroke, battle cerebral edema and alteration of
thromboembolism, and psychological consciousness, mortality is frequently dependent
complications, particularly depression. upon whether life-saving measures are taken.

MEDICAL DIAGNOSIS
◊ CT or MRI that is performed in the acute setting GENERAL HEALTHCARE MANAGEMENT
when evaluating for stroke.
MEDICAL MANAGEMENT

DIFFERENTIAL DIAGNOSIS ◊ Secondary stroke prevention is aimed at

modifiable risk factors, which were briefly
addressed in the section on etiology. Modifiable
Condition Presentation risk factors include diabetes, hypertension,
hyperlipidemia, and smoking.
Stroke Unilateral weakness and/or
numbness, facial droop, and speech SURGICAL MANAGEMENT
deficits ranging from mild dysarthria
and mild aphasia to global aphasia. ◊ Thrombectomy - the last known normal has to
be within 24 hours of intervention
Subdural Stroke-like symptoms based on
hematomas location or mass effect on the same PHARMACOLOGICAL MANAGEMENT
(SDH), structures in the brain that are ◊ IV tissue plasminogen activator (TPA) - this is
intracranial supplied by the MCA
done in the acute setting. the last known normal
hemorrhages
has to be within 4.5 hours of the administration
(ICH), or
of the thrombolytic.
masses

Status Can mimic stroke due to gaze OTHER HEALTHCARE MANAGEMENT

epilepticus deviation and loss of movement, as ◊ Occupational Therapists provide a holistic
well as global aphasia due to loss of approach (mind, body, spirit, and emotion) to
consciousness. help people reach the greatest level of function
(activities of daily living) and independence to
Multiple May also be confused with stroke achieve the best result for health improvement
sclerosis given presentations consistent with during stroke recovery.
vision loss and numbness or ◊ Speech Language Pathologists - Therapists who
weakness that typically will favor a assess and treat communication and swallowing
particular extremity. disorders after stroke.
PHYSICAL THERAPY, EXAMINATION, EVALUATION,
Toxic, Sepsis, uremia, hypo and AND DIAGNOSIS
infectious, hyperglycemia, hyponatremia, and
and hyperkalemia can all cause POINTS OF EMPHASIS ON EXAMINATION
metabolic symptoms that resemble a stroke. General Points of Examination
differentials ◊ Subjective
◊ Pain
Complex Typically there will be a headache ◊ Cognition
migraines associated with the symptoms, and ◊ Perception
the patient will likely have a history ◊ Behavior
of migraines and similar symptoms ◊ Signs of increased intracranial pressure
in the past. ◊ Level of consciousness
◊ Emotional status & behavior
Psychiatric Some experience unilateral
◊ Cognition
disorders numbness or weakness. Examples
◊ Communication & language
of these are conversion disorder
◊ Integumentary integrity
and panic attacks.
◊ Vital signs
◊ Aerobic capacity/endurance
◊ Sensory examination
PROGNOSIS ◊ Cranial & peripheral nerve integrity
◊ Neuromuscular & reflexes
◊ The most essential factors in determining ◊ Fine Motor Skills
prognosis are the size of the stroke, whether the ◊ Musculoskeletal
patient received thrombolytic therapy and/or o ROM
thrombectomy, and access to rehabilitation o MMT
following the stroke. o MBT
◊ Patients who suffered smaller cortical strokes ◊ Balance & tolerance
typically recover rapidly within a few weeks and ◊ Coordination
then begin to level out over a few months. ◊ Gait & locomotion
◊ For larger strokes, it can be challenging to give a ◊ Functional Assessment
prognosis in even the first three months because
40
 PT PROBLEM LIST
Spasticity To improve motor Roods
● Spasticity function and technique
● Decrease of ROM at the C/L dominantly in UE decrease spasticity (inhibitory
● Weakness of Strength on C/L UE in UE techniques) x 10
● Loss of sensation at the C/L UE mins
● Impaired eye and hand Coordination
● Impaired Gait Electromyograp
● Impaired ADLs hic biofeedback
(EMG-BFB) x
PT DIAGNOSIS 10 mins
◊ Neuromuscular Practice Pattern D: Impaired
Motor Function & Sensory Integrity Associated Gentle Passive
With Non-Progressive Disorders of the Central Stretching on
Nervous System - Acquired in Adolescence or affected UE
Adulthood structures x 10
reps x 2 sets x 5
PT PROGNOSIS SH
♢ In the upper extremity with severe impairment
and/or poor prognosis for recovery (Chedoke LOM on C/L To improve range Progression to
McMaster Stroke Assessment (CMSA) of Arm UE of motion of UE PROM ->
and Hand < Stage 4) treatment should focus on and improve AAROM ->
maintaining a comfortable, pain-free, mobile arm functional AROM
and hand independence exercises x 2
sets x 8 reps
♢ Brunnstrom’s Stages of Motor Recovery
♢ Impairment may begin to subside once brain US x 5 mins on
swelling subsides within 3 weeks. Residual affected limbs in
neurological impairments are those that persist preparation for
longer than 3 weeks & may lead to lasting stretching to
disability increase tissue
♢ The first three months of recovery is the MOST extensibility
important month - golden period percent for
Stretching
treating cva patients as it reveals most
Hold-Relax
measurable neurologic recovery and the
technique in
potential for plasticity of the nervous system
sitting position
PHYSICAL THERAPY PLAN OF CARE
for 10 reps x 2
sets
PT LONG AND SHORT TERM GOALS
◊ LTG: LTG: Pt will present an improvement of
function in the affected UE extremities in ROM, Weakness at To improve muscle Strengthening
strength, fine motor skills, posture, and gait in the C/L UE performance of UE exercises with
order to functionally perform basic ADLs and and increase progressive use
improve quality of life. functional of theraband
◊ Pt. will present a decrease in spasticity from independence colors x 2 sets x
grade 3 to 1 p 10 PTR to be able to perform 10 reps
ROM exercises and functional activities.
◊ Pt. will manifest an increase in range of motion Isometric
in UE p 10 PTR sessions to improve functional exercise on
independence affected
◊ Pt. will manifest an ↑ of 1 grade in muscle muscles x 3 6
strength in UE within 10 PTR sessions to secs hold x 10
improve muscle performance. and increase reps x 2 sets
functional performance
◊ Pt. will demonstrate an ↑ in sensation from a Progressive
score of 0 to 1 in sensory assessment p 10 PTR resistive
session to improve functional performance. strength training
◊ Pt. will exhibit improvements in coordination p on UE x 10 reps
13 PTR sessions to improve performing multiple x 2 sets x 10 SH
functional activities independently
◊ Pt. will exhibit an improved posture in 10 PTR
sessions to ↑ safety & functional independence
◊ Pt will manifest ↑ independence as to self-care &
mobility within 25 PTR sessions to ↑ functional Loss of To improve Desensitization
independence Sensation at sensory through
the C/L UE awareness and application of
PT INTERVENTIONS prevent secondary multiple types of
complications texture that can
promote
Problem POC Intervention sensory

41
 stimulation by and uneven
stroking material surfaces,
over the patient ascending and
X 10 mins. descending
stairs
Pin-prick
sensation X 10 Gait training c
times while Pt gait belt and
has eyes close contact
opened and guard from PT
closed. performing X 10
mins
Thermal
sensation Hall ambulation
desensitization while performing
by application of two activities
warm and cold through walking
temperature on while engaging
Pt X 10 times in conversation
while Pt has with a therapist
eyes opened x 10 mins.
and closed.
Impaired To promote
Impaired To improve eye performance independence and Fine motor
balance and and hand Balloon toss of ADLs improve functional exercises, finger
coordination coordination in exercises on performance of opposition, UE
in UE performing both hands x 10 patients. D1 √/ & D2 √/
functional activities reps x 2 sets strengthening
exercises c
Hand and foot thera band
coordination
exercises in
sync to the beat
of a music x 10
reps x 2 sets

Throwing a ball REFERENCES

against the wall
and catching it Books:
as it bounces x ◊ O’Sullivan, S.B., Schmitz, T.J., & Fulk, G.D.
10 reps x 2 sets (2014). Physical Rehabilitation (6th ed.).
Progress to Websites:
perturbation
exercises as ◊ Navarro-Orozco, D., Sánchez-Manso, JC.
tolerated (2020). Neuroanatomy, Middle Cerebral Artery.
StatPearls. Treasure Island (FL): Retrieved at
https://www.ncbi.nlm.nih.gov/books/NBK526002/
◊ Nogles TE, Galuska MA. (2020). Middle
Cerebral Artery Stroke. StatPearls. Treasure
Impaired To correct postural Postural Island (FL). Retrieved from:
Posture deviations and correction https://www.ncbi.nlm.nih.gov/books/NBK556132/
improve body exercises done ◊ Slater, D. MD. (2019). Middle Cerebral Artery
image while in front of a Stroke. Retrieved from Medscape:
providing tactile, mirror x 10-15 https://emedicine.medscape.com/article/323120-
verbal cues, min overview
feedback, head ◊ Ausmed. (June 2020). Different Types of Stroke.
straps Progress to Retrieved from:
perturbation https://www.ausmed.com/cpd/articles/different-ty
exercises as pes-of-strokes
tolerated

Stretching of
tight muscles 10
reps x 2 sets

Impaired Gait To improve gait Progression of

cycle and increase gait training
endurance. from parallel
bars to even

42
POSTERIOR CEREBRAL ARTERY SYNDROME
degree of macular sparing intention tremor,
hemiballismus
GENERAL MEDICAL BACKGROUND
Visual agnosia Contralateral hemiplegia
DEFINITION
◊ Occlusion of the posterior cerebral artery (ICA) Prosopagnosia Weber’s syndrome
due to atherosclerosis produces massive Oculomotor nerve palsy
infarction in the region of the brain supplied by and contralateral
the artery including the occipital lobe and medial hemiplegia
and inferior temporal lobe.
◊ Also affects the upper brainstem, midbrain, and Dyslexia Paresis of vertical eye
posterior diencephalon. movements, slight miosis
and ptosis, and sluggish
EPIDEMIOLOGY pupillary light response
◊ The incidence of PCA strokes can be estimated
between 5% to 10%. Some studies include only Memory defect
pure PCA. One study shows that pure PCA
strokes account for 232 (6.1%) cases of stroke Topographic disorientation
(n = 3808).
COMPLICATIONS
ETIOLOGY ◊ Limb shaking as a hemodynamic compromise
◊ The most common causes of PCA strokes in ICA occlusion.
include atherosclerosis, small artery disease and o complain of repetitive involuntary
embolism. movements of one or both limbs on one
side.
RISK FACTORS o misdiagnosed as partial seizures
◊ Risk of developing stroke after TIAs is as high ◊ Retinal claudication resulting from an increase in
metabolic demand in the retina on the
as 20% within the 1st month. If untreated, TIAs
background of an already reduced perfusion.
result in development of stroke within 2 years.
◊ Chronic ocular ischemia occurs when severe
Risk of stroke events remains high for 10 to 15
occlusion develops and the patient complains of
years after TIAs.
progressive loss of visual acuity.
◊ Risk factors for development of PCA are similar
to those for CAD and other peripheral vascular
◊ Anticoagulation-associated intracranial,
gastrointestinal, or retroperitoneal hemorrhaging
disease. These risk factors include:
dyslipidemia, hypertension, diabetes, advanced ◊ Stroke associated Epilepsy
glycation end products (AGEs) and its receptors, ◊ Hemorrhage into infarcted brain tissue
obesity, cigarette smoking, lack of exercise, age,
and C-reactive protein. MEDICAL DIAGNOSIS
◊ Bio-markers
PATHOMECHANICS / PATHOPHYSIOLOGY o Blood analysis
◊ This syndrome results from bilateral medial ▪ Serum electrolyte levels
thalamic infarction. The presentation in these ▪ lipid panels
patients varies from lethargic to obtunded to ▪ Renal and hepatic tests
comatose, but some patients may be agitated ▪ urinalysis
and may have associated hemiplegia or ◊ Cerebrovascular Imaging
hemisensory loss. Occasionally, the cranial ◊ Computed Tomography
nerve III nucleus is involved, with resultant ◊ MRI - dx of ischemia within the brain almost
ophthalmoplegia. immediately after the onset
◊ Patients may take days to weeks to recover and ◊ PET (Positron Emission Tomography) Scan
seem to be in a sleeplike state. Although ◊ MRA and US
alertness generally returns, prognosis for good ◊ Arteriography and DIgital Subtraction
functional recovery is poor because of severe Angiography
memory dysfunction. ◊ Chest X-rays & ECGs
◊ The syndrome may result from a “top of the
basilar” artery embolus. The artery of Percheron DIFFERENTIAL DIAGNOSIS
may be involved.
Ischemic Stroke Caused by a blockage cutting
CLINICAL PRESENTATION
off the blood supply to the
brain
Peripheral Territory Central Territory Most commonly type

Contralateral Central post-stroke pain, Hemorrhagic Caused by a bleeding in our

homonymous spontaneous pain and Stroke around the brain
hemianopsia dysesthesias; sensory
impairments Transient Ischemic Same as stroke except that
Attack the symptoms only last for a
Bilateral homonymous Involuntary movements; short amount of time because
hemianopsia with some choreoathetosis, the blockage that stops the

43
 blood getting to your brain is
temporary
caused by the restriction of
blood supply on the medial
aspect of the cerebral
hemisphere (frontal and
parietal lobes) and subcortical
Anterior Cerebral
structures; problems with
Artery
imitation & bimanual tasks,
apraxia, unresponsiveness,
slowness, delay, lack of
spontaneity, motor inaction
condition involving the
restriction of blood flow which
supplies the parts of the
frontal, tempora, and parietal
lobes of the brain including its
Middle Cerebral deeper structures; problem
Palsy with perceptual deficits, fluent
aphasia, global aphasia,
aprosody, affective agnosia,
apraxia, frontal gaze palsy,
premotor hemiplegia,
Gerstmann syndrome
PROGNOSIS
◊ Mortality associated with isolated posterior
cerebral artery (PCA) stroke is low; therefore,
the prognosis is generally good. Visual field
deficits improve to varying degrees; however,
they may be permanent and associated with
morbidity.
GENERAL HEALTHCARE MANAGEMENT
MEDICAL MANAGEMENT
◊ Immediate emergency care is crucial for a
hemorrhagic stroke. This treatment focuses on
controlling the bleeding in your brain and
reducing the pressure caused by the bleeding.
SURGICAL MANAGEMENT
◊ Surgery may be indicated to repair a superficial
ruptured aneurysm or AVM, prevent rebleeding,
and evacuate a clot (hematoma).
PHARMACOLOGICAL MANAGEMENT
◊ Antiplatelets (clopidogrel and plavix)
o Can be used to help prevent blood clots.
They work by making it more difficult for
the platelets in your blood to stick
together, which is the first step in the
formation of blood clots
OTHER HEALTHCARE MANAGEMENT
◊ Occupational Therapy
◊ Speech Therapy
◊ Nutritionist
PHYSICAL THERAPY, EXAMINATION, EVALUATION,
AND DIAGNOSIS
POINTS OF EMPHASIS ON EXAMINATION
General Points of Examination
◊ Subjective
◊ Pain
◊ Signs of increased intracranial pressure
◊ Level of consciousness
◊ Emotional status & behavior
◊ Cognition
◊ Communication & language
◊ Integumentary integrity
◊ Vital signs
◊ Aerobic capacity/endurance
◊ Sensory examination
◊ Cranial & peripheral nerve integrity
◊ Neuromuscular & reflexes
◊ Fine Motor Skills
◊ Musculoskeletal
o ROM
o MMT
o MBT
◊ Balance & tolerance
◊ Coordination
◊ Gait & locomotion
◊ Functional Assessment
PT PROBLEM LIST
◊ Pain
◊ Spasticity
◊ Impaired memory
◊ Decrease of ROM at the C/L dominantly in UE &
LE
◊ Weakness of Strength on C/L UE & LE
◊ Loss of sensation at the C/L UE & LE
◊ Impaired coordination
◊ Impaired Gait
◊ Impaired ADLs
◊ Presence of movement disorders like
choreoathetosis, hemiballismus, and intention
tremor
PT DIAGNOSIS
◊ Neuromuscular Practice Pattern D: Impaired
Motor Function & Sensory Integrity Associated
With Non-Progressive Disorders of the Central
Nervous System - Acquired in Adolescence or
Adulthood
PT PROGNOSIS
◊ Impairments may resolve spontaneously as
brain swelling subsides (reversible ischemic
neurological deficit), within 3 weeks. Residual
neurological impairments are those that persist
longer than 3 weeks & may lead to lasting
disability
PHYSICAL THERAPY PLAN OF CARE
◊ Refer to Middle Cerebral Artery Syndrome or
Anterior Cerebral Artery Syndrome Subjective
REFERENCES
Books:
◊ O’Sullivan, S.B., Schmitz, T.J., & Fulk, G.D.
(2014). Physical Rehabilitation (6th ed.).
◊ Ciccone, C. D. (2021). Pharmacology In
Rehabilitation. S.L.: F A Davis.
Websites:
◊ Helseth, E. K., et al. (2018). Posterior Cerebral
Artery Stroke. Retrieved from
https://emedicine.medscape.com/article/212810
0-overview#a4 on May 28, 2021.
44
 NEUROMUSCULAR CONDITIONS REVA COMPILATION
VELEZ COLLEGE PHYSICAL THERAPY BATCH 2022
TRAUMATIC BRAIN INJURY
WHAT’S INSIDE
Primary Injury
1. Diffuse Axonal Injury (DAI)
2. Focal injury
3. Coup/Counter coup injury
4. Closed/Open injury
Blast Injury
Secondary Injury
GENERAL MEDICAL BACKGROUND
DEFINITION
◊ An “alteration in brain function, or other evidence
of brain pathology, caused by an external force”
◊ Among the effects of Traumatic Brain Injury or
(TBI), are impairments in cognition, movement,
sensation, emotion, as well as behavioral
responses.
◊ Although moderate to severe injuries result in
worse outcomes, a diminished or altered state of
consciousness appears during initial onset,
regardless of the severity of the injury.
EPIDEMIOLOGY
◊ Leading cause of injury related death and
disability in the US, an average of 1.4 million TBI
occur each year, including 1.1 million emergency
department visits, 235,000 hospitalizations, and
50,000 deaths.
◊ Peaks at 3 different age levels:
o Early childhood (1-2years) - often
related to child abuse
o Late adolescence & early adulthood
(15-24 years in M; 18-25 years in F) -
related to risk-taking behaviors
o Elderly - related to falls
◊ Usually occurs as a consequence of:
o Falls (32%)
o MVA (19%)
o Struck by or against events (18%)
o Assault (10%)
ETIOLOGY
TBIs are a heterogenous injury, meaning that they have
a wide variety of pathophysiologic mechanisms:
◊ In open head injuries, the meninges have been
breached, leaving the brain exposed
◊ In closed head injuries, there is no skull fracture
or laceration of the brain, but the soft tissue of
the brain is forced into contact with the skull.
PATHOMECHANICS / PATHOPHYSIOLOGY
Primary and secondary injury cause damage to the
neuronal tissues of the brain.
Primary Injury
● Focal Injury
● Diffuse Axonal Injury
● Coup-counter coup
● Closed/open Injury
Secondary Injury
To ensure continuous cerebral blood flow and oxygen
supply to the brain, the normal brain vascular
autoregulation involves a pressure and volume
monitoring mechanism.
Vasoconstriction and vasodilation are very important
mechanisms to maintain the cerebral pressure in
response to changing systemic arterial pressure.
Cerebral pressure autoregulation maintains cerebral
blood flow ~50 - 150 mmHg.
when trauma occurs
↓
internal or extremity injuries
↓
excessive bleeding and decrease of blood pressure
↓
infarction within the cortical gray matter
● Occipital blows likely result in contusion injuries
compared to the frontal or lateral blows.
● mc injured::
➢ anterior poles
➢ undersurface of the temporal lobes
➢ undersurface of the frontal lobes
Vascular changes
Normally, acetylcholine gives rise to the dilation of the
vessels through the release of endothelium-derived
releasing factor which results in relaxation of the smooth
muscle in the vessel wall. Following a brain injury, there
are changes in the endothelium and the walls of the
blood vessels which causes abnormal vasoconstriction.
It can also result into:
● disturbed blood-brain barrier
● leakage of serum proteins and neurotransmitters
into the parenchyma which causes edema
Hypoxia
● d/t the blockages which results in the:
○ ↓ blood in the brain
○ ↓ oxygen in the blood because of the
concomitant pulmonary insult
○ internal or extremity injuries that cause
excessive blood loss.
● Ischemia occurs within the first few hours after
severe injury d/t the decrease in cerebral blood
flow around and at the impact side.
● vascular volume in the skull can increase if
venous outflow is blocked or loss of
autoregulation.
↑ Intracranial pressure (ICP)
Cause:
○ ↑ in the cranial blood volume after
trauma
○ Bleeding in the epidural compartment
that creates a mass effect that can
displace the brain and ↑ ICP
○ The shear and tensile forces of
traumatic injury create a subdural
hematoma by disruption of the bridging
veins.
 ○ Cerebrospinal blood volume increases
which blocks the outflow pathways or
interference with reabsorption.
○ To compensate for the slow volume
change, the ICP will rise.

→ The reason for these vascular changes is the

↓ ability of the cerebral vessels to basically
maintain homeostasis.

Parenchymal changes
axonal injury
↓
the shear and tensile forces disrupt the axolemma
↓ CLASSIFICATION
distal axon segment detaches
↓ 1. Primary Brain Injury - A blow or jolt to the head
trigger wallerian degeneration (skull, bullet, instrument) and involves rapid
↓ acceleration/deceleration of the brain.
myelin sheath pulls away from the axon

● This primary injury triggers a metabolic cascade Diffuse Axonal Injury (DAI)
that can add to secondary injury through ● Acceleration and deceleration of the
excitotoxicity and free radical formation. brain cause shear, tensile, and
● Secondary cell death by necrosis of the cellular compression forces.
membrane can be a result of edema. ● Responsible for initial loss of
consciousness in TBI patients if the
● Apoptosis may result in cell loss that occurs
corpus callosum, midbrain, pons, and
days, weeks, or months after injury white matter of cerebrum are affected.
● Excitotoxicity results in an increase in ● Most often occurs in discrete areas:
extracellular neurotransmitters such as ○ parasagittal white matter of the
glutamate and aspartate and increased cerebral cortex
potassium, which causes a massive ○ corpus callosum
depolarization of the injured brain. ○ pontine mesencephalic junction
adjacent to superior cerebellar
○ Glutamate rises to above normal or peduncles
abnormal amounts following brain injury ● mc: high speed MVA’s and sports
○ A complex interaction of the various related traumatic injuries
amino acids and neurotransmitters, may
affect postsynaptic functions, resulting in Focal Injury
secondary injury of the neural ● Occurs on the isolated area in the brain
● Common areas of focal injury:
mechanisms of the brain.
○ Ant. temporal pole
○ Inhibition function of the synaptic ○ Frontal poles
receptors can be altered, and may relate ○ Lateral & Inf. temporal cortex
to both functional and behavioral ○ Orbital & frontal cortex
changes. ● mc: contusions, lacerations, and
intracerebral hematomas
Compressive Damage
Coup or counter coup injury
● Intracranial hypertension and mass bleeding can
● Coup injury - at the point of impact
result in herniation which causes compression of (frontal lobe)
the brainstem, pituitary, and other delicate brain ● Countercoup - opposite point of impact
structures. (occipital lobe)
● The brainstem is responsible for the body’s
major visceral functions and involvement in this Closed or open head injury
may lead to paralysis or death in severe cases. ● Closed head injury - dura is intact; skull
can be fractured but not a necessary
thing.
○ mc: concussion
● Open head injury - object pierces the
skull or dura matter
○ gunshots wounds, knife stabs,
sharp object penetration, and
direct trauma)

2. Blast Injury - When an explosive device

detonates a transient shock wave is produced,
which can cause brain damage.

2
 ● Results in edema, confusion, DAI,
● Impaired perception of stimuli
hematomas and hemorrhage.

3. Secondary Brain Injury - A cascade of

biomechanical cellular & molecular events that ◊ Loss of consciousness (LOC)
would evolve over time because of initial injury & ◊ Altered level of consciousness
injury related hypoxia, edema, and ICP.
● Occurs 12-24 hours after trauma and
may occur up to 5-10 days. Alert Awake and easily arousable
● Normal ICP = 5-2 cm of water
Lethargic Difficult to arouse
○ S/sx: headache, vomiting w/o
(somnolent Drowsy, thinking is slow but still appropriate
nausea, ocular palsies, altered
) Fall asleep when not stimulated
LOC, back pain, papilledema,
pupillary dilation, abducens
Obtunded Sleeps most of the time
palsy, cushing’s triad (HTN,
Confused when aroused
bradycardia, & Abn respiration
Speech is mumbled
(Cheyne-stokes)).
Dulled/Blunted sensitivity and have
decreased interest in environment
SEVERITY
Delayed reaction to stimulus
Mild Moderate Severe
TBI TBI TBI Stupor Aroused only briefly with vigorous repeated
(Semi-com Sensory stimulation (shaking, pain
LOC < 30 30 mins - > 24 hrs atose) stimulation)
mins 24 hrs Non-verbal

AOC brief brief brief Comatose No response to pain, no eye opening, no

(24 hrs) (24 hrs) (24 hrs) sleep-wake cycle, inability to follow
commands, inability to talk, no auditory or
PTA < 1 day < 1 wk > 1 wk visual function
Usually ventilator dependent
GCS 13 - 15 9 - 12 >9 Usually those with DAI or compressions of
the diencephalon
Neuroim Normal Normal
aging /Abnormal
◊ Cognitive and behavioral impairments
o Affects immediate recall, STM, LTM
o Inability to learn and carry over new
CLINICAL PRESENTATION tasks and contribute to confusion.
o Inability to interact effectively with the
◊ Post traumatic amnesia (PTA) environment.
o Impaired initiation, especially the first
o Time between injury & pt. recall events; action steps or stages of a task,
loss of ability to retain new information. affecting the patient’s ability to live
o Used as an indicator for extent of independently.
damage o ↓ in safety awareness, delays in
o MC with acceleration-deceleration type
processing information, loss of
of injuries and foal injuries as well.
executive functions, Behavior may be
Memory excessive or disinhibited.
o There may be inappropriate social and
Procedural Skills
interpersonal behaviors
memory
o There may be mood disturbances which
Declarative Facts include depression, anxiety.
memory o Pseudobulbar affectation and motor,
sensory, and verbal perseveration.
Retrograde ● Frontal lobe affectation
o Can also be imitation of gestures,
amnesia ● Inability to remember events
before the injury restlessness, agitation, aggression, and
● Progressively decreases irritability
recovery o Often refuse to cooperate, apathetic,
impulsive, and hyperactive.
o Sometimes have psychosis, low
Anterograde ● Temporal lobe affectation frustration tolerance, and mental
Amnesia ● Inability to create new inflexibility
memories ◊ Communication, respiratory and swallowing
● Last to recover after a comatose impairments
state o usually non aphasic in nature
Contributing factors: o Disorganized or tangential oral or written
● Poor attention
communication, imprecise language,
● Distractibility
3
 word retrieval difficulties, and
irregularities,
disinhibited and socially inappropriate sialorrhea, loss of
language sensation, and gag
o Difficulties communicating in distracting reflex of the palata, loss
environments, reading social cues, and of taste in the posterior
adjusting communication to meet the 3rd of tongue, voice
demands of the situation. may be hoarse,
dysphagia, deviation of
o apneustic breathing - TBI within the
the tongue to the side
lower pons. of lesion.
▪ Prolonged inspiration followed
by a short and ineffective X ● Least affected
expiration. XI
o Dysphagia - difficulty in the four stages
of chewing and swallowing d/t CN ◊ Neuromuscular impairments
damage o UE or LE paresis, coordination, and
◊ Pain postural control impairments, rigidity
o May have head and neck pain which is o Tone can fluctuate as a result of the
common in whiplash-associated changes in the patient's position,
volitional movement, medication,
disorders.
infections or illness, and increase in pain
o May have neuropathic, myofascial, or discomfort or even a change in
fibromyalgia, and chronic pain emotion.
o (+) Ataxic gait
◊ CN damage o (+) tremors and chorea
I ● 1st CN to be damages, but o (+) dystonia (least common)
the last to recover o (+) primitive reflexes (ATNR, STNR, etc)
● usually d/t fx of the cribriform o Decerebrate positioning → WORSE
plate PROGNOSIS
Characterized by: ▪ d/t UE and LE extension; affects
● ↓ ability to smell (anosmia, the pons and midbrain
hyposmia) o Decorticate positioning → GOOD
● rhinorrhea PROGNOSIS
▪ d/t UE in flexion while LE in
II ● monocular blindness extension; affectation of
● responsible for pupillary light thalamus and corticospinal tract
reaction = anisocoria ▪ best motor response for TBI
● loss of direct pupillary response ◊ Dysautonomia
but there is brisk consensual o elevated SNS activity occurring as a
response to light. normal response to trauma ff. TBI
▪ This response may become
III ● 2nd mc affected overactive resulting in ↑ HR,
● responsible for EO, holding RR, & BP.
eyelids up, if affected = ® ptosis ▪ There may be diaphoresis,
hyperthermia, alterations in
LOC, reflexive motor response
IV ● Least affected to stimulation, and agitation.
● if damaged: ▪ Other s/sx include decerbrate
○ vertical diplopia, and decorticate posturing,
mimicking a CN 3 palsy. hypertonia, and teeth grinding.
▪ Best describes Dysautonomia:
V ● May present with anesthesia of Paroxysmal Sympathetic
a portion of the nose, eyebrow, Hyperactivity
and forehead.
Sympathetic Storming
VII ● mc affected ● Can occur d/t hypothalamic simulation of the
○ facial palsy usually d/t SNS with an ↑ in the circulating corticoids and
temporal fx catecholamines (stress response)
● Post-traumatic seizures
VIII ● d/t petrous or mastoid fx ○ Abn. electrical activity of the brain d/t
● can have an escape of CSF but injury
from the auditory canal ○ Signs assoc. with isolated lesions of the
(otorrhea) cortex
● Battle Sign: Hemorrhage at the ○ Signs assoc. with lobe affectation
mastoid process d/t mastoid fx.
Recovery Stages from DAI
IX ● Least affected: Coma *Refer to levels of consciousness*
CN 9-12:
● may have cardiac Vegetative State ● Higher CNS centers are

4
 not integrated with the stress.
brainstem (manages basic
cardiac, respiratory, &
other vegetative functions;
can be weaned of COMPLICATIONS
ventilator
● Dissociation between ◊ Hydrocephalus - the enlargement of the head
wakefulness & awareness; due to fluid build up in the brain, resulting in
inability to interact with the swelling and an increased intracranial pressure.
environment; decreased
level of awareness with Types:
eye opening & sleep-wake ● Obstructive/non communicating -
cycle; cannot follow blockage in any part of the ventricle
commands/speak; may ● Non obstructive/communicating -
startle & briefly orient to problems with CSF absorption
audiovisual stimuli; reflex Triad
smiling/crying; withdrawal 1. Dementia/mental deterioration
to noxious stimulus; 2. Ataxia/ataxic gait disturbances
non-purposeful, reflexive, 3. Urinary incontinence
non-reproducible ◊ Heterotrophic ossification - onset is typically
movements in response to 4-12 weeks post TBI
external stimuli ◊ Headaches
◊ Seizures
Persistent ● Present for at least 1 ◊ Infections - skull fractures and penetrating
Vegetative State month; no meaningful wounds may tear the meninges that surround
motor or cognitive the brain, leading to meningitis
function; complete ◊ Blood vessel damage
absence of awareness to ◊ Hypothalamic and endocrine dysfunction
the environment & self for ◊ Psychiatric problems
>1year after TBI or 3 ◊ Peripheral nerve damage
months after anoxic brain ◊ Sensory problems - the loss of light touch,
injury sharp/dull differentiation, proprioception,
kinesthesia, stereognosis, taste/smell deficits,
Minimally ● Minimal evidence of cranial nerve involvement
Conscious State self/environment ◊ Pneumonia, deconditioning, decreased
or Mute awareness; inconsistent, endurance
Responsiveness reproducible/sustained ◊ Chronic pain
cognitive behavior; ◊ DVT, pressure sores, contractures, fractures,
sleep-wake cycle is atrophy
present; can localize ◊ Degenerative brain diseases (AD, PD)
noxious stimuli; ◊ Dementia pugilistica - chronic traumatic
inconsistently reaches for encephalopathy with characteristics of dementia
objects; localizes sound (common in boxers, wrestlers,and athletes in
location; demonstrates sports that suffer from repeated concussions)
sustained visual fixation &
pursuit MEDICAL DIAGNOSIS
Confusional ● Disturbance of attention ◊ CT scan
State mechanisms; all cognitive o Indicated in the early stages of
operations are affected; is post-injury; can show potential fractures,
unable to form new detail hemorrhages and hematomas in
memories; hyper/hypo the brain, contusions, and swelling
arousal; ◊ MRI
o Is used once the pt is medically stable;
Emerging ● Confusion starts to clear;
gives a more detailed view of brain
Independence some memory is possible;
tissue
significant cognitive
problems; limited insight;
DIFFERENTIAL DIAGNOSIS
frequently uninhibited
social behaviors Repeated TBI can cause chronic traumatic
encephalopathy, characterized clinically by amnesia,
Intellectual or ● Increasing independence; executive dysfunction, aggression, depression, and
Social cognitive, behavioral, and parkin- sonism. It is characterized pathologically by
Competence social difficulties/problems tau-immunoreactive neurofibrillary tangles pref- erentially
persist; pt can plateau or involving the superficial cortical layers, astrocytic
regress (due to /repetitive tangles, and neurities. Stroke may be yet another
brain injury & stress) long-term complication of TBI.

Note: patients can plateau at any of these stages and

can regress under conditions of repetitive brain injury or CVA TBI

5

- sudden loss of
neurological
function caused
by an interruption
of the blood flow
to the brain
etiology: vascular
compression
onset: sudden,
progressive
age: MC 40 y.o onwards
pathophysiology: blood
turbulence leading to
intimal wall damage
clinical manifestation:
loss of motor function,
sensation, weakness, CN
involvement, seizures,
neglect
involvement:
unilateral/bilateral
cognition: usually not
impaired, (-) gestures
visual: normal, may be
accompanied with visual
neglect
speech and hearing: N,
slurred
prognosis: recover,
depending on severity of
CVA
Anoxic brain injury
- brain damage
from the lack of
oxygen to the
brain
Metabolic
encephalopathy
- systemic disorder
with diffuse brain
damage affecting
the hemispheres,
brain stem, and
reticular
activating system.
- not caused by
head injury but
caused by
chemical
imbalance in the
blood
PROGNOSIS
◊ Factors that affect outcome can be categorized
in 3 major areas:
o Injury severity - with severe injury, the
possibility of cognitive and behavioral
deficits increases; cognitive deficits that
- brain damage is
due to direct or
indirect trauma to
the skull, brain, or
both.
etiology: sudden, trauma
from external forces
onset: acquired,
non-progressive
age: MC 15-25 y.o
pathophysiology:
concussion, associated
with DAI, focal injury &
coup & counter coup;
hemorrhage
clinical manifestation:
vomiting, LOC,
aggression, behavioral
changes seizures, battle’s
sign, racoon’s eyes, PTA
involvement: bilateral
cognition: may be
impaired
visual: loss of conjugate
eye movement,
nystagmus
speech and hearing:
aphasia may be present
prognosis: depending on
GCS and RLA
GENERAL HEALTHCARE MANAGEMENT
affect motivation, attention, emotion,
memory, or learning may limit recovery
o Preinjury factors (e.g. history of
substance abuse, low educational level,
prior brain injury, psychiatric disorders)
can limit success; neuropsychological
dysfunction appears greater in those
aged >30y.o. who sustain injury, as well
as those with less education
o Postinjury factors (e.g. access to
appropriate care, adequate support) are
critical to optimize recovery
◊ Low initial scores on the GCS may be a
predictor of poor recovery in patients with
moderate-severe TBI
◊ Petechial hemorrhages, subarachnoid bleed,
obliteration of the third ventricle or basal
cisterns, midline shift, and subdural hematoma
findings are also predictive of poor outcomes
◊ Loss of pupillary light reflexes reflects significant
damage to the brainstem and may indicate a
poor prognosis; oculomotor deficits are often a
sign of cerebral damage, resulting in severe
cognitive deficits.
◊ The degree of hypoxemia and hypotension
during the early stages may also effect long-term
prognosis
◊ Duration of PTA may also predict recovery (<27
days likely to be employed; <34 days likely to
have good overall recovery; <53 days likely to
live without assistance)
◊ Lack of awareness of deficits, as well as a lack
of social skills reduces an individual’s ability to
reintegrate into the community
◊ Family and social supports are key factors in
recovery. Families require education and support
in order to understand how to best help their
family member. Often it becomes difficult to
sustain relationships that were stable before the
injury. Working with professionals who recognize
these deficits and are trained to treat them will
improve the chances of increasing quality of life
after brain injury.
MEDICAL MANAGEMENT
◊ Early resuscitation to stabilize the cardiovascular
& respiratory systems in order to maintain
adequate blood flow & oxygen to the brain
◊ Upon arrival to the medical center, the primary
goals are to minimize secondary brain injury by
optimizing cerebral blood flow & oxygenation,
stabilize VS, perform a complete examination,
identify & treat any non-neurological injuries,
and continuously monitor the patient
◊ SBP should be kept <90mmHg & oxygen
saturation above 90%
◊ Patients with severe injuries and some with
moderate injuries will need to be intubated
◊ Patient’s neck should be stabilized with a collar
& the head elevated to 30° to protect the spine &
avoid an increase in ICP
◊ Use GCS to determine severity
◊ X-rays and other neuroimaging tests, such as
MRI and CT may provide additional information
regarding the extent of the injury
6
 ◊ A neurological exam is performed to determine ◊ Arousal, attention, and cognition
whether surgery is warranted ◊ Pain
◊ ICP monitoring is recommended for patients with
GCS levels of <8, any acute abnormality on CT, ◊ Mental functions
an SBP of <90mmHg, or an age of >40 years o Coma Recovery Scale–Revised
◊ Elevated ICP can be treated with sedating o Disorders of Consciousness Scale
medications, moderate head-up positioning o Rancho Los Amigos Levels of Cognitive
(elevated to 30°), osmotherapy, hypothermia, Functioning
surgical decompression, and barbiturates o Moss Attention Rating Scale
◊ ICP should be <20mmHg & the CPP >60mmHg o Test of Everyday Attention
◊ If ICP cannot be treated successfully, inducing a o Trail Making Test Part B
pharmacologic coma or surgical decompression
o Galveston Orientation and Amnesia Test
may be necessary.
o Orientation Log
SURGICAL MANAGEMENT ◊ Aerobic capacity/endurance
◊ Surgery may be used to address the ff problems: ◊ Ventilation and respiration
◊ Integumentary integrity
o removing clot blood (hematomas)
o repairing skull fractures ◊ Balance
o opening a window in the skull o Berg Balance Scale
◊ It can be done through: o Community Balance and Mobility Scale
o Surgical Decompression o High-Level Mobility Assessment Tool
o Craniectomy
o Craniotomy ◊ Behavioral status
o External Ventricular Drain o Supervision Rating Scale,
Neurobehavioral Rating
PHARMACOLOGICAL MANAGEMENT o Scale–Revised, Agitated Behavior Scale
◊ Hypertension ◊ Community, Social, and Civic Life
o Beta blockers, ACE inhibitors, Ca o Mayo-Portland Adaptability Inventory
channel blockers, diuretics o Community Integration Questionnaire
◊ Diabetes Insipidus/Syndrome of inappropriate o Quality of Life After Brain Injury
ADH secretion ◊ CN integrity
o Control fluid & electrolyte intake
◊ Heterotrophic ossification ◊ Sensory integrity
o Early phase: disphosphonates ◊ Reflex integrity
o Intermediate phase: NSAIDS ◊ Joint integrity and mobility
o Late phase: surgery ◊ ROM
◊ Spasticity ◊ MMT - Muscle performance, including strength,
o Dantrolene sodium, baclofen, diazepam, power, and endurance
botulinum toxin ◊ Motor function
◊ Nutrition & feeding ◊ Neuromotor development and sensory
o High intake of calories & protein; NGT processing
feeding for obtunded patients ◊ Posture
◊ Bladder dysfunction
◊ Gait
o Frequent toileting; anticholinergics to
increase bladder capacity o Rancho Los Amigos (RLA) OGA System
◊ Depression o 10-Meter Walk Test
o Antidepressants o 6-Minute Walk Test
◊ Tonic arousal o Modified Walking and Remembering
o Bromocriptine, methylphenidate Test
◊ Reduced initiation ◊ Self-care and domestic life
o Amitriptyline, sinemet, bromocriptine ◊ Functional Independence Measure, Functional
Assessment Measure
◊ Mobility
OTHER HEALTHCARE MANAGEMENT o Functional Independence Measure
◊ Physician o Functional Assessment Measure
◊ Work life
◊ Rehabilitation Nurses o Mayo-Portland Adaptability Inventory,
◊ SLP Community
◊ OT o Integration Questionnaire
◊ Neuropsychologist o Quality of Life After Brain Injury
◊ Social workers
◊ Caregivers PT PROBLEM LIST
◊ Pain 2° to trauma
◊ Headache, Nausea, Dizziness
PHYSICAL THERAPY, EXAMINATION, EVALUATION,
◊ Confusion and disorientation.
AND DIAGNOSIS
◊ Impaired static & dynamic balance
◊ Impaired posture
POINTS OF EMPHASIS ON EXAMINATION ◊ Impaired gait
◊ Medical records review ◊ LOM
◊ ↓ muscle strength
7
 ◊ Fatigue, Decreased aerobic capacity
◊ Impaired reflexes
◊ Impaired concentration and cognition
◊ Loss of coordination
◊ Impaired fine motor skills
◊ Slurred speech
◊ ↑ Risk for Falls
◊ Impaired function independence
◊ Difficulty swallowing
◊ Light sensitivity
◊ Noise sensitivity
◊ Difficulty hearing
◊ Eyestrain, Visual difficulties
◊ Feeling confused or foggy
◊ Frustration, Irritable, More emotional
PT DIAGNOSIS
◊ Practice Pattern 5D – impaired motor function
and sensory integrity associated with
non-progressive disorders of the central nervous
system – acquired in adolescence or adulthood.
◊ Practice Pattern 4B – impaired posture
◊ Practice Pattern 4C – impaired muscle
performance
◊ Practice Pattern 5A – primary prevention/risk
reduction for loss of balance and falling
◊ Practice Pattern 7B – impaired integumentary
integrity associated with superficial skin
involvement
PT PROGNOSIS
◊ Patients with mild head injury (usually defined as
GCS score on admission of 13-15) tend to do
well.
◊ Moderate Head Injury
o Approximately 60 percent will make a
positive recovery and an estimated 25
percent left with a moderate degree of
disability. Death or a persistent
vegetative state will be the outcome in
about 7 to 10 percent of cases. The
remainder of patients will have a severe
degree of disability.
◊ Severely head-injured patients have the worst
outcomes.
o Only 25 to 33 percent of these patients
have positive outcomes.
◊ Moderate disability and severe disability each
occur in about a sixth of patients, with moderate
disability being slightly more common.
o About 33 percent of these patients do
not survive. The remaining few percent
remain persistently vegetative.
◊ Once head-injured patients leave the acute-care
hospital, some benefit from a rehabilitation
program
◊ Prime candidates for rehabilitation are patients
with less severe initial injuries or those that
started to show significant improvement.
◊ Patients with moderate or mild injuries, or
severely injured patients who have improved
sufficiently, are likely candidates for outpatient
therapy.
PHYSICAL THERAPY PLAN OF CARE
PT LONG AND SHORT TERM GOALS
◊ ↓ Pain to provide comfort, facilitate functional
independence, and avoid harmful muscle
compensatory strategies
◊ ↑ muscle strength to improve muscle
performance for amb. or transfers, and facilitate
functional independence
◊ ↑ ROM to improve functional mobility and joint
mobility
◊ Improve posture to avoid deviations from
developing
◊ Improve gait pattern to improve functional
mobility and transfers
◊ ↑ static & dynamic balance to facilitate
independence in amb. and transfers, enhance
performance, prevent injuries and ↓ fear of
falling
◊ Improve coordination to facilitate functional
independence and improve personal self-care.
◊ ↓ Fatigability to facilitate an improvement in
muscle performance for amb. transfers, and
self-care.
◊ Improve fine motor skills to facilitate functional
independence in self-care and ADLs.
◊ ↓ Risk for Falls to prevent injuries
◊ Improve functional independence to facilitate an
improved performance in ADLs.
PT INTERVENTIONS
◊ Pain
o Conventional TENS pulse width: 140;
frequency: 50 Hz; constant, duration:
10 mins for pain relief, with constant
feedback.
o Gentle massage x 15min to increase
circulation, promote muscle relaxation,
decrease spasticity and to promote pain
relief.
o Hydrotherapy c therapist supervision c
water temperature of 29-30 °C for 20
mins. to decrease pain, increase
strength, and increase aerobic capacity.
◊ LOM
o AAROM stretching exercises 15SH x
10reps x 3 sets to increase ROM and
prepare muscles for exercise
o Hold-Relax PNF Stretching Technique x
30SH x 10 reps x 2 sets to ↑ mobility,
joint ROM and joint flexibility.
o Yoga x 20min. ↑ flexibility, increase
aerobic capacity & improve posture
◊ Strength
o PREs using PNF patterns and
Theraband 5SH x 10reps x 3 sets to
increase strength of muscles.
o Biceps curls using 5lbs dumbbells on
bilat. UE x 10 reps x 3 sets to increase
UE strength.
o Sitting strengthening exercise on bilat.
LE c light ankle cuff weights x 5SH x 5
reps x 3sets to ↑ bilat LE strength.
◊ Coordination
o Frenkel’s exercises c therapist guarding
the side x 2 sets x 10 reps to improve
coordination as to sitting and standing
Sitting
8
 ▪ One leg stretching to slide the
heel to a position indicated by a
mark on the floor
▪ The alternate leg stretching &
lifting to place the heel on the
marked point
▪ From stride sitting posture pt. is
asked to stand and then sit
▪ Rise and sit c knees together
▪ Sitting hip abduction & o Walking x 10 mins to improve gait &
adduction
Standing
▪ In stride standing, weight is
transferred from one foot to
another.
▪ Place foot forward and
backward on a straight line.
▪ Walk sideways by placing feet
on the marked point
◊ Fine motor skills
o Hand Therapy Ball Exercises x 15min.
to improve fine motor skills
▪ Power Grip
▪ Pinch
▪ Table Roll
▪ Finger Flexion
▪ Finger Squeeze
◊ Aerobic capacity
o Stationary cycling x 15 min. to increase
aerobic endurance, increase LE
strength, and promote balance in sitting
o Diaphragmatic Breathing Exercises x 5
reps x 2 sets to control breathing and
facilitate oxygen uptake.
o Jogging on a treadmill mod. assist. +1 x
15 min. to increase aerobic endurance,
increase tolerance and improve dynamic
balance.
◊ Balance and Risk for falls
o Weight shifting exercises within // bars x
15 min. to promote an increase in
balance and tolerance in standing and
decrease risk for falls.
o Static Balance Control exercise:
Tandem stance & Single-leg stance for
15 mins on // bars to improve balance
and tolerance
o Standing balance training in tandem
stance x15 min. on // bars to improve
balance and tolerance
◊ Posture
o Postural awareness training in front of
mirror c verbal, auditory cues and
positive reinforcement to improve
postural alignment
◊ Gait
o Gait Training on parallel bars c footsteps
as guide for 10 minutes to improve
ambulation & gait.
◊ Functional training x 5 reps x 2 sets c guidance
of therapist to improve performance in ADLs
o Supine ↔ sit
o Sit ↔ stand
◊ HEP:
o HMP x 20 mins to decrease pain and inc
blood circulation
o Self-stretching Exercises using (B)
Symmetrical PNF D2 flexion UE & D1
extension LE patterns x 15 SH x 10 reps
x 3 sets to improve flexibility and ↑ ROM
o Strengthening Exercises using 5 lb
dumbbells and ankle weights to all the
major muscle groups of the body x 10
o reps x 2 sets to increase muscle
strength and increase functional
capacity.
o Postural correction techniques in front of
the mirror x 10 mins in order to improve
posture.
aerobic functional capacity.
o Yoga x 10mins. to ↑ flexibility, increase
aerobic capacity & improve posture
◊ Pt. Education
o Education on the condition
o Use of diary/notebook to keep track of
daily activities
o Benefits of referral to SLP for dysphagia
and OT for impaired fine motor skills
o Wound care management
o Information on proper progression &
healing of incision site
o Importance of proper body mechanics in
performing exercises and amb. training
& safety
o Fall safety awareness c supervision
o Energy conservation techniques
o Avoid valsalva maneuver
◊ Precautions:
o Minimize external noise during
treatment to avoid annoyance and
improve focus in doing tasks.
o Give simple instructions as to not
confuse or agitate the patient.
o Reduce level of stimulation in the
environment
o Place in a private/quiet room
o Remove noxious stimuli if there is any
o Limit unnecessary sounds/noises
o Provide frequent orientation to time,
date, place, and activities that they will
be doing.
o Provide emotional support, encourage
socialization, behavioral control and
motivation.
o Pt. should have frequent rest intervals
between exercises or activities in order
to avoid fatigue.
o Using of warm colors to prevent
agitation from light sensitivity
REFERENCES
◊ Books:
o O'Sullivan, S. B., & Schmitz, T. J.
(2007). Physical rehabilitation.
Philadelphia, PA: F.A. Davis.
o Goodman, C. C. & Fuller K. S. (2015).
Pathology: Implications for the Physical
Therapist (4th ed.). Elsevier.
o Ciccone, Charles D., 1953-. (2007).
Pharmacology in rehabilitation.
Philadelphia :F.A. Davis Co.,
o Jameson, J. L., & Loscalzo, J. (2015).
Harrison's principles of internal medicine
(19th edition.). New York: McGraw Hill
Education.
◊ Websites
o https://www.physio-pedia.com/Overview
_of_Traumatic_Brain_Injury
9
o https://www.mayoclinic.org/diseases-con
ditions/traumatic-brain-injury/symptoms-
causes/syc-20378557

10
PHARMACOLOGICAL MANAGEMENT SUMMARY

Medications Functions Side Effects PT Implications

Antihypertensives Anti-HTN medication; lowers BP Blunted HR, Dizziness, OH ● Use RPE to monitor exercise intensity
(Beta-blockers, ACE ● Pt may be at risk for falls
inhibitors, Ca channel
blockers, Diuretics)
Disphosphonates Used as treatment and prophylaxis for HO GI irritation ● PTs must pay attention for any signs of adverse drug
NSAIDS Used as treatment and prophylaxis for HO Long-term use may result in GI problems effects
Dantrolene sodium Used to treat spasticity of CNS origin Drowsiness, weakness, dizziness, nausea ● Best to treat pt during peak effect of these
Diazepam Relaxes skeletal muscles; reduces spasticity medications
Baclofen Inhibits spinal reflexes; reduces spasticity ● PTs must pay attention for any signs of adverse drug
Botulinum toxin Used for the treatment of focal spasticity reactions
Antidepressants Reduces symptoms of depression (fatigue, Sedation, OH, seizures, cardiac arrhythmias, ● Pt may be at risk of falls
loss of appetite, etc) anticholinergic effects ● PTs must pay attention for any signs of adverse drug
reactions
Methylphenidate May be used to address tonic arousal Dizziness, nausea,behavioral changes ● PTs must pay attention for any signs of adverse drug
reactions
Sinemet May be used to address reduced initiation GI problems, cardiovascular problems, ● PTs must pay attention for any signs of adverse drug
dyskinesia reactions
Bromocriptine May be used to treat tonic arousal and Nausea, headaches, vomiting, GI irritation ● PTs must pay attention for any signs of adverse drug
reduced initiation reactions

PT PLAN OF CARE SUMMARY

PROBLEM GOAL INTERVENTION

Pain 2° to trauma Pt. will present with pain relief to promote comfort in the
performance of activities.
LOM Pt. will show an increase in ROM c increments of 5° or 10° to
improve mobility, joint extensibility and improve performance of
ADLs.
↓ muscle strength Pt.will be able to increase muscle strength to enable better
performance of ADLs or to promote a stable base of
support when performing activities in standing or something
like that.
Conventional TENS pulse width: 140; frequency: 50 Hz; constant, duration:
10 mins for pain relief, with constant feedback.
Gentle massage x 15min to increase circulation, promote muscle relaxation, decrease
spasticity and to promote pain relief.
Hydrotherapy c therapist supervision c water temperature of 29-30 °C for 20 mins. to
decrease pain, increase strength, and increase aerobic capacity.
AAROM stretching exercises 15SH x 10reps x 3 sets to increase ROM and prepare muscles
for exercise
Hold-Relax PNF Stretching Technique x 30SH x 10 reps x 2 sets to ↑ mobility, joint ROM and
joint flexibility.
Yoga x 20min. ↑ flexibility, increase aerobic capacity & improve posture
PREs using PNF patterns and Theraband 5SH x 10reps x 3 sets to increase strength of
muscles.
Biceps curls using 5lbs dumbbells on bilat. UE x 10 reps x 3 sets to increase UE strength.
Sitting strengthening exercise on bilat. LE c light ankle cuff weights x 5SH x 5 reps x 3sets to
↑ bilat LE strength.
11
Loss of coordination Pt. will show an improved coordination to facilitate improved
coordination skills and promote better performance in ADLs
Impaired fine motor skills Pt. will show an improvement in fine motor skills to promote
better performance in ADLs as to self-care, eating, dressing,
and personal hygiene.
Decreased aerobic capacity Pt. will show an improved aerobic capacity to facilitate
endurance & improved performance in ADLs č ↓ fatigue
Impaired static & dynamic Pt. will show an improvement in static and dynamic balance to
balance and risk of falls decrease the risk of falls, prevent injuries, and to facilitate
functional ADLs.
Impaired posture Pt. will be able to improve and correct posture in order to
improve quality of life and prevent injuries or conditions related
to posture.
Impaired gait Pt. will be able to amb. with the proper gait pattern with an
improved balance and tolerance to walking to prevent falls and
to promote functional independence as to ambulation.
Impaired functional Pt. will be able to perform functional activities with minimal
independence assistance to promote independence in performing ADLs.
Frenkel’s exercises c therapist guarding the side x 2 sets x 10 reps to improve coordination as
to sitting and standing:
Sitting
● One leg stretching to slide the heel to a position indicated by a mark on the floor
● The alternate leg stretching & lifting to place the heel on the marked point
● From stride sitting posture pt. is asked to stand and then sit
● Rise and sit c knees together
● Sitting hip abduction & adduction
Standing
● In stride standing, weight is transferred from one foot to another.
● Place foot forward and backward on a straight line.
● Walk sideways by placing feet on the marked point
Hand Therapy Ball Exercises x 15min. to improve fine motor skills
● Power Grip
● Pinch
● Table Roll
● Finger Flexion
● Finger Squeeze
Stationary cycling x 15 min. to increase aerobic endurance, increase LE strength, and
promote balance in sitting
Diaphragmatic Breathing Exercises x 5 reps x 2 sets to control breathing and facilitate oxygen
uptake.
Jogging on a treadmill mod. assist. +1 x 15 min. to increase aerobic endurance, increase
tolerance and improve dynamic balance.
Weight shifting exercises within // bars x 15 min. to promote an increase in balance and
tolerance in standing and decrease risk for falls.
Static Balance Control exercise: Tandem stance & Single-leg stance for 15 mins on // bars to
improve balance and tolerance
Standing balance training in tandem stance x15 min. on // bars to improve balance and
tolerance
Postural awareness training in front of mirror c verbal, auditory cues and positive
reinforcement to improve postural alignment
Gait Training on parallel bars c footsteps as guide for 10 minutes to improve ambulation &
gait.
Functional training x 5 reps x 2 sets c guidance of therapist to improve performance in ADLs
Supine ↔ sit
Sit ↔ stand
12
 HOME EXERCISE PROGRAM PRECAUTIONS
1. HMP x 20 mins to decrease pain and inc blood circulation 1. Minimize external noise during treatment to avoid annoyance and improve focus in
2. Self-stretching Exercises using (B) Symmetrical PNF D2 flexion UE & D1 extension LE doing tasks.
patterns x 15 SH x 10 reps x 3 sets to improve flexibility and ↑ ROM 2. Give simple instructions as to not confuse or agitate the patient.
3. Strengthening Exercises using 5 lb dumbbells and ankle weights to all the major muscle 3. Reduce level of stimulation in the environment
groups of the body x 10 reps x 2 sets to increase muscle strength and increase 4. Place in a private/quiet room
functional capacity. 5. Remove noxious stimuli if there is any
4. Ball squeezing and rolling exercises x 15min. to improve fine motor skills 6. Limit unnecessary sounds/noises
5. Postural correction techniques in front of the mirror x 10 mins in order to improve 7. Provide frequent orientation to time, date, place, and activities that they will be doing.
posture. 8. Provide emotional support, encourage socialization, behavioral control and
6. Walking x 10 mins to improve gait & aerobic functional capacity. motivation.
7. Yoga x 10mins. to ↑ flexibility, increase aerobic capacity & improve posture 9. Pt. should have frequent rest intervals between exercises or activities in order to
avoid fatigue.
10. Using of warm colors to prevent agitation from light sensitivity

13
 NEUROMUSCULAR CONDITIONS REVA COMPILATION
VELEZ COLLEGE PHYSICAL THERAPY BATCH 2022
PARKINSON’S DISEASE &
PARKINSONISM
WHAT’S INSIDE
1. Parkinson’s Disease
2. Secondary Parkinsonism
a. Postencephalitic Parkinsonism
b. Toxic Parkinsonism
c. Drug Induced Parkinsonism
d. Metabolic Parkinsonism
e. Vascular and Tumors
3. Post-Traumatic Parkinsonism
a. Dementia Pugilistica
4. Parkinson-Plus Syndrome
PARKINSON’S DISEASE
GENERAL MEDICAL BACKGROUND
DEFINITION
◊ A chronic progressive disorder of the Central
Nervous System (CNS) with motor and non
motor symptoms due to the degeneration of
dopaminergic substantia neurons and nigra
striatal pathways.
◊ Also known as the shaking palsy or paralysis
agitans, it is most commonly characterized by its
four cardinal features of bradykinesia, rigidity,
tremors, and postural instabilities.
◊ Parkinsonism is an umbrella term that
categorizes a group of disorders with the same
symptoms or presentation of Parkinson’s
Disease but does not necessarily mean that
there is a primary disturbance in the
dopaminergic system of the basal ganglia.
◊ Parkinson’s Disease is the most common form
of parkinsonism and is often termed as primary
or idiopathic parkinsonism.
EPIDEMIOLOGY
◊ Affects around 1 million Americans and around
7-10 million people worldwide.
◊ The average age of onset is around 50-60 years
old.
◊ For early onset/young onset PD, it affects
individuals aged 21 - 40 years old.
◊ For juvenile onset PD, it affects individuals less
than 21 years old.
◊ Prevalence among White Americans, <50%
among African American & Asian Americans.
◊ To this day, there is no data available on the
prevalence of PD in the Philippines. In
record-based studies, the prevalence of PD in
Asia is 35.8-68.3/100,000 (age standardized to
WHO population) and 51.3-176.9/100,000 in
door-to-door surveys.
ETIOLOGY
◊ There is no known cause for Idiopathic
Parkinson’s Disease although genetic and
environmental influences have been identified.
◊ Genetic causes of PD include both autosomal
dominant and autosomal recessive inherited
mutationsAutosomal dominant forms involve
mutations in the LRRK2 and SNCA genes.
◊ Autosomal recessive forms involve mutations in
the PARK2, PINK1, and DJ-1.
◊ For Secondary Parkinsonism, this usually results
from a number of different identifiable causes
including viruses, toxins, drugs, & tumors.
RISK FACTORS
◊ Increasing age and having an affected family
member can be a risk factor for PD.
◊ Exposure to pesticides, particularly those
containing DDT and rotenone can cause, or
have been found to cause PD.
◊ Cigarette smoking and caffeine have been also
found to predispose PD.
PATHOMECHANICS / PATHOPHYSIOLOGY
◊ Prior to recorded EMG activity in the muscles
engaged in a movement, the basal ganglia are
active.
◊ Lesions do not cause paralysis or weakness;
instead, they alter the nature of movement,
resulting in a loss of adaptive control, slowed
movement, and poor coordination.
◊ The basal ganglia are large subcortical
structures that are functionally placed between
the cortex and the thalamus and are linked.
o The limbic lobe, frontal cortex, and
brainstem all have direct links to them.
◊ The failure to facilitate desired behaviors and
simultaneously inhibit unwanted behaviors may
be responsible for the cognitive, emotional, and
memory problems that coexist with movement
disorders.
◊ The degeneration of a nucleus that is part of the
basal ganglia, the substantia nigra, leads to loss
of its ability to produce dopamine, a
neurotransmitter necessary to normal function of
basal ganglia neurons.
o Before clinical indications of the disease
appear, 70 to 80 percent of the
dopamine in the brain is thought to be
depleted.
◊ The system adjusts at first, and
dopamine-dependent pathways become more
efficient, but as dopamine depletion persists,
function diminishes.
CLASSIFICATION
Primary Parkinsonism
Variant ● Tremor Predominant
- Tremors are a predominant
manifestation
- It is the most common variant.
● Postural Instability
- Manifestations are predominantly
due to abnormalities of posture
and balance
Onset ● Early-onset (<40 years;
often familial)
- Young-onset (>21 years)
- Juvenile (<21 years)
● Late (>40 years; generally
 sporadic) include decreases in mental
activity, memory problems, dizzy
Genetic - This classification represents only spells, loss of balance, tremors
<10% of cases and either be and coordination, speech
because of: problems, paratonia, and
● Casual Gene parkinson symptoms.
● Associated Gene
Parkinson-Plus Syndrome
Secondary Parkinsonism
- A group of neurodegenerative diseases that
Postencephalitic - This type of parkinsonism affect the substantia nigra and produce
Parkinsonism occurred due to the influenza parkinsonian symptoms along with other
epidemic way back in 1917 to neurological signs.
1926.
- Parkinsonism symptoms were
noted in individuals several years CLINICAL PRESENTATION
after the epidemic which gave rise
to a theory that the brain was Primary Motor Symptoms (Cardinal Features)
infected slowly by the virus. ◊ Rigidity
- This type of parkinsonism is no o Pt. ℅ “heaviness” and “stiffness” of
longer seen as there have been no limbs.
recent outbreaks of influenza. o Fairly constant regardless of the task,
amplitude, or speed of movement
Toxic - This type of parkinsonism is o Often asymmetrical (especially in the
Parkinsonism caused by exposure to early stages of PD)
environmental toxins such as o Proximal affectation (shoulder & neck
industrial chemicals & pesticides muscles) first, then distal affectation
containing DDT & rotenone. (muscles of face and extremities)
- Manganese is the most common o Types:
toxin that represents serious Cogwheel - Jerky, ratchet-like resistance
occupational hazards for miners Rigidity to passive movement as
due to prolonged exposure. muscles alternately tense
- Other toxins that could cause and relax
parkinsonism are carbon disulfide, - occurs when tremor coexists
carbon monoxide, methanol, & with rigidity
cyanide.
Lead pipe - Sustained resistance to
Drug Induced - Drugs have been found to Rigidity passive movement, with no
Parkinsonism interfere with dopaminergic fluctuations
(DIP) mechanisms, either presynaptically
or postsynaptically.
● Neuroleptic drugs
- Chlorpromazine, Haloperidol, ◊ Bradykinesia
Thiothixene. o slowness of movement
● Antidepressant drugs o prolonged movement and reaction times
- Amitriptyline, Amoxapine, → leading to ↑ time on task &
Trazodone. dependence on daily activities
● Anti-hypertensive drugs o Akinesia
- Methyldopa, reserpine ▪ poverty of spontaneous
movement
▪ Ex. Absence of associated
Metabolic - Metabolic disorders can cause movement (arm swing during
Parkinsonism parkinsonian symptoms such as walking), or Freezing (sudden
Wilson’s disease, hyperthyroidism, stops in movement).
hyperparathyroidism, o Hypokinesia
hypoparathyroidism & Spatz ▪ slowed and reduced movements
disease. ▪ Examples:
● Moderate or Severe PD:
Vascular and - Secondary parkinsonism can also handwriting that may
Tumors be attributed to development of start out strong but
vascular causes and tumors in becomes smaller and
certain areas of the brain. smaller as writing
proceeds
Post-Traumatic Parkinsonism (micrographia).
● During walking,
Dementia - Also termed as ‘punch drunk rotational movements of
Pugilistica syndrome’, it is a type of chronic the trunk with arm swing
traumatic encephalitis with may also start out
characteristics of dementia. strong and decrease
- Manifestations of dementia over time.
◊ Tremor
2
 o involves involuntary shaking or
gigantocellular reticular nucleus, and
oscillating movement of a part or parts
coeruleus-subcoeruleus complex.
of the body resulting from contractions
of opposing muscles
3 ◊ Involvement of the nigrostriatal system
o Resting Tremor
is apparent (pars compacta of the
▪ present at rest
substantia nigra).
▪ suppressed briefly by voluntary
movement
4 ◊ Lesions are also found in the cortex
▪ disappears with sleep
(temporal mesocortex and allocortex).
▪ slight tremor of the hand or foot
on one side of the body, or less
5 ◊ Pathology is extended to involve the
commonly in the jaw or tongue.
sensory association areas of the
o Postural Tremor
neocortex and prefrontal cortex.
▪ can be seen when muscles are
used to maintain an upright
6 ◊ Pathology is extended to involve the
posture against gravity
sensory association areas of the
▪ tremor of the head and trunk
neocortex and premotor areas.
o Action Tremor
▪ tremor that continues with
movement COMPLICATIONS
▪ can occur in patients with
advanced disease Secondary Motor Symptoms
▪ Tremor tends to be less severe
when the patient is relaxed and
unoccupied. Motor ◊ ↓ torque production
▪ aggravated by emotional stress Performance ◊ Fatigue
or excitement ◊ Contractures and deformity
common
◊ Postural Instability ◊ Masked face
o due to abnormalities of posture and ◊ Micrographia
balance
o Pts. demonstrate abnormal and Motor ◊ Start hesitation
inflexible postural responses controlling Planning ◊ Freezing episodes
their center of mass (COM) within their ◊ Poverty of movement
base of support (BOS)
o Response to instability is an abnormal Motor ◊ Slower learning rates, reduced
pattern of coactivation → resulting in a Learning efficiency
rigid body and an inability to utilize ◊ ↑ context-specificity of learning.
normal postural synergies to recover ◊ Procedural learning deficits for
balance complex and sequential tasks
o Pts. also demonstrate difficulty in
Gait ◊ Reduced stride length; ↑
regulating feed-forward, anticipatory
step-to-step variability
adjustments of postural muscles during
◊ Reduced speed of walking
voluntary movements.
◊ Cadence (steps per minute)
typically intact; may be ↓ in
advanced PD
◊ Difficulty walking (starting and stopping,
◊ ↑ time: double-limb support
misjudging corners, abnormal shoe wear)
◊ Insufficient hip, knee, and ankle
◊ Resting tremors (usually unilateral at onset)
flexion: shuffling steps
◊ Bradykinesia
◊ Insufficient heel strike with
◊ Difficulty balancing (carrying items while walking
increased forefoot loading
difficult, frequent falls)
◊ ↓ trunk rotation: ↓ or absent arm
◊ Depression/sadness (often precedes onset of
swing
motor signs)
◊ Festinating gait: anteropulsion
◊ Loss of motor skills
common
◊ Handwriting (micrographia, tremulous)
◊ Freezing of gait (FOG) Difficulty
◊ Voice and speech changes/difficulty
turning: increased steps per turn
(hypophonia, dysarthria).
◊ Difficulty with dual tasking:
◊ Loss of memory/dementia (mild or severe)
simultaneous motor and/or
◊ Skin disorders (dry skin, rough skin, dandruff of
cognitive tasks
scalp).
◊ Difficulty with attentional demands
of complex environments
STAGES OF PARKINSON’S DISEASE
Posture ◊ Kyphosis with forward head
1 ◊ Lesions are found in the medulla ◊ Leaning to one side with tonal
oblongata (dorsal IX/X nucleus, or asymmetries Increased fall risk
intermediate reticular zone)
Sensation ◊ Paresthesias
2 ◊ Pathology expanded to involve lesions ◊ Pain
of the caudal raphe nuclei, the ◊ Akathisia

3
 ◊ Corticobasal degeneration (CBD)
Speech, ◊ Hypokinetic dysarthria
◊ Lewy Body Dementia (LBD)
Voice, and ◊ Dysphagia
◊ Alzheimer’s Disease
Swallowing
◊ Huntington’s Disease
◊ Parkinson-plus syndromes
Cognition ◊ Dementia
Function & ◊ Bradyphrenia Essential Tremor Essential tremor
Behavior ◊ Visuospatial deficits doesn't cause
◊ Depression associated health
◊ Dysphoric mood problems, while
Parkinson's carries
Autonomic ◊ Excessive sweating other symptoms,
Nervous ◊ Abnormal sensations of heat and such as stooped
System cold posture and balance
◊ Seborrhea problems.
◊ Sialorrhea
◊ Constipation Essential tremors are
◊ Urinary bladder dysfunction usually felt more in
motion, Parkinson’s
Cardiopulmo ◊ Low resting BP tremors are felt more
nary function ◊ Compromised cardiovascular while resting
response to exercise
◊ Impaired respiratory function Progressive People with PSP tend
Supranuclear Palsy to stand straight or tilt
Skin ◊ Dry skin (PSP) their heads
Disorders ◊ Rough skin backwards (resulting
◊ Dandruff of scalp in backwards falls),
while people with
Parkinson's usually
bend forwards.
MEDICAL DIAGNOSIS
◊ No single definitive test Problems with
o Accurate diagnosis is only possible with speech and
continued observation of evolving swallowing tend to be
clinical signs & symptoms more common and
◊ Based on history & clinical examination severe in PSP than in
o Handwriting samples, speech analysis, Parkinson's and are
interview questions that focus on often more apparent
developing symptoms, and physical earlier.
examination are used
◊ Preclinical stage: nonmotor sx predominate Multiple System Nerve destruction in
o There is an increasing focus on use of Atrophy (MSA) Parkinson's tends to
questionnaires & tests (e.g., olfactory occur in the areas of
testing, imaging of cardiac sympathetic the brain that control
innervation) that focus on emerging movement, whereas
nonmotor symptoms MSA affects what's
o Sx present many years before an official called the autonomic
dx of PD: loss of smell, sleep nervous system
disturbances, vivid dreams with REM
alterations, foot dystonia & foot Corticobasal Corticobasal
cramping similar to restless legs Degeneration (CBD) Degeneration (CBD)
syndrome, orthostatic hypotension, and is a rare type of
constipation parkinsonism that
◊ Diagnosis of PD is typically made if at least 2 of affects people from
4 cardinal motor features are present the age of 40,
o Cardinal motor features: tremor, rigidity, typically between the
bradykinesia, postural instability ages of 50 to 70. It
◊ Exclusion of Parkinson-plus syndromes tends to affect one
o Presence of extrapyramidal signs that side of the body more
are bilaterally symmetrical and do not than the other initially,
respond to L-dopa & dopamine agonists gradually spreading
(apomorphine test) are suggestive of over a few years.
these syndromes, not PD.
◊ Imaging to rule out other pathologies Lewy Body Dementia The difference lies
◊ PET scan to aid in determining dopamine levels (LBD) largely in the timing of
◊ MRI result: absence/abnormal swallow tail sign cognitive (thinking)
◊ Postmortem exam: presence of lewy bodies and movement
symptoms. In
DIFFERENTIAL DIAGNOSIS dementia with Lewy
◊ Essential Tremor bodies, cognitive
◊ Progressive Supranuclear Palsy (PSP) symptoms develop
◊ Multiple System Atrophy (MSA)
4
 within a year of Rigidity Akinesia
parkinsonism—any
condition that Tremor predominant variant Gait dysfunctions
involves the types of
movement changes, Younger onset Partial instabilities
such as tremor or
muscle stiffness, Cognitive dysfunctions
seen in Parkinson's
disease. Later age of onset

Alzheimer’s Disease Alzheimer's affects

◊ With L-dopa therapy, progression is generally
language and
slower with overall improvement in mortality rate
memory, while
◊ PD does not significantly reduce life span in
Parkinson's affects
most persons who develop the generalized form
problem solving
between 50 and 60 years of age. However,
(executive function),
deterioration continues until death occurs.
speed of thinking,
o Most common causes of death:
memory and other
cardiovascular disease & pneumonia
cognitive functions,
◊ Hoehn-Yahr Classification of Disability Scale
as well as mood.
provides a broad measure for charting the
progression of the disease using motor signs &
Huntington’s Disease In Parkinson's, it's
elements of functional status
alpha-synuclein. In
Huntington's, it's
huntingtin HOEHN-YAHR CLASSIFICATION OF DISABILITY

Parkinson-Plus Parkinsonism is a Stage Character of Disability

Syndromes general term that
refers to a group of I ◊ Minimal or absent; unilateral if present
neurological
disorders that cause II ◊ Minimal bilateral midline involvement
movement problems ◊ Balance not impaired
similar to those seen
in Parkinson's III ◊ Impaired righting reflexes
disease such as ◊ Unsteadiness when turning or rising from
tremors, slow chair. Some activities are restricted, but
movement and patient can live independently & continue
stiffness. some forms of employment.

IV ◊ All symptoms present and severe

PROGNOSIS
◊ Progressive with a long subclinical period s̅
apparent clinical manifestations estimated to be
at least 5 years
◊ Mean PD duration: approx. 13 years
◊ All clinical manifestations worsen progressively
◊ Rate of progression is variable
o Young age at onset or who are tremor
predominant = more benign progression
o Pts who present with postural instability
& gait disturbances = more pronounced
deterioration with a more rapid disease
progression
▪ Neurobehavioral disturbances &
dementia are more common in
this group
o Older age at onset & rigidity/hypokinesia
as an initial sx = more rapid rate of
motor progression; earlier development
of cognitive decline & dementia
◊ Presence of associated comorbidities (stroke,
auditory deficits, visual impairments) & male sex
may be used to predict faster rate of motor
progression
GOOD PROGNOSIS BAD PROGNOSIS
Family history Bradykinesia
◊ Standing and walking possible only with
assistance
V ◊ Confined to bed or wheelchair
GENERAL HEALTHCARE MANAGEMENT
MEDICAL MANAGEMENT
◊ Currently no cure for PD; palliative care is given
◊ No single intervention has proven to be disease
modifying
◊ Treatment is to preserve patient’s independence
& quality of life;
◊ Directed at slowing disease progression using
neuroprotective strategies, and symptomatic
treatment of motor and nonmotor symptoms
◊ Combined approach of physical therapy and
pharmacological intervention plays a key role in
the management of patients with PD
o Variety of interventions to maximize
functional ability & minimize secondary
complications are used
o Early intervention is critical
o Interventions also focus on improvement
of motor function, exercise capacity,
functional performance, and activity
participation
SURGICAL MANAGEMENT
◊ Deep brain stimulation
5
 o subthalamic stimulation - most effective
for tremor; less effect on dyskinesia and
rigidity
o globus pallidus stimulation - has good
initial effect; but chances of psychosis
and punding activity over time
◊ Fetal cell transplantation
◊ Stem cell transplantation
◊ Stereotactic procedure
o Thalamotomy
o Pallidotomy
PHARMACOLOGICAL MANAGEMENT
◊ Drug therapy is adapted to the person’s needs,
which may vary with the stage of the disease
and the predominant manifestations.
◊ Levodopa is usually taken simultaneously with
other anti-PD drugs
◊ Levodopa (L-dopa)
o Mechanism of action: resolves
dopamine deficiency by being converted
to dopamine after crossing BBB
o Effect: improves tremor, rigidity,
bradykinesia, and walking problems
o Side-effect: fluctuations of dyskinesias
that produce chorea, athetosis,
dystonia, tics, and myoclonus; sleep
disturbances; depression; disabling
psychiatric toxicity (hallucinations,
delusions, paranoia); cardiovascular
changes (hypotension dizziness,
arrhythmias; genitourinary changes
(dysuria); and gastrointestinal changes
(nausea, dry mouth)
o Suddenly becomes less effective and
causes worsening of symptoms (“off”
state). Although the most effective for
PD, early use may contribute more
disability at later stages when the effect
fluctuates and ultimately decreases.
o Levodopa with Carbidopa (Sinemet)
▪ Carbidopa enables more
levodopa to reach the brain
before being converted to
dopamine
▪ decreases the amount of
levodopa needed to achieve
desired effect
o Is ineffective when taken with protein;
amino acids compete with levodopa for
transport across intestinal mucosa
o Should not be taken by pts with
malignant melanoma or active peptic
ulcers.
◊ Catechol-O-methyltransferase (COMT) inhibitors
o MOA: slow the breakdown of dopamine
o effect: same as Levodopa, reduce
levodopa off time and allow for
decreased dosing of levodopa
o side effect: same as in Levodopa,
dizziness, muscle pain/cramps
◊ Dopamine agonists (bromocriptine (Parlodel),
pramipexole (Mirapex), ropinirole (Requip))
o MOA: act directly on dopamine
receptors in basal ganglia
o effect: same as in Levodopa
o side-effect: same as in Levodopa
o May produce fewer side effects
(dyskinesias, fluctuations); early use
may delay disease progression
◊ Anticholinergics
o MOA: inhibits excessive ACh influence
caused by dopamine deficiency
o Effect: same as in Levodopa
o Side effect: same as in Levodopa
o use is limited by frequent side effects
◊ Monoamine oxidase type B (MAO-B) inhibitors
(Selegiline (Eldepryl) and rasagiline (Azilect))
o MOA: block MAO-B effect that naturally
breaks down chemicals in the brain;
therefore allow more dopamine to be
available
o effect: same as Levodopa
o side-effects: same as Levodopa,
dizziness and headache
o usually used early in treatment when
symptoms are mild; can be included
when incidence of wearing off occur
◊ Amantadine (Symmetrel)
o effect: same as in Levodopa
o side effects: same as in other anti-PD
drugs but milder
o recommended for pts with mild
symptoms but no disability
OTHER HEALTHCARE MANAGEMENT
◊ Physician
◊ Nurse
◊ Speech Language Pathologist for dysphagia
◊ Psychiatrist for sleep disorder, anxiety,
depression, etc.
◊ Nutritionist
◊ Occupational therapist
PHYSICAL THERAPY, EXAMINATION, EVALUATION,
AND DIAGNOSIS
POINTS OF EMPHASIS ON EXAMINATION
◊ Mini-Mental Status Examination (MMSE)
o A 30-item questionnaire to assess
cognition function (memory, orientation,
conceptual reasoning, problem solving,
and judgement; speed of information
processing, attention, and concentration
can suspect bradyphrenia)
o impaired cognition = score of <24
MMSE
max score
“What is the year? Season? Date? Day? 5
Month?”
“Where are we now? State? County? Town/city? 5
Hospital? Floor?”
The examiner names three unrelated objects 3
clearly and slowly, then the instructor asks the
patient to name all three of them. The patient’s
response is used for scoring. The examiner
repeats them until patient learns all of them, if
possible.
“I would like you to count backward from 100 by 5
sevens.” (93, 86, 79, 72, 65, …) Alternative:
“Spell WORLD backwards.” (D-L-R-O-W)
“Earlier I told you the names of three things. Can 3
you tell me what those were?”
6
 o blurred vision
Show the patient two simple objects, such as a 2
o comorbid pathologies associated with
wristwatch and a pencil, and ask the patient to
aging (cataracts, glaucoma, diabetic
name them.
retinopathy, SMD)
o fuzzy vision d/t antidepressants and
“Repeat the phrase: ‘No ifs, ands, or buts.’” 1
anticholinergic
◊ ROM
“Take the paper in your right hand, fold it in half, 3
o decreased hip and knee ext, DF,
and put it on the floor.” (The examiner gives the
shoulder flex, elbow ext, neck ext, and
patient a piece of blank paper.)
spinal ROM
◊ Posture
“Please read this and do what it says.” (Written 1
o kyphosis
instruction is “Close your eyes.”)
o shadow pillow posture (flexed posture
with forward head in supine)
“Make up and write a sentence about anything.” 1
◊ MMT
(This sentence must contain a noun and a verb.)
o muscle weakness
“Please copy this picture.” (The examiner gives 1 ◊ Modified Ashworth Scale (MAS)
the patient a blank piece of paper and asks o assesses muscle tone
him/her to draw the symbol below. All 10 angles o rigidity grade 4, asymmetrical
must be present and two must intersect.) ▪ neck and shoulders → trunk and
extremities
o decreased facial mobility
MAS

0 = No increase in muscle tone

/30 1 = Slight increase in muscle tone, with a catch
and release or minimal resistance at the end of
the range of motion when an affected part(s) is
◊ Geriatric Depression Scale - Short (GDS-S) moved in flexion or extension
o A short 15-item questionnaire yes/no 1+ = Slight increase in muscle tone, manifested
questions that will assess the as a catch, followed by minimal resistance
psychosocial function through the remainder (less than half) of the
o possible depression = score of <6 range of motion
GDS-S 2 = A marked increase in muscle tone
throughout most of the range of motion, but
1. Are you basically satisfied with your life? yes no yes affected part(s) are still easily moved
no yes no yes no yes no yes no yes no yes no yes no 3 = Considerable increase in muscle tone,
yes no yes no yes no yes no yes no passive movement difficult
2. Have you dropped many of your activities and 4 = Affected part(s) rigid in flexion or extension
interests?
3. Do you feel that your life is empty? ◊ Coordination
4. Do you often get bored? o bradykinesia
5. Are you in good spirits most of the time? ◊ Functional assessment
6. Are you afraid that something bad is going to o tremors
happen to you? o dyskinesia
7. Do you feel happy most of the time? ◊ Berg Balance Scale (BBS)
8. Do you often feel helpless? o an objective measure of static and
9. Do you prefer to stay at home, rather than going dynamic balance abilities
out and doing things? o at risk for falls = BBS <45
10. Do you feel that you have more problems with o decreased postural control
memory than most?
11. Do you think it is wonderful to be alive now? BBS 0-4
12. Do you feel worthless the way you are now?
13. Do you feel full of energy? 1. Sitting unsupported
14. Do you feel that your situation is hopeless? 2. Change of position: sitting to standing
15. Do you think that most people are better off 3. Change of position” standing to sitting
than you are? 4. Transfers
5. Standing unsupported
scoring: yes for bolded questions = 1 point. A score of 6. Standing with eyes closed
5 or more suggests depression. 7. Standing with feet together
8. Tandem standing
9. Standing on one leg
◊ Sensation 10. Turning trunk (feet fixed)
o sensory changes d/t aging or co-morbid 11. Retrieving objects from floor
pathology (stroke, DM, etc.) 12. Turning 360 degrees
◊ Pain 13. Stool stepping
o Mild aching and cramp-like sensations 14. Reaching forward while standing
o Aches and pains d/t immobility, impaired
posture, or ligamentous strain total /56
◊ Vision
o Visual changes ◊ 10-Meter Walk Test
7
 o shuffling gait
o decreased cardiopulmonary endurance
◊ Fatigue Severity Scale (FSS)
o easily fatigued = low FSS score
FSS
strongly disagree → strongly agree
1. My motivation is lower when I am
fatigued.
2. Exercise brings on my fatigue.
3. I am easily fatigued.
4. Fatigue interferes with my physical
functioning.
5. Fatigue causes frequent problems for me.
6. My fatigue prevents sustained physical
functioning.
7. Fatigue interferes with carrying out certain
duties and responsibilities.
8. Fatigue is among my most disabling
symptoms.
9. Fatigue interferes with my work, family, or
social life.
total
PT PROBLEM LIST
◊ Rigidity
◊ Impaired posture / Postural Instability
- kyphosis with forward head
◊ ↓ muscle strength
◊ Easily fatigued
◊ Impaired gait (shuffling)
◊ Dysphagia
◊ OH
CARDINAL FEATURES:
◊ rigidity
◊ bradykinesia
◊ tremor (intentional)
◊ postural instability
PT DIAGNOSIS
◊ Practice Pattern E: Impaired motor function and
sensory integrity associated with progressive
disorders of the central nervous system.
PT PROGNOSIS
◊ Patients with a young age at onset or who are
tremor predominant typically demonstrate a
more benign progression.
◊ Patients with PD who present with postural in-
stability and gait disturbances (the PIGD group)
tend to have more pronounced deterioration with
a more rapid disease progression.
PHYSICAL THERAPY PLAN OF CARE
PT LONG AND SHORT TERM GOALS
LONG TERM GOAL:
◊ Pt. will be able to reduce difficulty in moving
(laterality) UE, reduce tremor, improve mobility
and function, prevent falls, and maintain overall
quality of life within _____ PTR sessions.
SHORT TERM GOALS:
◊ Will manifest decrease in muscle tone within __
PTR session to improve joint mobility and
function
◊ Will manifest an improved posture within __ ptr
session to enhance performance on ADLs
◊ Will manifest an increase of 1 grade higher in
ms strength of (specify muscles) within __ ptr
1-7
session to improve functional performance.
◊ Will manifest an increase of cardiopulmonary
endurance within __ ptr sessions
◊ Will manifest an improved gait pattern in __ ptr
sessions to increase safety and enhance
performance in ADLs
◊ Will manifest a decrease in occurence of
dysphagia within __ ptr sessions to enhance
performance of ADLs
◊ Will manifest a decrease in occurrence of
orthostatic hypotension within ___ ptr sessions
to improve quality of life.
PT INTERVENTIONS
RIGIDITY:
/63 ◊ ROODS inhibitory techniques on (laterality)
UE/LE x __ reps x __ sets to decrease muscle
tone and promote relaxation
a. gentle shaking
b. slow rolling
c. rhythmic initiation
POSTURE:
◊ Postural correction exercises
a. isometric rows x __ reps x __ sets to
correct kyphotic posture
b. Chin tucks x __ reps X __ sets to
decrease forward head posture
c. Mirror imaging in standing position for 5
mins to correct posture
DECREASE MUSCLE STRENGTH:
◊ Strengthening exercises on (laterality) (specific
muscles), neck and trunk muscles to increase
muscle strength
a. wall slides
b. shoulder blade squeeze in sitting
c. resistance band exercises c yellow
resistance band x __ reps x __ sets
i. chest pull in sitting
ii. seated in hip abduction
iii. hip extension in standing
EASILY FATIGUED:
◊ aerobic exercises to improve cardiovascular
function, enhance performance of ADLS, and
reduce bradykinesia
a. cycling on stationary bicycle x 15 mins
b. swimming x 15 mins
c. walking on treadmill x 15 mins
GAIT
◊ Gait training to improve balance, coordination
and ambulation
a. treadmill x 15 mins
b. tandem walking x 10 meters x 2 rounds
c. dual task exercise. Instruct patient to
walk for 10 m while holding a cup on
(laterality) hand x 2 rounds
OH
8
 ◊ Tilt table. Tilt for 10-15 degrees and check BP
after tilting.

REFERENCES
Books:
◊ Goodman, C.G., & Fuller, K.S. (2015).
Pathology: Implications for the Physical
Therapist. 4th ed. St. Louis, MO: Elsevier.
◊ O’Sullivan, S.B., Schmitz, T.J., & Fulk, G.D.
(2014). Physical Rehabilitation. 6th ed.
Philadelphia, PA: F.A. Davis Company.
◊ Ciccone, C.D. (2016). Pharmacology in
Rehabilitation. Philadelphia, PA; F.A. Davis
Company.

Websites:
◊ Folstein MF, Folstein SE, McHugh PR:
“Mini-mental state: A practical method for
grading the cognitive state of patients for the
clinician.” J Psychiatr Res 1975;12:189-198.
Retrieved from
http://www.fammed.usouthal.edu/Guides&JobAi
ds/Geriatric/MMSE.pdf
◊ Jamora, R., & Miyasaki, J. M. (2017). Treatment
gaps in Parkinson's disease care in the
Philippines. Neurodegenerative disease
management, 7(4), 245–251.
https://doi.org/10.2217/nmt-2017-0014
◊ The use of Rating Depression Series in the
Elderly, in Poon (ed.): Clinical Memory
Assessment of Older Adults, American
Psychological Association, 1986 Retrieved from
https://geriatrictoolkit.missouri.edu/cog/GDS_SH
ORT_FORM.PDF.

◊ U.S. Department of Health and Human Services.

(n.d.). What Is Lewy Body Dementia? National
Institute on Aging.
https://www.nia.nih.gov/health/what-lewy-body-d
ementia#:~:text=The%20difference%20lies%20l
argely%20in,stiffness%2C%20seen%20in%20P
arkinson's%20disease.

◊ https://www.movementdisorders.org/MDS-Files1
/PDFs/MDS-UPDRS-Rating-Scales/scale_rush_
dyskinesia.pdf

9
PHARMACOLOGICAL MANAGEMENT SUMMARY

Medications Functions Side Effects PT Implications

Levodopa (L-dopa) Improves tremor, rigidity, Decreased effectiveness or ineffective Monitor changes and symptoms
bradykinesia, and overtime. Schedule PTR after breakfast dose of LevodopaPTR is best
walking. Ineffective when taken with protein. when pt has NOT eaten his daily protein in the day.
Fluctuations Should not be taken by pts with malignant melanoma or active
Gastrointestinal problems peptic ulcers.
Cardiovascular changes Carefully observe posture and instruct to avoid sudden
Behavioural changes postural adjustments
Catechol-O-methyl transferase (COMT) inhibitors same as Levodopa same as Levodopa Like with Levodopa, monitor changes and symptoms
Dopamine agonists Apply needed interventions and precautions
Anticholinergics
Monoamine oxidase type B (MAO-B) inhibitors
Amantadine (Symmetrel)
Dopamine agonists (bromocriptine - Parlodel, same as Levodopa same as Levodopa May produce fewer side-effects (dyskinesia, fluctuations);
pramipexole - Mirapex, ropinirole - Requip) early use may delay disease progression
Anticholinergics same as Levodopa same as levodopa Inhibits ACh influence caused by dopamine deficiency
Monoamine oxidase type B (MAO-B) inhibitors same as Levodopa same as Levodopa, dizziness and headache. block MOA-B effect that naturally breaks down chemicals in
(selegiline - Eldepryl, rasagiline - Azilect) the brain; therefore allow more dopamine to be available.
Amantadine (Symmetrel) same as Levodopa same as in other anti-PD drugs but milder Recommended for patients with mild symptoms but no
disability

PT PLAN OF CARE SUMMARY

PROBLEM GOAL INTERVENTION

Rigidity to decrease muscle tone and promote relaxation to improve ROODS inhibitory techniques on (laterality) UE/LE x __ sets x __ reps.
quality of life a. gentle shaking
b. slow rolling
c. rhythmic initiation
Posture ● to improve and correct posture and to improve quality of Postural correction exercises
life a. isometric rows
● to correct kyphotic posture b. chin tucks
● to decrease forward head posture c. mirror imaging in standing position
Decrease Muscle Strength to increase muscle strength to be able to carry objects without Strengthening exercises on (laterality) (specific muscles), neck and trunk muscles to increase
difficulty muscle strength
a. wall slides
b. shoulder blade squeeze in sitting
c. resistance band exercises c yellow band
i. chest pull in sitting
ii. seated in hip abduction
iii. hip extension in standing
10
Easily Fatigued to improve cardiovascular function, enhance performance of a. cycling on stationary bicycle x 15 mins
ADLs, and reduce bradykinesia b. swimming x 15 mins
c. walking on treadmill x 15 mins

Gait to improve balance, coordination, and ambulation and to reduce a. treadmill x 15 mins
risk of falls b. tandem walking x 10 meters x 2 rounds
c. dual task exercise. Instruct patient to walk for 10 m while holding a cup on (laterality)
hand x 2 rounds
OH to reduce risk of falls Tilt table.
- tilt for 10-15 degrees and check BP after tilting.
HOME EXERCISE PROGRAM PRECAUTIONS
1. walking on treadmill x 15 mins 1. use gait belt during exercises all the time
2. chin tucks 2. avoid using valsalva maneuver
3. mirror imaging in standing position 3. avoid overuse, overstress and overload
4. wall slides 4. put emphasis on diaphragmatic breathing during exercise
5. shoulder blade squeeze in sitting 5. respect any signs of pain and discomfort

11
 NEUROMUSCULAR CONDITIONS REVA COMPILATION
VELEZ COLLEGE PHYSICAL THERAPY BATCH 2022

MULTIPLE SCLEROSIS ◊ Unknown

ETIOLOGY

◊ theory - This is induced by implicated viruses

WHAT’S INSIDE such as human herpesvirus-6 and Chlamydia
pneumoniae
◊ The immune system responds with activated
1. Relapsing Remitting Multiple Sclerosis myelin-reactive lymphocytes when exposed to a
2. Secondary Progressive Multiple Sclerosis viral agent.
3. Primary Progressive Multiple Sclerosis
4. Progressive Relapsing Multiple Sclerosis RISK FACTORS
◊ Geographical gradient
◊ Vitamin D Deficiency
◊ Smoking
GENERAL MEDICAL BACKGROUND
◊ Obesity
DEFINITION ◊ Infectious Factors (measles, canine distemper,
human herpes virus-6, Epstein-Barr Virus,
◊ An autoimmune disease characterized by: Chlamydia pneumonia)
o Inflammation
o Demyelination (Selective) PATHOMECHANICS / PATHOPHYSIOLOGY
o Gliosis
◊ Can cause acute and chronic symptoms which
may result in severe disability and impaired
quality of life
◊ Characterized by the Charcot’s Triad
o Scanning Speech
o Intention tremor
o Nystagmus

EPIDEMIOLOGY

◊ Affects 2.1 million worldwide

◊ Females > Males; ratio of 2:1 to 3:1
◊ Rare in children, as is the onset of symptoms in
adults > 50 y.o.
◊ Onset: 20-40 y.o.
◊ Predominant in white populations
◊ African Americans demonstrate ~ half the risk of
acquiring the disease
◊ Low rates in Asians & Native Americans
◊ Geographical Pattern:
High-frequency Temperate Zones:
● Northern US
● Northern Europe
● New Zealand
● Scandinavian countries
● Southern Canada
● Southern Australia

Medium-frequency Closer to the equator:

● Southern US
● Southern Europe
● The rest of Australia

Low-frequency Tropical areas:

● 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
 CLASSIFICATION
Relapsing- ● Characterized by discrete
Remitting attacks of neurological deficits
MS (relapse) with either full or
(RRMS) partial recovery (remission) in
subsequent weeks to months.
● Periods between relapses are
characterized by lack of
disease progression.
● The stable patient may have
local inflammatory activity that
is clinically silent.
● Affects ~85% of patients with
MS at diagnosis.
▪ Numbness of face, body or
extremities
▪ Position sense disturbance
▪ LE vibratory sense impairment
o Rare
▪ Anesthesia
◊ Pain (2nd most common complaint)
o Anxiety & fear worsens pain
o Types
▪ Trigeminal Neuralgia - touching
or moving face triggers pain
▪ Lhermitte’s Sign - neck flexion
produces electric-like sensation
through spine to lower extremity
◊ Paroxysmal Limb Pain
o burning, aching dysesthesia
o lower extremity
o worse at night & after exercise

◊ Hyperpathia
Secondary ● Characterized by an initial o minor stimuli hypersensitivity
-Progressi relapsing-remitting course, ◊ Headache
ve MS followed by a change in clinical o Migraine headache
(SPMS) course with progression to o Tension headache
steady and irreversible decline ◊ Chronic Neuropathic Pain
with or without continued acute o burning pain
attacks. ◊ Musculoskeletal Pain
● May be d/t progressive axonal o muscle pain
loss rather than new lesions. o ligament pain
● Before newer treatments, the ◊ Vision Changes
majority of patients with RRMS o Optic Neuritis - first symptom; ice
progressed to SPMS. pick-like pain behind eye with blurring or
graying of vision or total blindness in
Primary-Pr ● Characterized by disease one eye
ogressive progression and steady o Scotoma/Scotomata -
MS functional decline from onset; break/interruption/dark spots in visual
(PPMS) patients may experience field
modest fluctuations in o Marcus Gunn Pupil (Relative Afferent
neurological disability but Pupil Defect [RAPD]) - no consensual
discrete attacks do not occur. light reflex on good eye, pupils dilate
● Associated with later onset with light
(mean age 40 years) and more o Nystagmus - involuntary cyclical eyeball
equal gender distribution. movement; gaze-induced
● Affects ~10% of patients with o Internuclear Ophthalmoplegia
MS. o Diplopia - eye muscles incoordination
▪ Horizontal - CN VI
▪ Vertical - CN IV
Progressiv ● Characterized by a steady o Homonymous Hemianopsia - rare
e-Relapsin deterioration in disease from ◊ Motor
g MS onset (similar to PPMS) but o slow, stiff, weak movements
(PRMS) with occasional acute attacks. o reduced strength, endurance,
● Intervals between attacks are synergistic relationship
characterized by continuing o secondary muscle weakness
disease progression. ◊ Spasticity
● Affects ~5% of patients with o also with increased DTR
MS. o cause pain, contractures, abnormal
posture, decreased skin integrity & falls
◊ Involuntary flexor & extensor spasms
CLINICAL PRESENTATION ◊ (+) Babinski Sign
◊ Early ◊ Loss of precise autonomic control
o fatigability (most common complaint) ◊ Adaptive muscle shortening
o visual disturbance o pectoralis major & minor, and posterior
o weakness neck musculature, iliopsoas,
o paresthesia -> numbness hamstrings, gastrocnemius
◊ Advanced ◊ Fatigue
o Multiple symptoms with varying o abrupt
involvement o overwhelming sleepiness & tiredness,
weakness
◊ Sensory o worsens throughout the day
o Common o one of the most troubling
▪ Paresthesia ◊ Coordination & Balance
2
 o Ataxia - uncoordinated movements o Uhthoff’s Phenomenon - pseudo-attack;
o Postural Tremor - shaking back and reaction to heat that increases body
forth heat (fever, prolonged exercise, sun
o Intention Tremor exposure, hot baths, temperature) which
o Sensory Ataxia - feet numbness worsens symptoms & resolves < 24
◊ Gait & mobility hours
o Ataxic gait - drunken gait (uneven steps,
poor foot placement, uncoordinated COMPLICATIONS
limb) ◊ Musculoskeletal
o Scissoring gait - due to severe lower
extremity spasticity, particularly o Osteoporosis
adductors o Fibrosis/ankylosis
o Circumduction, hip hiking, vaulting, o Decrease in contractile strength
backward trunk lean, foot drop, shuffling o Decreased muscle endurance
◊ Speech & swallowing o Atrophy
o Dysarthria - slurred, poorly articulated ◊ Digestive
speech with low volume, unnatural o Appetite loss
emphasis & slow rate o Constipation
o Dysphonia - harshness, hoarseness, o Poor nutrition
breathlessness or hypernasal o Delayed healing
o Dysphagia - difficulty swallowing ◊ Respiratory
o Impaired coughing
◊ Cognition o Increased risk of respiratory infections
o Short term memory o Decreased vital capacity
o Attention & concentration o Decreased endurance
o Verbal fluency ◊ Neuromuscular
o Executive functions o Decreased sensory input
o Information processing - concept o Decreased motor control
information, processing, abstract o Poor coordination
reasoning, problem solving, planning & ◊ Autonomic ability
sequencing o Renal Urinary stasis
o Visuospatial functions o Increased urinary infections
◊ Emotional o Renal calculi
o Depression ◊ Cardiovascular
o Pseudobulbar affect / Emotional lability / o Decreased physical work capacity
Emotional dysregulation - sudden o Thrombophlebitis
crying, laughing & other emotional o Orthostatic hypotension
displays ◊ Psychosocial
o Euphoria - exaggerated feeling of o Anxiety/depression
wellbeing, incongruent with o Detachment
incapacitating disability o Intellectual deficit Integumentary
o Biploar affective disorder o Skin atrophy
◊ Bladder o Decubiti
o Urge incontinence
o Overflow incontinence
o Dyssynergic bladder MEDICAL DIAGNOSIS
◊ Bowel ◊ CSF Examination
o Constipation o ↑ in protein (myelin basic 25%),
o Bowel impaction oligoclonal IgG bands, and WBCs
o Diarrhea ◊ Evoked Potentials (EP)
o Incontinence o Demonstrates presence of
◊ Sexual demyelinating lesions on visual,
o Women auditory, and somatosensory pathways
▪ Sensation changes o Visual Evoked Potentials - most
▪ Vaginal dryness sensitive indicator for optic nerve
▪ Trouble reaching orgasm o Brainstem Auditory Evoked Response -
▪ Libido loss to check out auditory pathway
o Men o Somatosensory Evoked Response - to
▪ Impotence check out the somatosensory pathway
▪ Decreased sensation ◊ Lumbar Puncture with CSF Analysis
▪ Difficulty or inability to ejaculat o Elevated total IgG in CSF
▪ Libido loss o Presence of oligoclonal IgG
◊ Deconditioning o ↑ CSF proteins during relapses
o ↑ T-lymphocytes
◊ Exacerbating Factors ◊ MRI
o Exacerbation/Relapse - new & recurrent o Greatest sensitivity for the diagnosis
symptoms > 24 hours due to viral or
bacterial infection, major organ system
disease or stress
o Pseudo-exacerbation - temporary
worsening of symptoms < 24 hours
3
Diagnostic Criteria for MS (Simplified)
● Long interval ● Minimal recovery
between 1st & between relapses
Possible MS History of relapsing and may be 2nd relapses ● Multifocal onset
remitting without prior neurogenic
● Low lesion load ● High early
symptomatology
on MRI relapse rate
Probable 2 documented attacks with clinical, ● Presentation of ● Large lesion load
MS laboratory, or imaging evidence of at optic neuritis & brain atrophy
least 1 lesion or 1 documented attack ● Full recovery on MRI
with clinical, laboratory, or imaging from
evidence of at least 2 lesions exacerbations
Definite MS 2 attacks separated by at least one
month with clinical, laboratory, or GENERAL HEALTHCARE MANAGEMENT
imaging evidence of at least 2 lesions
MEDICAL MANAGEMENT

SURGICAL MANAGEMENT
◊ Deep Brain Stimulation
o A surgical procedure that permanently
DIFFERENTIAL DIAGNOSIS implants electrodes in the thalamus.
o A battery is implanted near the
collarbone, which sends electric pulses
MS SLE to the electrodes that blocks abnormal
nerve signals that are believed to cause
MRI brain periventricular; Gray & white tremors.
lesion Drawson’s matter lesion; o Used to control tremors associated with
fingers; small to small, rarely MS; doesn’t cure MS
large large ◊ Neurectomy
o To address trigeminal neuralgia 2˚ MS
MRI cord < 1 segment rare extensive o Can be performed on peripheral
lesion myelopathy branches of trigeminal nerve like the
supraorbital, infraorbital, lingual, and the
Relapse Rate every 2 years ~ every 5 years alveolar nerves.
o Can be accomplished by alcohol
Progression 10% Primary Stepwise &
injection, incision, cryotherapy, or
Progressive MS gradual
radiofrequency lesioning.
@ onset multi-organ
o Peripheral neurectomy can be safe in
85% Relapsing failure
elderly patients in remote and rural
Remitting MS ->
areas, where neurosurgical facilities are
Secondary
not readily available.
Progressive MS
o Evidence regarding these peripheral
@ 8 - 15 years
techniques is inconclusive.
◊ Rhizotomy
CNS Pathology Demyelination Vasculopathy ->
o Involves cutting away a section of a
-> Axonal loss Cognitive
nerve.
o Helps address facial pain d/t severe
CSF High IgG Normal
nerve pain

PHARMACOLOGICAL MANAGEMENT
PROGNOSIS

The prognosis and severity of the disease vary between Corticosteroid Prednisone, methylprednisolone
patients.The condition is often mild early on in the Therapy
disease and worsens as time progresses.
Anti-Spasticity Baclofen – 1st drug of
intervention
Good Prognosis Bad Prognosis Others: tizanidine, dantrolene,
diazepam
● Female ● Male
● Relapsing course ● Progressive Carbomazepine – used for
● Mild relapses course reducing sudden spasms
● Good recovery ● Primarily
Phenol nerve blocks – can be
between pyramidal/cerebel
effective until 6 months
exacerbations lar symptoms
● Primarily sensory ● More frequent Botulism toxin (Botox) – same
symptoms relapses time frame with phenol nerve

4
 o Paresthesia
blocks
o Hyperpathia
o Dysesthesia
o Trigeminal neuralgia
Pain Relievers Carbamazepine
o Lhermitte’s SIgn
Amitryptiline
◊ ROM
Phenytoin
◊ Vision
Diazepam
o Diplopia
Gabapentin
o Blurred vision
◊ Muscle Tone
Fatigue Amantadine hydrochloride
o Spasticity is common
(Symmetrel) – first-line therapy
◊ DTR
o Hyperreflexia is seen due to pyramidal
tracts lesions
Tremor Atarax
◊ MMT
Clonazepam
o N/A if spasticity is severe
Propanolol
o Paresis is common
Buspirone
◊ Coordination assessment
Primidone
o Ataxia
o Intention tremors
Immunosuppressive Drugs, Drugs for bowel and
o Dysmetria
bladder management, Intravenous immunoglobulin
o Dysdiadochokinesia
◊ Balance and tolerance
◊ Research is still ongoing for “Disease Modifying ◊ Gait assessment
o Ataxic gait
Therapies” given orally or intravenously. Table at ◊ Respiratory status
the end explains the different DMT ◊ Functional status
◊ Test and measures
o Expanded disability status scale
OTHER HEALTHCARE MANAGEMENT (Kurtzke)
◊ Neurologist o Minimum record of disability
◊ Neurosurgeon o Modified fatigue impact scale (Fisk)
◊ Physician
◊ IM PT PROBLEM LIST
◊ Orthopedic Surgeon ◊ Sensory deficit
◊ Cardiologist
◊ Visual changes
◊ Pulmonologist
◊ Surgeon ◊ Pain
◊ Anesthesiologist ◊ Spasticity
◊ Psychiatrist ◊ Weakness
◊ Nutritionist, Dietician ◊ Fatigue
◊ Nurse, Caregivers ◊ Ataxia/ Impaired Coordination
◊ Medical Technologists ◊ Decrease cardiorespiratory function
◊ Psychiatrist
◊ Cognitive and behavioral function
◊ Speech Therapist
◊ Occupational Therapist ◊ Speech and feeding problem
◊ Physical Therapist ◊ Psychosocial issues
◊ Dietician ◊ Bowel and bladder dysfunction
◊ Social Worker/Psychologist ◊ Risk of falls

PT DIAGNOSIS
PHYSICAL THERAPY, EXAMINATION, EVALUATION,
AND DIAGNOSIS ◊ Neuromuscular Pattern E: Impaired Motor
Function and Sensory Integrity Associated with
POINTS OF EMPHASIS ON EXAMINATION Progressive Disorders of the Central Nervous
System.
◊ History Taking
o Symptoms experienced by the pt.
o Disease progression PT PROGNOSIS
o Deficits in function
◊ Cognitive/behavioral status ◊ Depending on the patient’s presentation,
o Mild to moderate cognitive impairment individuals with MS have good prognosis with
are common PTR as they may benefit from strengthening
o Euphoria exercises, balance exercises, ROM exercises,
o Emotional dysregulation etc. Risks of falls are also reduced with PT.
◊ Communication
o Scanning speech
o Dysarthria
o Dysphasia
◊ Integumentary assessment
o Skin integrity and condition
◊ Sensory assessment
5
PHYSICAL THERAPY PLAN OF CARE
Aerobic Training Strength Training
PT LONG AND SHORT TERM GOALS
How 2x/ week. Both can be done on the same
often day.
◊ Exhibit improved sensation as to
superficial/deep/combined cortical to facilitate a Rest muscles for at least 1 day between
better sense of the environment & movement strength training sessions
when doing ADLs
◊ Exhibit a ↓ in pain to improve activity tolerance & How Initially, 30 mins 10-15 reps/set
performance. much per session. Then Gradually increase
◊ Exhibit a ↓ in spasticity to facilitate movement of gradual increase. to 2 sets.
the extremities in preparation for exercises or
activities. How hard Moderate intensity; Resistance heavy
◊ Exhibit an ↑ muscle strength to improve better usually 5 or 6 / 10 enough to safely
performance of ADLs, in preparation for for the pt. (10 finish the last set.
ambulation, promote safety & stability. being highest
◊ Exhibit an improved static & dynamic balance & intensity) Rest intervals for
tolerance to promote safety, ↓ risk of falls, and 1-2 mins every
improved ADL performance. Pt must be able to after set
◊ Exhibit improved coordination to facilitate talk during the
improved coordination skills and promote better activity
performance in ADLs
◊ Exhibit improved aerobic capacity to facilitate How to Arm cycling, Resistance bands,
endurance & improved performance in ADLs č ↓ walking, elliptical weight machines,
fatigue trainer free weights.
◊ Exhibit N˚ gait pattern to promote safe
ambulation in performing ADLs. Derived from: Canadian Physical Activity Guidelines for
Adults with MS

PT INTERVENTIONS
◊ For full list of PT interventions, see table at the
end. This section will contain principles for
intervention.
◊ DURING THE TIME OF DX:
o Explain benefits of physiotherapy
o Identifying areas of of physical abilities
and areas of improvement
o Goal setting
o Initiation of care
o Establishing regular exercise
◊ DURING TIMES OF STABILITY:
o Monitoring pt mobility
o Regular PT consultation
◊ During and After Relapse:
o Regain previous level of function
o Respect fatigue
o Reevaluation and continuing rehab
sessions
◊ With Increasing Progression:
o Need for assistive aides
o Re-prioritizing exercises that
accommodate ability level of pt
o Respect cognitive changes
◊ All exercises should be a challenge, but never a
struggle
◊ Sensory retraining
◊ Pain management
◊ Therapeutic exercises
◊ Proper positioning
◊ Mechanical aides
◊ Splinting and casting
◊ Postural exercises
◊ Functional gait exercises
◊ Coordination exercises (Frenkel’s exercises)
REFERENCES
◊ Please cite accordingly.
Books:
Cifu, D. X. (2015). Chapter 46: Multiple Sclerosis. In
Braddom's physical medicine and rehabilitation (5th
ed.). Elsevier Health Sciences.
O'Sullivan, S. B., Schmitz, T. J., & Fulk, G. (2013).
Chapter 16: Multiple Sclerosis. In Physical rehabilitation
(6th ed.). F.A. Davis.
Websites:
Costello, MS, ANP-BC, MSCN – N, K. (2014, July). The
Use of Disease Modifying Therapies in Multiple
Sclerosis: Principles and Current Evidence. National
Multiple Sclerosis Society.
https://www.nationalmssociety.org/getmedia/5ca284d3-fc
7c-4ba5-b005-ab537d495c3c/DMT_Consensus_MS_Co
alition_color
Rohrig, PT, DPT, MSCS, M. (2018). A RESOURCE
FOR HEALTHCARE PROFESSIONALS Physical
Therapy in Multiple Sclerosis. National Multiple
Sclerosis Society.
https://www.nationalmssociety.org/NationalMSSociety/m
edia/MSNationalFiles/Brochures/Clinical_Bulletin_Physi
cal-Therapy-in-MS-Rehabilitation.pdf
Deep Brain Stimulation. Multiple Sclerosis Trust.
https://mstrust.org.uk/a-z/deep-brain-stimulation#:~:text=
Deep%20brain%20stimulation%20is%20sometimes,is%
20implanted%20near%20the%20collarbone. Updated
March 2019. Accessed April 29, 2021.
Johnson, J. What to know about surgery for MS.
MedicalNewsToday.
https://www.medicalnewstoday.com/articles/325462.
Published June 13, 2019. Accessed April 29, 2021.

6
Shankar Kikkeri N, Nagalli S. Trigeminal Neuralgia. In:
StatPearls. Treasure Island (FL): StatPearls Publishing;
November 20, 2020. Accessed May 2, 2021.

Tafti D, Ehsan M, Xixis KL. Multiple Sclerosis. In:

StatPearls. Treasure Island (FL): StatPearls Publishing;
January 7, 2021. Accessed May 2, 2021.

7
PHARMACOLOGICAL MANAGEMENT SUMMARY

Medications Functions Side Effects PT Implications

glatiramer acetate ❖ Promotes differentiation in Th2 1. Injection-site reactions ● Immediate transient post-injection reaction (flushing,
(Copaxone®) and T-reg cells leading to 2. Lipoatrophy chest pain, palpitations, anxiety, dyspnea, throat
bystander suppression in CNS 3. Vasodilation, rash, dyspnea constriction, and/or urticaria)
-Increases release of neurotrophic 4. Chest pain ● Lipoatrophy and skin necrosis
factors from immune cells 5. Lymphadenopathy ● Potential effects on immune response
❖ Deletion of myelin-reactive T cells

interferon beta-1a ❖ Promotes shift from Th1-Th2 1. Flu-like symptoms ● Monitor VS

(Avonex®) ❖ Reduces trafficking across BBB 2. Depression ● Respect pt behavioral problems
❖ Restores T-reg cells 3. Elevated hepatic transaminases ● Seizure care
❖ Inhibits antigen presentation 4. Depression, suicide and/or psychosis
❖ Enhances apoptosis of 5. Anaphylaxis and other allergic reactions
autoreactive T-cells 6. CHF
7. Lower peripheral blood counts
8. Seizures
interferon beta-1a 1. Injection-site reactions ● Monitor VS
(Rebif®) 2. Flu-like symptoms ● Respect pt behavioral problems
3. Abdominal pain ● Seizure care
4. Depression ● Exercise prescription for low blood count
5. Elevated hepatic transaminases
6. Hematologic abnormalities
7. Anaphylaxis and other allergic reactions
8. Lower peripheral blood counts
9. Seizure
interferon beta-1b 1. Flu-like symptoms ● Monitor VS
(Betaseron®) 2. Injection-site reactions ● Respect pt behavioral problems
(Extavia®) 3. Elevated hepatic transaminases ● Seizure care
peginterferon 4. Low WBC ● Exercise prescription for low blood count
beta-1a (Plegridy®) 5. Depression and/or suicide
6. CHF
7. Injection-site necrosis
8. Low WBC
9. Flu-like symptoms
10. Seizures
cladribine ❖ Cytotoxic effects on B and T 1. Upper respiratory tract infection ● Pain during exercise
(Mavenclad®) lymphocytes through impairment 2. Headache ● Energy conservation
of DNA synthesis resulting in 3. Lymphopenia ● Monitor VS
depletion of lymphocytes. 4. Nausea ● Respect pt behavioral problems
5. Back pain
6. Arthralgia and arthritis
8
 7. Insomnia
8. Bronchitis
9. Hypertension
10.Fever
11.Depression
dimethyl fumarate ❖ Promote anti-inflammatory and 1. Anaphylaxis and angioedema ● Consider discontinuing treatment in patients with
(Tecfidera®) cytoprotective activities mediated 2. PML persistent lymphopenia (<500) lasting over 6 months)
by Nrf2 pathway. 3. Lymphopenia
4. Elevated AST
5. Liver injury
6. Flushing
7. GI symptoms
8. Pruritis
9. Rash
fingolimod ❖ Blocking of S1P receptor on 1. Headache ● Bradyarrhythmia and/or atrioventricular block
(Gilenya®) lymphocytes thus preventing their 2. Influenza following first dose
egress from secondary lymph 3. Diarrhea ● Risk of infections including serious infections
organs. 4. Back pain ● monitor for infection during treatment and for 2
5. Elevated hepatic enzymes months after d/c
6. Cough ● Low pulmonary function tests (FEV1)
7. Bradycardia following first dose ● Monitor VS
8. Macular edema
9. Lymphopenia
10.Increased BP
11.Bronchitis/pneumonia
Alemtuzumab ❖ Binding to CD52, a cell surface 1. Skin rash, fever, headache, muscle aches and/or ● Infusion reactions
(Lemtrada®) molecule present on T and B temporary reoccurrence of previous neurologic ● Autoimmunity (thyroid disorders, immune
lymphocytes, and on natural killer symptoms. thrombocytopenia (ITP)
cells, monocytes and 2. More serious but uncommon infusion reactions ● Infection
macrophages. This results in include anaphylaxis and/or hear
antibody-dependent cellular
cytolysis and complement
mediated lysis
mitoxantrone ❖ Disrupts DNA synthesis and repair 1. Temporary blue discoloration of sclera and urine ● Monitor VS
(Novantrone®) ❖ Inhibits B cell, T cell, and 2. Nausea ● Infection
macrophage proliferation 3. Alopecia
❖ Impairs antigen presentation 4. Menstrual disorders including amenorrhea and
❖ Impairs secretion of interferon infertility
gamma, TNFα and IL-2 5. Infections (URI, UTI, stomatitis)
6. Cardiac toxicity (arrhythmia, abnormal EKG and/or
congestive heart failure)

9
 natalizumab ❖ Block α4integrin on lymphocytes, 1. Headache ● Monitor VS
(Tysabri®) thus reducing trafficking of 2. Fatigue ● Energy conservation
lymphocytes into the CNS. 3. Urinary tract infection ● Exercise prescription
4. Lower respiratory tract infection
5. Arthralgia
6. Urticaria
7. Gastroenteritis
8. Vaginitis
9. Depression
10. Diarrhea
Orange= Self-injected ; Green = orally ; Blue = intravenous

PT PLAN OF CARE SUMMARY

PROBLEM GOAL INTERVENTION

Sensory Deficit Exhibit improved sensation as to superficial/deep/combined
cortical to facilitate a better sense of the environment &
movement when doing ADLs
Desensitization on bilat. UE and LE for 5 reps x 3 sets to normalize response to sensation and
enhance sense of environment.
Proprioceptive compensatory techniques – make use of alternative sensory systems for
feedback and movement control (verbal cues, biofeedback, etc.)

Pain Exhibit a ↓ in pain to improve activity tolerance & performance. Therapeutic USD for 15 mins. @ 2.5 W/cm2 c circular strokes on each major muscle group of
LE c therapist supervision in order to ↓ pain.

Spasticity Exhibit a ↓ in spasticity to facilitate movement of the extremities 1. Stretching

in preparation for exercises or activities. 2. ROM
3. Strengthening of opposite muscles
4. NMES
5. Positioning
Weakness Exhibit an ↑ muscle strength to improve better performance of Strengthening exercises on bilat. LE for 2 sets x 10 reps x15 SH c red thera band to ↑ muscle
ADLs, in preparation for ambulation, promote safety & stability. strength, to decrease hip hiking and preparation for gait training
a. Trunk rotation
b. Single- leg bridge
c. Side-lying hip abduction
d. Leg curl
e. 4 way ankle
Resistance Training

10

Fatigue Exhibit improved aerobic capacity to facilitate endurance &
improved performance in ADLs č ↓ fatigue
Frequency: 2-3 sessions/week Intensity: 1-3 sets, 8-15 repetitions at 60-80% 1 repetition
maximum
Increase resistance 2-5% once 15 repetitions is consistently achieved
Prioritize large, multi-joint muscle groups
Stationary cycling for 15 mins to ↑ aerobic capacity & improve functional performance.
Arm ergometry 15 mins x 2 sets c 2 min. rest interval to improve aerobic capacity

Energy Conservation/Management
4 Ps: Pacing, planning, prioritizing, positioning
Task Simplification
Adaptive equipment/assistive devices
Environmental modifications
Strategic rest breaks
Ataxia / Impaired Exhibit improved coordination to facilitate improved coordination Light weights on extremities
Coordination skills and promote better performance in ADLs Bracing/splinting
Balanced Based Torso Weighting

Frenkel’s exercises c therapist guarding the side x 2 sets x 10 reps to improve coordination as
to:
a. Sitting
i. One leg stretching to slide the heel to a position indicated by a mark
on the floor
ii. Alternate leg stretching & lifting to place the heel on the marked point
iii. From stride sitting posture pt. is asked to stand and then sit
iv. Rise and sit c knees together
v. Sitting hip abduction & adduction
b. Standing
i. In stride standing, weight is transferred from one foot to another.
ii. Place foot forward and backward on a straight line.
iii. Walk sideways by placing feet on the marked point.
Decreased Exhibit improved aerobic capacity to facilitate endurance & Frequency of 3-4 session/week Intensity
cardiorespiratory function improved performance in ADLs č ↓ fatigue Rating of Perceived Exertion (RPE) Warm Up/Cool Down 1-2/10
Rating of Perceived Exertion (RPE) Duration Exercise Intensity 3-5/10
Goal to achieve 20-30 minutes

DBE 5 reps x 3 sets c 1 min. rest interval to facilitate oxygen uptake.

Respiratory muscle training 3 sessions/week for 30 minutes has demonstrated improvement
Option for “fatigue” days
Speech and feeding Exhibit speech & feeding function to perform better ADLs with Refer to SLP
problem no problems.

11
Bowel and bladder Exhibit improved bowel & bladder function to perform better Timed voiding
dysfunction ADLs with no problems. Strengthen PFM if needed (Kegel’s Exercises)

Gait problems Exhibit N˚ gait pattern to promote safe ambulation in performing 1. Gait Training on even and uneven surfaces to promote functional mobility
ADLs. 2. Functional Electrical Stimulation
3. AFOs (if needed) to prevent foot slap
4. Hip Flexion Assist Device (if needed) to promote proper gait pattern
Impaired Balance/ Risk of Exhibit an improved static & dynamic balance & tolerance to Tai Chi
Falls promote safety, ↓ risk of falls, and improved ADL performance. Yoga
Aquatics
Core strengthening
Pilates
Vestibular exercises
Progressively challenging manipulation of somatosensory input during sitting, standing, and
walking
Cognitive dual task added to traditional balance exercises
HOME EXERCISE PROGRAM PRECAUTIONS
1. DBE 5 reps x 3 sets c 1 min. rest interval 1. Always emphasize on visual and auditory cues.
2. Self-stretching on affected areas 5 reps x 3 sets x 15 SH to improve flexibility 2. Avoid environmental clutter.
3. PRE using 2 lbs weights 5 reps x 3 sets to improve strength 3. Focus on safety and slowing down the movements.
4. Frenkel’s Exercises 5 reps x 3 sets 4. Do not exercise when feeling unwell (dizziness, SOB, nausea, vomiting)
5. Yoga x 15 mins to improve balance 5. Avoid valsalva maneuver
6. Rest in between exercise to minimize effects of fatigue
7. Use of gait belt for safety and to reduce risk of falls.
8. Stop the exercise when pain persists
9. Activity pacing to prevent fatigue
10. Observe proper body mechanics at all times when doing the exercise
11. List down all activities and tasks to reinforce memory.

12
 NEUROMUSCULAR CONDITIONS REVA COMPILATION
VELEZ COLLEGE PHYSICAL THERAPY BATCH 2022

◊ Dopamine antagonists - haloperidol,

MOVEMENT, CEREBELLAR, metoclopramide
AND VESTIBULAR DISORDERS ◊ Dopamine agonists - levodopa
◊ Antihypertensives - methyldopa, monoamine
MOVEMENT DISORDERS OF THE CNS oxidase inhibitors
◊ Athetosis ◊ Antiepileptics - phenytoin, carbamazepine,
◊ Chorea valproic acid, gabapentin, felbamate
◊ Ballismus ◊ Adrenergic agents - amphetamines,
◊ Dystonia methylphenidate, caffeine, b-Adrenergic
◊ Tics agonists
◊ Tremors ◊ Others - antihistamines, tricyclic
◊ Myoclonus antidepressants, buspirone, lithium, cimetidine,
oral contraceptives, cocaine, selective serotonin
GENERAL MEDICAL BACKGROUND reuptake inhibitors.

DEFINITION PATHOMECHANICS / PATHOPHYSIOLOGY

Complex, multi-system disorders characterized by ◊ Firing rate model: activity imbalance between
abnormal protein aggregates that accumulate in select the direct and indirect pathways changes the
regions in central, peripheral & autonomic nervous mean firing rate of output nuclei of the basal
systems. Neurologic syndromes, characterized by either ganglia and induces hypokinetic or hyperkinetic
an excess of movement or a paucity of voluntary and movement disorders;
automatic movements, unrelated to weakness or
spasticity. ◊ Firing pattern model: oscillatory and/or
synchronized activity observed in the basal
EPIDEMIOLOGY ganglia disturbs information processing in the
Epidemiology of Diseases Associated with Movement basal ganglia, resulting in motor symptoms;
Disorders ◊ Dynamic activity model: movement-related
◊ Huntington’s Disease - Onset most often occurs activity changes through the direct and indirect
between ages 35 and 50, with the condition pathways disrupt balance between
progressing without remission over 10 to 25 movement-related inhibition and surrounding
years. Huntington's disease affects an estimated excitation in the output nuclei, and induce motor
one in every 10,000 people in the U.S. symptoms.
◊ Parkinson’s Disease - affects approximately 10
to 20 in every 100,000 individuals in the CLASSIFICATION
worldwide population and 1 in 100 Americans
ages 60 years older.42 PD is currently the ◊ Hyperkinetic Disorders - characterized by an
second most common age-related excess/excessive movement
neurodegenerative disease after Alzheimer ◊ Hypokinetic Disorders - characterized by a
disease.
paucity of movement or hypokinesia
◊ Wilson’s Disease - a rare disorder that affects
males and females in equal numbers. The
disease is found in all races and ethnic groups. Hypokinetic Disorders Hyperkinetic Disorders
Although estimates vary, it is believed that
Wilson’s disease occurs in approximately one in Apraxia Ataxia
30,000 to 40,000 people worldwide. Onset most Rigidity Athetosis
often occurs between ages 35 and 50, with the Bradykinesia Chorea
condition progressing without remission over 10 Dystonia
to 25 years. Approximately one in 90 people Tics
may be carriers of the disease gene. Tremors
◊ Multiple System Atrophy - adult onset; affects Dysmetria
both sexes equally. The estimated prevalence of
MSA is 3 per 100,000.10 The mean age of onset
for MSA is around 55 years.
◊ Tourette’s Syndrome - Affects nearly 4% of Classification of Tremors
young people between ages 5 – 18.
◊ Restless Leg Syndrome- prevalence of RLS is Tremor Type Description
2% to 15%.42 It is slightly more common in
women and in individuals of Northern European Action - Postural Occurs when the body
descent. occurs with part is voluntary
voluntary maintained against
ETIOLOGY contraction gravity
Diseases Causing Movement Disorders of muscle Includes: essential,
◊ Huntington’s Disease physiologic, cerebellar,
◊ Restless Leg Syndrome dystonic, and
◊ Multiple System Atrophy drug-induced tremors
◊ Parkinson’s Disease
◊ Progressive Supranuclear Palsy Kinetic Occurs with any form of
◊ Tourette Syndrome voluntary movement
Includes: classic
Some Medications that may Induce Movement Disorders essential, cerebellar,
 COMPLICATIONS
dystonic, and
drug-induced tremors ◊ Falls
◊ Fractures
Intention Subtype of kinetic tremor ◊ Destruction of objects
amplified as the target is ◊ Anxiety
reached. The presence of ◊ Depression
this type of tremor implies
that there is a MEDICAL DIAGNOSIS
disturbance of the ◊ Movement Disorders are often associated with
cerebellum or its other diseases or conditions.
pathways. ◊ Electromyography - Surface EMG forms the
foundation of movement neurophysiology and
Rest Occurs in a body part that can clarify muscle discharge timing and spatial
is relaxed and completely relationships, as well as frequency information.
supported against gravity. This is useful for distinguishing tremor types,
Most commonly caused tremor versus myoclonus, and which muscles
by parkinsonism, but are involved in dystonia. Common modalities
may also occur in severe that are simultaneously recorded with EMG are
essential tremor EEG and motion detectors.
◊ CT Scan
◊ Conventional magnetic resonance imaging
CLINICAL PRESENTATION (MRI) weighted to detect T 1 - and T 2
-relaxation times of water protons can sensitively
◊ Akinesia - inability to initiate movements exclude structural causes of parkinsonism.
commonly seen in patients with PD ◊ Transcranial sonography (TCS) reveals
◊ Bradykinesia - slow movements structural midbrain and striatal changes in
parkinsonian disorders as hyperechogenic
◊ Asthenia - generalized weakness, secondary to signals
cerebellar pathology ◊ Serum levels
◊ Ataxia - inability to perform coordinated ◊ Complete Blood Count
movement
DIFFERENTIAL DIAGNOSIS
◊ Athetosis - condition that presents with ◊ Compulsive behaviors
involuntary movements combined with instability ◊ Generalized Hyperactivity
of postures, peripheral movement occur without ◊ Mannerisms
central stability
◊ Chorea - movements that are sudden, random, Combinations Possible Associated
and involuntary Disease
◊ Clonus - characteristic of UMNL, involuntary,
Tremor and Akinesia Parkinson;s Disease or
alternating, spasmodic contractions of a muscle
Atypical Parkinsonism
precipitated by a quick stretch reflex
◊ Lead-pipe rigidity - a form of rigidity, where there
Parkinsonism, ataxia, Multiple System Atrophy
is uniform and constant resistance to ROM
autonomic dysfunction,
often associated with lesions of the basal
spasticity, myoclonus
ganglia.
◊ Cogwheel rigidity - a form of rigidity where
Vertical supranuclear Progressive Supranuclear
resistance of movement has a phasic quality to
gaze palsy and falls, Palsy
it, often seen with Parkinson’s disease
symmetrical parkinsonism
◊ Clasp knife response - a type of resistance seen
during ROM of a hypertonic joint when there is
Akinesia, rigidity, Corticobasal
greatest resistance at the initiation of the range
myoclonus, dystonia and degeneration
that lessens with movement though the ROM
apraxia, asymmetrical
◊ Dysdiadochokinesia - inability to perform rapid
clinical phenotype
alternating movements (RAMs).
◊ Dysmetria - inability to control the range of the
Chorea, dystonia, and Huntington Disease
movement and the force of a muscular activity
bradykinesia
◊ Dystonia - closely related to athetosis, however,
there is a larger axial muscle involvement rather Dystonia plus tremor Primary Dystonia
than the appendicular muscles
◊ Fasciculations - muscular twitch caused by Tremor (rest and Wilson Disease
random discharges of LMN and its muscle postural), dystonia,
fibers; suggestive of LMNL akinetic-rigid syndrome
◊ Hemiballismus - involuntary and violent
movement of a large body part Ataxia and myoclonus Mitochondrial disease;
◊ Kinesthesia - ability to perceive the direction and (Ramsay Hunt syndrome, celiac disease;
extent of movement of a joint or body part ‘progressive myoclonic Overricht-Lundborg
◊ Tremor - involuntary, rhythmic oscillatory ataxia’) disease
movements secondary to basal ganglia lesion.

2
 ● Deep brain stimulation, a surgical treatment
option that uses an implant to stimulate the
Chorea Ballismus Athetosis
areas of your brain that controls movement
Rapid Rapid Slow

Involuntary Involuntary Involuntary SURGICAL MANAGEMENT

◊ Deep Brain Stimulation - is an elective surgical
Non- Non- Non- procedure in which electrodes are implanted into
stereotypical stereotypical stereotypical certain brain areas. These electrodes, or leads,
generate electrical impulses that control
Semi-purposeful abnormal brain activity. The electrical impulses
can also adjust for the chemical imbalances
Dance-like Violent flinging Writhing within the brain that cause various conditions;
movement controls patient’s symptoms (e.g., tremors),
improves motor function. This can help facilitate
More on distal More on Has propensity physical therapy treatment.
proximal affecting upper ◊ Thalamotomy involves lesioning the portions of
limb the thalamus that cause the tremors. Different
types include radiofrequency thalamotomy, laser
induced thermal therapy, magnetic resonance
guided focused ultrasound, focused thermal
Tremor Syndromes lesions and gamma knife thalamotomy. This can
facilitate physical therapy treatment.
Tremor Syndrome Clinical Features
PHARMACOLOGICAL MANAGEMENT
Cerebellar Tremor Intention or postural tremor;
ipsilateral involvement to ◊ Hyperkinetic Disorders
lesion, imbalance, hypotonia
Medication Class Indication
Enhanced Physiologic Postural tremor, lower
Tremor amplitude
Deutetrabenazine VMAT-2 Huntington’s
(Austedo) inhibitor Disease;
Essential Tremor Postural tremor, symmetric,
Tardive
involves hands, wrists, lower
Dyskinesia
extremities, head or voice
Valbenazine VMAT-2 Tardive
Parkinsonian Tremor Rest tremor, asymmetric,
(Ingrezza) inhibitor dyskinesia
involves distal extremities,
decreases with voluntary
Extended-release NMDA Parkinson’s
movement, bradykinesia,
amantadine antagonist disease,
postural instability, and
(Gocovri) dyskinesia
rigidity

Psychogenic Tremor Abrupt onset, spontaneous ◊ PTR is best scheduled at times where the
remission, extinction with medication is not at peak dose because side
distraction, changing tremor effects of these medications would include
characteristics sedation and drowsiness.

◊ Hypokinetic Disorders
PROGNOSIS
Medication Indication
In many cases, movement disorders cannot be cured,
and the goal of treatment is to minimize symptoms and Levodopa, carbidopa Parkinson’s disease.
relieve pain. Some are severe and progressive,
impairing the ability to move and speak. Dopamine agonists Increase dopamine levels

GENERAL HEALTHCARE MANAGEMENT Monoamine oxidase Slow the breakdown of

(MAO)-B inhibitors dopamine in the brain.
MEDICAL MANAGEMENT
Treatment of movement disorders would vary depending Catechol-O-methyltransfe Slow the breakdown of
on the underlying cause of the condition. Options may rase (COMT) inhibitors levodopa in the body,
include: allowing more levodopa
● Drug therapies to control symptoms to reach the brain.
● Physical or occupational therapy to help
maintain or restore the ability to control Anticholinergic Drugs Decrease the brain
movements chemical acetylcholine
● Botulinum toxin injections to help prevent and help restore balance
muscle contractions between acetylcholine
and dopamine.

3
 ◊ NM Pattern 5E: Impaired Motor Function and
Amantadine Increases dopamine
Sensory Integrity Associated With Progressive
activity in the brain. It also
Disorders of the Central Nervous System
affects the glutamate
system in the brain,
reducing uncontrolled
PT PROGNOSIS
body movements.
Pt’s prognosis depends on the following:
◊ Motivation
◊ PTR is best scheduled during the peak time
◊ Comorbidities
effect of these medications controlling the
involuntary movements. ◊ Prior physical functioning
◊ Lifestyle

OTHER HEALTHCARE MANAGEMENT PHYSICAL THERAPY PLAN OF CARE

◊ Occupational Therapy - for individuals who have PT LONG AND SHORT TERM GOALS
problems with fine motor skills.
◊ LTG: To improve patient’s quality of movements
◊ Speech Language Pathology - for individuals
who have problems with speech. by increasing patient’s stability in standing,
sitting, and walking to increase tolerance in
◊ Psychologist - for individuals who have mental ADLs.
health issues. STGs:
◊ Orthotist - for individuals who need orthosis. ◊ To increase ROM to improve patient’s quality of
movements in preparation for performing ADLs.
PHYSICAL THERAPY, EXAMINATION, EVALUATION, ◊ To increase muscle strength to improve patient’s
AND DIAGNOSIS stability in performing activities in preparation for
performing ADLs.
POINTS OF EMPHASIS ON EXAMINATION ◊ To improve fine motor skills in order to improve
◊ Patient Demographics dexterity and grip functions in preparation for
performing ADLs.
◊ Fall History
◊ To improve coordination in order to allow
◊ Medications
synchronous movements of the extremities in
◊ HFD
preparation for performing ADLs.
◊ Observation
◊ To improve balance in order to provide a stable
◊ Ocular Inspection
base of support for stability in performing ADLs.
◊ Sensory Assessment
◊ To improve gait in order to help the patient safely
◊ Deep Tendon Reflexes
perform activities and decrease risk for falls
◊ ROM Assessment
◊ To increase independence with ADLs to improve
◊ MMT
overall quality of life.
◊ Fine Motor Assessment
◊ Coordination Assessment
PT INTERVENTIONS
o Finger-to-nose test
o Heel-to-shin test
◊ Balance Assessment ◊ Strengthening Exercises to improve muscle
o Functional Reach Test strength and coordination to reduce severity of
o Berg Balance Scale symptoms
◊ Gait Assessment o Resistance training using ankle weights
◊ Functional Assessment and/or dumbbells. x 10 reps x 2 sets
o FIM o Progressive resistive exercises using
yellow theraband. x 5 SH x 10 reps x 2
PT PROBLEM LIST sets
◊ Decreased ROM ◊ Balance Exercises
◊ Decreased Muscle Strength o Standing with feet together x 10 SH x 5
◊ Impaired Fine Motor Skills (if upper extremity, or reps x 2 sets
hand affectation) o Romberg stance x 10 SH x 5 reps x 2
◊ Impaired Coordination sets
◊ Impaired Balance (if lower extremity affectation) o Standing on one leg x 10 SH x 5 reps x
◊ Impaired Gait (if lower extremity affectation) 2 sets
◊ Decreased independence in ADLs especially o Walking heel-to-toe for 3 minutes
with self-care, ambulation, and transfers. ◊ Coordination Exercises - Frenkel’s Exercises
o Supine
PT DIAGNOSIS ▪ Flex and extend one leg by the
Movement Disorders are often associated with certain heel sliding down a straight line
conditions; the following are the practice patterns that on the table.
may be used: ▪ Abduct and adduct hip smoothly
◊ NM Pattern 5A: Primary Prevention/Risk with knee bent and heel on the
table.
Reduction for Loss of Balance and Falling ▪ Abduct and adduct leg with
knee and hip extended by

4
 sliding the whole leg on the 2. Frontera W, DeLisa J. Delisa's Physical
table. Medicine And Rehabilitation Principles And
▪ Flex and extend hip and knee Practice. 5th ed. Philadelphia: Lippincott
with heel off the table. Williams & Wilkins; 2010:670-685.
▪ Flex and extend both the legs 3. Martin S, Kessler M. Neurologic Interventions
together with the heel sliding on For Physical Therapy. 3rd ed. St. Louis, MO:
the table. Elsevier Saunders; 2016:437-450.
▪ Flex one leg while extending the
other. Websites:
▪ Flex and extend one leg while 1. Crawford P, Zimmerman E. Tremor: Sorting
taking the other leg into Through the Differential Diagnosis. Aafp.org.
abduction and adduction. https://www.aafp.org/afp/2018/0201/p180.html.
▪ Heel of one limb to opposite leg Published 2018.
(toes, ankle, shin, patella). 2. Movement Disorders. Neuroscience.ubc.ca.
▪ Heel of one limb to opposite http://neuroscience.ubc.ca/CourseMat/0_Movem
knee, sliding down the crest of ent_Disorders_2011_Clinical.pdf.
tibia to ankle. 3. Pilitsis J, Khazen O, Patel S. Deep Brain
o Sitting Stimulation – Advantages, Risks and Conditions
▪ One leg is stretched to slide the Treated. Aans.org.
heel to a position indicated by a https://www.aans.org/en/Patients/Neurosurgical-
mark on the floor. Conditions-and-Treatments/Deep-Brain-Stimulati
▪ The alternate leg is lifted to on.
place the heel on the marked
point.
▪ From stride sitting posture
patient is asked to stand and
then sit.
▪ Rise and sit with knees together.
▪ Sitting hip abduction and
adduction.
◊ Transfer Training
o Sit-to-stand
o Standing pivot
o Bed to wheelchair (if applicable)
◊ Gait Training in parallel bars
Home Exercise Program
◊ Biceps curls, wrist flexion, and extension x 10
reps x 2 sets
◊ Balance exercises for 10 reps x 2 sets
o Romberg Stance
o Weight shifting
o Standing on one leg
o Walking in a straight line
◊ Frenkel's exercises 5 reps x 3 sets
◊ Home Ambulation for 30 minutes daily with
frequent rest intervals.
Precautions
◊ Use of gait belt especially during gait and
transfers to prevent falls
◊ Avoid environmental clutter
◊ Activity Pacing
◊ Proper Body Mechanics

Patient and Family Education

◊ Explain the condition to the patient and his/her
family
◊ Encourage the patient to assist the patient in
doing daily activities
◊ Fall Prevention Techniques
◊ Falling Techniques
REFERENCES
Books:
1. Cifu D. Braddom's Physical Medicine And
Rehabilitation. 5th ed. St. Louis, MO: Elsevier;
2016:1017-1027.

5
CEREBELLAR DISORDERS
GENERAL MEDICAL BACKGROUND
DEFINITION
◊ Cerebellar disorders occur when the cerebellar
function is affected through several
mechanisms, which often combine reduced
blood flow, edema, mechanical compression,
invasion of cerebellar parenchyma, inflammatory
response, immune process, cytotoxic effect, and
neurodegeneration.
◊ The hallmark feature of cerebellar damage is
incoordination of movements without overt
muscle weakness.
EPIDEMIOLOGY
◊ Recent global studies on ataxia reported an
estimated overall prevalence rate of 26/100,000
in children
◊ prevalence rate of dominant hereditary
cerebellar ataxia of 2.7/100,000
◊ prevalence rate of recessive hereditary
cerebellar ataxia of 3.3/100,000
◊ Men demonstrate more neurological gait
problems compared to women
ETIOLOGY
◊ Congenital malformation
o almost always sporadic, often occurring
as part of complex malformation
syndromes that affect other parts of the
CNS.
o manifest early in life and are
non-progressive.
◊ Hereditary ataxias- may be autosomal recessive
or autosomal dominant
o Autosomal recessive ataxias:
▪ Friedreich ataxia (the most
prevalent)
▪ Ataxia-telangiectasia
▪ Abetalipoproteinemia
▪ Ataxia with isolated vitamin E
deficiency
▪ Cerebrotendinous
xanthomatosis
o Autosomal dominant ataxia:
▪ Spinocerebellar ataxias
◊ Acquired conditions
o may result from non hereditary
neurodegenerative disorders , systemic
disorders, multiple sclerosis, cerebellar
strokes, repeated traumatic brain injury,
or toxin exposure, or they may be
idiopathic.
RISK FACTORS
◊ Viral infections
◊ Bacterial infections
◊ Exposure to certain toxins, such as lead ,
mercury, thallium, alcohol , and some
insecticides
◊ Paraneoplastic syndromes
◊ Bleeding, abscess, blood clots, or blockage in
the cerebellum
PATHOMECHANICS / PATHOPHYSIOLOGY
◊ In serious and continuing dysfunction, the
cerebellar lesion is extensive and usually
involves one or more of the deep cerebellar
nuclei in addition to the cerebellar cortex.
◊ Lateral portions of the cerebellar hemispheres
and the associated dentate nuclei play important
roles in the planning and programming of
movement. This is particularly so in multi joint
movements and in those requiring fine dexterity
in the distal extremities. Lesions on either side of
the dentate nuclei or the overlying cortex can
interfere with programming, resulting in delays in
both the initiation and the termination of
movement.
◊ Many of the signs and symptoms associated
with cerebellar damage can also be caused by
lesions outside the cerebellum itself. Ataxia, for
example, can be caused or exacerbated by a
variety of extracerebellar lesions. Conditions that
disrupt the spinocerebellar tracts can cause
dysmetria and ataxia by depriving the
cerebellum of proprioceptive input. These kinds
of defects underlie Friedreich's ataxia and many
of the cerebellar findings of multiple sclerosis.
By the same token, disruption of somatosensory
nerves in the peripheral nervous system can
impair the proprioceptive sense enough to cause
a sensory ataxia, such as might be observed in
alcoholic or other types of peripheral neuropathy.
Disorders of the vestibular system, by interfering
with balance and equilibrium, can mimic and
exacerbate the gait problems associated with
cerebellar damage.
◊ There are a large number of processes that
injure the cerebellum. Ethanol and many
anticonvulsant medications (such as phenytoin
and carbamazepine) are cerebellar toxins and
as well as certain types of cancer chemotherapy,
such as cytosine arabinoside (Zawacki et al,
2000) and lithium, given for manic-depressive
disorder. Ethanol characteristically causes
atrophy of the cerebellar vermis. This is true
even for exposure in utero (Autti-Ramo et al,
2002).
◊ Antibodies or other immune system
disturbances (i.e. paraneoplastic cerebellar
degenerations and in celiac disease (Gluten
enteropathy)
◊ In spinocerebellar ataxias, they may be due to
trinucleotide repeats (Wallace and Bird, 2018).
Trinucleotide repeats are abnormal "nonsense"
areas in human DNA that tend to get bigger with
time.
6
 CLASSIFICATION MEDICAL DIAGNOSIS
◊ 2 Distinguishable Cerebellar Syndromes:
- Midline Cerebellar Syndromes ◊ Imaging: Brain and spinal cord MRI
→ characterized by imbalance ◊ Some blood tests:
→ persons are unsteady, they are unable to o CBC with ESR
stand in Romberg with eyes open or closed, and o Liver function tests
are unable to perform tandem gait. o Vitamin B12 level
→ Severe midline disturbance causes "trunkal o TSH, fT3, fT4
ataxia" a syndrome where a person is unable to o Copper level studies
sit on their bed without steadying themselves. → o Paraneoplastic screen
Some persons have "titubation" or a bobbing o Anti-tissue transglutaminase antibody,
motion of the head or trunk. o Screen for infection and inflammation,
→ also often affect eye movements. There may o Some drug levels (carbamazepine,
be nystagmus, ocular dysmetria and poor phenytoin, lithium)
pursuit. o Lumbar puncture (to examine CSF for
- Hemispheric Cerebellar Syndromes oligoclonal bands)
→ characterized by incoordination of the limbs. o Electromyography (EMG) and nerve
→ There may be decomposition of movement, conduction studies (NCS)
dysmetria, and rebound. o Visual evoked potentials
→ Dysdiadochokinesis is the irregular ◊ Genetic testing
performance of rapid alternating movements. ◊ ENG or rotatory chair testing
Intention tremors may be present on an attempt
to touch an object. DIFFERENTIAL DIAGNOSIS
→ Kinetic tremor may be present in motion.
→ The finger-to-nose and heel-to-knee tests are
classic tests of hemispheric cerebellar Sensory Cerebellar Vestibular
dysfunction.
Vertigo Absent May be Present
→ While reflexes may be depressed initially with
hemispheric cerebellar syndromes, this cannot present
be counted on.
Nystagmus Absent May be Present
→ Speech may be dysarthric, scanning, or have
irregular emphasis on syllables. present

Dysarthria Absent Present Absent

CLINICAL PRESENTATION
Limb ataxia Present Usually Absent
◊ Headache (typically present (one
◊ Nausea/ vomiting legs) limb,
◊ Dizziness unilateral,
legs only, or
◊ Dysmetria
all limb)
◊ Dysarthria
◊ Dyssynergia Vibration & Impaired Normal Normal
◊ Dysdiadochokinesia position
◊ Rebound phenomenon sense
◊ Scanning speech
◊ Hypotonia Ankle Depressed Normal Normal
◊ Nystagmus reflexes or absent
◊ Blurred vision, impaired visual acuity
◊ Tremor Stance Often able to Unable to May be
◊ Hearing loss, tinnitus stand with stand with able to
◊ Memory difficulties feet together feet together stand with
◊ Swallowing difficulties & eyes open & eyes feet
◊ Fatigability but not with either open together;
◊ Titubation eyes closed or eyes typically
◊ Ataxic gait (Romberg worse with
sign) eyes closed
COMPLICATIONS

◊ Risk for falls PROGNOSIS

◊ Paralysis of eye muscle (ophthalmoplegia)
◊ Dizziness ◊ The prognosis of cerebellar disturbances
◊ Gait disorders and bed-bound state depends on the etiology.
◊ Worsening tremor ◊ Metabolic and nutritional etiologies of cerebellar
◊ Psychosocial stigma dysfunction have a relatively good prognosis.
◊ Raised intracranial pressure ◊ Some neurologic diseases must be treated
◊ Developmental milestone delay in case of symptomatically only, and often worsen over
children time.

7
GENERAL HEALTHCARE MANAGEMENT ◊ Coordination Ax
◊ Balance Ax
MEDICAL MANAGEMENT o determine abnormalities in postural
◊ There is no cure for hereditary forms of control
cerebellar degeneration. Treatment is usually o Increased fall risk
supportive and is based on the person's o Tests:
symptoms. - Berg Balance Scale
◊ For example, drugs may be prescribed to ease - POMA
gait abnormalities. Physical therapy can - Balance Evaluation System Test
strengthen muscles. Other disorders that may (BESTest)
contribute to the cerebellar degeneration may - Mini BEST
have treatment options that ease symptoms. - Functional Reach Test
- Timed Up and Go (TUG)
SURGICAL MANAGEMENT - Romberg’s Test
- Sharpened Romberg’s Test
◊ Surgery for structural lesions (tumor, ◊ Gait Ax
hydrocephalus) is beneficial o Cerebellar ataxic gait
o to relieve increased intracranial o Tests:
pressure and - Dynamic Gait Index (DGI)
◊ prevent life-threatening herniation. - Walkie Talkie Test
◊ Deep brain stimulation
o may improve postural/kinetic tremor in ◊ Functional Ax
selected cases o Functional Independence Measure
o Functional Assessment Measure
PHARMACOLOGICAL MANAGEMENT
PT PROBLEM LIST
◊ Aminopyridines (e.g. 4-aminopyridine) for
downbeat nystagmus (DBN) and episodic ataxia ◊ Decreased aerobic capacity
type 2 (EA2) ◊ Decreased ROM
o side effects: vertigo, headache, nausea ◊ Decreased muscle strength
o cardiac arrhythmia (rare but a severe ◊ Impaired balance and coordination
side effect) ◊ Postural instability
◊ Acetazolamide for EA2 ◊ Cerebellar ataxic gait
o side effects:development of kidney ◊ Impaired function in ADLs
stones ◊ Increased fall risk
◊ Zn supplementation
◊ Gabapentin
PT DIAGNOSIS
See Pharmacological Summary table at the end ◊ NM PATTERN C - Impaired motor function and
sensory integrity associated with
OTHER HEALTHCARE MANAGEMENT non-progressive disorders of the central nervous
system- congenital origin or acquired in infancy
◊ Neurologist or childhood
◊ Neurosurgeon
◊ Dietician PT PROGNOSIS
◊ Endocrinologist
◊ Geneticist ◊ The long-term outlook varies depending on its
◊ Psychiatrist underlying cause.
◊ PT ◊ Patients relatively have good prognosis
◊ OT
◊ Social worker PHYSICAL THERAPY PLAN OF CARE

PHYSICAL THERAPY, EXAMINATION, EVALUATION, PT LONG AND SHORT TERM GOALS

AND DIAGNOSIS
◊ To relieve pain through physical modalities,
POINTS OF EMPHASIS ON EXAMINATION ROM & stretching exercises
◊ History Ax ◊ To maintain, and improve joint range of motion
◊ Cardiopulmonary Ax through ROM & stretching exercises
o Aerobic capacity ◊ To improve strength through resistance
◊ Musculoskeletal Ax
exercises
o Muscle Tone
o ROM ◊ To improve endurance through aerobic
o MMT exercises
◊ Neurological Ax ◊ To improve motor skills and coordination through
o Sensation
o Reflexes balance and coordination exercises
◊ Motor Skills Ax ◊ To improve gait and stability through ambulation
o determine abnormalities in motor training
learning ◊ To improve postural stability through postural
- Motor Function Test training
8
 Websites:
PT INTERVENTIONS
◊ AROM/AAROM/PROM x 10 reps x 3 sets to
increase ROM
◊ Eye-head coordination exercises x 10 reps x 2
sets to improve coordination
◊ Frenkel’s exercises x 10 reps x 2 sets to improve
coordination
◊ Aerobic Training (e.g. cycling, lap swimming) x
30 mins. to increase aerobic capacity, increase
LE strength and enhance coordination
◊ Biofeedback therapy x 20 mins. to enhance
stability and postural control
◊ Postural training in front of mirror x 10 mins to
decrease postural instability
◊ Locomotion training on treadmill with weight
support x 30mins. to improve ambulatory
functions
See Plan of Care Summary table at the end
HEP
◊ Self-stretching x 15SH x 10 reps x 2 sets to
increase ROM
◊ Eye-head coordination exercises x 10 reps x 2
sets to improve coordination
◊ Frenkel’s exercises x 10 reps x 2 sets to improve
coordination
◊ Aerobic Training (e.g. stationary cycling) x 30
mins to increase aerobic capacity, increase LE
strength and enhance coordination
◊ Postural training in front of mirror x 10 mins to
decrease postural instability
◊ Gonzales-Usilgi, H. Cerebellar Disorders.
Updated in May 2020. Accessed on May 19,
2021.
https://www.msdmanuals.com/professional/neur
ologic-disorders/movement-and-cerebellar-disor
ders/cerebellar-disorders#:~:text=Cerebellar%20
disorders%20have%20numerous%20causes,im
aging%20and%20sometimes%20genetic%20tes
ting.
◊ Neupsy Key. Disorders of Equilibrium. Accessed
on May 26, 2021.
https://neupsykey.com/disorders-of-equilibrium/
◊ Cerebellar Disorders. Accessed on May 26,
2021.
dizziness-and-balance.com/disorders/central/cer
ebellar/cerebellar.htm.
Cerebellar Degeneration Information Page.
National Institute of Neurological Disorders and
S.
www.ninds.nih.gov/Disorders/All-Disorders/Cere
bellar-Degeneration-Information-Page.
Published March 27, 2019. Accessed May 26,
2021.

PATIENT EDUCATION
1. Proper warm-up activities and post-exercise
cool-down stretching
2. Proper breathing techniques during lifting
weights
3. Demonstrate proper use of assistive device
4. Proper positioning techniques
5. Home environment modifications for safe
mobility

REFERENCES

Books:
◊ Gruol, D L, Koibuchi, N, Manto, M, Molinari, M,
Schmahmann, J. D. Essentials of Cerebellum
and Cerebellar Disorders. Springer International
Publishing AG Switzerland; 2016.
Journals:
◊ Zesiewicz TA, Wilmot G, Kuo SH, et al:
Comprehensive systematic review summary:
Treatment of cerebellar motor dysfunction and
ataxia. Report of the Guideline Development,
Dissemination, and Implementation
Subcommittee of the American Academy of
Neurology. Neurology 90 (10):464–471, 2018.
doi: 10.1212/WNL.0000000000005055.
◊ Zawacki et al. Cerebellar toxicity of cytosine
arabinoside: clinical and neuropsychological
signs. Neurology 55, 1234, 2000
◊ Diego et al. Vestibular and hearing
manifestations of phenytoin toxicity: a
retrospective review. ENT journal, 80, 404-409,
2001

9
 VESTIBULAR DISORDERS Hypofunction) leading to a decreased
or eliminated receptor
Vestibular Disorders input.
● BPPV Trauma: vestibular
● UVH symptoms are usually
● BVH seen in 30%-60% in
● Central Vestibular Hypofunction patients c TBI.
● Meniere’s Disease -Vestibular Neuronitis
● Perilymphatic Fistula and Labyrinthitis-an
● Vestibular Schwannoma acute infection with
● Motion Sickness prolonged attacks of
● Migraine-related Dizziness symptoms persisting for
● Multiple Sclerosis several days or weeks
● Multiple System Atrophy that is caused by viral or
bacterial infection and
GENERAL MEDICAL BACKGROUND can cause UVH
-Tumors-acoustic
DEFINITION neuromas, gliomas, ot
brainstem or cerebellar
◊ Damage to the vestibular system which includes medulloblastomas can
also cause UVH
the parts of the inner ear in the brain that help
-Meniere’s Disease
control balance and eye movements.
◊ Damage may be d/t a disease, aging or injury. BVH (Bilateral -Auto-toxicity/auto-toxic
◊ Most common complaint: dizziness with Vestibular drugs
increasing prevalence with age. Hypofunction) -Bilateral infection:
neuritis and meningitis
EPIDEMIOLOGY -Vestibular neuropathy
-Osteosclerosis: Paget’s
◊ Mean age of onset is in the fifth decade of life Disease
◊ In the US, 5.5% experience dizziness (>15 CENTRAL
million per year) Cerebrovascular Insults involving AICAs, PICAs, and
o 32% of emergency department visits for insults vertebral arteries
dizziness have otologic/vestibular VBI Most commonly caused by MVA
pathology as the number one cause (Vertebrobasilar
o >70% of patients with initial complaints Insufficiency)
of dizziness will not have a resolution of TBI D/t labyrinthine or skull fractures,
symptoms at a 2-week follow-up demyelinating diseases s/a MS are some
o 63% of patients with persistent dizziness CNS pathologies
report recurrent symptoms continuing
beyond 3 months RISK FACTORS
◊ Disorders of the Peripheral vestibular system
o 22% presented with balance complaints ◊ Head trauma
◊ 38% with peripheral disturbances and 21% with ◊ Vestibular neuritis
◊ Viral neurolabyrinthitis
central disturbances had balance complaints ◊ Systemic disorders (HTN, diabetes, OA,
◊ Odds ratio (OR) of syncope was 21 times higher osteoporosis, and depression)
than that the general pediatric population in ◊ Migraine
patients with unspecified dizziness, and
sensorineural hearing loss was 43 times higher in
PATHOMECHANICS / PATHOPHYSIOLOGY
those with peripheral vestibular disorders
◊ With vestibular schwannoma, ~3000 cases are ◊ Receptors in this fluid-filled SCC detects angular
diagnosed each year in the US alone with a acceleration of the head motions of the fluid
prevalence of about 1 in 100,000 worldwide would tell us if we are moving
o It comprises 5-10% of all intracranial ◊ Vestibule – region of the inner where the SCC
neoplasms in adults would converge close to the cochlea (hearing
o It peaks in the 5th & 6th decade of life organ)
o M=F ◊ Vestibular system works with the visual system
to keep objects in focus when the head is
ETIOLOGY moving which makes the VOR. Rotation of the
head causes a flow of a fluid of the endolymph
PERIPHERAL which in turn causes displacement of the top
Mechanical BPPV (Benign - May be related to portion of the hair cells that are embedded in the
Paroxysmal degenerative processes jelly-like cupula, movement of the otoconia,
Positional or mechanical which is responsible for the inertial mass which
Vertigo) impairments of moves the hair cells in the jelly-like cupula
peripheral vestibular ◊ SCCs are particularly sensitive to fast head
system movements such as during walking or episodes
Decreased UVH (Unilateral -Viral insults, trauma, of imbalance s/a slips, trips, stumbles
Receptor Input Vestibular and vascular events
10
◊ Receptors in the otoliths, the utricles and ▪ balance portions of both inner
saccules detect linear acceleration and head ears are damaged
position with response to gravity ◊ Central Nervous System Pathology
◊ Hair cells in the otolith organs are blanketed in a o Central Vestibular Hypofunction
jelly-like layer studded with tiny calcium stones ◊ Specific vestibular disease
called otoconia o Meniere’s disease
◊ When the head is tilted or body position is ▪ There is increase endolymphatic
changed with respect to gravity, the fluid causing distention in the
displacement of the stones would cause the hair membranous tissues
cells to bend. ▪ Chronic Meniere’s disease can
◊ Otoliths respond to slow head movements such result in a unilateral vestibular
as those movements observed during postural hypofunction which is indicative
sway. of rehabilitation
◊ Vestibular system cannot, by itself, give o Perilymphatic fistula
information about the position of the body, such ▪ There is rupture of the oval
as simple head nods on a stable trunk versus window, the membrane
head nods with a moving trunk. separating the middle ear from
◊ Mechanoreceptors in the neck must provide the inner ear
information to the CNS in order to know the o Vestibular Schwannoma/Acoustic
position of the body part relative to the whole. Neuroma
Not just the neck but includes the ankles, knees, ▪ A benign primary intracranial
feet, hips, trunk, etc. tumor of myelin forming cells of
◊ Vestibular system works with the visual and the CN 8
skeletal systems for the sensors and muscles o Motion/ travel sickness
and joints to maintain orientation and balance. ▪ The sensory conflict theory that
◊ If there are any impairments in these systems, it explains when visual
can lead to vestibular disorders. proprioception and vestibular
inputs do not match each other
CLASSIFICATION ▪ A condition in which a
disagreement exists between
◊ Peripheral Pathology visually perceived movement
and the vestibular system sense
o Mechanical- BPPV of movement
▪ most common peripheral o Migraine- related dizziness
vestibular pathology ▪ Can be deceptively similar to a
▪ most common cause of vertigo peripheral vascular lesion,
▪ Described as a brief intense however the reason being the
sensation of spinning that vascular event occurs in a
occurs when there are changes vestibular structure such as a
in the position of the head with vestibular nuclei
respect to gravity o Multiple Sclerosis (MS)
Benign: Doesn’t cause further illness ▪ Can cause vestibular diseases
Paroxysmal: Temporary and sudden onset ▪ Can affect CN 8, where it enters
Positional: Related to changes in body position the brainstem and causes
Vertigo: The false sensation of spinning identical symptoms identical to
UVH
o Canalithiasis o Multiple System Atrophy (MSA)
▪ The otoconia are floating freely ▪ Progressive degenerative
in one of the SCC disease of the nervous system
▪ BPPV occurs on the turned involving 4 clinical domains:
head ● Cerebellar ataxia
o Cupulolithiasis ● Autonomic dysfunction
▪ Fragments of the otoconia break (AD)
away and adhere to the cupula ● PD- like symptoms
of one of the SCC ● Corticospinal
▪ BPPV is on the side of the dysfunction
vertigo
CLINICAL PRESENTATION
◊ Decreased sensory input Often associated with one or more of these sx:
o UVH (Unilateral Vestibular ◊ Dizziness: light-headed, floating, or rocking
Hypofunction)
sensation, faintness, increased risk of falls;
▪ 1 sided/unilateral vestibular
sensation of being heavily weighted or pulled in
lesion
one direction.
▪ One of the two vestibular
nerves, which are nerves that ◊ Dysequilibrium: sensation of being off-balance
run from each ear to the o May be caused by BVH, chronic
brainstem is not functioning unilateral vestibular hypofunction, LE
properly somatosensation loss, upper
o BVH (Bilateral Vestibular Hypofunction) brainstem/vestibular cortex lesion,
cerebellar and motor pathway lesions
11
◊ Lightheadedness: a feeling of faintness
MEDICAL DIAGNOSIS
o Maybe caused by OH, hypoglycemia,
anxiety, and cardiac in origin ◊ Electronystagmography (ENG)- group of eye
◊ Vertigo: a sense that the environment is moving movement tests that look for signals of a
or spinning; if severe, accompanied by nausea vestibular dysfunction or neurological problems
and vomiting by measuring nystagmus and other eye
o Peripheral Vertigo: episodic & has a movements
o Negative results: no involuntary eye
short duration; autonomic sx are present
movements during the test
s/a pallor, nausea, sweating & vomiting;
▪ Nystagmus may occur normally
auditory fullness & tinnitus may be
when head is moved
present
o Positive results: ENG detects an
▪ Can be caused by BPPV.
involuntary eye movement during the
Meniere’s Disease, trauma,
test
infection, tumor, or metabolic
disorders s/a DM, acute alcohol ◊ Rotation Test- another way of evaluating how
intoxication, and sensory neural well the eyes and inner ear work together for
hearing loss may be (+) every head movement in one direction
o Central Vertigo: LOC, (+) neurological ▪ Negative results: no eye
sx, diplopia, hemiplegia, weakness, movement in the opposite
numbness, ataxia, dysarthria usually d/t direction
meningitis, migraine, H/A ▪ Positive results: there is eye
◊ Cognitive changes: movement in the opposite
o Diff. concentrating and paying attention direction
o Easily distracted o Auto-head rotation
o Forgetful ▪ The person being tested is
o STM lapses asked to look at a fixed target
o Confused and move his/her head back
o Disoriented and forth or up/down for short
o Difficulty comprehending periods of time
instructions/directions o Rotatory Chair test
o Difficulty following speakers in ▪ A computerized chair that
conversations esp. c background moves for the person being
noise/movement present tested
◊ Hearing changes: ◊ Vestibular-Evoked Myogenic Potential (VEMP)-a
o Hearing loss
laboratory test used to evaluate whether the
o Distorted or fluctuating hearing
saccule and inferior vestibular nerve are intact
o Tinnitus (Meniere’s Disease)
and functioning normally
o Sensitivity to loud noise; may increase
o Negative results: presence of initial
sx of vertigo, dizziness or imbalance
inhibitory potential of 13 ms after the
◊ Other manifestations:
click and an excited or potential of 20
o (+) imbalance & spatial disorientation
sec after the click
o (+) disequilibrium or postural instability
o Positive results: absence of the clicks or
d/t vestibulospinal reflex; there may be
excitatory and inhibitory potentials on
ataxia, gait disturbances, increased risk
one side of the lesion is indicative of
for falls
UVH
o Vision disturbances
◊ Computerized Dynamic Posturography
o Discomfort from busy visual
(CDP)-assess a patient’s ability to integrate
environment
vestibular, visual, and somatosensory
o Sensitivity to: light esp fluorescent lights,
information for maintenance of postural control
certain types of computer monitors &
under six sensory conditions.
digital TV
o Negative result: there is no exaggerated
o Increased night blindness
body sway
o Poor depth perception
o Positive result: there is exaggerated
◊ Other symptoms:
body sway
o Nausea
◊ Cervical and Ocular Vestibular-Evoked
o Vomiting
Myogenic Potential (cVEMP) - use to stimulate
o Hangover
the sensory tissue within the otolithic organs
o Slurred speech
cVEMP Responses
o H/A
o Sensitivity to pressure, temperature, Pathological Absent Reduced Enhanced
Condition amplitude amplitude amplitude
wind currents, pain pressure or other
Otologic
symptoms c certain dietary changes like
high sodium Meniere disease ✓ ✓ ✓
Superior canal ✓
COMPLICATIONS dehiscence
Neurolabyrinthitis ✓ ✓
◊ Injury from falling
Vestibular neuritis ✓ ✓
◊ Reduced quality of life
◊ Discomfort Neurologic
◊ Anxiety and depression
12
 Migraine ✓ ✓
Spinocerebellar
✓ movement.
degeneration
Multiple sclerosis ✓ o Acute phase is the horizontal nystagmus
Brainstem stroke
✓ ◊
◊ Hearing Tests-audiometry measures of hearing
function
o Pure Tone Audiometry-a response is
requested when sound are heard of
different pitches through the
headphones
o Speech Audiometry Tests- sometimes
referred to as speech discrimination
where the repetition or recognition of
words is requested as they are
presented at different intervals or
intensities
▪ Negative result: 90% to 100% of
the words on the list are
correctly identified
▪ Positive result: 90% to 100% of
the words on the list are
incorrectly identified
o Tympanometry- examines the function
of the middle ear and Eustachian tube
o Acoustic-Reflex Testing- measures the
reflex of the stapes, one of the tiny
bones of the middle ear
◊ Scans
o MRI- in and around the inner ear
▪ Vascular loop or sling can be
identified on MRI.
▪ Inflammatory lesions can be
identified with MRI, including
labyrinthitis and inflammatory
lesions of the eighth cranial
nerve.
▪ Dizziness can be experienced
during an MRI leading to
nystagmus and a sense of
rotation, or floating.
o Computed Tomography (CT Scan)-
specifically done on the temporal lobe
within which the inner ear resides; used
to rule out causes of symptoms that are
unrelated to vestibular system
▪ Negative result:
▪ Positive result:
DIFFERENTIAL DIAGNOSIS
◊ Nystagmus from a cerebellar lesion may be in a
pure vertical direction.
◊ Pendular nystagmus is indicative of congenital
disorders s/an absence of central vision or
cortical visual processing nystagmus from a
central vestibular lesion.
◊ Lateropulsion is manifested by central lesions
above the level of the vestibular nuclei.
◊ Vestibular neuritis or acute unilateral
vestibulopathy
o Acute onset of constant rotational
vertigo, positional imbalance
nystagmus, and nausea without hearing
loss that last 24-72 hours after the
patient is able to begin moving.
o Complaints of varying degrees of
dizziness or imbalance with head
test & significant postural instability
Chronic phase
o (+) Unilateral head thrust
o (-) Audiograms for hearing loss
◊ Labyrinthitis
o Sx of vestibular neuritis with addition of
hearing loss & tinnitus.
o May d/t coral or bacterial agents
o (+) Audiograms for hearing loss
o Ddx with Meniere’s disease wherein
there’s repeated spontaneous attacks of
vertigo.
o Vertigo is also accompanied by tinnitus,
reduced hearing, oral fullness or
auditory fullness, postural imbalance,
nausea, and or vomiting.
o Usually free of symptoms between
attacks and there may be progressive
hearing loss and imbalance.
o Reduced caloric response unilaterally in
the acute phase, horizontal nystagmus,
significant postural instability, and
decreased hearing on audiogram.
◊ Bilateral vestibular disorders
o Postural imbalance or severe
dysequilibrium, especially in the dark or
on uneven surfaces
o Occasional dizziness
o Gait ataxias
o Oscillopsia
o Falls on compliant surfaces with eyes
closed
◊ Meniere’s disease
o Meniere's disease (endolymphatic
hydrops, ELH) is a common disorder of
the inner ear characterized by episodic
true vertigo.
o It is preceded by an increasing
sensation of aural fullness or aching in
the affected ear, by tinnitus, and by
fluctuating hearing loss.
o Nausea and vomiting can occur at the
time of the vertiginous.
o Classic feature: Low-frequency
sensorineural hearing loss with
moderate impairment of speech
discrimination.
◊ Perilymphatic fistula (PLF)
o It is defined as an abnormal
communication through which perilymph
passes from inner ear to middle ear.
o The most common causes of PLF are
complications from ear surgery, head
trauma such as basilar skull fracture,
whiplash injury from a motor vehicle
accident, barotrauma (e.g., a rupture of
the round window during scuba diving),
puncturing injury through the tympanic
membrane, coughing, straining, nose
blowing, and other such maneuvers that
increase intrathoracic and cerebrospinal
fluid (CSF) pressures and rupture the
labyrinthine window.
o Symptoms associated with PLF result
from an imbalance in pressure of
endolymphatic and perilymphatic fluid.
13
 ◊ Acoustic neuroma
o Acoustic neuroma may present as
Meniere's disease except that attacks
are usually not followed
asymptomatic periods.
o Vertigo is usually associated with
hearing loss and tinnitus.
o An acoustic neuroma originates in the
vestibular division of the eighth nerve
just within the internal auditory canal.
o As it grows, it occupies the posterior
fossa at the cerebellopontine angle.
o Facial weakness, facial sensory loss,
unilateral ataxia of limbs, and gait
abnormality may be present.
◊ Herpes zoster oticus
o A viral syndrome involving the eighth
nerve and is also known as the Ramsey
Hunt syndrome.
o In this syndrome, the zoster virus
remains dormant in the seventh and
eighth nerve ganglia and is reactivated
during periods of lower immunity.
o Patients can develop hearing loss,
vertigo, and facial weakness before or
after developing vesicular eruption or
burning pain in the ear.
◊ Motion sickness
o A normal sensation, that in some people
becomes debilitating.
o The predominant explanation for motion
sickness is the sensory conflict theory.
o The three inputs of proprioception,
vestibular and visual information do not
match stored neutral patterns the brain
expects to recognize.
o As a result, persons experience pallor,
nausea, emesis, diaphoresis, and
motion sensitivity.
◊ Multiple sclerosis (MS)
o MS can affect cranial nerve VIII where it
enters the brainstem and causes
identical symptoms to unilateral
vestibular pathology.
◊ Multiple system atrophy (MSA)
o A progressive degenerative disease of
the nervous system involving four
clinical domains: cerebellar ataxias,
autonomic dysfunction, Parkinson’s
disease like symptoms,
corticospinal dysfunction.
o Has been found to be a cause of
dizziness and imbalance.
Central Vestibular Peripheral Vestibular
Pathology Pathology
Ataxia is often severe Mild ataxia
Abnormal smooth pursuit and Smooth pursuit and
abnormal saccadic eye saccades usually normal;
movement tests positional testing may
reproduce nystagmus
Sx usually do not include Sx may include hearing loss
hearing loss; if so, it is often (insidious - may recover),
sudden & permanent fullness in ears, tinnitus
SX of acute vertigo not SX of acute vertigo usually
usually suppressed by visual suppressed by visual fixation
fixation
Pendular nystagmus (eyes Nystagmus will incorporate
oscillate at equal speeds) slow and fast phases (jerk
nystagmus)
Pure persistent vertical Spontaneous horizontal
by nystagmus persists nystagmus usually resolves
regardless of positional within 7 days in a patient
testing (persistent downbeat with UVH
nystagmus in Hallpike-Dix
may indicate anterior canal
BPPV)
SX might include diplopia, altered consciousness,
lateropulsion
PROGNOSIS
◊ When there is a unilateral lesion in the
peripheral vestibular system and the CNS is
intact, recovery of function is possible.
◊ Recovery rate in a central vestibular system
disorder causing dizziness or disequilibrium
depends on the nature of the lesion and the
concomitant neurologic dysfunction.
◊ A disease such as MS can cause episodes of
symptoms and progressive dysfunction with
poor adaptation and compensation because of
the other damage within the CNS.
GENERAL HEALTHCARE MANAGEMENT
SURGICAL MANAGEMENT
◊ Ablative surgery
◊ Surgically implanted vestibular prosthesis can
also be done for worst case bilateral vestibular
hypofunction.
PHARMACOLOGICAL MANAGEMENT
◊ Vestibular suppressants
o First-line treatment
▪ Anticholinergic
▪ Antihistamines
o Second- line treatment
▪ Lorazepam
▪ Clonazepam
o Third-line in-hospital treatment, only with
close Supervision
▪ Diphenidol
and ◊ Antiemetics
o Phenothiazine
▪ Prochlorperazine
▪ Promethazine
▪ Thiethylperazine
▪ Trimethobenzamide
◊ Prednisone
o Long term suppression of symptom is
not recommended since the body must
experience the symptom in order to
develop compensatory strategies
OTHER HEALTHCARE MANAGEMENT
◊ Nutritionist- focuses on regulating the body’s
fluid balance to stabilize the volume and
electrolyte concentration of the ear’s endolymph
fluid
14
 o May include alternating intake of ● Negative
substances like sodium and sugar, ▪ UVH
managing fluid intake, eliminating ● Positive, eyes closed
caffeine & alcohol, avoiding substances ▪ BVH
likely to trigger symptoms (nicotine, ● Positive
aspirin, NSAIDs) ▪ Central Lesion
◊ Psychologist- recommended if pt. has difficulty ● Positive
o Single-legged stance
coping with or has been disabled by the
▪ BPPV
symptoms or when pt experiences the ff:
● Negative
o Depression
▪ UVH
o Stress
● May be positive
o Anxiety
▪ BVH
o Other feelings of isolation
● Acute: positive
● Chronic - negative
PHYSICAL THERAPY, EXAMINATION, EVALUATION,
▪ Central Lesion
AND DIAGNOSIS
● May be unable to
perform
POINTS OF EMPHASIS ON EXAMINATION o Turn head while walking
▪ BPPV
◊ History taking ● May produce light
o Symptoms unsteadiness
o Duration and frequency ▪ UVH
▪ BPPV - lasts seconds to ● Acute: may not keep
minutess balance
▪ Meniere’s - lasts minutes to ● Compensated: normal
hours ▪ BVH
▪ Vestibular neuronitis, migraine ● May not keep balance
associated dizziness - lasts for or slows cadence
days ▪ Central Lesion
o Determine under what circumstance ● May not keep balance,
symptoms occur increased ataxia
◊ Positional and Diagnostic Testing:
◊ Attention, Arousal & Cognition
o Dix-Hallpike test
◊ Cardiopulmonary assessment ▪ Most common positional test
◊ Cranial nerve assessment used to examine for BPPV
◊ Sensory assessment ▪ Positive result: occurence of
◊ Tolerance assessment nystagmus
◊ Postural assessment o Roll test
o Abnormal shift of COG to the side of ▪ Performed if horizontal SCC
lesion BPPV is suspected
◊ ROM ▪ Positive result: occurrence of
o Decreased cervical motions nystagmus and vertigo
◊ MMT o Dynamic visual acuity (DVA)
o Decreased strength to cervical ▪ Used to measure visual acuity
musculature during horizontal motion of the
◊ Gait assessment head to identify the functional
o Instability may be noted significance of vestibular
o BPPV - normal hypofunction.
o UVH - acute: wide-based, slow, ▪ Positive result: a 3-line or more
decreased arm swing & trunk rotation; decrement in visual acuity
compensated: normal during head movement
o BVH - acute: wide-based, slow, ▪ Negative result: head movement
decreased arm swing & trunk rotation; results in little or no change of
compensated: mild gait deviation visual acuity
o Central lesion - pronounced ataxia o Head impulse test (HIT)
◊ FIM ▪ Used to examine semicircular
◊ Balance tests: canal function.
o Romberg ▪ Bilateral loss of vestibular
▪ BPPV function
● Negative ● Will make corrective
▪ UVH saccades after a HIT to
● Acute - positive either side
● Chronic - negative ▪ Unilateral peripheral lesion or
▪ BVH pathology of the central
● Acute: positive vestibular neurons
● Chronic: negative ● Will not be able to
▪ Central Lesion maintain gaze when the
● Often negative head is rotated quickly
o Tandem Romberg toward the side of lesion
▪ BPPV
15
 o Head shaking induced nystagmus
(HSN)
▪ To diagnose unilateral
peripheral vestibular defect
▪ Positive result: manifest a
horizontal HSN
◊ Standard tests/Outcome Measures:
o Visual analogue scale
▪ Effective technique to obtain
subjective intensity ratings of
vertigo, lightheadedness,
dysequilibrium, and oscillopsia.
o Dizziness Handicap Inventory (DHI)
▪ Used to measure a patient’s
self-perceived handicap as a
result of vestibular disorders.
▪ Score > 60 is associated with
severe dizziness and recurrent
falls
o Vestibular Rehabilitation Benefit
Questionnaire (VRQB)
▪ Used to specify the benefit from
vestibular physical therapy and
includes questions that address
avoidance behavior.
o Motion Sensitivity Quotient
▪ Provide a subjective score of an
individual’s sensitivity to motion.
▪ A score of 0 indicates no
symptoms whereas a score of
100 means severe dizziness in
all positions.
PT PROBLEM LIST
◊ Occurence of clinical presentations c head
movements
◊ LOM on cervical motions 2º apprehension of
aggravating clinical presentation
◊ Decreased muscle strength on cervical
musculature 2º apprehension of aggravating
clinical presentation
◊ Impaired posture
◊ Impaired balance
◊ Impaired gait
◊ Decreased performance in doing ADLs
PT DIAGNOSIS
◊ Neuromuscular Practice Pattern A: Primary
Prevention/Risk Reduction for Loss of Balance
and Falling
PT PROGNOSIS
◊ The physical therapist plays a major role in the
multidisciplinary approach to the man- agement
of symptoms.
◊ When symptoms are due to a peripheral
vestibular lesion, functional recovery will begin
within 2 days to 4 weeks through the adaptive
mechanism of the brain.
PHYSICAL THERAPY PLAN OF CARE
PT LONG AND SHORT TERM GOALS
LTG
◊ Pt. will be able to perform head movements s
increased occurrence of clinical manifestations
to improve overall performance of ADLs.
STG
◊ Pt. will be able to reduce incidence of clinical
presentation to perform ADLs without
discomfort.
◊ Pt. will be able to demonstrate an increase in
range of motion to improve functional mobility.
◊ Pt. will be able to demonstrate increased
muscular strength to improve functional
performance.
◊ Pt. will be able to demonstrate improved posture
to correct postural alignment and avoid
secondary impairments.
◊ Pt. will be able to demonstrate improved balance
to reduce risk of falls and reduce instability.
◊ Pt. will be able to demonstrate improved gait
performance to enhance safety.
◊ Pt. will be able to demonstrate improved
performance in doing ADLs to enhance quality
of life.
PT INTERVENTIONS
For BPPV
Objective of care:
❏ The otoconia will be returned into the vestibule.
The patient will demonstrate reduced vertigo
associated with head motion.
❏ The patient demonstrates improved balance.
❏ The patient will demonstrate enhanced
decision-making skills regarding self-treatment
strategies as a form of prophylaxis.
❏ The patient will demonstrate independence in
daily activity (BALD; IADL) involving head
motion.
Interventions:
◊ Canalith repositioning maneuver (based on
canalithiasis theory) x 1-2 mins waiting time for
each step or until the vertigo and nystagmus has
stopped to resolve s/sx of BPPV and replace the
otoconia into the vestibule, where the calcium
crystals can be reabsorbed.
◊ Liberatory (Semont) maneuver (based on
cupulolithiasis theory) x 1 min. each through
rapid moving the Pt. to dislodge the debris from
the cupula
◊ Brandt- Daroff exercises x 5-10 reps x 3x/day
until Pt. has no vertigo for 2 consecutive days to
relieve vertigo and dizziness
o Pt. Education
▪ Explain to the patient that the
movements must be performed
rapidly and that this will
probably provoke the patient’s
vertigo
▪ Patients should also be
informed that it is normal to
have some residual symptoms
of dysequilibrium and nausea on
completing the exercises
▪ Residual symptoms are usually
temporary and patients need to
continue the exercise
◊ Modified Epley Maneuver on a plinth x 30 SH x
1 set for every position x 15 mins. to reposition
canalith in the SCC to treat BPPV
For UVH:
16
Objective of care:
Practice walking 5 Making smaller Turning
❏ The patient will demonstrate improved stability steps and turning turns. Close provides a
of gaze during head movement. 180° (left and eyes. greater
❏ The patient will demonstrate diminished right) challenge to the
sensitivity to motion
vestibular
❏ The patient will demonstrate improved static and
system
dynamic postural stability
Interventions: Walk and move Counting Use distracting
Interventions: the hand backwards from cognitive or
◊ Gaze stability exercises x 8 reps x 1 set x 5 SH side-to-side, up 100 by 3s motor demands
x 1 min. rest in between set to address VOR, and down to challenge
improve cervical spine ROM & muscle strength,
balance
and correct habitual compensatory posture
o Cervical spine lateral rotation
▪ First two reps = 0°-30° then ◊ Habituation exercises (only when a patient with
30°-0° a UVH has continual complaints of dizziness) x
▪ Third to sixth rep = 0°-40° then 30 sec. or when symptoms abate, whichever
40°-0° comes first to reduce response to a repeatedly
▪ Seventh and eight reps = performed movement
0°-<50° then <50°-0°
o Cervical spine flexion and extension For BVH
▪ First two reps = 0°-20° then Objectives of care
20°-0° ❏ The patient will demonstrate reduced subjective
▪ Third to sixth rep = 0°-30° then complaints of gaze instability.
30°-0° ❏ The patient will demonstrate improved static and
▪ Seventh and eight reps = dynamic balance
0°-<35° then <35°-0° ❏ The patient will be independent in proper
o Cervical spine lateral flexion performance of a HEP that includes walking.
▪ First two reps = 0°-20° then ❏ The patient will demonstrate enhanced decision
20°-0° making skills regarding performance of daily
▪ Third to sixth rep = 0°-30° then activity (BADL; IADL) made more challenging
30°-0° owing to the disorder.
▪ Seventh and eight reps = Interventions:
0°-<35° then <35°-0° ◊ Gaze stability exercises similar to the X1
◊ Postural stability exercises 3x/day x 1-2 mins/ paradigm described in treatment for UVH x 8
reps to improve balance by encouraging the reps x 1 set x 5 SH x 1 min. rest in between set
development of balance strategies within the to address VOR, improve cervical spine ROM &
limitations of the patient, be they somatosensory, muscle strength, and correct habitual
visual, or vestibular. compensatory posture

For CVH
Begin with: Progress to: Purpose: Objectives of care
❏ The patient will demonstrate enhanced decision
Stand with feet Bring feet closer Enhance the making skill regarding fall prevention strategies
shoulder-width together. Close use of vestibular and necessary safety precautions to allow safe
apart, arms eyes. Stand on cues for balance
across chest
functioning within the home and community.
a sofa, cushion, by decreasing ❏ The patient will demonstrate enhanced decision
or foam base of support. making skill regarding use of compensatory
Eyes closed strategies to assist in gaze stability.
increases ❏ The patient will be independent in performance
reliance on of a HEP that includes walking.
vestibular cues Interventions:
for balance ◊ The PT intervention for a central vestibular
lesion at the level of the brainstem (vestibular
Practice ankle Doing circle Teaches the nuclei) likely will be similar to a UVH, with the
sways: sways. Close patient to use a same expectations for recovery.
medial-lateral and eyes. correct ankle
anterior-posterior ◊ Habituation exercises x 30 sec. or when
strategy symptoms abate, whichever comes first to
reduce response to a repeatedly performed
Attempt to walk Do the same Enhance the movement.
with heel touching exercise on use of vestibular ◊ Gait and balance exercises designed to
toe on firm carpet cues for balance
surface incorporate somatosensory, visual, and
by decreasing vestibular contributions are also effective means
base of support with this patient population.
Doing the on o Walking on a treadmill with feedback as
carpet alters to deviations with posture and gait
proprioceptive pattern.
input, increasing o Standing shoulder-width apart stance
difficulty o Standing Romberg stance, feet together
o Tandem stance

17
Pt. and family education or HIP:
◊ Pt. and family will be educated about the O’Sullivan S, Schmitz T, Fulk G. Physical Rehabilitation.
disorder and its manifestations 6th edition. Philadelphia: F.A. Davis Co; c2014
◊ Recovery time after initiating vestibular
rehabilitation for UVH averages 6 to 8 weeks
Websites:
◊ Pt. should be should be reminded that there is
Johns Hopkins Medicine. What causes vestibular
presence of dizziness when doing the
balance disorders.
interventions, and the dizziness is necessary to
https://www.hopkinsmedicine.org/health/conditions-and-
determine if there is any progress
diseases/vestibular-balance-disorder#:~:text=Infections,
◊ If vertigo arises, rest until symptoms subside
such%20as%20traumatic%20brain%20injury. Published
◊ Prepare a bucket within the area (near the bed
2021. Accessed on May 13, 2021.
or sofa) in case Pt. will feel nauseous and about
to vomit
◊ Pt./ Family may resort to traditional/home
remedies (Vicks, efficascent, white flower) when
preferred to address nausea
◊ Count when doing exercises and make sure the
exercise area is well lit
◊ Pt. will be taught of about energy conservation
techniques
◊ Pt. will be encouraged to focus on the quality of
movement rather than the quantity
◊ Pt. will be given a copy of pictures of exercises
to follow
HEP:
◊ Brandt-Daroff exercises in the bed or on the
couch and incorporates bed mobility to relieve
vertigo and dizziness.
◊ Mirror therapy for postural awareness training to
improve posture and standing tolerance c/s
supervision.
◊ Walking around the house/community to
improve coordination, tolerance and improve
performance on ADLs.
Precautions:
◊ Ease the Pt. into the therapy, make sure the Pt.
will not be shocked or surprised
◊ Preparer a bucket within the area in case the Pt.
feels nauseous and about to vomit
◊ Do not exercise when feeling unwell (dizziness,
SOB, nausea, vomiting)
◊ Rest in between exercises to minimize effects of
fatigue and dizziness
◊ Activity pacing to prevent fatigue and occurrence
of dizziness
◊ Do proper breathing techniques during exercises
◊ Always emphasize on visual and tactile cues
◊ Avoid environmental clutter
◊ Focus on safety and slowing down the
movements
◊ Use of gait belt for safety and in reducing risk of
falls
◊ Educate on risk of falls, how to prevent falls, and
proper falling techniques
◊ Observe proper body mechanics at all times
when doing the exercise
◊ List down all activities and tasks to reinforce
memory

REFERENCES

Books:
Braddom L, Chan L, Harrast M. Physical medicine and
rehabilitation. 5th edition. Philadelphia, PA:
Saunders/Elsevier; c2016

Goodman C, Fuller K. Pathology Implications for

Physical Therapist. 4th ed. St. Louis, Missouri:
Elsevier Saunders; c2015

18
PHARMACOLOGICAL MANAGEMENT SUMMARY

Medications Functions Side Effects PT Implications

CEREBELLAR DISORDER
Aminopyridines Improves attacks in patients with EA‐2 by Vertigo Monitor VS
blocking potassium channels, subsequently Headache Use RPE to monitor exercise intensity
improving regulation of the PC pacemakers. Nausea
Cardiac arrhythmia (rare but severe)
Acetazolamide Inhibits carbonic anhydrase, which results in Mild transient hand dysesthesia Monitor VS
brain acidosis and reduction of brain lactate Asymptomatic mild hypotension Immediate care for hypotension
and pyruvate levels. Ureteric calculus
Development of kidney disease
Gabapentin Stimulates alpha‐2‐delta P/Q calcium Mild transient giddiness Monitor VS
channels, enhancing GABA transmission Abdominal pain Respect patient’s behavioral problems
Impotence
VESTIBULAR DISORDER
Vestibular suppressants Reduces the intensity of vertigo and ● Prostatic enlargement; sedation can Monitor VS
● First-line treatment nystagmus evoked by a vestibular imbalance worsen dizziness of non labyrinthine Respect patient’s behavioral/cognition problems
○ Anticholinergi causes
c ● Sedation, drug dependency
○ Antihistamine ● Hallucinations, disorientation,
s confusion
● Second- line
treatment
○ Lorazepam
○ Clonazepam
● Third-line in-hospital
treatment, only with
close Supervision
○ Diphenidol
Antiemetics Used to treat motion sickness and is Effective Sedation Monitor VS
● Phenothiazine against nausea and vomiting Respect patient’s behavioral/cognition problems
○ Prochlorperaz Long term suppression of symptom is not
ine recommended since the body must
○ Promethazine experience the symptom in order to develop
○ Thiethylperazi compensatory strategies
ne
○ Trimethobenz
amide
Prednisone Vestibular suppressants Adverse reactions: Monitor VS
Increase BP Respect patient’s behavioral/cognition problems
Sodium retention
19
 GI irritation Long term suppression of symptoms is not recommended
Muscle wasting since the body must experience the symptom in order to
Osteoporosis

PT PLAN OF CARE SUMMARY

PROBLEM GOAL INTERVENTION

Decreased aerobic capacity Exhibit an increase in aerobic capacity to be able to improve Aerobic exercises x 30 mins to increase aerobic capacity, increase strength and enhance
tolerance and performance in ALDs coordination
- Arm and leg ergometer
- Brisk walking
- Stationary cycling
- Swimming

LOM Exhibit an increase in ROM to be able to maintain joint mobility
and improve overall functional performance
Decreased muscle strength Exhibit an increase in muscle strength to be able to improve
performance in ADLs and promote stability
Impaired coordination Exhibit an improved coordination to promote better performance
in executing movement and in overall ADLs
PROM & AROM exercises
PNF diagonal patterns x 10 reps x 2 sets
- D1 UE & LE flexion and extension
- D2 UE & LE flexion and extension
Strengthening exercises on bilat. UE& LE x 10 reps x 2 sets c red theraband to increase
muscle strength and improve motor function
- Biceps curls
- Wrist flexion & extension
- Partial squats
- Lateral walking
- Leg curl
- Heel-toe raie
Eye-head coordination exercises x 10 reps x 2 sets to improve coordination
Frenkel’s exercises c therapist guarding the side x 2 sets x 10 reps to improve coordination in
bilat. UE & LE
● UE
○ Touches each object with the right hand and then the left hand
○ Flexes the right shoulder to 90 degree with elbow and wrist extended
○ Takes his or her right index finger and touches the tip of his or her nose,
repeat with the left hand
○ Exercise is performed alternating right and left index finger
○ Taps bilateral hands on bilateral thighs while alternating palmer and dorsal
surfaces as fast as possible
● LE: in lying
○ Flex and extend one leg by the heel sliding down a straight line on the table.
○ Abduct and adduct hip smoothly with knee bent and heel on the table.

20
 ○ Abduct and adduct leg with knee and hip extended by sliding the whole leg on
the table.
○ Flex and extend hip and knee with heel off the table.
○ Flex and extend both the legs together with the heel sliding on the table.
○ Flex one leg while extending the other.
○ Flex and extend one leg while taking the other leg into abduction and
adduction.
○ Heel of one limb to opposite leg (toes, ankle, shin, patella).
○ Heel of one limb to opposite knee, sliding down crest of tibia to ankle
● Sitting
○ One leg is stretched to slide the heel to a position indicated by a mark on the
floor.
○ The alternate leg is lifted to place the heel on the marked point.
○ From stride sitting posture patient is asked to stand and then sit.
○ Rise and sit with knees together.
○ Sitting hip abduction and adduction.
● Standing
○ In stride standing weight is transferred from one foot to other.
○ Place foot forward and backward on a straight line.
○ Walk along a winding strip.
○ Walk between two parallel lines
○ Walk sideways by placing feet on the marked point.
○ Walk and turn around
○ Walk and change direction to avoid obstacles.

Locomotion training on treadmill with weight support x 30mins. to improve ambulatory

Impaired postural control &
balance
Exhibit an improved postural control and balance to promote
greater postural stability, decrease the risk for falls and improve
overall movement and performance in ADLs.
functions
Biofeedback therapy x 20 mins. to enhance stability and postural control
Postural training in front of mirror x 10 mins to decrease postural instability
Rhythmic trunk stabilization x 10 mins to improve range of motion, muscle strength, and
postural stability.

Balance exercises x 10 reps x 2 sets to improve static and dynamic balance and decrease risk
for falls
- Lateral weight shift in sitting and standing
- Single leg stance
- Romberg stance (EO, EC) ➝ progress to using balance platform
- Tandem stance (EO, EC) ➝ progress to using balance platform
HOME EXERCISE PROGRAM PRECAUTIONS
1. Frenkel’s exercises 1. Risk for falls
2. PNF diagonal patterns x 10 reps x 2 set 2. Avoid exercising when feeling unwell
a. D1 UE & LE flexion and extension 3. Avoid environmental clutter
21
 b. D2 UE & LE flexion and extension 4. Energy conservation techniques
3. Strengthening exercises c resistance 5. Proper warm-up activities and post-exercise cool-down stretching
a. Biceps curl 6. Proper breathing techniques during exercise to avoid Valsalva maneuver
b. Wrist flexion 7. Demonstrate proper use of assistive device
c. Partial squats 8. Proper positioning techniques
d. Leg curls 9. Proper body mechanics
e. Heel-toe raise 10. Home environment modifications for safe mobility
4. Postural control and balance exercises
a. Lateral weight shift in sitting and standing
b. Single leg stance
c. Romberg stance (EO, EC)
d. Tandem stance (EO, EC)

22
 NEUROMUSCULAR CONDITIONS REVA COMPILATION
VELEZ COLLEGE PHYSICAL THERAPY BATCH 2022
SPINAL CORD INJURY
GENERAL MEDICAL BACKGROUND
DEFINITION
◊ Spinal cord injury (SCI) is a relatively
low-incidence, high-cost injury that results in
tremendous change in an individual’s life. Spinal
cord injuries can be grossly divided into two
broad etiological categories: traumatic injuries
and nontraumatic damage. Trauma is the most
frequent cause of injury in adult rehabilitation
populations. Nontraumatic damage in adult
populations generally results from disease or
pathological influence.
EPIDEMIOLOGY
◊ SCI primarily affects young adults, with most
injuries occurring between the ages of 16 and
30, but over time the average in 30% of all
pediatric cases.
◊ Males are twice as likely to have a SCI as
females, with an overall mean age of 14.6 years.
◊ Incidence of pediatric SCI varies by region, with
the South and Midwest regions having almost
twice as many as in the Northeast.
◊ Every year, around the world, between 250 000
and 500 000 people suffer a spinal cord injury
(SCI).
◊ There is no reliable estimate of global
prevalence, but estimated annual global
incidence is 40 to 80 cases per million
population.
ETIOLOGY
◊ The primary cause of SCI is motor vehicle
accidents, accounting for nearly 40% of SCIs.
◊ Falls are the second most common cause at
28%.
◊ Approximately 15% of SCIs are caused by
violence; these include job-related injuries to
security guards, policemen, workers shot during
robberies, victims of violent crimes, and others.
◊ The likelihood of SCI from a gunshot wound
appears to be higher among those who have
had previous gunshot wounds (30%) or who
have had prior involvement in the criminal justice
system (52%)
RISK FACTORS
◊ Male, Early 40’s
PATHOMECHANICS / PATHOPHYSIOLOGY
◊ The pathophysiology of SCI may be divided into
phases. Primary injury refers to the structural
damage occurring instantly after the traumatic
event. Trauma to the spinal cord results in
primary destruction of neurons at the level of the
injury by disruption of the membrane,
hemorrhage, and vascular damage.
◊ Secondary injury refers to a pathophysiologic
cascade initiated shortly after injury, including
such insults as ischemia, hypoxia, edema, and
various harmful biochemical events. The spread
of damage is thought to be due to initiation of
biochemical events leading to necrosis and
excitotoxic damage and can continue for hours,
days, or weeks.
CLASSIFICATION
◊ Topographical Classification
o Tetraplegia
▪ Complete paralysis of all four
extremities, trunk and
respiratory muscles
▪ Results from lesions of the
cervical cord
o Paraplegia
▪ Complete paralysis of all or part
of the trunk and both lower
extremities
▪ Results from lesions of the
thoracic or lumbar spinal cord or
cauda equina
◊ Designation of Lesion Level
o Neurological level
▪ Most caudal level of the spinal
cord with normal motor and
sensory function on both the left
and right sides of the body
o Motor level
▪ Most caudal segment of the
spinal cord with normal motor
function bilaterally
o Sensory level
▪ Most caudal segment of the
spinal cord with normal sensory
function bilaterally
◊ Broad Functional Categories
o Complete
▪ No sensory or motor function in
the lowest sacral segments (S4
and S5)
▪ Determined by anal sensation
and voluntary external anal
sphincter contraction
▪ Zones of partial preservation
(ZPP) - Areas of intact motor
and/or sensory function below
the neurological level except S4
and S5
o Incomplete
▪ Preservation of motor and/or
sensory function below the
neurological level including
sensory and/or motor function at
S4 and S5
Types of Incomplete Lesions/Clinical Syndromes:
A. Anterior Cord Syndrome
◊ Related to flexion injuries of the cervical region
damaging the anterior portion of the cord and/or
its vascular supply from the anterior spinal artery
◊ Features:
 o Preservation of proprioception, light ◊ Spinal Shock
touch, and vibratory sense o Characterized initially by an absence of
o Bilateral loss of motor function, pain and all reflex activity, impairment of
temperature sensation below the level of autonomic regulation resulting in
the lesion hypotension and loss of control of
o Worst prognosis of incomplete SCI sweating and piloerection
o Loss of deep tendon reflexes,
B. Brown-Sequard Syndrome bulbocavernosus reflex, cremasteric
◊ Occurs from hemisection of the spinal cord reflex, a Babinski response, and a
◊ Typically caused by penetration wounds such as delayed plantar response
gunshot or stab o Phases
◊ Features: ▪ Initial period of total areflexia:
o Contralateral loss of pain, temperature 0-24 hours
and light touch ▪ Gradual return of reflexes: 1-3
o Ipsilateral loss of motor function days
proprioception, vibration and kinesthesia ▪ Period of increasing
o Good prognosis for recovery hyperreflexia : 1-4 weeks
▪ Final hyperreflexia: 1-6 months
C. Central Cord Syndrome ◊ Neurogenic Shock
◊ Most common SCI syndrome o Defined as a systolic blood pressure
◊ Occurs from hyperextension injuries to the less than 100 mmHg, with a heart rate
less than 80 beats per minute
cervical region and associated with congenital or
degenerative narrowing of the spinal canal ◊ Spasticity
o An indication of an upper motor neuron
◊ Features: lesion
o More severe neurological involvement of
o Velocity-dependent increase in muscle
UE than LE tone in response to passive movement
o With complete preservation of sacral ◊ Respiratory Impairments
tracts, normal sexual, bowel, and o With high spinal cord lesions at C1 and
bladder function may be retained C2, phrenic nerve innervation and
o Good prognosis for walking recovery spontaneous respiration are lost.
D. Posterior Cord Syndrome o Paralysis or paresis of the muscles of
◊ Rare respiration leads to poor ventilation,
which may then cause impaired
◊ Occurs as a result of damage to the posterior respiration leading to atelectasis and
columns of the spinal cord and can be due to pneumonia.
spinal cord compression from tumors o Neurological Level of Spinal Cord Injury
◊ Features: and Muscles of Respiration
o Preservation of motor function, pain,
temperature and light touch Level of Injury Respiratory Muscles
o Loss of proprioception and vibration
o Wide based gait pattern C1–C2 Sternocleidomastoid,
upper trapezius, cervical
E. Conus Medullaris Syndrome extensors
◊ Injury to the conus medullaris and lumbar nerve
C3–C4 Partial diaphragm,
roots scalenes, levator scapulae
◊ Features:
o No lower extremity reflexes C5–C8 Diaphragm, pectoralis
o Bowel, bladder and sexual dysfunction major and minor, serratus
anterior, rhomboids,
F. Cauda Equina Syndrome latissimus dorsi
◊ Results from compression and disruption of the
T1–T5 Some intercostals, erector
nerve roots of the cauda equina spinae
◊ Lower motor neuron injuries
◊ With same potential to regenerate as peripheral T6–T10 Intercostals and
nerves but full return of innervation is abdominals
uncommon
T11 and below All of the muscles above
◊ Features:
o Loss of motor and sensory function in
the lower extremities and bladder ◊ Thermoregulation impairments
o Areflexic bowel and bladder and saddle o Loss of internal thermoregulatory
anesthesia responses
◊ Bowel and Bladder Dysfunction
CLINICAL PRESENTATION o Center of micturition: S2–S4

2
 o Urinary tract infections are a major o LMNL – Lesions at the conus medullaris
cause of mortality and morbidity in or cauda equina
people with SCI A. Male Response
◊ Erectile capacity
Types of Bladder Dysfunction: o UMNL > LMNL
A. Hyperreflexic / Automatic / Spastic bladder o Incomplete SCI > Complete SCI
◊ UMNL o Reflexogenic erection
◊ Lesions that occur above the conus medullaris ▪ UMNL > LMNL
and sacral segments
▪ Response to external physical
◊ Intact reflex arc
◊ Reflexively empties in response to a certain stimulation of the genitals or
level of filling pressure perineum
◊ Detrusor muscle is hyperreflexive ▪ An intact reflex arc is required
◊ Management (mediated through S2-S4)
o Triggered by stroking, kneading, tapping o Psychogenic erection
the suprapubic region, thigh, or lower ▪ LMNL > UMNL
abdomen; or pinching or hair pulling at
▪ Occur through cognitive activity
the area
such as erotic fantasy
B. Areflexic / Autonomous / Flaccid bladder ◊ Ejaculation
◊ LMNL o LMNL > UMNL
◊ Lesion of the sacral segments or conus o Incomplete SCI > Complete SCI
medullaris o A physical occurrence compared to
◊ Absent reflex arc orgasm which is a cognitive
◊ Flaccid because there is no reflex action of the psychogenic event
detrusor muscle
◊ Management
o Increasing intra abdominal pressure - B. Female Response
Can be emptied using crede's maneuver ◊ Vaginal lubrication, Labial engorgement, &
(compressing the lower abdomen) Clitoral erection
o UMNL > LMNL
Types of Bowel Dysfunction: o Occur through reflexogenic stimulation
A. Spastic Bowel ◊ Psychogenic response
◊ Spinal cord lesions above S2 o LMNL > UMNL
◊ Lesions above the center of defecation ◊ Fertility and pregnancy
◊ Intact defecation reflex o Fertility is not affected as severely in
◊ Spastic contraction of anal sphincters women as men with SCI
◊ Management
o Menstrual cycle typically is interrupted
o Regularly scheduled evacuation
▪ Exact time of day is chosen by for a period of 4 to 5 months following
the patient based on lifestyle injury
needs and should be done o Women with SCI who want to bear
consistently at the same time of children should be closely supervised
day during pregnancy.
o Use of suppositories and digital
o Labor and delivery must be monitored.
stimulation techniques to cause a reflex
defecation
◊ Autonomic dysreflexia
B. Flaccid Bowel o Lesions above T6
◊ S2–S4 lesions o Initiating Stimuli
◊ Lesions in conus medullaris or cauda equina ▪ Bladder distention ƒ
(sacral nerve roots) ▪ Rectal distention ƒ
◊ Loss of spinal defecation reflex ▪ Stimuli that would normally be
◊ Management painful below level of lesion
o Regularly scheduled evacuation ▪ Gastrointestinal irritation
o Manual evacuation techniques ▪ Pressure sores ƒ
o Gentle Valsalva maneuver ▪ Urinary stones ƒ
▪ Bladder infections ƒ ƒ
▪ Kidney malfunction ƒ
Safe bowel program includes eating a diet with ▪ Environmental temperature
appropriate amount of fiber, fluid intake, physical activity, changes
stool softeners, laxatives, and bulking agents. ▪ Labor
▪ Skeletal fracture below level of
◊ Sexual Dysfunction injury
o Characterized by physiological ▪ Electrical stimulation below level
dysfunctions with sensory and motor of lesion
impairments o Manifestations
▪ Hypertension (rise in systolic BP
o UMNL – Lesions above conus
20–30 mmHg)
medullaris (above S2-S4) ▪ Bradycardia
3
 ▪ Severe headache
▪ Feeling of anxiety
▪ Constricted pupils
▪ Blurred vision
▪ Flushing and piloerection above
level of lesion
▪ Dry, pale skin below level of
lesion (due to vasoconstriction)
▪ Nasal congestion
▪ Increased spasticity
▪ May be asymptomatic
can define bone, disk and other
problems
◊ Magnetic resonance imaging (MRI)
o MRI uses a strong magnetic field and
radio waves to produce
computer-generated images. This test is
very helpful for looking at the spinal cord
and identifying herniated disks, blood
clots or other masses that may be
compressing the spinal cord

COMPLICATIONS DIFFERENTIAL DIAGNOSIS

◊ Pressure ulcers
o Major complication of SCI
o Frequently seen with complete and
Spinal Cord CVA Vertebral
tetraplegic patients
Injury Fracture
o Ulcerations of soft tissue caused by
unrelieved pressure and shearing forces
Traumatic Sudden loss of Discontinuity in
damage to the neurological a bone resulting
◊ Deep Vein Thrombosis
spinal cord or function caused from mechanical
o Results from development of a
nerves at the by an forces that
thrombus within a vein
end of the spinal interruption of exceed the
o Due to lack of mobility and active
canal. the blood flow to bone's ability to
muscle contraction of the LEs
the brain withstand them.
◊ Contractures
- Spinal shock, - Sudden
o Develop secondary to prolonged - Chronic back
neurogenic weakness or
shortening of structures across and pain in thoracic
shock, numbness of
around a joint, resulting in limitation in and/or lumbar
spasticity, the face, arm, or
motion region
respiratory leg
impairments - Sudden - Decreased
◊ Pain
and dimness or loss thoracic and
o Common occurrence in the acute and
thermoregulatio of vision, lumbar range of
chronic stages of recovery
n impairments particularly in movement
o Can limit the performance of activities of
one eye
daily living, affect sleep, and contribute - Impaired
- Sudden
to a lower quality of life pulmonary
difficulty
o 2 broad categories function
speaking
▪ Nociceptive Pain
- Sudden severe
▪ Neuropathic pain - Increased
headache with
kyphosis
no known cause
◊ Heterotopic ossification
- Unexplained - Neurological
o Osteogenesis in soft tissues, usually
dizziness, deficits due to
near joints, below the level of the lesion
unsteadiness, or narrowing of
sudden falls spinal canal
◊ Osteoporosis
o Reduction in bone mineral density is
due primarily to combination of no or
limited muscle action and limited PROGNOSIS
weight-bearing
o Most common in the LEs ◊ The prognosis for recovery depends on the level
of the injury, muscle strength, and ASIA
◊ Edema Impairment scale at the initial injury.
o Osteogenesis of soft tissues near joint ◊ The age of the individual also seems to
below the level of lesion contribute to recovery, with the best potential
related to a younger age.
◊ Those with Asia Impairment Scores (AIS) of D at
MEDICAL DIAGNOSIS
any level have higher life expectancy rates as
◊ X-rays compared to those with AIS A–C. Clients with
o X-rays can reveal vertebral (spinal paraplegic injuries live longer than those with
column) problems, tumors, fractures or low cervical and high cervical injuries.
degenerative changes in the spine ◊ Preservation of pinprick sensation at 4 months
◊ Myelogram after injury in the LEs or sacral region is
o An X-ray of the spine taken after a dye associated with a good prognosis for motor
is injected. recovery at 1 year after injury
◊ Computerized tomography (CT) scan ◊ Experience significant problems in a number of
o This scan uses computers to form a areas of life, resulting in ongoing stress related
series of cross-sectional images that to pain, lack of income and financial problems,
spasticity, stress, and difficulty in their sex lives.

4
 optimize function, mobility, and
GENERAL HEALTHCARE MANAGEMENT engagement in the community.
o Provide training in the use of low- and
MEDICAL MANAGEMENT high-tech assistive technology (e.g.,
adapt a smartphone for use by a person
◊ Use of a rigid collar and spinal board with limited hand function; train an
◊ Traditional cardiopulmonary resuscitation (CPR) individual to use voice recognition
methods - minimize trauma to a potentially software).
unstable cervical spine that is utilizing the ◊ Speech Therapy
jaw-thrust maneuver to access the airway. ◊ Respiratory
◊ Oxygen and medication to control the ◊ Orthopedic
hyperperfusion and swelling of the spinal cord. ◊ Cardiovascular
◊ Cardiac, hemodynamic, and respiratory status
are closely monitored. PHYSICAL THERAPY, EXAMINATION, EVALUATION,
◊ High cervical injuries require immediate AND DIAGNOSIS
placement of ventilation equipment - intermittent
positive-pressure breathing, bronchodilators, POINTS OF EMPHASIS ON EXAMINATION
and mucolytics. A. Inspection
◊ A urinary catheter typically is inserted, and
a. general appearance
secondary injuries are addressed.
i. body type
◊ The goal is to restore spinal alignment, establish
ii. presence of assistive device
spinal stability, and prevent further neurologic
b. mental status: (SCI pt.’s may present
deterioration, enhancing recovery.
with accompanying TBI)
i. orientation as to P/P/T
SURGICAL MANAGEMENT
ii. determine level of
consciousness
◊ Closed and open reduction of the vertebrae iii. memory & attention
◊ Decompression of the spinal cord c. communication skills
◊ Surgery, including fusion and internal fixation - B. Cardiopulmonary assessment
most common procedure performed prior to use a. vital signs
of an orthosis for 8 to 12 weeks. b. Chest expansion measurement
c. auscultation
PHARMACOLOGICAL MANAGEMENT d. aerobic capacity
◊ Note: A complete table for medication - its C. Integumentary assessment:
function, side effects and PT implication; is a. skin presentation
found at the end portion of the file. i. scars or wounds
ii. swelling
◊ Gabapentin(Neurontin) - treating spasticity
iii. inflammation
associated with spinal cord injury. iv. pressure ulcers
◊ Botulinum toxin - used to treat patients with 1. braden scale
hyperactive bladder following a spinal cord D. Neurological assessment:
injury. a. ASIA - Impaired or absent sensation
◊ Opioids - The preferred route of administration below the level of lesion.
for strong opioid drugs is oral administration. b. DTRs - hyperreflexive DTRs
Durations of strong opioid medications such as E. Musculoskeletal assessment:
morphine last up to 4-5 hours, with peak a. ROM - decreased ROM
analgesic effects taking place 60 minutes after b. MMT - absent or decreased muscle
oral administration. strength below level of lesion.
◊ Benzodiazepines - prescribed to address c. MBT - disuse atrophy may be present.
spasticity on a short-term basis. Spasticity is d. Muscle Tone - hypertonia or spasticity
estimated to affect 70% of individuals with a SCI, below the level of the lesion; initial
and is distinguished by hypertonicity, flaccidity: spinal shock
hyperreflexia, and painful spasms. F. Examination for coordination:
◊ Baclofen - acts as an allosteric modulator to a. fine motor assessment
GABA b receptors which leads to the inhibition b. equilibrium and non-equilibrum
of alpha motor neurons within the spinal cord. coordination tests
◊ Corticosteroids - used to control the G. Balance and tolerance assessment:
inflammatory sequelae after the initial tissue a. Sitting balance score
damage associated with a spinal cord injury. b. Motor assessment scale
c. Functional Reach Test
H. Postural assessment: Impaired sensation below
OTHER HEALTHCARE MANAGEMENT the level of lesion.
I. Gait assessment: Impaired or absent gait below
◊ Occupational Therapy
the level of lesion.
o Optimize upper extremity function and
a. 10 meter walk test
prevent deformities (e.g., fabricate an
b. 6 minute walk test
orthosis to enable the use of a
c. Timed walking test
keyboard; fit mobile arm supports to
J. Functional assessment:
support weak muscles).
a. FIM
o Evaluate and recommend wheelchair
b. Wheelchair Skills Test
seating and positioning systems to
c. SCIM
5

PT PROBLEM LIST
1. Pt. may manifest with impaired cognition.
2. Pt. has imapired or absent sensation below the
level of lesion.
3. Pt. has hypertonia/spasticity below the level of
the lesion; initial flaccidity: spinal shock
4. Pt. has increased hyperreflexia
5. Pt. has decreased ROM
6. Pt. has decreased or absent muscle strength
below the level of the lesion; paraplegia or
tetraplegia
7. Pt. manifests with atrophy (disuse atrophy)
8. Pt. manifests with involuntary movement and
spasms.
9. Pt. has impaired posture below level of lesion
10. Pt. has impaired or absent gait: depends on
level of lesion
11. Pt. has impaired ventilation
12. Pt. is at risk for developing pressure sores.
13. Pt. has impaired aerobic capacity
14. Pt. has decreased functional independence in
ADLs.
PT DIAGNOSIS
Neuromuscular Practice Pattern H – impaired motor
function, peripheral nerve integrity and sensory integrity
associated with non-progressive disorders of the spinal
cord
PT PROGNOSIS
The potential for recovery from SCI is directly related to
the neurological level of lesion and completeness of the
injury. An incomplete lesion (ASIA B, C, or D) is a good
prognostic indicator of greater likelihood of recovery of
motor function. Even with complete lesions (ASIA A),
70% patients with cervical level injuries are likely to
experience one level of motor recovery below the
original neurological level. Preservation of pinprick
sensation at 4 months after injury in the LEs or sacral
region is associated with a good prognosis for motor
recovery at 1 year after injury. Recovery of motor
function generally plateaus around 12 to 18 months after
injury. Specific factors related to prognosis of walking
ability are discussed below.
PHYSICAL THERAPY PLAN OF CARE
PT LONG AND SHORT TERM GOALS
LTG
Pt. will manifest an ↑ in bilat. LE AROM & muscle
strength, improved posture, balance and tolerance, and
coordination p 30 PTR sessions to be able to walk on
even terrain c an assistive device s difficulty & improve
overall mobility.
STG
1. Pt. will demonstrate an ↑ in sensation from a
score of 0 to 1 in sensory assessment p 9 PTR
session to improve functional performance.
2. Pt. will exhibit decreased mm tone from a grade
1 to grade 0 p 10 PTR sessions to increase
functional performance
3. Pt. will manifest an increased mm tone from a
grade of 0 to grade 1 p 10 PTR sessions to
increase functional performance.
4. Pt. will show an increase ROM c increments of
5° p 10 PTR sessions to improve mobility and
muscle performance.
5. Pt. will manifest an ↑ of 1 grade in muscle
strength within 10 PTR sessions to improve
muscle performance.
6. Pt. will manifest increase in mm bulk from
increments of 0.2 in p 10 PTR sessions to
improve mm performance.
7. Pt. will demonstrate ↓ involuntary movement &
spasms p 8 PTR sessions to increase functional
performance
8. Pt. will exhibit an improved posture in 12 PTR
sessions to ↑ safety & functional independence
9. Pt. will show an improved gait within 15 PTR
sessions to ↑ safety and achieve better mobility
independence
10. Pt. will demonstrate an improved ventilation p 13
PTR sessions to achieve mobility and functional
independence.
11. Pt. will exhibit awareness about pressure sores
p 6 PTR sessions to decrease complications
and increase functional independence
12. Pt. will manifest an increase aerobic capacity
from a grade of 6 to grade 5 on RPE to improve
functional independence.
13. Pt will manifest ↑ independence as to self-care &
mobility within 20 PTR sessions to ↑ functional
independence
PT INTERVENTIONS
1. Sensory re-education techniques on affected
area c eyes opened and progress c eyes closed
to improve sensation
2. Stretching exercises on affected areas x 5 reps x
3 sets to ↓ hypertonicity.
3. Rood’s inhibitory technique x 10 mins to ↓
hypertonicity
a. Neutral warmth
b. Gentle shaking/rocking
4. Rood’s facilitatory techniques x 10 mins to ↑ mm
tone
a. A-icing
b. Tapping
c. Vibration
5. ROM exercises on affected joints x 10 reps x 2
sets to improve range of motion.
a. PROM
b. AAROM
c. AROM
6. Manual Strengthening x 5 reps x 3 sets to ↑ mm
strength & ↑ mm bulk.
a. CKC exercises like push-ups & squats
b. OKC exercises like bench press & bicep
curls
7. Resistance Bands Strengthening on affected
mm x 5 reps x 3 sets to ↑ mm strength & ↑ mm
bulk.
8. Stretching and manual massage (effleurage /
kneading) on affected mm x 15 mins to ↓ mm
spasms.
9. Massage on affected mm x 1 mins to ↓ mm
spasms.
a. effleurage
6
 b. kneading
10. Postural awareness exercises in front of a mirror
c verbal & tactile cues x 20 mins to improve
posture.
11. Stretching exercises on tight mm x 5 reps x 3
sets x 8 SH to ↑ tissue extensibility & improve
posture.
12. Strengthening exercises on weak muscles x 5
reps x 3 sets to improve posture
a. CKC exercises like push-ups & squats
b. OKC exercises like bench press & bicep
curls
13. Gait training / Treadmill / Parallel bar exercises c
gait belt x 5 rounds to ↑ gait.
14. Transfer exercises x 5 reps x 3 sets to ↑
functional independence
a. W/c↔bed
b. W/c↔toilet
c. W/c↔mat
15. Respiratory Management x 10 reps x 2 sets to ↑
respiration & respiratory endurance
a. Deep-Breathing Exercises
b. Glossopharyngeal Breathing
c. Air Shift Maneuver
d. Respiratory Muscle Strengthening
e. assisted coughing
f. Abdominal Binder
g. Manual Stretching
16. Skin Care to promote integumentary integrity.
a. Positioning
b. Consistent and effective pressure relief
c. Skin inspection
17. Cardiovascular/Endurance Training x 10 reps x
2 sets to ↑ cardiopulmonary endurance
a. Arm ergometry
b. Swimming
Precautions:
1. Orthopedic/stress at the fracture site
2. Skin integrity
3. Fall risk
4. Overstretching
5. Overuse
6. Always monitor vital signs before and after
performing exercises.
7. Avoid valsalva maneuver to prevent increase in
blood pressure.
8. Pt. must be encouraged to rest intervals
between exercises or activities in order to avoid
fatigue.
9. Maintain proper posture during exercises.
10. Avoid activities that worsen the condition.
11. Always wear a seat belt while in a vehicle.
12. Take precautions to avoid falls by adding
environmental modifications such as handrails,
non slip mat etc.
Pt. Education
Living with a SCI requires significant adaptations and
changes on the part of the patient and his or her family.
In order to meet the challenges presented by a SCI,
patients must fully understand all the consequences of
the injury. Patient and family/caregiver education should
begin early after injury about the impact of SCI on the
different body systems, secondary complications, and
prognosis. Later in the recovery process it may be
particularly helpful to have the patient meet individuals
with long-standing SCI who have completed
rehabilitation and are functioning in the community to
gain an appreciation of the impact of the injury on
day-to-day life. Pt. will also be educated about pressure
sores and its prevention and health and wellness.
Home Exercise Program
1. Pressure relief techniques x 30 seconds every
15 mins (on wheelchair) or every 2 hours (on
bed) to relieve pressure from the ischial
tuberosities and to prevent formation of pressure
ulcers.
a. On wheelchair
● Sitting push-ups
● Alternative pressure relief
method to avoid stress to the
wrist structures, adjust position
by shifting the trunk forward or
to each side
b. On bed
● Supine to sidelying
2. Self-stretching exercises x 8 reps x 2 sets x 8
SH to maintain range of motion and improve
joint integrity.
3. Handgrip exercises on bilat. hands in sitting
position x 8 reps x 2 sets to improve handgrip
strength.
4. Manual Strengthening x 5 reps x 3 sets to ↑ mm
strength & ↑ mm bulk.
a. CKC exercises like push-ups & squats
b. OKC exercises like bench press & bicep
curls
5. Self stretching on UE or LE x 8 reps x 2 sets c 8
SH to inc LE ROM & dec spasticity.
Wheelchair Prescription
A wheelchair prescription will vary according to the
level and extent of injury.
General considerations are the following:
1. Seat depth should be approximately 1 to 2 in
(2.5 to 5.1 cm) back from the popliteal space to
allow an even weight distribution on the thighs
and to prevent excessive pressure on the ischial
tuberosities.
2. Floor-to-seat height. The type and dimensions
of the cushion or custom-made seat must be
known so that seat height can be measured
accurately, allowing adequate (2 in [5.1 cm])
clearance from the floor to the foot pedals and
provide slightly greater than a 90° angle at the
hips.
3. Back height. If the patient will not be pushing
the wheelchair, a high back may be desired for
added comfort and stability. A patient with
tetraplegia who will be pushing the wheelchair
requires a back height that is below the inferior
angle of the scapula so that the axilla is free of
the handles during functional activities. Most
patients with paraplegia prefer a lower back
height, especially if they have intact abdominal
muscles.
4. Seat width and depth are variable and should
be fitted to the anthropometric characteristics of
the. patient. The patient should be fitted in the
narrowest chair possible, but have adequate
space between the lateral edges of the thighs
7
 and wheelchair armrests or wheels to avoid skin
irritation.
5. Removable armrests and detachable
swing-away leg rests are important
components of wheelchairs used by many
patients with SCI.
6. Additional wheelchair accessories may be
required to meet specific patient needs. Several
features that warrant consideration include
enlarged release mechanisms on the leg rests, a
friction surface on the hand rims, brake
extensions, anti-tipping devices, and grade aids
(which decrease backward movement of the
chair while ascending inclined surfaces).

REFERENCES
◊ Please cite accordingly.
Books:
● Ciccone, C. D. (2002). Pharmacology in
rehabilitation. Philadelphia: F.A. Davis Co.
● O’Sullivan (2018). National Physical Therapy
Examination Review and Study Guide. Evanston
Illinois. Therapy Ed. Ltd
● Goodman, Catherine Cavallaro. (2015).
Pathology: implications for the physical therapist
(4th. Ed). St. Louis, Missouri: Elsevier Saunders.

Websites:
● Pharmacological management of spinal cord
injuries. (n.d.). Retrieved May 16, 2021, from
Physio-pedia.com website:
https://www.physio-pedia.com/Pharmacological_
Management_of_Spinal_Cord_Injuries
● No title. (n.d.). Retrieved May 16, 2021, from
Aota.org website:
https://www.aota.org/About-Occupational-Thera
py/Professionals/RDP/spinal-cord-injury.aspx
● Assessment of spinal cord injury. (n.d.).
Retrieved May 16, 2021, from Physio-pedia.com
website:
https://www.physio-pedia.com/Assessment_of_S
pinal_Cord_Injury
● How is SCI diagnosed? (n.d.). Nih.Gov.
Retrieved May 16, 2021, from
https://www.nichd.nih.gov/health/topics/spinalinj
ury/conditioninfo/diagnosed
● Dave, S., & Cho, J. J. (2021). Neurogenic
Shock. In StatPearls. StatPearls Publishing.
● Spinal Cord Injury. (n.d.). Who.Int. Retrieved
May 20, 2021, from
https://www.who.int/news-room/fact-sheets/detai
l/spinal-cord-injury

8
PHARMACOLOGICAL MANAGEMENT SUMMARY
Medications Functions
Gabapentin(Neurontin) Developed originally as an anticonvulsant;
may also be helpful as an adjunct to other
drugs in treating spasticity associated with
spinal cord injury.
Botulinum toxin This intervention may help normalize bladder
function and allow more effective voiding or
intermittent catheterization.Likewise, injection
of botulinum toxin into the bladder detrusor
muscle can help reduce the incidence of
stress urinary incontinence in people with
idiopathic overactive bladder syndrome that is
resistant to oral drug therapy and other
interventions.
Opioids Strong-agonist opioids such as morphine
remain the most popular drugs used to treat
severe pain due to their high affinity for
mu-receptors located in the CNS.
Benzodiazepines Used to treat musculoskeletal pain resulting
from acute or chronic injury to musculature
and surrounding tissue.
Baclofen Baclofen, commonly known as Kemstro or
Lioresal, is a medication used in the treatment
of spasticity in spinal cord injuries. This drug
acts as an allosteric modulator to GABA b
receptors which leads to the inhibition of alpha
motor neurons within the spinal cord.
Corticosteroids Used to control the inflammatory sequelae
after the initial tissue damage associated with
a spinal cord injury.
Side Effects
The primary side effects of this drug are
sedation, fatigue, dizziness, and ataxia.
Such effects include generalized muscle
weakness, difficulty speaking or swallowing,
and respiratory distress.
Common side effects of opioid use include
drowsiness, nausea, and mood changes. A
chief concern for patients who are prescribed
opioids is the risk for addiction.
Benzodiazepines cause depression of the
CNS and related side effects such as
dizziness, drowsiness, and lethargy. Another
potential side effect of Diazepam is the
“hangover effect” which is caused by a half-life
ranging from 20-50 hours in adults.
The main adverse effects are nausea,
dizziness, drowsiness, fatigue, and weakness.
Noted complications such as wound
infections, sepsis, and pneumonia are
prevalent in patients with spinal cord injuries.
PT Implications
● Monitoring of Vital signs
● Energy Conservation Techniques
● Balance Exercises
● strengthening exercises
● breathing exercises
● patient education on the potential side effects of
opioids
● planning optimal treatment times
● monitor signs of addiction in patients
● To achieve optimal outcomes from physical therapy, it
is imperative for spinal cord patients to follow dosage
schedules and to report noticeable side effects of
opioid use with their care team.
● Orthostatic hypotension is a frequent complication in
patients with a SCI.
● Proper monitoring of vital signs
● fall prevention program
● patient education on possible side effects of
medication
● Physical therapists must implement other techniques
to manage pain and spasticity as a primary treatment
option or adjunct to medication.
● patient education on safety and medication
withdrawal
● proper scheduling of therapy sessions
● The therapist must be mindful of the systemic effects
and their respective presentation.
9
 ● limitations on the interventions available to the
therapist, particularly high-velocity manipulations.

PT PLAN OF CARE SUMMARY

PROBLEM GOAL INTERVENTION

Imapired or absent sensation Pt. will demonstrate an ↑ in sensation from a score of 0 to 1 in a. Sensory re-education techniques on affected area c eyes opened and progress c
below the level of lesion sensory assessment p 9 PTR session to improve functional eyes closed to improve sensation.
performance.
Hypertonia/spasticity a. Stretching exercises on affected are x 5 reps x 3 sets to ↓ hypertonicity.
Pt. will exhibit decreased mm tone from a grade 1 to grade 0 p
b. Rood’s inhibitory technique x 10 mins to ↓ hypertonicity
10 PTR sessions to increase functional performance
i. Neutral warmth
ii. Gentle shaking/rocking
Flaccidity Pt. will manifest an increased mm tone from a grade of 0 to a. Rood’s facilitatory techniques x 10 mins to ↑ mm tone
grade 1 p 10 PTR sessions to increase functional performance. i. A-icing
ii. Tapping
iii. Vibration
Decreased ROM Pt. will show an increase ROM c increments of 5° p 10 PTR a. ROM exercises on affected joints x 10 reps x 2 sets to improve range of motion.
sessions to improve mobility and muscle performance. i. PROM
ii. AAROM
iii. AROM
Decreased or absent muscle Pt. will manifest an ↑ of 1 grade in muscle strength p 10 PTR a. Manual Strengthening
strength sessions to improve muscle performance. i. CKC exercises like push-ups & squats
ii. OKC exercises like bench press & bicep curls
b. Resistance Bands Strengthening
c. Weights
Atrophy Pt. will manifest increase in mm bulk from increments of 0.2 in p a. Manual Strengthening x 5 reps x 3 sets to ↑ mm strength & ↑ mm bulk.
10 PTR sessions to improve mm performance. i. CKC exercises like push-ups & squats
ii. OKC exercises like bench press & bicep curls
b. Resistance Bands Strengthening on affected mm x 5 reps x 3 sets to ↑ mm strength
& ↑ mm bulk.
Involuntary movement and Pt. will demonstrate ↓ involuntary movement & spasms p 8 PTR a. Stretching and manual massage (effleurage / kneading) on affected mm x 15 mins to
spasms sessions to increase functional performance. ↓ mm spasms.
b. Massage on affected mm x 1 mins to ↓ mm spasms.
i. effleurage
ii. kneading
Impaired posture Pt. will exhibit an improved posture p 12 PTR sessions to ↑ a. Postural awareness exercises in front of a mirror c verbal & tactile cues x 20 mins to
safety & functional independence improve posture.
b. Stretching exercises on tight mm x 5 reps x 3 sets x 8 SH to ↑ tissue extensibility &
improve posture.
c. Strengthening exercises on weak muscles x 5 reps x 3 sets to improve posture
i. CKC exercises like push-ups & squats

10
 ii. OKC exercises like bench press & bicep curls
Impaired gait Pt. will show an improved gait p 15 PTR sessions to ↑ safety a. Gait training / Treadmill / Parallel bar exercises c gait belt x 5 rounds to ↑ gait.
and achieve better mobility independence
Impaired ventilation Pt. will demonstrate an improved ventilation p 13 PTR sessions a. Respiratory Management x 10 reps x 2 sets to ↑ respiration & respiratory endurance
to achieve mobility and functional independence. i. Deep-Breathing Exercises
ii. Glossopharyngeal Breathing
iii. Air Shift Maneuver
iv. Respiratory Muscle Strengthening
v. assisted coughing
vi. Abdominal Binder
vii. Manual Stretching
Risk for pressure sores Pt. will exhibit awareness about pressure sores p 6 PTR a. Skin Care to promote integumentary integrity.
sessions to decrease complications and increase functional i. Positioning
independence ii. Consistent and effective pressure relief
iii. Skin inspection
Impaired aerobic capacity Pt. will manifest an increase aerobic capacity from a grade of 6 a. Cardiovascular/Endurance Training x 10 reps x 2 sets to ↑ cardiopulmonary
to grade 5 on RPE to improve functional independence. endurance
i. Arm ergometry
ii. Swimming
Decreased functional Pt will manifest ↑ independence as to self-care & mobility p 20 a. Transfer exercises x 5 reps x 3 sets to ↑ functional independence
independence in ADLs PTR sessions to ↑ functional independence i. W/c↔bed
ii. W/c↔toilet
iii. W/c↔mat

HOME EXERCISE PROGRAM PRECAUTIONS

1. Pressure relief techniques x 30 seconds every 15 mins (on wheelchair) or every 2 hours 1. Orthopedic/stress at the fracture site
(on bed) to relieve pressure from the ischial tuberosities and to prevent formation of 2. Skin integrity
pressure ulcers. 3. Fall risk
4. Overstretching
a. On wheelchair
5. Overuse
● Sitting push-ups 6. Always monitor vital signs before and after performing exercises.
● Alternative pressure relief method to avoid stress to the wrist structures, 7. Avoid valsalva maneuver to prevent increase in blood pressure.
adjust position by shifting the trunk forward or to each side 8. Pt. must be encouraged to rest intervals between exercises or activities in order to
b. On bed avoid fatigue.
● Supine to sidelying 9. Maintain proper posture during exercises.
2. Self-stretching exercises x 8 reps x 2 sets x 8 SH to maintain range of motion and improve 10. Avoid activities that worsen the condition.
joint integrity. 11. Always wear a seat belt while in a vehicle.
12. Take precautions to avoid falls by adding environmental modifications such as
3. Handgrip exercises on bilat. hands in sitting position x 8 reps x 2 sets to improve handgrip
handrails, non slip mat etc.
strength.
4. Manual Strengthening x 5 reps x 3 sets to ↑ mm strength & ↑ mm bulk.
11
 c. CKC exercises like push-ups & squats
d. OKC exercises like bench press & bicep curls
5. Self stretching on UE or LE x 8 reps x 2 sets c 8 SH to inc LE ROM & dec spasticity.

12
 NEUROMUSCULAR CONDITIONS REVA COMPILATION
VELEZ COLLEGE PHYSICAL THERAPY BATCH 2022
MOTOR NEURON DISORDERS
MOTOR NEURON LESION
WHAT’S INSIDE
1. Upper Motor Neuron Disorders
a. Primary Lateral Sclerosis
b. Tropical Spastic Paraparesis
c. Lathyrism
d. Epidemic Spastic Paraparesis
e. Familial (Hereditary) Spastic
Paraplegia
f. Pseudobulbar Palsy
2. Lower Motor Neuron Disorders
a. Poliomyelitis
b. Post-polio Syndrome
c. Spinal Muscular Atrophy
i. SMA Types 1, 2, 3, 4, 0
ii. Distal SMA
iii. Progressive Bulbar Palsy
iv. Kennedy’s Disease
3. Combined Upper and Lower Motor Neuron
Disorders
a. Classic ALS
b. Familial ALS
c. Juvenile ALS
d. Western Pacific ALS – Parkinsonism
Dementia Complex
e. Groote Eylandt Motor Neuron Disease
f. Postencephalitic (Encephalitis
Lethargica) ALS
g. Progressive Bulbar Palsy
PRIMARY LATERAL SCLEROSIS
GENERAL MEDICAL BACKGROUND
DEFINITION
◊ Primary lateral sclerosis (PLS) is a rare
neuromuscular disease with slowly progressive
weakness in voluntary muscle movement. PLS
belongs to a group of disorders known as motor
neuron diseases.
◊ Affects the upper motor neurons (also called
corticospinal neurons) in the arms, legs, and
face. It occurs when nerve cells in the motor
regions of the cerebral cortex (the thin layer of
cells covering the brain which is responsible for
most higher level mental functions) gradually
degenerate, causing movements to be slow and
effortful.
◊ The disorder often affects the legs first, followed
by the body, trunk, arms and hands, and finally
the bulbar muscles (muscles that control
speech, swallowing, and chewing).
EPIDEMIOLOGY
◊ 0.01/100,000
◊ Males>Females
◊ In most cases, the disorder occurs during the
fifth decade. However, according to the medical
literature a familial form may exist that affects
children.
◊ The exact prevalence of primary lateral sclerosis
and motor neuron diseases is unknown.
ETIOLOGY
◊ Similar to other sporadic MNDs, the etiology is
not known.
PATHOMECHANICS / PATHOPHYSIOLOGY
◊ Loss of Betz cells in the precentral gyrus
◊ Degeneration of CST
CLASSIFICATION
◊ Mills Syndrome
o A hemiplegic variant of PLS
o Often associated with unilateral
presentation of UMN signs in the UE
and LE.
◊ Juvenile Onset PLS
o Chromosome 2q33
o Gene mutations
▪ PLS: Deletion in exon 9
▪ ALS2: Mutation in another
region of alsin gene
▪ Familial spastic paraparesis,
infantile onset
o Clinical
▪ Onset: Childhood
▪ Spasticity: Bulbar; Extremities
▪ Gaze paresis
▪ Normal: Cognition; Sensation
o Laboratory
▪ Central motor conduction times:
Delayed or Unrecordable
▪ EMG: No denervation
CLINICAL PRESENTATION
◊ Is defined as having little or no LMN involvement
clinically or by electromyography (EMG). In spite
of this, most patients with PLS eventually have
fasciculations and cramps
◊ PLS progresses much more slowly than
ALS—studies show an average life span of
between 8 and 15 years after diagnosis.
◊ Most patients with PLS have unilateral leg
spasticity, later involving the other leg DIFFERENTIAL DIAGNOSIS
approximately 1 to 2 years after, then ◊ The differential diagnosis for PLS includes other
progressing to the upper limbs 3 to 4 years later, central nervous system disorders; ALS and
and eventually showing pseudobulbar hereditary spastic paraparesis are two important
involvement 1 to 2 years later conditions. Consideration should be given to
◊ The primary findings on examination and the genetic analysis for hereditary spastic
cause of disability in PLS are spasticity and paraparesis, particularly in patients with
clumsiness rather than weakness, consistent relatively symmetrical lower limb involvement.
with a UMN syndrome. ◊
◊ Eventually, bulbar dysfunction is seen in nearly
all patients. Unlike ALS, symptoms of bladder Similarities Differences
dysfunction are common late in the disease.
ALS -Both -Degeneratio
COMPLICATIONS conditions n in PLS is of
are motor only the UMN
◊ Respiratory failure and death
neuron whereas in
◊ Pneumonia d/t infection or aspiration
diseases, ALS it is of
◊ UTI
-some forms both the
◊ Constipation
of ALS UMN and
◊ Spasticity and cramping of muscles
mainly affect LMN.
◊ Depression
the UMN (at -Muscle
◊ Loss of speech as means of communication
least at first), wasting,
◊ Immobility and attendant disability
and progress Charley
◊ Complications of immobility such as skin
more slowly, Horse
infections/bedsores and ulcers
making it cramps, and
difficult to significant
distinguish weakness
MEDICAL DIAGNOSIS
from PLS, seen in ALS
◊ Pringles’ Diagnostic Criteria Most cases is the result
o Criteria: that look like of LMN
o Insidious onset PLS are degeneration.
o Spastic paresis beginning in LE but may actually early -In general,
appear in bulbar or UE first stages of both the
o Adult onset 50 yo or older UMN-predom speed of
o No family history of PLS inant ALS progression
o Gradual progression of dse (3 yr or that and extent of
more) eventually disease are
o Usually associated c CST dysfunction: develop into greater in
symmetrical distribution ultimately ALS. For this ALS possibly
developing severe spastic spinobulbar reason, a because both
paresis diagnosis of levels of
◊ MRI BRAIN PLS should motor
o Atrophy of frontoparietal region only be made neurons
◊ MRI SPINE after degenerate.
o Normal symptoms
◊ MRS have been
o Abnormal NAA / Creatine ratio present for at
◊ SPECT least three to
o Decrease uptake of motor cortex four years.
◊ PET
o Decrease glucose consumption
◊ Electrodiagnostic studies should be performed PROGNOSIS
to exclude LMN involvement and should be
carried out on all patients. ◊ PLS is not fatal. There is no cure and the
◊ Most neurologists follow an affected individual's progression of symptoms varies. Some people
clinical course for at least 3 to 4 years before may retain the ability to walk without assistance,
making a diagnosis of PLS. but others eventually require wheelchairs,
canes, or other assistive devices.

2
 ◊ The rate at which your symptoms appear and
progress varies from person to person. It is
usually very slow and occurs over years or
decades. There may be periods of time with little
or no decline; if progression becomes more
rapid, revaluation by your healthcare provider is
important to determine whether another
condition is responsible.
◊ Many factors appear to influence the severity
and progression of your PLS, including your
general health, nutrition, and other factors such
as your genetic code.
TROPICAL SPASTIC PARAPARESIS
GENERAL MEDICAL BACKGROUND
DEFINITION
◊ Increased HTLV-1 proviral loads.
HTLV-II-associated disease appears to be milder
and has a more slowly progressive course.
PATHOMECHANICS / PATHOPHYSIOLOGY
◊ The pathogenesis of this entity is not completely
known and involves a multivariable phenomenon
of immune system activation against the
presence of HTLV-I antigens, leading to an
inflammatory process and demyelination, mainly
in the thoracic spinal cord.
◊ A retrovirus - human T-lymphotropic virus type 1
(HTLV-1) - has been recently implicated as a
possible etiology of the syndrome.
CLINICAL PRESENTATION
◊

◊ Tropical spastic paraparesis/human T-cell Disturbances Sx S

leukemia type I-associated myelopathy
(TSP/HAM) is caused by a human T-cell Motor Gait Stumbling
leukemia virus type I (HTLV-I) after a long disturbance, and leg
incubation period. tendency to weakness
fall Spastic hyperreflexia
◊ TSP/HAM is characterized by a chronic para paresis, lower limb,
progressive paraparesis with sphincter weakness clonus,
disturbances, no/mild sensory loss, the absence Plantar
of spinal cord compression and seropositivity for extensor
HTLV-I antibodies.
◊ Symptoms can begin long after the original Sensory Pain, feet
infection, sometimes decades after. numbness at paresthesia,
lumbar level loss of light
EPIDEMIOLOGY and touch
◊ As per WHO estimate worldwide 10-20 million backache sensory level
peoples are carrying HTLV1 and 5% of it are at lower
affected with TSP thoracic level
◊ TSP is very common in Latin America, the
Caribbean Basin, sub-Saharan Africa and Japan Autonomic urinary neurogenic or
◊ in approximately 2-3% of HTLV-1 affected dysfunction, overactive
person, it’s common among: constipation, bladder
o common among females Sexual diminished
o age group: 30-50 years dysfunction peristalsis,
Erectile
ETIOLOGY dysfunction
◊ The possible mechanism by which HTLVI
infection contributes to the pathogenesis of
TSP/HAM is unknown
COMPLICATIONS
◊ The common mode of transmission of this virus
◊ Same as PLS
is through [15-16] 1. Breastfeeding 2. Sharing
infected needles during intravenous drug use 3.
Sexual activity MEDICAL DIAGNOSIS
◊ Serologic and polymerase chain reaction (PCR)
RISK FACTORS tests of serum and CSF
◊ Older age at disease onset o If the CSF-to-serum ratio of HTLV-1
antibodies is > 1 or if PCR detects
HTLV-1 antigen in CSF, the diagnosis is
very likely.
3
 o Protein and Ig levels in CSF may also
be elevated, often with oligoclonal
bands; lymphocytic pleocytosis occurs
in up to 50% of patients.
◊ MRI
o Spinal cord lesions often appear
hyperintense on T2-weighted MRI
DIFFERENTIAL DIAGNOSIS
◊ Where HTLV-I is endemic, many disorders may
occur in asymptomatic carriers of the virus. The
etiological relation of FITLY-I to tropical spastic
paraparesis is accepted, but the disorders for
which HTLV-I is responsible are uncertain.
o Adult T-cell leukaemia/lymphoma (ATLL)
o Polymyositis Chronic arthritis
o Uveitis
o Motor neuron disease-like disorder
o Sicca syndrome
o Lymphocytic alveolitis
o Chronic infective dermatitis
PROGNOSIS
◊ TSP is a slowly progressive disease, but it is
rarely fatal. Most individuals live for several
decades after the diagnosis.
◊ Their prognosis improves if they take steps to
prevent urinary tract infection and skin sores,
and if they participate in physical and
occupational therapy programs.
LATHYRISM
GENERAL MEDICAL BACKGROUND
DEFINITION
◊ Synonymous to neurolathyrism
◊ A neurodegenerative disease that is caused by
heavy consumption of grass pea, Lathyrus
sativus.
EPIDEMIOLOGY
◊ The prevalence varies from country to country.
◊ The disease occurs in remote areas and affects
poor farmers with no access to medical care.
◊ The areas are mostly inaccessible for
epidemiological surveys. so there aren’t that
many epidemiological studies.
◊ Mean Prevalence:
o Ethiopia 6 per 1000
o India 5.3 per 1000
o Bangladesh 1.4 per 1000.
◊ Males>Females
ETIOLOGY
◊ Oral daily consumption of the chickling pea
vetch (lathyrus sativus)
RISK FACTORS
◊ Heavy physical activity
◊ Male gender
◊ Young age (15-25 years)
◊ Micro nutrient deficiency (Zn,Cu, Vit C, Vit A)
◊ Diarrhea and febrile illnesses are also
predisposing factors.
PATHOMECHANICS / PATHOPHYSIOLOGY
◊ Toxicological cause of the disease is attributed
ODAP is a neurotoxin that acts as a structural
analogue of the neurotransmitter glutamate.
Legumes containing the toxin is, although
knowledge about how to neutralize Lathyrus is
present, but drought can lead to shortages of
fuel and water, preventing the necessary steps
that can be taken, particularly in poor countries.
◊ Lathyrism usually occurs when the despair of
poverty and malnutrition leaves a few other
dishes. Lathyrism can also be caused by the
falsification of food products.
CLASSIFICATION
◊ Osteolathyrism
o It affects the bone and connective tissue
rather than the nervous system. It is a
skeletal disorder caused by the toxin
beta-aminopropionitrile BAPN, and
characterized by hernias, aortic
dissection, the exostoses, and
kyphoscoliosis and other skeletal
deformities, apparently as the result of
defective aging of collagen tissue.
o The cause of this disease is attributed to
beta-aminopropionitrile, which inhibits
the copper-containing enzyme lysyl
oxidase responsible for cross-linking
procollagen and proelastin. BAPN is
also a metabolic product of a compound
4
 present in sprouts of grass pea, pea and ◊ There are no specific clinical or laboratory tests
lentils.
for lathyrism.
◊ The clinical chemistry profile of lathyrism is not
CLINICAL PRESENTATION reported and is not of significance in clinical
◊ Upper motor neuron disorder with symmetrical diagnosis of the disease.
spastic paralysis. ◊ Routine and research electrophysiological
◊ Patients have difficulty in walking studies have been performed, but none is
needed for diagnosis
◊ with exaggerated deep tendon reflexes and ◊ Pt’s symptoms and diet are enough to diagnose
clonus. lathyrism
◊ Patients walk with a typical adductor gait with or o Absence of cassava consumption
without a walking cane. o (+) grass pea consumption
◊ Weakness and heaviness in lower limbs.
◊ Sensation and sphincters are spared. DIFFERENTIAL DIAGNOSIS
◊ A unique symptom of lathyrism is the atrophy of ◊
gluteal muscles of the buttocks.
◊ Similarities Differences
Stages of the Disease
Konzo -rapid onset attributed to
-non weeks of high
Stage I - No stick spastic gait with no
progressive cyanide
stage need to use a walking
course exposure
stick and no Babinski
from cassava
sign.
-Pyramidal
signs in the
Stage II - One stick spastic gait with the
UE are more
stage need of one walking
common
stick. Ankle clonus
-objective
and Babinski sign
sensory loss
present.
in the lower
extremities,
Stage III - Two sticks Spastic cross
signs of
stage adductor gait with the
amyotrophy,
need of two walking
subtle
sticks. Ankle clonus
changes in
and Babinski sign
mental
present.
status, and
the
Stage IV - Crawler There is bed ridden
progressive
stage (wheel chair) state
course of the
with loss of leg use
viral disease
and contracture.
Arms are strong and ◊
pyramidal signs
present.
PROGNOSIS

◊ ◊ Reversible leg dysfunction if consumption of the

offending agent is discontinued in the prodromal
COMPLICATIONS phase
◊ Same as PLS ◊ The symptoms are irreversible once the
spasticity occurs
◊ None of the neurolathyrism cases are so far
MEDICAL DIAGNOSIS
cured successfully or controlled pathologically.

5
 ◊ Some of the patients with long lasting PATHOMECHANICS / PATHOPHYSIOLOGY
neurolathyrism have been reported to develop a ◊ Exact pathogenic mechanisms of the disease
clinical course resembling that of ALS with
progressive worsening of the manifestations and remain unknown.
involvement of the LMN. Cognitive, sensory, ◊ Biochemical & toxicological studies suggest that
cerebellar, cranial nerve function and life metabolites of linamarin
expectancy do not decline. (α-Hydroxyisobutyronitrile β-Dglucopyranosid,
main casava cyanogen), notably cyanide
(mitochondrial toxin), thiocyanate (AMPA
EPIDEMIC SPASTIC PARAPARESIS chaotropic agent), & cyanate (protein
carbomylating agent) may play an important role
GENERAL MEDICAL BACKGROUND in the pathogenesis of Konzo

DEFINITION
◊ Are epidemics of neurodegenerative disease
putatively caused by food toxins which have
reported in the tropics with no clear
understanding of pathologic mechanisms
◊ These diseases include the disease named
Konzo that has been well documented in
sub-Saharan Africa
o Konzo means “tired legs” in the native
language of the yaka tribe of Congo
◊ Konzo is a distinct neurological entity with
selective upper motor neuron damage,
characterized by an abrupt onset of an
irreversible, non-progressive, and symmetrical
spastic para/tetraparesis
EPIDEMIOLOGY
◊ Epidemiological studies consistently show an
association between the outbreak of the disease
& chronic dietary reliance on insufficiently
processed cyanogenic cassava (or tapioca).
◊ Epidemics occur when these conditions coincide
at times of severe food shortage. Up to 1993,
outbreaks in poor rural areas in Africa
contributed to more than 3,700 cases of konzo.
The number of affected people is
underestimated.
◊ Mostly among children and women of
childbearing age.
ETIOLOGY
◊ The disease is associated with prolonged high
dietary cyanogen consumption from insufficiently
processed roots of bitter cassava combined with
a protein-deficient diet low in sulphur amino
acids (SAAs)
CLINICAL PRESENTATION
◊ Symmetrical permanent & irreversible
paraparesis with no signs of sensory
genitourinary impairments.
◊ Transient non motor symptoms like paresthesia,
cramping pain, or LBP.
◊ (+) hyperreflexia
◊ (+) babinski
◊ Contracture may develop in later stages
◊ Cognitive impairment developmental delays
have been reported among school aged & very
young children
◊ Walks on balls of the feet with rigid legs
◊ Speech difficulties
◊ Blurred vision
◊
COMPLICATIONS
◊ Same as PLS
MEDICAL DIAGNOSIS
◊ The following criteria are used:
o (1) a visible symmetric spastic
abnormality of gait while walking or
running;
o (2) a history of onset of less than one
week followed by a nonprogressive
course in a formerly healthy person;
o (3) bilaterally exaggerated knee or ankle
jerks without evidence of sensory loss
o (4) absence of grass pea consumption
◊ Urine specimens from a sample of the
population should be collected and analyzed for
thiocyanate, the main metabolite of cyanide.

RISK FACTORS
DIFFERENTIAL DIAGNOSIS
◊ Factors of susceptibility, including genetics, poor
nutrition, poverty, dietary, cyanogen exposure or
their interactions have been suggested. Similarities Differences

6
 o Onset: Any age ranging from early
Lathyrism -rapid onset caused by
childhood to late adulthood
-non weeks of high
◊ Compex HSP
progressive Lathyrus
o combination of the symptoms of Pure
course consumption
HSP with concomitant neurologic
disorders (seizures, impaired cognition,
dementia, extrapyramidal disturbance,
PROGNOSIS or peripheral).

◊ Non-progressive
CLINICAL PRESENTATION
◊ Non-remitting
◊ A good and varied diet, and immediate ◊ Progressive spasticity
treatment with high doses of multivitamins, but ◊ Weakness of the lower limbs
especially vitamin B12, is recommended to ◊ Hypertonic urinary bladder
avoid possible increased neurodamage due to ◊ Progression of this condition leads to a caudal to
concurrent vitamin B deficiency. rostral degeneration of the CST and the slight or
◊ Physical rehabilitation with crutches has proven mild involvement of the dorsal columns of the
successful in achieving independent locomotion. SC
◊ Impaired vibration sense
FAMILIAL (SPASTIC) PARAPLEGIA ◊ Muscular atrophy
◊ Pure HSP
GENERAL MEDICAL BACKGROUND o Gradual weakness in the legs
o Increase muscle tone and stiffness or
DEFINITION spasticity
o Excessive urge to urinate
◊ Genetically heterogeneous group of o Lack of sensation on the feet
neurodegenerative disorders that mainly affect ◊ Complicated HSP
the neurons of the SC o Peripheral neuropathy
◊ Caudal to rostral degeneration of the CST o Epilepsy
◊ Likelihood: o Ataxia
o Usually AD o Retinopathy
o Sometimes AR o Optic Neuropathy
o Rarely X-linked recessive o Dementia
o Icthyosis
EPIDEMIOLOGY o Learning and development problems
o Hearing loss
◊ Children and early adulthood o Speech, breathing, swallowing problems
◊ May occur at any age
COMPLICATIONS
ETIOLOGY
◊ Shortening and hardening of calf muscles
◊ Faulty gene from 1 or both parents ◊ Cold feet
◊ Extreme fatigue
◊ Back and knee pain
PATHOMECHANICS / PATHOPHYSIOLOGY ◊ Stress
◊ Depression
◊ Gene abnormality causes the long nerves in the
spine to deteriorate
MEDICAL DIAGNOSIS
CLASSIFICATION
◊ MRI scans of the brain and spine
◊ Pure HSP ◊ CSF analysis
o Considered more classic patterns ◊ Nerve conduction tests
o Presents with: ◊ EMG
▪ Spasticity
▪ Urinary Disturbance
▪ Vibration sense impairment DIFFERENTIAL DIAGNOSIS
7
 ◊ Dysphagia
◊ MS
◊ CP COMPLICATIONS

PROGNOSIS ◊ Poor nutrition

◊ Psychological dysfunction
◊ Life expectancy of Pure HSP = normal ◊ Progression of disease
◊ Progresses slowly throughout the years without ◊ Aspiration pneumonia
exacerbations, remissions, or periods of abrupt ◊ Severe dysphagia
worsening. ◊ Social withdrawal
◊ Disability from spasticity and weakness is
common but life expectancy remains normal
MEDICAL DIAGNOSIS
PSEUDOBULBAR PALSY
◊ CBC
GENERAL MEDICAL BACKGROUND ◊ Electroencephalogram
◊ CSF analysis
DEFINITION ◊ CT scan or MRI of the brain
◊ Motor and sensory evoked potential tests
◊ Results from a disease in the corticobulbar ◊ Videofluoroscopic swallowing study
tracts ◊ Speech assessment
◊ Bilateral damage must occur

EPIDEMIOLOGY DIFFERENTIAL DIAGNOSIS

◊ Prevalence in individuals above 50 years old ◊ Alcohol withdrawal seizure

◊ Incidence is higher in males in all age groups ◊ Delirium tremens
◊ Metabolic encephalopathy
ETIOLOGY

◊ CVA PROGNOSIS
◊ Demyelinating disorders
◊ MND ◊ Would vary depending on severity
◊ High brainstem tumors ◊ Symptoms may improve
◊ Head injury ◊ Would depend on the underlying etiology
◊ Neurosyphilis

RISK FACTORS LOWER MOTOR NEURON DISORDERS

POLIOMYELITIS
◊ Stroke
◊ MND GENERAL MEDICAL BACKGROUND
◊ MS
◊ CVA DEFINITION

PATHOMECHANICS / PATHOPHYSIOLOGY ◊ AKA as:

o Acute Anterior Poliomyelitis
◊ Nerves carrying signals from the cerebral cortex o Infantile Paralysis
to areas of the lower brainstem are o Heine Medin Disease
damaged/affected. ◊ Crippling and deadly infectious disease caused
by the polio virus which affects the person's SC
CLINICAL PRESENTATION and brain
◊ anterior horn cells of the grey matter (SC ad
◊ Paralyzed tongue brain) are affected
◊ Palatal movements are absent ◊ High risk individuals:
◊ Paralyzed facial muscles o Severely immunocompromised
◊ Exaggerated reflexes o Not Vaccinated
◊ Nasal regurgitation
◊ Dysphonia EPIDEMIOLOGY
8
 o Paralysis may occur at anytime during
◊ Prevalent in countries with poor healthcare the febrile period
◊ Average age of onset : 5-10 y/o o Maximum severity occurs within first 48
◊ Males > Females hours
◊ Children > Adults o Tremors, muscle weakness, and
◊ Affects children < 3 y/o. (Common among constipation
infants) o 2 groups:
▪ Spinal
ETIOLOGY ▪ Bulbar
● Diplopia
◊ Poliovirus is a human enterovirus (RNA) and a ● Facial weakness
member of the Picornaviridae ● Dysphagia
◊ Commonly acquired through the fecal-oral route ● Dystonia
◊ Incubation period of 5 to 35 days ● Nasal voice
◊ Infectivity is at its maximum during the 1st week ● Weakness of traps and
◊ Virus exits the body through stools in the SCM
following weeks ● Respiratory impairment

COMPLICATIONS
PATHOMECHANICS / PATHOPHYSIOLOGY
◊ Pain
◊ The virus enters the fecal-oral or respiratory ◊ Muscle Weakness
route, then enters into the lymphoid tissues of ◊ LOM
the GI tract. ◊ Contractures
◊ A primary (minor) viremia follows the spread of ◊ Spasticity
the virus to the reticuloendothelial viremia. ◊ Impaired Gait Pattern
◊ At this point, the infection may either be ◊ Impaired Respiration
contained or may further multiply and cause ◊ Swallowing Difficulty
several days of secondary viremia which will ◊ Speech Problem
culminate and develop symptoms and ◊ Easily Fatigable/Decreased Endurance
antibodies.
◊ Predilection for motor neurons in the lateral
anterior horn causes paralysis. MEDICAL DIAGNOSIS
◊ 50% of the original number of motor neurons
can be lost without the muscle losing clinical ◊ Oropharyngeal secretions
normal strength. ◊ Stool
◊ Blood samples
CLASSIFICATION ◊ Biopsy

◊ Abortive Poliomyelitis (Non-Paralytic) DIFFERENTIAL DIAGNOSIS

◊ Paralytic Poliomyelitis
Criteria GBS Poliomyelitis
CLINICAL PRESENTATION
Location PNS PNS
◊ Abortive Poliomyelitis Structures Myelin Sheath Anterior Horn
o Fever, headache, vomiting, diarrhea, Involved Cells
constipation, and sore throat
o Non progressive Cause Idiopathic Virus
o Non-paralytic poliomyelitis
o Virus stays in the bloodstream Distribution Symmetrical Asymmetrical
o Abdominal pain
o Lethargic and irritable Pattern Distal to Proximal to
o Muscle spasms are always present in Proximal Distal
the extensors of the neck and back and
may affect hamstrings and other Pain Common Not Common
muscles.
◊ Paralytic Poliomyelitis
9
Sensory Common (Mild) Rare
Symptoms
MEDICAL DIAGNOSIS

◊ Clinical Criteria
PROGNOSIS o Confirmed history of paralytic polio
o Partial to fairly complete neurologic and
◊ In nonparalytic poliomyelitis, recovery is functional recovery
complete. o Neurologic and functional stability for a
◊ In paralytic poliomyelitis, about two-thirds or minimum of 15 years
66% of patients have residual permanent o Onset of 2 or more of the following
weakness. conditions since achieving a period of
◊ Bulbar paralysis is more likely to resolve stability such as:
compared to peripheral paralysis. ▪ Unaccustomed fatigue
◊ Bulbar poliomyelitis has the highest mortality ▪ Mm or joint pain
rate. (4%-6% but increases to 10%-20% in ▪ New weakness in mm
adults) previously affects and
unaffected
▪ Functional loss
POST - POLIO SYNDROME ▪ Cold intolerance
▪ New atrophy
GENERAL MEDICAL BACKGROUND o No other medical diagnosis that is tied
to these health problems
DEFINITION ◊ Electrophysiological Tests
◊ Laboratory tests
◊ Occurrence of new health problems after several ◊ Imaging
years of acute poliomyelitis ◊ CSF Sampling
◊ Pt. exhibits new health problems ◊ Biopsy
◊ Fatigue is described as a “Hitting the wall”
phenomenon
◊ Fatigue happens at the late afternoon to night SPINAL MUSCULAR ATROPHY
but improves with rest SMA TYPES 1, 2 , 3 , 4 , 0
◊ Unknown cause
GENERAL MEDICAL BACKGROUND

RISK FACTORS DEFINITION

◊ Prior paralytic poliomyelitis ◊ Also known as Proximal Hereditary Motor

◊ Period of partial or complete functional recovery Neuropathy
of after acute-paralytic poliomyelitis , followed by ◊ Characterized by weakness and wasting on
an interval usually 15 years or more of stable muscles used for movement/ skeletal muscles;
neuromuscular function. loss of specialized nerve cells called motor
◊ Symptoms persist for at least a year neurons that control muscle movement
◊ Prolonged hospitalization ◊ Weakness tends to be more severe in the
◊ Respiratory involvement muscles that are close to the center of the
◊ Onset after 10 years old body compared to distal muscles.
◊ Severe and extensive poliomyelitis
EPIDEMIOLOGY
◊ The incidence of SMA is around one in 10,000
CLINICAL PRESENTATION live births with a carrier frequency of
approximately 1 in 50 individuals.
◊ Fatigue ◊ The mortality and/or morbidity rates of spinal
◊ Mm pain
muscular atrophy are inversely correlated with
◊ Joint pain
the age of onset.
◊ Weakness on the previously affected or
unaffected mm ◊ Higher death rates are associated with early
◊ Difficulty in walking, stair climbing, and dressing onset disease in patients with SMA Type 1
10
◊ The median survival rate is around seven the formation of the spliceosome, which
removes introns in pre- mRNA into functional
months of age with a mortality of around 95% by
mRNA.
the age of 18 months
◊ The damage motor neurons specifically to either
neuronal sensitivity to spliceosome malfunction
ETIOLOGY directly or indirectly through incorrectly spliced
◊ In 95% of cases, SMA results from a mRNA creating dysfunctional proteins key to
homozygous deletion of SMN1 on chromosome neuronal function
5q13; however, this does not explain how there
can be significant clinical heterogeneity in CLASSIFICATION
phenotype.[6] The answer lies in there being two
versions of SMN: 1) telemoeric version (SMN1)
2) centromeric version (SMN2) with individuals SMA CLINICAL SUBTYPES
varying in the number of copies of SMN2 they
possess Type 1 SMA/ Acute Infantile/ Onset: Before 6
◊ Each individual has 2 SMN gene: SMN 1 & SMN Werdnig - Hoffman Disease months
2. More than 95% of patients with SMA have Milestones: No sitting
homozygous disruption in SMN 1 gene under
chromosome 5q caused by mutation or Type 2 SMA/ Chronic Infantile Onset: 6 - 18 months
rearrangement. All patients with SMA retain at Milestones: Sitting
least 1 cup of their SMN 2 which generates only only no walking
10% of the amount of full length SMN proteins
VS SMN 1. This genomic organization still Type 3 SMA/ Chronic Juvenile Onset: Childhood
provides a therapeutic pathway to promote SMN after 12 months
2 existing in all patients to function like the Milestones: Walking
missing SMN 1 gene.
Type 4 SMA Onset: After 30 years
old
RISK FACTORS
◊ Respiratory infections account for most of the
deaths. CLINICAL PRESENTATION
◊ In estimating patients in Type 2 SMA, the age of
death varies, but death is most often because of
respiratory complications. SMA CLINICAL S/SX
◊ Male individuals are most commonly affected, SUBTYPES
especially with early onset forms of spinal Spinal Muscle Atrophy ● Muscle weakness
muscular atrophy. Like your type one and Type 2 Type 1 at birth
as it makes. ● Cannot control
head movements
PATHOMECHANICS / PATHOPHYSIOLOGY or hold head when
◊ The precise role SMN protein plays in neuronal pulled to sitting
function and development is not fully position
understood, and its subsequent absence ● Deep tendon
causing such devastating deficits has so far reflexes are absent
eluded precise pathophysiological descriptions. ● Abnormall bell -
SMN protein is found in all eukaryotic cells and shaped chest that
has shown to play a crucial role in all cells with prevents lungs
regards to homeostatic cellular pathway from fully
◊ Several hypotheses surrounding SMN protein expanding
and its role in SMA exist, two main hypotheses ● Sphincter
relate to SMN protein’s role in 1) The neuronal abnormalities
cytoplasm and 2) the neuronal nucleus. SMN ● Arthrogyposis
protein in the cytoplasm has demonstrated a ●
vital role in mRNA transport through axons, actin
dynamics, and vesicle release in the synapse. In Spinal Muscle Atrophy ● Characterized by
the nucleus, SMN protein forms small nuclear Type 2 (Chronic Infantile muscle weakness
RNA’s (snRNA) and therefore plays a key role in
11
SMA) that develop in tremors and mild
children between breathing
ages 6 to 12 problems
months and as ● Patients are
well as 6 to 18 basically similar to
months SMA Type 3 in
● Can sit without presentation and
support, although clinical findings,
they may need although the
help getting overall degree of
to a seated motor weakness is
position. less severe
● The lifespan of ● Normal life
individuals with expectancy
SMI Type 2 varies
but many live into Spinal Muscle Atrophy ● Arthrogryposis
their 20s or 30s. Type 0 Multiplex
● Most common Congenita.
form of SMA ● Affected infants
● Most children would move less in
present between in the womb of the
the ages of 6 and ● mother and as a
18 months or 6 to result they are
12 months often born with
joint deformities or
Spinal Muscle Atrophy ● Slow progressive contractures.
Type 3 (Chronic Juvenile proximal weakness ● They have
SMA) ● Typically causes extremely weak
muscle weakness muscle tone or
after early hypotonia at
childhood around 2 birth respiratory
to 17 years of age
● Can stand and
walk unaided, but COMPLICATIONS
overtime walking ◊ Individuals with SMA suffer from respiratory,
as well as climbing gastrointestinal, orthopedic complications that
stairs may become affect the quality of life and can potentially be
increasingly life-threatening, for example, chest infections
difficult for these secondary to aspiration due to inadequate
individuals. swallowing and muscle weakness. Patients with
● They may also SMA are prone to suffer from metabolic acidosis,
have problems especially during periods of illness or fasting, the
with running, underlying etiology of this predisposition is
climbing stairs and unknown, and there have been suggestions that
getting up from the dysfunctional glucose metabolism secondary to
chair. pancreatic abnormalities may play a role
● Many affected
individuals would DISTAL SMA
require wheelchair
● assistance later in GENERAL MEDICAL BACKGROUND
life.
DEFINITION
Spinal Muscle Atrophy ● Rare and often
Type 4 (Adult Onset SMA) begins in early
adulthood ◊ Mimics Spinal (Charcot Marie Tooth Disease)
● Usually experience ◊ Characterized by peroneal, muscular atrophy,
mild to moderate weakness and wasting in the legs
muscle weakness,
12
 ◊ There would be high foot arches or pes cavus
since it basically mimics your CMT.
◊ DTRs are reduced or absent.
EPIDEMIOLOGY
◊ It's an extremely rare autosomal recessive. In
mild cases, juvenile onset is around 2 to 10
years of age. In severe cases, they usually
occur four months of age up to 20 years of age.
◊ It can also be an autosomal dominant SMA. In
KENNEDY’S DISEASE
juvenile, 2 to 20 years of age, or it can also
occur in adults 20 to 40 years old.
GENERAL MEDICAL BACKGROUND
CLINICAL PRESENTATION
◊ Clinical manifestations basically consists of
weakness and atrophy distally in the legs,
especially in the anterior tibial muscles and
peroneal muscles which may also involve fine
muscles.
◊ There's foot drop distal muscle involvement in
the LE, below knee atrophy, no sensory and
autonomic dysfunction
◊ There may be UE involvement, weakness and
atrophy which are initially noted
◊ Complaints or manifestations distally in the legs,
especially in your TAs and peroneal muscles as
well as atrophy of your intrinsic foot muscles
◊ Pes cavus may also be present.
◊ If the upper extremities are involved, they are
usually involved in the later stages because
more or less upper extremities are usually
spared
PROGRESSIVE BULBAR PALSY
GENERAL MEDICAL BACKGROUND
DEFINITION
◊ It is a juvenile bulbar palsy or bulbar hereditary
motor neuropathy type 1 and 2
◊ Bullbar HMN 1is an autosomal recessive
syndrome that begins in the second decade of
life.
EPIDEMIOLOGY
◊ The onset is around 18 months, even up to 31
years of age, again at similar risk recessive and
slowly progressive for some time, as bilateral
CLINICAL PRESENTATION
◊ Characterized by facial weakness, dysphagia
and dysesthesia followed by facial weakness
and compromised respiratory function.
◊ The distinguishing feature of this syndrome is
the development of bilateral sensorineural
hearing loss.
◊ Cranial nerves affected are 7 and 12, but it can
also affect cranial nerves 3, 5 and 6.
DEFINITION
◊ X - linked lower motor neuron disorder
◊ Increase rates of type 2 diabetes, infertility, and
hand tremors
EPIDEMIOLOGY
◊ Progressive weakness and wasting of the limbs
and bulbar muscles begin in males and mid
adult 20 to 40 years of age
ETIOLOGY
◊ Results from a triple repeat mutation of your
cytosine adenine guanine or CAG in the exon 1
of the androgen receptor gene on the X
chromosome
CLINICAL PRESENTATION
◊ (+) weakness and wasting of facial, bulbar, and
extremity muscles
◊ Limb weakness and wasting: asymmetrical
◊ Weakness: proximal>distal; more weakness is
seen in dominant side
◊ Weakness: difficulty climbing stairs and walking
long distance
◊ (+) tremors in hand, hyperlordotic posture, IR
arms, gait disturbances, falls, troubles with
stairs, complaints of cramps and fasciculations
and myalgia, sensory abnormality
◊ (+) Hanging jaw/jaw drop, fasciculations of lips,
perioral muscles, and tongue, irregular endges
or furrowing of tongue, dysphagia, dysarthria,
nasal voice d/t palatal weakness, laryngeal
spasms, twitching mvmts of chin,postural
tremors of jaw
◊ M/C symptom: gynecomastia
13
◊ Reduced fertility d/t testicular atrophy,
asospermia, oligospermia, endrogen resistance,
erectile dysfunction, reduced libido, diabetes
◊ (-) DTR
◊ Slow, progressive disorder
◊ Remain ambulatory until later stage; some
confined to w/c at later dse
◊ Lifespan: normal.
◊ Common cause of death: pneumonia and
respiratory failure
MEDICAL DIAGNOSIS
1. Genetic testing of both parents but specific
genetic testing can be done prenatally or
postnatally
● Homozygous SMN 1 gene deletion is
seen in number of patients
- Sensory nerve conduction: normal in
SMA pts
- Compound motor action potentials: low
normal or reduced depending on
severity
- Motor velocities: normal in SMA pts
1. Muscle biopsy in order to differentiate SMA
from other neuromuscular DO if genetic is
unrevealing or nonspecific
● Muscle selection should be considered
on clinically affected muscles, but not to
the degree that degeneration would
render the tissue
unrecognizableAdequate results Can be
obtained by open or needle biopsy as
long as physician has adequate
experience in procedure and processing
of tissue
2. Histologic Findings
● Initial changes include: atrophy of
muscle fibers with compensatory
hypertrophy resulting in a group of large
and small fibers during the first 6-8
weeks of life, differentiating congenital
fiber type disproportion in SMA may be
difficult
● In the chronic form of SMA, secondary
myopathic changes may be seen in
additional 2-type grouping and may
histologically resemble muscular
dystrophy
● Classic histologic findings
- Degeneration and loss of spinal motor
neurons with a neurogenic pattern of
muscle morphology
- Occasional neuronal chromatolysis c
loss of myelinated axons in both ant and
post roots
- Disproportionate loss of myelin in the
thoracic and lumbar segments esp in
the CST c relative sparing of the cervical
cord
- Motor neurons in the brainstem, notably
in the hypoglossal nucleus
3. Molecular genetic testing on blood sample for
CAG trinucleate repeat expansion in the
autosomal recessive gene
- Individuals c >36 CAG trinucleate repeats in the
autosomal recessive gene are dx with
Keneddy’s disease.
DIFFERENTIAL DIAGNOSIS
● Congenital - <6months: Pompe disease,
Prader-Willi syndrome, Myotonic dystrophy type
1, Sellweger spectrum disorder, Congenital
myasthenic syndromes, X-linked infantile spinal
muscular atrophy. It is essential to consider
congenital myopathies, disorders of metabolism,
and disorders of mitochondria.
● Childhood: Botulism, hexosaminidase A
deficiency, Guillain-Barré, Duchenne muscular
dystrophy, Fazio-Londe syndrome, Hirayama
disease
● Adulthood: Amyotrophic lateral sclerosis, spinal,
and bulbar muscular atrophy
PROGNOSIS
Historically prognosis has been dependent on SMA type
with type 0 being the worst and individuals dying within
the first months of life and type IV having a mild disease
that does not affect the life expectancy. However, with
the recent introduction of disease-modifying agents such
as onasemnogene abeparvovec, there have already
been reported cases of SMA type I patients living longer
than the historical cohort data would suggest, prognosis,
therefore could potentially be much improved and is the
source of ongoing study.
COMBINED UPPER AND LOWER MOTOR NEURON
DISORDERS
CLASSIC ALS
GENERAL MEDICAL BACKGROUND
DEFINITION
◊ Amyotrophic Lateral Sclerosis (ALS) commonly
known as Lou Gehrig’s Disease, is the most
common and devastatingly fatal MND among
14
 adults. ALS is characterized by the degeneration
farmers, industrial
and loss of motor neurons in the spinal cord,
occupations)
brainstem, and brain, resulting in a variety of
● Diet
UMN and LMN clinical signs and symptoms.
(e.g., high fat intake
[saturated >
EPIDEMIOLOGY
monounsaturated],
◊ Currently 30,000 individuals in US have ALS, & high glutamate intake,
15 cases are diagnosed every day, except in a low fiber intake, low
very few high incidence areas like Guam & Kii antioxidant intake)
Peninsula of Japan ● Trauma
(e.g., skeletal
◊ Overall incidence of ALS is in the range of ~
trauma, fractures,
0.4-2.4 cases per 100,000 severe electrical
◊ the incidence of ALS increasing c each decade shock with
of life until at least 7th decade unconsciousness)
● Vigorous physical
◊ Prevalence is 4-10 cases per 100,000
activity (e.g., heavy
manual labor,
ETIOLOGY athleticism)
◊ Unknown etiology, no one single mechanism but
multiple/cumulative, including: oxidative stress,
exogenous neurotoxicity, excitotoxicity, impaired PATHOMECHANICS / PATHOPHYSIOLOGY
axonal transportation, protein aggregation,
◊ Amyotrophic lateral sclerosis is characterized by
apoptosis, & lifestyle factors.
o Superoxide dismutase (SOD)- a group a progressive degeneration and loss of motor
of enzymes that eliminate oxygen free neurons in the spinal cord, brainstem, and motor
radicals that although products of cortex.
normal cell metabolism have been
implicated in neurodegeneration for ALS Affected Unaffected/Lesser Extent
o Glutamate Toxicity - Glutamate is an
excitatory neurotransmitter & has also ● UMN in CST ● Sensory system
been implicated in degeneration ● Brainstem nuclei & SCT, some
o Clumping of Neurofilament Proteins- for CN studies suggest
Clumping of neurofilament proteins into 5,7,9,10,12 & ant that sensory
spheroids in the cell body & proximal horn cells in SC neurons may be
axon is one of the histopathological ● Morphological involved (but
characteristics of ALS studies have lesser extent)
found that ● CN 3,4,6
RISK FACTORS peripheral ● Onuf’s nucleus –
sensory nerves aka Onufrowicz
exhibit axonal nucleus is located
Known Risk Factors Possible Risk Factors
atrophy, in the ventral
for ALS for ALS
demyelination & margin of anterior
degeneration & horn in S2.
● Disease-causing ● Neurotoxicant
dorsal root Control striated
mutations (e.g., exposures (e.g., lead,
ganglion cells at ms in pelvic floor
SOD1, alsin) mercury, pesticide
autopsy revealing including anal &
● Clusters (e.g., exposure, solvent
loss of large external urethral
Western Pacific exposure)
ganglion cells. sphincters
ALS/PDC) ● Lifestyle factors (e.g.,
degeneration of
● Family history cigarette smoking,
Clark’s nucleus &
● Age alcohol intake,
SCT
● Gender (male > anthropometric
female) measures)
● Certain occupation ◊ As motor neurons degenerate, they can no
characteristics (e.g.,
electrical workers, longer control the muscle fibers they innervate.

15
 Healthy, intact surrounding axons can sprout
cramping, difficulty c fine motor activities
and reinnervate the partially denervated muscle
◊ Reinnervation can compensate for the
Stage 2 Moderate weakness, ms wasting, possible
progressive degeneration until motor unit loss is
atrophy, affectations in ADLs (modified
about 50% and electromyography (EMG)
indep
studies have found evidence of motor unit
reinnervation in individuals with ALS
Stage 3 Severe weakness, c functional limitations &
◊ As the disease progresses, reinnervation cannot
use of assist. devices but remained
compensate for the rate of degeneration, and a
ambulatory
variety of impairments develop
Stage 4 Severe weakness, c LE wasting & mild UE
CLINICAL PRESENTATION wasting. w/c bound
◊ Muscle Weakness
o Focal, asymmetrical ms weakness Stage 5 Dec mobility & endurance, UE & LE
beginning weakness, no head control
o Considered as cardinal sign of ALS in
LE/UE/bulbar ms Stage 6 Bedbound, progression of dse, respi sx or
o Cervical extensor weakness is very respiratory distress syndrome (RDS)
typical
Stage 7 Death (some references)
◊ Spasticity
o spasticity will eventually lead to
contractures, deformities & dyssynergic COMPLICATIONS
mvmt patterns ◊ Respiratory Impairments - orthopnea, dyspnea
◊ Fasciculation at rest, paradoxical breathing, accessory muscle
o Random spontaneous twitching of ms use and weak cough
fibers often seen through the skin are ◊ Cognitive Impairments- Severe frontotemporal
also common in ALS, rarely the initial sx Dementia
◊ Ophthalmoplegia - Complete ocular paralysis
◊ Hyperreflexia, clonus, & presence of
pathological reflexes (Babinski, Hoffman sign or
babinski like responses) MEDICAL DIAGNOSIS
◊ Hyporeflexia, dec/absent reflexes, dec ms tone
◊ Pt. c clinical presentation of ALS, laboratory
(flaccidity)
◊ Muscle Cramps studies, EMG, NCV studies, ms & nerve biopsy
o Can occur in uncommon sites (tongue, & neuroimaging studies are needed to support
jaw, neck, abdomen & UE, hands, calf, the dx of ALS & exclude other diagnoses
thighs
◊ Cadaveric hand – most striking feature of ALS. Required Absence of
flattening of thenar eminence c guttering & claw
hand ● Presence of LMN ● Electrophysiological
◊ Dysarthria signs by clinical, & pathological
◊ Spastic Dysphagia electrophysiological evidence of other dse
◊ Flaccid Dysphagia or neuropathological that may explain
◊ Pseudobulbar Affect examination UMN & LMN signs
◊ Respiratory Impairments- m/c cause of death ● Presence of UMN by ● Neuroimaging
◊ Mild deficit to severe frontotemporal dementia clinical examination evidence of other dse
◊ Extraocular muscle - spared but if degeneration ● Dse progression processes that may
occurs it does so in later stages of the dse within a region or to explain the observed
course other regions by clinical &
◊ Urinary sx: urgency, obstructive micturition, or clinical examination electrophysiological
both or via medical hx signs

Stages of ALS
◊ El Escorial Criteria
Stage 1 Mild, focal asymmetrical weakness o EMG criteria: signs of active denervation
affecting the hand, fasciculations, hand (like fibrillation potentials & positive
sharp waves) & signs of chronic
16
 denervation (large motor unit potentials, impairments, activity limitations & participation
inc duration proportion of polyphasic restrictions are inevitable in ALS pt.
potentials, inc amplitude, unstable ◊ The time from onset to death ranges from
motor unit potentials)
several mo to 20 yrs max.
◊ Average duration of ALS is ~27-43 months c the
Clinically Both UMN & LMN signs in at least 3-4
mean duration between 23-52 months
Definite regions OR Both UMN & LMN signs in
◊ 5 yr survival rate - 9-40%
bulbar & at least 2spinal regions
◊ 10 yr survival rate -8-16%
Clinically UMN & LMN in 2 regions c at least 1 ◊ Death usually occurs 3-5 yr after dx & results
Probable UMN from respiratory failure
rostral to LMN sign
Good Prognosis Bad Prognosis
Clinically UMN & LMN signs in 1 region only
Probable c OR UMN signs alone in 1 regions & LMN <35-40 yo onset/dx
laboratory signs defined by EMG criteria present in
support at least 2 regions Limb onset ALS (37-44% 5 Bulbar onset ALS (9-
yr survival rate) 16%)
Clinically UMN & LMN signs found together in 1
Possible region OR UMN signs alone in =/>2 Other factors: Psychological distress
regions OR LMN signs rostral to UMN o Less severe (higher mortality rate)
signs & inability to establish a dx of involvement at the time
clinically probable supported ALS of dx
o longer interval between
the onset & dx
DIFFERENTIAL DIAGNOSIS
o absence of sx of
dyspnea at onset
ALS Myasthenia Gravis o pt c psychological well
being
Disease of the motor Disorder at the
neuron neuromuscular junction
FAMILIAL ALS
50-60 yrs old ● Peaks in women
GENERAL MEDICAL BACKGROUND
20-30 yrs old
● Peaks in men 50-60
DEFINITION
yrs old

● Progressive ● Ocular sx ◊ Familial ALS (FALS) is an inherited autosomal

● No loss of sexual
function
● Pseudobulbar
palsy
● No sensory loss
● Weakness may trait that occurs 5% to 10% of all ALS cases.
fluctuate throughout ◊ Clinically identical to ALS but it’s hereditary
the day but most ◊ The identification of at least one additional family
commonly worsens member with ALS in successive generations is
later in the day essential for the diagnosis of FALS.

EPIDEMIOLOGY
Diagnosis: Diagnosis: Anti-acetylcholine
electrophysiological receptor antibody, ◊ about 10% of the entire ALS cases and the
examination, NCV studies, Edrophonium, MUSK onset is 46 yrs old
ms & nerve biopsy antibodies ◊ Familial ALS tend to have an early onset of
about ten years, more than patients with
sporadic disease
◊ C9ORF72 is the best-known gene to be
PROGNOSIS associated with ALS and accounts for 40% of
familial patients and 8% of sporadic patients in
European and North American societies
◊ ALS has a progressive & deteriorating dse
ETIOLOGY
trajectory & the progression from pathology, ◊ Genetic studies have identified mutations in
multiple genes, including those encoding the
17
 protein C9ORF72 (OPEN READING FRANCE ◊ El Escorial Criteria - widely accepted criteria
72 on chromosome) considered standard for the diagnosis of ALS
◊ Copper and zinc superoxide dismutase (SOD1)
gene mutation may account for approximately
15% of cases of FALS DIFFERENTIAL DIAGNOSIS
◊ RNA binding proteins TBP43 which is encoded
by TAR DNA binding proteins gene and FUS
TLS (fused sarcoma or translocated in
liposarcoma) as the m/c cause of FALS Familial ALS Sporadic ALS

46 years old 56 to 63 yrs old

PATHOMECHANICS / PATHOPHYSIOLOGY
Bulbar Features: 20-30% Bulbar Features: Unusual
◊ The mutated SOD1 appears to cause increased
reactivity to hydrogen peroxide and lead to an
Leg Involvement: common Leg Involvement:
increase in free radicals
occasional
◊ Copper ions in a reduced state will cause this
process to become harmful to the neuron.
Oxidative damage and glutamate toxicity may
interact or potentiate each other. PROGNOSIS

CLINICAL PRESENTATION
Good Prognosis Bad Prognosis
◊ Spasticity
<35-40 yo onset/dx
o As dse progresses, UMN may decrease,
spasticity will eventually lead to
Limb onset ALS (37-44% 5 Bulbar onset ALS (9-
contractures, deformities, and
yr survival rate) 16%)
dyssynergic movement patterns
◊ Hyperreflexia, clonus, and presence of
Other factors: Psychological distress
pathological reflexes (Babinski, Hoffman sign or
o Less severe (higher mortality rate)
babinski-like responses)
involvement at the time
◊ Abnormal timing of movement, loss of dexterity
of dx
and fatigue, all of which would affect motor
o longer interval between
control and function
the onset & dx
◊ Spastic Dysarthria
o absence of sx of
◊ Spastic Dysphagia
dyspnea at onset
◊ Pseudobulbar Affect
o pt c psychological well
◊ Respiratory impairments - m/c cause of death
being
◊ Urinary and Bowel Impairments

COMPLICATIONS
◊ Respiratory Impairments - orthopnea, dyspnea
at rest, paradoxical breathing, accessory muscle
use and weak cough
◊ Cognitive Impairments- Severe frontotemporal
Dementia
◊ Ophthalmoplegia - Complete ocular paralysis
MEDICAL DIAGNOSIS
◊ Genetic Testing- help determine the cause of
Familial ALS in a family
o About 60-70 percent of individuals with
Familial ALS will have a positive genetic
test result (meaning a mutation has
been identified).
JUVENILE ALS
GENERAL MEDICAL BACKGROUND
DEFINITION
◊ Juvenile amyotrophic lateral sclerosis (JALS) is
a very rare severe motor neuron disease
characterized by progressive upper and lower
motor neuron degeneration causing facial
spasticity, dysarthria, and gait disorders with
onset before 25 years of age.
EPIDEMIOLOGY
◊ The prevalence and incidence of JALS are not
known. A small number of cases have been
18
 reported to date. The disorder has been
described in various ethnic groups. MEDICAL DIAGNOSIS
◊ Motor evoked potential studies show absent or
ETIOLOGY reduced action potentials.
◊ Electromyography demonstrates signs of
◊ Mutations in the following genes have been denervation, while nerve conduction velocities
found in patients presenting with JALS: ALS2 are normal.
(2q33-q35), and rarely SIGMAR1 (9p13.3), ◊ Magnetic resonance imaging (MRI) scans of the
SPG11 (15q13-q15) and FUS (16p11.2).
Mutations in the latter gene are sporadic and brain and spinal cord are normal.
appear to be associated with a severe and
aggressive course.
DIFFERENTIAL DIAGNOSIS
PATHOMECHANICS / PATHOPHYSIOLOGY
◊ Gene mutation leads to C-terminal truncation of Juvenile ALS SMA Type 1
the FUS protein, resulting in loss of the nuclear
localization sequence (NLS), redistribution of the Onset before 25 yrs old At birth
FUS protein from the nucleus to the cytoplasm,
mutations in these genes: caused by defects in both
dislocation and abnormal deposition of protein
ALS2 (2q33-q35), and copies of the survival
cytoplasm, and formation of basophilic inclusion
rarely SIGMAR1 motor neuron 1 gene
bodies. Then, the abnormally-localized FUS
(9p13.3), SPG11 (SMN1) on chromosome
protein is assembled into stress particles, which
(15q13-q15) and FUS 5q
increase the stress response and cause
(16p11.2).
pathogenicity, indicating the importance of the
function of the mutant region
Overactive reflexes Deep tendon reflexes are
(hyperreflexia) absent
CLASSIFICATION

◊ Dominant Form- onset is usually at 2nd

decade, primarily presenting with UMNL signs PROGNOSIS
◊ Recessive Form - onset is usually in the 2st
decade with UMNL signs and 2nd decade with
LMNL signs
Good Prognosis Bad Prognosis

<35-40 yo onset/dx
CLINICAL PRESENTATION
◊ Babinski sign Limb onset ALS (37-44% 5 Bulbar onset ALS (9-
◊ Muscle spasms yr survival rate) 16%)

◊ Overactive reflexes (hyperreflexia) Other factors: Psychological distress

◊ muscle wasting (atrophy) o Less severe (higher mortality rate)
◊ muscle weakness involvement at the time
◊ muscle twitches of dx
◊ Facial spasticity o longer interval between
◊ Slurred speech (dysarthria) the onset & dx
◊ Spastic gait o absence of sx of
dyspnea at onset
COMPLICATIONS o pt c psychological well
being
◊ Respiratory Impairments - orthopnea, dyspnea
at rest, paradoxical breathing, accessory muscle
use and weak cough
◊ Cognitive Impairments- Severe frontotemporal WESTERN PACIFIC ALS - PARKINSONISM
Dementia DEMENTIA COMPLEX
◊ Ophthalmoplegia - Complete ocular paralysis
GENERAL MEDICAL BACKGROUND

19
 DEFINITION ◊ Bulbar symptoms include dysarthria and
dysphagia
◊ Amyotrophic Lateral Sclerosis and
Parkinsonism-Dementia Complex (ALS-PDC) is COMPLICATIONS
a disappearing neurodegenerative disorder of ◊ Respiratory Impairments - orthopnea, dyspnea
apparent environmental origin formerly
at rest, paradoxical breathing, accessory muscle
hyperendemic among Chamorros of
use and weak cough
Guam-USA, Japanese residents of the Kii
◊ Cognitive Impairments- Severe frontotemporal
Peninsula, Honshu Island, Japan and
Dementia
Auyu-Jakai linguistic groups of Papua-Indonesia
◊ Ophthalmoplegia - Complete ocular paralysis
on the island of New Guinea.

EPIDEMIOLOGY
MEDICAL DIAGNOSIS
◊ The crude incidence rate of Guam ALS was
◊ basic blood chemistry and metabolic labs, with
7.5/100,000/year, which was much higher than
consideration of thyroid studies, Lyme serology,
the rates of sporadic ALS, 2.3/100,000/year in
acetylcholine receptor antibody, and
Rochester and 0.6/100,000/year in Hokkaido,
cerebrospinal fluid analysis when clinically
although it was markedly low as compared with
appropriate.
that in the most frequent period between
1950-1960s. ◊ Urine evaluation for arsenic, lead, and mercury
may occasionally be helpful.
ETIOLOGY ◊ EMG is essential to confirm the presence of both
◊ exposure to genotoxins in seed of neurotoxic acute and chronic denervation in multiple limbs,
cycad plants formerly used for food and/or and muscle biopsy is occasionally needed to
medicine. exclude muscle diseases such as inclusion body
myositis.
RISK FACTORS ◊ An MRI of the cervical spine may be helpful to
◊ environmental origin formerly hyperendemic exclude cervical myelopathy.
among Chamorros of Guam-USA, Japanese
residents of the Kii Peninsula, Honshu Island,
Japan and Auyu-Jakai linguistic groups of DIFFERENTIAL DIAGNOSIS
Papua-Indonesia on the island of New Guinea.
Groote Eylandt MND Western Pacific ALS
PATHOMECHANICS / PATHOPHYSIOLOGY
◊ Experimental animal studies show that single Low calcium and iron exposure to genotoxins in
systemic doses of MAM can induce dysplasia of and high manganese seed of neurotoxic cycad
the developing cerebellum, features that are levels plants
represented in a proportion of Guamanian and
Kii-Japan subjects with ALS/PDC.
Guam-USA, Japanese Usually in northern
◊ The cerebellar pathology appears to result from
residents of the Kii Australian region
MAM-induced DNA damage in the form of Peninsula, Honshu
O6-methyguanine (O6-mG), which is subject to Island, Japan and
repair by O6-mG methyltransferase (MGMT). Auyu-Jakai linguistic
MAM-induced cerebellar damage is increased in groups of
transgenic animals lacking MGMT and Papua-Indonesia on
decreased in animals overexpressing MGMT the island of New
Guinea.

CLINICAL PRESENTATION
◊ dementia and extrapyramidal symptoms such as PROGNOSIS
rigidity of trunk and limbs, postural instability
◊ emotional lability

20
 ◊ Survival rates vary in relation to the decade of
onset: 15% of men and 29% of women who
developed symptoms in the 1950s lived beyond
10 years
◊ only 3% of men and 13% of women who
developed symptoms in the 1970s lived beyond
10 years.
◊ Death is most commonly associated with
pulmonary or urinary tract infection
◊ Respiratory Impairments - orthopnea, dyspnea
at rest, paradoxical breathing, accessory muscle
use and weak cough
MEDICAL DIAGNOSIS
◊ EMG is essential to confirm the presence of both
acute and chronic denervation in multiple limbs
◊ basic blood chemistry and metabolic labs- to
identify if there is a presence of high
manganese/ low iron

GROOTE EYLANDT MOTOR NEURON DISEASE

DIFFERENTIAL DIAGNOSIS
GENERAL MEDICAL BACKGROUND
Groote Eylandt MND Western Pacific ALS
DEFINITION
Low calcium and iron exposure to genotoxins in
◊ A syndrome associated with low calcium and and high manganese seed of neurotoxic cycad
levels plants
iron and high manganese levels

EPIDEMIOLOGY
Guam-USA, Japanese Usually in northern
◊ Usually located in northern Australian region residents of the Kii Australian region
◊ This neurological complex may be classed as Peninsula, Honshu
an ethnic-geographic isolate, a term suggested Island, Japan and
by Gajdusek1 to describe those diseases, Auyu-Jakai linguistic
usually rare, occurring with a high incidence in groups of
remote areas Papua-Indonesia on
the island of New
Guinea.
ETIOLOGY
◊ Low calcium and iron and high manganese
levels
◊ A study shows: gene mutation occurred on
Bickerton Island or the adjacent mainland PROGNOSIS

PATHOMECHANICS / PATHOPHYSIOLOGY Good Prognosis Bad Prognosis

◊ abnormal concentrations of manganese in the
brain, especially in the basal ganglia, are o Less severe Psychological distress
associated with neurological disorders involvement at the time (higher mortality rate)
of dx
o longer interval between
the onset & dx
CLINICAL PRESENTATION o absence of sx of
dyspnea at onset
◊ UMNL and LMNL signs together with cerebellar o pt c psychological well
extrapyramidal signs being
◊ CN and oculomotor muscle affectations
\GENERAL HEALTHCARE MANAGEMENT
COMPLICATIONS
MEDICAL MANAGEMENT

21
 ◊ MND’s are currently incurable, but are not
◊ HPI
untreatable.
o Age of onset
o An interdisciplinary approach is
o Initial presenting symptoms
preferable and more effective in
◊ PMH
treatment.
◊ Family History
SURGICAL MANAGEMENT ◊ Physical Examination
◊ Cardiovascular/Pulmonary Assessment
◊ Surgically implanted baclofen pump - for PLS o V/S
◊ In KD- surgery can be performed to suppress ◊ Sensory Examination
androgen activity ◊ Reflex Integrity
o Side effects: reduced mm strength, ◊ Developmental Reflex
osteoporosis, altered mood effects o Babinski Sign
◊ Surgical Revision- for SMA o Hoffman Sign
o may also provide stable correction of o Palmomental Reflex
spine and early orthopedic interventions ◊ CN Integrity
may be indicated in patients where o CN VII, IX, X, XII for facial nerve &
prolonged survival is anticipated pseudobulbar affect (gag reflex)
◊ Motor Function
o Hand function, modification, and control
PHARMACOLOGICAL MANAGEMENT of movement patterns should be
examined
◊ Riluzole (Rilutek) o MAS
◊ Adaravone, Radicava o DTR
◊ Nusinersen (Spinraza ™) ◊ MSK Assessment
◊ Muscle relaxants o ROM
o Baclofen o MMT
o tizanidine o MBT
o benzodiazepine o Posture
◊ Botulinum Toxin ▪ Static and dynamic postural
◊ Amitriptyline and atropine, botulinum Injections, alignment and body mechanics
glycopyrrolate during self-care
◊ Combinations of dextromethorphan and o Gait
quinidine ◊ Cardiorespiratory Endurance
◊ Anticonvulsants and NSAIDs ◊ Functional Assessment
◊ Antidepressants
◊ Benzodiazepines PT PROBLEM LIST
◊ Morphine ◊ Pain
◊ Opiates ◊ SOB
◊ LOM
◊ Spasticity
OTHER HEALTHCARE MANAGEMENT ◊ Weakness
◊ As there is no cure for MND’s, symptomatic and ◊ (+) contractures
supportive treatment can help people be more ◊ Impaired posture
comfortable while maintaining QOL ◊ Impaired balance and tolerance
◊ Multidisciplinary clinics with specialists from ◊ Circumduction gait
neurology, PT, RT, and social work are important ◊ Bowel/bladder alterations
in the care of pts ◊ Decreased endurance
◊ Dieticians are essential in maintaining weight
and strength PT DIAGNOSIS
◊ People who cannot chew or swallow may ◊ Neuromuscular Pattern 5A: Primary
require feeding tube or percutaneous prevention/risk reduction for loss of balance and
gastrotomy tube (PEG tube) to help with feeding falling
when strong enough for surgery ◊ Neuromuscular Pattern 5E: Impaired Motor
Function and Sensory Integrity Associated with
PHYSICAL THERAPY, EXAMINATION, EVALUATION, Progressive Disorder of the CNS.
AND DIAGNOSIS

POINTS OF EMPHASIS ON EXAMINATION

22
 ◊ Neuromuscular 5G: Impaired motor function and https://apps.who.int/iris/bitstream/handle/10665/265051/
sensory integrity associated with acute or PMC2536324.pdf?sequence=1&isAllowed=y
chronic polyneuropathies https://www.worldscientific.com/doi/abs/10.1142/978184
8161665_0017
https://www.vliruos.be/en/projects/project/22?pid=404
PT PROGNOSIS https://www.ennonline.net/fex/22/grass
https://jnnp.bmj.com/content/jnnp/43/8/661.full.pdf
◊ Varies on type of MND and age of onset
◊ PLS, KD are not fatal and progress slowly
◊ SMA may appear to be stable for long periods
but improvement should not be expected
◊ ALS, some forms of SMA are fatal

PHYSICAL THERAPY PLAN OF CARE

PT LONG AND SHORT TERM GOALS

◊ Maintain independent function and mobility

◊ Pt. will exhibit an increase in muscle strength in
all major mm groups in the body to increase
functional performance and be able to engage in
more physical activities.
◊ Pt. will exhibit improved dynamic balance and an
increase in dynamic balance as to standing and
walking to increase functional mobility and
improve ADL’s.
◊ Pt. will manifest an increase in sitting, standing,
walking tolerance to increase functional mobility.
◊ Pt. will experience a decrease/ total elimination
of pain
◊ Pt. will exhibit an increase in range of motion to
main joint integrity
◊ Pt. will show a decrease in spasticity to be able
to do functional movements
◊ Pt.will be able to regain near normal to
normal muscle strength to enable better
performance of ADLs.
◊ Pt. will manifest a decrease in postural
deviations to improve posture

PT INTERVENTIONS

REFERENCES

Books:

Websites:
https://www.ncbi.nlm.nih.gov/books/NBK553160/
https://www.nhs.uk/conditions/hereditary-spastic-paraple
gia/#:~:text=Hereditary%20spastic%20paraplegia%20is
%20a,paraparesis%20or%20Str%C3%BCmpell%2DLorr
ain%20syndrome.
https://patient.info/doctor/bulbar-and-pseudobulbar-palsy
https://www.healthline.com/health/pseudobulbar-palsy#o
utlook
https://journals.plos.org/plosntds/article?id=10.1371/jour
nal.pntd.0001051

23
PHARMACOLOGICAL MANAGEMENT SUMMARY

Medications Functions Side Effects PT Implications

Beta-blockers Anti-HTN medication or lowers BP Blunted HR, Dizziness, OH Use RPE to monitor exercise intensity
(Propanolol, [-olol]) Monitor pt. vital signs before, during and
after interventions.
Pt is at risk for falls
Dantrolene Blocks Ca++ release in the sarcoplasmic Drowsiness, dizziness, weakness, Monitor pt. vital signs before, during and
reticulum tiredness, nausea, and diarrhea after interventions.
Effective at reducing mm tone

Gabapentin decreases pseudobulbar affect Clumsiness, unsteadiness, Monitor pt. vital signs before, during and
constipation, diarrhea, drowsiness, after interventions.
tiredness, nausea
Acetaminophen and Relieve pain HA, drowsiness, dizziness Monitor pt. vital signs before, during and
other NSAID’s after interventions.
Botulinum toxin Used to treat jaw spasms and drooling HA, tiredness, blurred vision, muscle Monitor pt. vital signs before, during and
stillness, pain after interventions.
Muscle relaxants To treat spasticity Drowsiness, Dizziness, Agitation, Monitor pt. vital signs before, during and
such as baclofen, Irritability, HA, Decreased BP after interventions.
tizanidine, and
benzodiazepine
Riluzole (Rilutek ®) For ALS prolonging life for 2-3 months but does Dizziness, lightheadedness, Monitor pt. vital signs before, during and
not relieve sx drug reduces body’s production of drowsiness, tiredness, nausea, after interventions.
neurotransmitter glutamate which carries signals vomiting, diarrhea, loss of appetite,
to motor neurons stomach pain, or numbness/tingling
around the mouth
Adaravone, To slow clinical decline seen in pts with ALS Chest pain, change in walking and Monitor pt. vital signs before, during and
Radicava balance, clumsiness, unsteadiness, after interventions.
difficulty in breathing
Morphine To cope with MSK abnormalities or pain Drowsiness, stomach pain, HA, Monitor pt. vital signs before, during and
mood changes, difficulty urinating, after interventions.
small pupils

PT PLAN OF CARE SUMMARY

PROBLEM GOAL INTERVENTION

Pain Pt. will experience a decrease/ total elimination of pain Modalities such as: Hot Packs, Ultrasound, TENS
LOM Pt. will exhibit an increase in range of motion to main joint ROM Exercises such as: AROM, AAROM, PROM, and
integrity Stretching exercises
Spasticity Pt. will show a decrease in spasticity to be able to do Inhibitory Techniques and PNF Techniques
functional movements
24
Decreased muscle strength Pt.will be able to regain near normal to normal muscle Strengthening exercises such as:CKC exercises (squats,
strength to enable better performance of ADLs. lunges, push ups)OKC exercises using free weights,
theraband, etc. in accordance to the DAPRE, DeLorme or
Oxford regimen
Postural Deviations Pt. will manifest a decrease in postural deviations to improve Visual Feedback with mirror therapy to educate pt. with proper
posture postural alignment
Decreased Balance and Pt. will show an improvement in balance and an increase in Weight Shifting exercises
Tolerance sitting and standing tolerance to increase independence. One leg stance
HOME EXERCISE PROGRAM PRECAUTIONS
1. HMP, Conventional or Low Mode Frequency TENS x 15 mins 1. Avoid valsa maneuver
2. PROM ↔ AAROM ↔ AROM exercises 2. Energy conservation techniques
3. CKC exercises (squats, lunges, push ups)OKC exercises using free 3. Proper body positioning and body mechanics during exercise
weights 4. Change position every 2 hrs in bed, 30 mins in w/c
4. Mirror Therapy

25
 NEUROMUSCULAR CONDITIONS REVA COMPILATION
VELEZ COLLEGE PHYSICAL THERAPY BATCH 2022

PERIPHERAL NERVE INJURIES There will be compression

because of cervical rib seen
WHAT'S INSIDE in apical lung tumors or
malignant metastasis from
1.) UE the lungs and not the lower
2.) LE deep cervical lymph nodes.
3.) CN
4.) GBS Thoracic Outlet Term used to describe a
5.) CMTD Syndrome group of disorders that
6.) Diabetic Neuropathies would present with
7.) Toxic Neuropathies symptoms 2° neurovascular
8.) Leprosy compression of fibers of the
9.) CRPS brachial plexus.

GENERAL MEDICAL BACKGROUND Usually occurs between the

DEFINITION points of the interscalene
- Any disorder of the peripheral nervous system triangle as well as at the
(PNS) either involving the axon or myelin sheath inferior border of the axilla
because of trauma, metabolic disorders, or
genetic problems which can either be localized Compression of the nerves
or generalized. as well as the blood supply
- Either a proximal or distal affectation that results can also occur as they pass
in motor and sensory problems. over the first rib.

Upper Extremity Neuropathies Long Thoracic Nerve Aka knapsack nerve,

Injury external respiratory nerve
Upper Brachial Plexus Aka Erb Duchenne’s Palsy, of bell, nerve to serratus
Injury Birth Palsy, or Obstetric anterior, or posterior
Palsy thoracic nerve

Affects the upper trunk of the From the anterior rami of the
brachial plexus (C5 – C6) C5, C6, C7.

The affected nerves are Injuries to the long thoracic

those supplied by the C5 – nerve may be because of
C6 nerve roots the long course of the nerve
(suprascapular nerve, nerve and it is held in place by the
to subclavius, axillary nerve, scalene muscles and it slips
lateral pectoral nerve, upper off the serratus anterior.
and lower subscapular
nerves) Dorsal Scapular Nerve Comes from the anterior
Injury rami of C5.
There is also partial
paralysis of the long thoracic Often termed as posterior
and musculocutaneous scapular nerve or nerve to
nerves. rhomboids.

Frequently occurs as a Injury to the C5 root is more

result of birth injury. Also
because of compressed
stretch or torn C5 – C6
nerve roots.
Lower Brachial Plexus Also known as Klumpke’s
Injury Palsy
Affects C8 – T1 nerve roots
or the lower trunk of the
brachial plexus.
Usually an injury from
childbirth
Uncommon and can be
contrasted with Erb’s
Duchenne Palsy
Specific nerves involved are
– ulnar nerve (primarily),
median nerve (partially).
common than injury to the
nerve itself.
Inferior portion of the
scapula would wing
posteriorly often termed as
posterior winging because
of scalene hypertrophy
Axillary Nerve Injury Aka circumflex nerve
Arises from the posterior
cord of the brachial plexus
C5 – C6
Passes laterally through the
axilla and it courses behind
the surgical neck of the
humerus
Cutaneous innervation
would include the lower half
 of the deltoids
Suprascapular Nerve From the upper trunk of the
Injury brachial plexus C5 – C6
Innervates the posterior
capsule of the GH joint
Subscapular Nerve Upper and lower
Injury subscapular nerve which
arises from the posterior
cord of the brachial plexus
C5 – C6
Upper subscapular nerve is
aka short subscapular nerve
Thoracodorsal Nerve Posterior cord of the brachial
Injury plexus C6 – C8
Usually associated with
posterior cord injury.
Musculocutaneous Lateral cord of the brachial
Nerve Injury plexus C5, C7
Also known as antebrachial
cutaneous nerve
Radial Nerve Injury Most common injury to the
(level of spiral groove) radial nerve occurs at the
spiral groove from fracture of
the humerus as a result of
the nerve’s close association
with the humerus in the
spiral groove
PIN (Posterior Pure motor nerve and
Interosseous Nerve) injured in wounds of the
Syndrome elbow (low radial palsy), so
there is no wrist drop
anymore since the ECRL is
spared around that area
Patients are usually told to
wear a dorsal outrigger
splint
Compression is thought to
occur after takeoff of the
branches to the radial wrist
extensors as well as the
radial sensory nerve.
Wartenberg Syndrome Entrapment of the superficial
sensory branch of the radial
nerve.
Pronator Teres Compression neuropathy of
Syndrome the median nerve at the
elbow
Median Nerve Injury Aka Kiloh-Nevin Syndrome/
(Anterior Interosseous Entrapment at the Gantzer
Nerve Syndrome) muscle (accessory head of
the FPL below the radial
tuberosity)
Rare entrapment syndrome
which comparatively has
little epidemiologic data
Accounts for < 1% of
neuropathies of the UE.
It is a pure motor neuropathy
s/a the posterior
interosseous nerve injury
because it does not contain
any sensory fibers.
Carpal Tunnel Median nerve is compressed
Syndrome within the carpal canal,
approximately 1 to 2 cm
beyond the distal wrist
crease. It is more common
in women and is often
bilateral but more severe in
the dominant hand
Ulnar Nerve Injury Formed from the medial
(Cubital Tunnel epicondyle of the humerus,
Syndrome) olecranon process of the
ulna, and the tendinous arch
joining the humeral and
ulnar heads of the FCU.
Guyon’s Canal Ulnar nerve impingement
Syndrome along an anatomical space
in wrist between the hook of
hamate and pisiform.
EPIDEMIOLOGY
● Males > Females
● Also common in: athletes, desk jobs, elderly, and
those who are pregnant
● Most common UE PNI is CTS (Carpal Tunnel
Syndrome)
● Sensory > Mixed > Motor Nerves
ETIOLOGY
● Most common nerves affected:
○ Common Peroneal Nerve
○ Ulnar Nerve
● Peripheral Nerves can be damaged through:
Heredity
Trauma ● Compression Injuries (mc)
● Traction (brachial plexus
injury)
● Laceration
● Crush and percussions
(fractures, compartment
syndromes)
● Penetrating trauma (stab
wounds)
● High-velocity trauma (MVA)
Thermal ● Frostbite
Infections
Toxins ● Heavy metals (ie. lead for
radial nerve injuries)
2
 macrophages would clear the debris of the
Metabolic or
degenerating axon.
Systemic
● This would leave basically an empty tunnel of
Schwann cells as the axon is degenerating
Aging
● Once the damaged axon segments are removed
completely, the cell body starts to grow a new
Malignancies
axon in the empty tunnel left by the Wallerian
degeneration (Wallerian Regeneration).
Vascular
○ The success would depend on the
disorders
remaining Schwann cells as they
basically help guide the re-growing
Inflammatory ● Leprosy (usually affects the
axons to its correct destination.
disease ulnar nerve)
● Once the new axon would reach the injury site, it
tries to reconnect with the axon segments
across the injury site.
Carpal Tunnel Syndrome The most common ○ The success would depend on the injury
entrapment neuropathy itself.
Causes: Repetitive ● The Wallerian Regeneration can only bring a
trauma, obesity, newly formed axon to the site of the injury. The
pregnancy, lupus, etc axons need an intact myelin sheath to grow in a
correct direction. Without it, the axon would
basically get lost and wander about. This gives
Pronator Syndrome Trauma from repetitive
rise to a messy structure made of axons looking
overuse, tight casting,
like a ball of yarn.
penetrating injuries such
as intravenous catheter,
● If the damaged nerve has a large gap between
carrying a bag with the
the cut ends or if the myelin sheath is lost, the
arm flexed (“grocery bag
regeneration may not end in a functional
neuropathy”)
recovery. Also, if the neuron body is damaged
for some reason, the regeneration may fail
Anterior Interosseous Direct trauma,
altogether.
Nerve Syndrome inflammation, strenuous
○ The success of the repair would depend
exercise, fractures,
on the extent of the injury as well as the
variant of brachial
size of the damaged area.
neuritis, compression by
anomalous fibrous bands
CLASSIFICATION
in this region
Classification - Seddon & Sunderland
Seddon Sunderland Description
Median Nerve Caused by trauma or
Entrapment inflammation Neurapraxia First-Degree Focal conduction
block without
axonal damage
RISK FACTORS
Risk factors include:
Axonotmesis Second-Degree Axon damage with
● Superficial position,
Wallerian
● A long course through an area at high risk of
degeneration,
trauma, and;
supporting
● A narrow path through a bony canal.
structures intact
PATHOMECHANICS / PATHOPHYSIOLOGY Neurotmesis Third-degree Damage to axon
● All the injuries to the nerves are happening at Fourth-degree and endoneurium
the level of the cellular processes Fifth-degree
● Trauma, inherited disorders, environmental Damage to
toxins, metabolic or nutritional disorders may perineurium and
affect the myelin sheath in the axon or the endoneurium
adjacent motor units activated by the peripheral
nerves. Damage to axon
● Severity of the involvement causes changes in and all supporting
the nerve and muscle responses, determining structures
the amount of function lost.
● PNI almost always involve the axons only, not
the cell body itself. Classification – Based on Pathology
● After the injury, the part of the axon which is Distribution Proximal 1 nerve
severed from the main cell body would start to
disintegrate (Wallerian Degeneration à does Distal Multiple nerves
not affect the Schwann cells (provides the
myelin sheath in PNS)). If they are not destroyed Pathology Neuropraxia Myelin sheath
by the injury, the Schwann cells would not be
destroyed or affected. They, along with the Axonotmesis Axons

3
 ● Motor symptoms may include: fasciculations,
Neurotmesis Myelin sheath &
spasms, myalgias with inflammatory myopathy
Axons
may also occur
● Abnormalities in sensory perception.
Etiology Trauma, Toxic Myelin sheath
● Neuralgia à severe and multiple shock-like pains
OR axon
that would radiate from a specific nerve
distribution could occur
Hereditary, Myelin sheath
● Hyperalgesia à presents usually after a PNI.
Thermal AND axon

Endocrine, Axons Upper Brachial Plexus - Flaccid paralysis

Vascular, Injury - Sensory loss over
Ischemic the deltoid, anterior
radial surface of the
Post-Infectious, Myelin Sheath forearm, and hand
Autoimmune, - If amniotic bands
Nutritional were the congenital
cause, the child may
also show
Classification – Hereditary Types
characteristics like
Hereditary Disorders of Lipid Metabolism
underdeveloped
- Metachromatic leukodystrophy
extremity or
- Krabbe’s Disease (globoid cell leukodystrophy)
deformed area.
- Fabry’s Disease
- GH subluxation or
- Adrenoleukodystrophy/ Adrenomyeloneuropathy
D/L
- Refsum’s Disease
- Skeletal deformity
- Tangier Disease
- Poor bone growth
- Cerebrotendinous Xanthomatosis
- Learned pattern of
non-use of the UE.
Hereditary Ataxias with Neuropathy
● Friedrich’s Ataxia
Lower Brachial Plexus ● Paralysis or atrophy
● Vitamin E deficiency
Injury of the small hand
● Spinocerebellar Ataxia
muscles, and flexors
● Abetalipoproteinemia (Bassen-Kornzweigh
of the wrist
Disease)
● Produces flexion
and supination at
Disorders of Defective DNA Repair
the elbow, extension
- Ataxia-telangiectasia
of the wrist, and
- Cockayne’s Syndrome
hyperextension of
the MCP joints, as
Giant Axonal Neuropathy
well as flexion of IP
Porphyria
joints (basically
- Acute Intermittent Porphyria (AIP)
forms a claw hand
- Hereditary Coproporphyria (HCP)
deformity)
- Variegate Porphyria (VP)
● Edema, cyanosis, as
Familial Amyloid Polyneuropathy (FAP)
well as trophic
● Transthyretin-related
changes and
● Gelsolin-related
sensory loss in the
● Apolipoprotein A1-related
ulnar nerve
distribution
CLINICAL PRESENTATION ● Atrophy of the
Clinical Manifestations (General): intrinsic muscles of
● LMNL since it affects peripheral nerves. the hand and
● There would be weakness, paresis of sometimes long
denervated muscles, hypotonia, hyporeflexia, flexors of the
rapid atrophy, fatigue fingers.
● Sensory loss would correspond to motor
weakness as well. Long Thoracic Nerve - Paralysis of
● Proprioceptive losses may yield to sensory Injury serratus anterior
ataxia muscles (boxer’s
● Insensitivity may yield to limb trauma. muscle),
● Autonomic dysfunction would be evident in the - Leading to instability
form of vasodilation and loss of vasomotor tone. of the scapula,
● Dryness medial winging of
● Warm skin the scapula (known
● OH as the open book
● Edema deformity)
● Hyperexcitability of the remaining nerve fibers,
so there would be sensory dysesthesias, Musculocutaneous ● Weakness of
hyperalgesia, pins & needles, numbness, Nerve Injury shoulder and elbow
tingling, burning flexion as well as

4
 forearm supination Weakness Median at wrist
since the biceps is Ulnar at elbow
the main supinator
of the forearm
PROGNOSIS
COMPLICATIONS ● If nerve tissue is irritated from tension,
● Impaired sensory function compression, or hypoxia, damage may not be
● Impaired motor function permanent and show signs of recovery when
● Impaired dexterity irritating factors are eliminated.
● Impaired sensitivity to cold ● If nerve tissue is injured, recovery is dependent
● Eventual pain problems on several factors that includes:
o Extent of injury to the axon and its
MEDICAL DIAGNOSIS surrounding connective tissue sheath
o Nature and level of injury
1. Clinical presentation suggestive of peripheral o Timing and technique of the repair
nerve entrapment/ compression syndrome: o age and motivation of the person
history and physical examination
2. Electrodiagnostic confirmation of a nerve Lower Extremity Neuropathies
segment lesion GENERAL MEDICAL BACKGROUND
3. Correlate history, physical examination, and DEFINITION
electrodiagnostic findings
4. Electrodiagnostic excludes radiculopathy,
Lumbosacral Pathology affecting either the
plexopathy or peripheral polyneuropathy
Plexopathy lumbar or sacral plexus of
Electromyography (EMG). In an EMG, a thin-needle nerves.
electrode inserted into your muscle records your Are rare syndromes caused by
muscle's electrical activity at rest and in motion. damage to the nerve bundles
Reduced muscle activity can indicate nerve injury.
Lateral Femoral Divided into 2 branches:
Nerve conduction study. Electrodes placed at two
Cutaneous Nerve
different points in your body measure how well electrical
Injury Posterior branch provide
signals pass through the nerves.
cutaneous sensation from the
Magnetic resonance imaging (MRI). MRI uses a superior external part of the
magnetic field and radio waves to produce detailed buttocks
images of the area affected by nerve damage

Genetic Testing. Involves taking a blood sample and Anterior branch supply the outer
testing it for defective genes. surface of the thigh Meralgia
paresthetica if affected
Nerve Biopsy. In a small number of cases where other
tests have been inconclusive, a nerve biopsy may be
performed. This is a minor surgical procedure where a Meralgia A sensory disturbance in the
sample of a peripheral nerve is removed from the leg for Paresthetica lateral aspect of the thigh
testing.
Femoral Nerve Comes from the posterior
DIFFERENTIAL DIAGNOSIS primary rami of the L2-L4
Formed by L2-L4 roots and
Anatomic Area Symptom Nerve Injuries reaches the front of the leg by
to Consider penetrating the psoas muscle
before it exits the pelvis
Shoulder Pain or Axillary
Numbness Brachial Plexus Obturator Nerve Anterior rami of the femoral
nerve
Weakness Axillary
Brachial Plexus Arises from 3 anterior divisions of
Long Thoracic the lumbar plexus L2, L3, L4
Spinal descending through the obturator
Accessory canal in the medial obturator
Suprascapular foramen to the medial side of the
thigh.
Forearm Pain or Pronator Teres
Numbness Radial Tunnel
Superior Gluteal L4-S1
Weakness Posterior Nerve Supplies G. med & G. min.
Interosseous
Inferior Gluteal L5-S2
Hand Pain or Radial at wrist Nerve Supplies G. max, TFL (hip
Numbness Ulnar at wrist or FABIR), ITB
elbow

5
 Sciatica Pain cause by compression or Lumbosacral - Diabetic Amyotrophy
irritation of the sciatic nerve by a Plexopathy - Parsonage Turner
problem in the lower back Syndrome
- Tumors
Sciatic Nerve A complication of THA with an
Palsy incidence of 0.2-2.8% of the time
or within an incident of 1.7-7.6 Femoral Nerve ● Hemorrhage d/t hemophilia
following THA revision. ● Anticoagulation therapy
● Trauma
Tibial Nerve From the anterior primary rami of ● Direct Trauma d/t
the sacral plexus emerging as a penetrating wounds or
separate nerve proximal to the fractures of the hip or
popliteal fossa, containing fibers
pelvis.
from L4,L5,S1,S2 and S3
● Intrapelvic masses
Tarsal Tunnel A condition caused by ● Aortic Iliac Aneurysms
Syndrome compression of the tibial nerve or ● Lithotomy position during
associated branches as the childbirth
nerve passes underneath the
flexor retinaculum at the level of Obturator - Nerve root compression
the ankle or distally, it’s Nerve from herniated nucleus
analogous to CTS for the median
nerve pulposus
- Anterior D/L of the hip joint
Morton’s Interdigital nerves which are - Penetrating wounds
Neuroma thickened & irritated - Fixation of a femur fracture
gone wrong
Common Injury at the fibular head, where - THA
Peroneal Nerve the nerve would wind around the
- Pressure from gravid uterus
Syndrome fibular head.
- Difficult labor
Anterior Occurs as a result of an ↑
Compartment pressure within the anterior Sciatic Nerve ● Screw broken piece of
Syndrome compartment of the leg which Palsy trochanteric wire fragments
contains the deep peroneal nerve of methyl methacrylate
& tibial artery & muscles of the bone cement
anterior compartment. ● Burch-Schneider metal
cage

Tibial Nerve - Direct trauma s/a

EPIDEMIOLOGY penetrating wounds,
● There are several large studies on traumatic entrapment through narrow
nerve injuries. The frequency of the lower space, ischemia of the
extremity nerve injuries is assessed to posterior component of the
approximately 20 to 23% of the overall lesions to leg, compression for long
the peripheral nerve system. Peroneal division periods of time.
neuropathy is the most common lower extremity
nerve palsy. Tarsal Tunnel ● Extrinsic Causes:
Syndrome - External trauma d/t crush
ETIOLOGY injury, stretch injury,
There are various ways in which the lower limb nerves fractures, dislocation of the
are injured. Some of the common etiology is listed as ankle & hindfoot, and even
follows: severe ankle sprains
● Fractures, particularly the hip, femur, tibia, fibula, ● Local Causes:
and, occasionally, the ankle - Space occupying masses
● Crush injury - Localized tumors
● Knife assault - Bony prominences
● Gunshot - Venous plexus within the
● Iatrogenic tarsal tunnel
● Traction - Nerve compression d/t
● Blunt trauma valgus foot
● Radiation
Common ● Frequent Crossed leg
Iatrogenic injuries form a significant portion of injuries. Peroneal Nerve position
They are caused by Syndrome ● Sitting
● Intramuscular injection ● Squats
● Total hip prosthesis operation ● Fibular neck fracture
● Excision of tumor ● Compression from tight
● Tourniquet bandages
● Traction or pressure during operation ● Bedridden patients on a
frog leg position
6
 Anterior - Occurs as a result of an ↑ aspect of thigh, greatest at
Compartment pressure within the anterior the knee.
Syndrome compartment of the leg
which contains the deep Superior - (+) Trendelenburg sign on
peroneal nerve & tibial Gluteal Nerve single leg stance on the
artery & muscles of the paralyzed LE
anterior compartment. - Pt. presents with a waddling
gait/chorus girl gait, if there
RISK FACTORS is bilateral G. med or
Risk Factors (General): bilateral superior gluteal
● Diabetes, especially if your sugar levels are nerve injury
poorly controlled
● Alcohol abuse Inferior Gluteal ● Affects L5-S2 nerve roots,
● Vitamin deficiencies, particularly B vitamin Nerve targeting the G. max, TFL,
● Infections, such as Lyme disease, shingles, ITB
Epstein-Barr virus, hepatitis B and C, and HIV ● If tight ITB foot is held in
● Autoimmune diseases, such as rheumatoid pronation, there would be
arthritis and lupus, in which your immune system genu valgum & coxa vara
attacks your own tissues PFPS d/t weak G. med.
● Kidney, liver or thyroid disorders
● Exposure to toxins Sciatica - Numbness or weakness in
● Repetitive motion, such as those performed for the legs or feet
certain jobs - In severe cases, may
● Family history of neuropathy experience a loss of feeling
or movement.
Common Peroneal Nerve Injury - May feel the sensation of
- Thin (Anorexia Nervosa) pins and needles, which
- Certain autoimmune disorders (Polyarteritis involves a painful tingling in
Nodosa) the toes or feet.
- Nerve damage from other medical problems s/a
Bell’s Palsy ● Bell palsy, a common
diabetic/ alcohol use
clinical condition in which
- Have Charcot-Marie-Tooth Disease
the facial nerve (cranial
nerve [CN] VII) is
PATHOMECHANICS / PATHOPHYSIOLOGY
unilaterally affected and is
◊ See UE PNI Pathomechanics/ Pathophysiology characterized by facial
hemiparesis
CLINICAL PRESENTATION
Sciatic Nerve ● Sensory manifestations
Lumbosacral If symptoms cannot be localized to Palsy include posterior thigh pain
Plexopathy a single nerve, patients may ℅: at the level of the sciatic
notch, radicular pain along
- Neuropathic pain
the sciatic nerve distribution
- Numbness or weakness with hip and knee range of
- Muscle wasting motion, diminished
sensation, and
Meralgia ● (+) burning pain, paresthesias.
Paresthetica numbness, paresthesia, or
even anesthesia Tibial Nerve - (-) plantar flexion
- (-) flexion of toes
Femoral Nerve - Weakness - Weak inversion
- Acute severe pain in the Tarsal Tunnel ● Sensory disturbance that
groin, thigh, and lower Syndrome varies from sharp pain to
abdomen loss of sensation
- Medial leg & calf numbness ● Motor disturbance with
- Sensory loss in the anterior resultant atrophy of the
and medial sides of the intrinsic musculature,
● Gait abnormalities
thigh, medial side of leg,
(overpronation & a limp d/t
medial border of foot pain with weightbearing)
- ↓ patellar reflex
Morton’s - Pain & burning sensation of
Obturator ● Weakness in the Neuroma toes 2 - 4
Nerve adductors/internal &
external rotators of the hip, Common ● Foot drop
● Difficulty crossing the leg, Peroneal Nerve ● Sensory disturbance in the
Syndrome specific innervation
● Pain in the groin,
● Paralysis
specifically in the medial ● Paresis of anterior & lateral

7
 compartment muscles of and hip lateral rotation
the leg
● Steppage gait Superior L4, L5, S1
● At heel strike Lateral Gluteal Nerve Pain that increases during
border of the foot would ambulation in the gluteal region
also contact 1st Trendelenburg gait
● During loading response Weak Hip abductors
with Foot slap hip medially rotated
● During swing with
excessive hip flexion to
clear the foot Sciatica L4 - S3
● Paralysis of anterior & most commonly injured nerve in the
lateral compartment hip region
muscles Sensory alterations and
paresthesias
Anterior - Pain & paresthesia in the Muscle Weakness
Compartment extremity
Syndrome
Bell’s Palsy Acute Complications of Sarcoidosis
Benign Skull Tumors
COMPLICATIONS
Brainstem Gliomas
● Burns and skin trauma. Patients might not feel
Cerebral Aneurysms
temperature changes or pain in parts of the body
Meningioma
that are numb.
Tuberculous Meningitis
● Infection. The feet and other areas lacking
sensation can become injured without your Tibial Nerve L4- S3
knowing. Check these areas regularly and treat ● Tarsal Tunnel Syndrome
minor injuries before they become infected, most common foot entrapment
especially if one has diabetes. syndrome
● Falls. Weakness and loss of sensation may be (+) tinel’s sign
associated with lack of balance and falling. Burning pain and paresthesias at
● Deformities - severe peripheral neuropathies sole of foot and toes, worsens after
may cause deformities especially on the long periods of walking, pain may
muscles affected by the nerve radiate to the medial side of the
ankle distal to the medial malleolus
MEDICAL DIAGNOSIS Weakness of muscles during long
● “See UE Neuropathies for Medical Diagnosis” standing to muscles supplied
● Posterior fossa Entrapment
DIFFERENTIAL DIAGNOSIS Syndrome
Weakened dorsalis pedis pulse
Lumbosacral Local Pelvic Bone Infection Sensory alteration to the soles of
Plexopathy foot, presence of intermittent
Avascular Necrosis of the Hip
cramping
Radiation Induced Plexopathy Inability to PF and invert the foot,
fex or abd or add toes
Meralgia Lateral femoral Cutaneous Nerve
Paresthetica (L2, L3) Popliteal Artery Entrapment
Pressure or entrapment Syndrome
Trauma or Compression
Sensory Alteration only no motor Morton’s Stress Fracture
Neuroma Tendon Sheath Ganglion
presentation
Capsulitis
Burning, pain, numbness, dull, ache
Pain in lower back Common L4 - S2
Paresthesias Peroneal Nerve Most commonly injured in the LE
Syndrome Altered sensation around the head
Femoral Nerve L2, L3, L4 of the fibula
Decreased sensation to sensory Lateral aspect of leg abd dorsum of
foot
loss, medial aspect of distal thigh
Presence of weakness or paralysis
Not commonly injured, DTR lost to the supplied muscles
Quadriceps wasting most evident Steppage Gait
Due to trauma or compression
Anterior Osteomyelitis
Obturator L2, L3, L4 Compartment Necrotizing Fasciitis
Nerve Adductor Muscle Strain Syndrome Popliteal Artery Entrapment
Sensory deficits and present pain Syndrome
Weak adductors
Weak hip adduction, knee flexion
PROGNOSIS
8
 ● Neuropathy rarely leads to death if the cause is
determined and controlled. CLINICAL PRESENTATION
● The sooner the diagnosis is made and treatment Clinical Presentation (General):
is started, the greater the chance that nerve ● Pain
damage can be slowed or repaired. ● A tingling sensation
● Recovery, if it’s possible, usually takes a very ● Numbness
long time -- from months to even years. ● Skin that feels sensitive to the touch
● Some people live with a degree of neuropathy ● Weak or paralyzed muscles. This can cause
for the rest of their lives. drooling or slurred speech.
● Vision changes
CN
DEFINITION Clinical Presentation (Specific):
● Neuropathy is a disorder caused by nerve
Bell’s Palsy - Drooping of part of the face.
damage. It affects your ability to feel and move.
It usually affects only one
● The cranial nerves are those that arise directly
side of the face.
from your brain or brainstem. They often affect
areas like the face and eyes. When nerves in
Microvascular ● Double vision,
the brain or brainstem are affected, it is called
Cranial Nerve ● Droopy eyelid, and;
cranial neuropathy.
Palsy ● Other problems with
eyesight.
EPIDEMIOLOGY
● Cranial neuropathies occur in one-quarter of CN III Palsy - Eyelid will sag and droop,
patients with symptomatic neurosyphilis - Double vision,
● The frequency is highest (up to 50%) in acute - Trouble moving the eye, and;
syphilitic meningitis - Pupils that are bigger than
normal.
ETIOLOGY
CN IV Palsy - Eye or eyes turn abnormally.
● Infections. Infections in the spinal fluid can It sometimes makes them
irritate cranial nerves. For example, Lyme see double.
disease often affects the seventh nerve. But it - It may force them to tilt their
can cause problems with any cranial nerve. head when looking
● Cancer. Cancer cells can spread to the spinal
fluid and damage one or more cranial nerves. CN VI Palsy ● Cause abnormal movement
Sometimes cancer can press on cranial nerves of the eye and double vision.
as they run through the skull.
● Increased intracranial pressure from a tumor,
head trauma, or brain swelling. This can injure COMPLICATIONS
cranial nerves. Pressure can also be raised in ● Cranial nerve disorders can affect smell, taste,
certain headaches. Cranial nerves 3, 4, and 6 vision, sensation in the face, facial expression,
are most often affected. hearing, balance, speech, swallowing, and
● Congenital cranial neuropathies. These are muscles of the neck.
nerve injuries from trauma that occurs at birth.
Or they can occur before birth from MEDICAL DIAGNOSIS
developmental problems or infection. ● “See UE Neuropathies for Medical Diagnosis”
● Microvascular cranial nerve palsy. This can ● Nervous system exam to test sensation,
develop in people who have high blood pressure reflexes, balance, and mental status
or other vascular risks, such as diabetes or ● Blood tests to look for infections or health
smoking. Poor circulation to the cranial nerves conditions such as diabetes
injures them. It most often affects cranial nerves ● Electromyography (EMG), which measures the
3, 4, and 6. electrical activity of muscles when working and
● Autoimmune abnormalities. These occur at rest
when the immune system attacks one's own ● CT or MRI scans, which are imaging tests that
cranial nerves. This can happen in allow healthcare providers to see the brain
Guillain-Barré syndrome or lupus. ● Nerve conduction velocity tests to help find
● Aneurysm. This can press on nearby nerves. It out how and where the nerve is damaged
most often affects cranial nerves, 3, 4, and 6. ● Biopsies of the skin and nerves to find out
how severely nerves are damaged
● Inflammatory diseases. These include
● Hearing tests
sarcoidosis and multiple sclerosis.
● Spinal tap (lumbar puncture) to look for
RISK FACTORS infection or inflammation in the spinal fluid
● Patients with: ● Angiography, which is a special X-ray that uses
○ Poorly controlled diabetes contrast dye and takes pictures of your heart
○ High Blood Pressure and blood vessels
○ Head Injuries
○ Infections DIFFERENTIAL DIAGNOSIS
○ Strokes ● Bell’s Palsy
○ Brain Tumors ● Microvascular Cranial Nerve Palsy
PATHOMECHANICS / PATHOPHYSIOLOGY ● CN III Palsy
● See UE PNI Pathomechanics/ Pathophysiology ● CN IV Palsy
● CN VI Palsy
9
 (<50%) activation
PROGNOSIS and
● Cranial neuropathies are often not dangerous. lymphocytic
They may get better on their own with time. But infiltration;
they can certainly be bothersome for the people variable
who have them. secondary
● The best strategy for managing a cranial axonal
neuropathy is to manage possible causes. damage
These include diabetes, high blood pressure,
Acute Motor Children Axonal 1st attack on
infections, and brain tumors; one should also Axonal and young motor nodes
prevent head injury. Neuropathy adults; of ranvier,
(AMAN) prevalent in few
GUILLAIN-BARRE SYNDROME China and lymphocytes
DEFINITION Mexico; , frequent
● Progressive, symmetrical weakness of the limbs, may be periaxonal
with hyporeflexia or areflexia, with or without seasonal; macrophage
recovery s; extent of
sensory abnormalities
rapid; axonal
● Maximal Weakness occurs within 4 weeks, anti-GD1a damage
although typically peaks by 2 weeks antibodies highly
● Now recognized to a group of disorders variable

EPIDEMIOLOGY Acute Motor Mostly Axonal Same as

- Most common cause of neuromuscular paralysis Sensory adults; AMAN, but
in the Western World with an annual incidence Axonal uncommon; also affects
of 1 to 2 per 100,000 Neuropathy recovery sensory
(AMSAN) slow; often nerves and
incomplete; roots; axonal
ETIOLOGY closely damage
● Several things are known to trigger GBS. About related to usually
two-thirds of people with GBS had diarrhea or a AMAN severe
respiratory illness several weeks before
developing symptoms. Miller Fisher Adults and Axonal or Few cases
● Infection with Campylobacter jejuni, which Syndrome children; demyelinatin examined;
causes diarrhea, is one of the most common risk (MFS) ophthalmop g resembles
legia, AIDP
factors for GBS.
ataxia and
● People also can develop GBS after some other areflexia
infections, such as flu, cytomegalovirus, Epstein with
Barr virus, and Zika virus. Very rarely, people anti-GQ1b
have developed GBS in the days or weeks after antibodies
receiving certain vaccines. (90%)
.
About 1 in every 1,000 reported Campylobacter illnesses
CLINICAL PRESENTATION
leads to GBS. As many as 40% of GBS cases in the
United States are thought to be triggered by ● Presents with progressive onset of limb
Campylobacter infection. weakness both proximally weakness both
proximally and distally that is typically
symmetrical with strength nadir in 2 to 4 weeks
RISK FACTORS
● Sensory loss is variable
- Anyone can develop GBS; however, in the ● Cranial Nerves can be affected with facial palsy
United States, it is more common in men and and bulbar weakness
adults older than 50. ● Muscle of respiration are frequently affected with
decline of vital capacity and ventilatory support
PATHOMECHANICS / PATHOPHYSIOLOGY is required in 25% of cases
● Antecedent infection with 3 weeks of onset of ● Autonomic System can be affected causing
weakness tachycardia, hypertension, and cardiac
● Most commonly defined infectious agent is arrhythmias
Campylobacter jejuni ● Pain can be a significant complaint; might
● Other causative agents are cytomegalovirus precede onset of clinical weakness
(CMV) ○ Acute Stages: Deep and Aching
affecting back, buttocks, and posterior
CLASSIFICATION thigh
● Later Neuropathic pain can be described with
SUBTYPES FEATURES ELECTRODI PATHOLOG degeneration and regeneration of sensory
AGNOSIS Y nerves
● Fatigue
Acute Adults> Demyelinatin 1st attack on
Inflammatory children in g Schwann COMPLICATIONS
Demyelinatin western; cell surface; ● Severe GBS may lead to paralysis
g recovery widespread ● Respiratory Impairment and Failure
Polyneuropa rapid; anti myelin
● Autonomic instability: tachycardia, arrhythmias,
thy (AIDP) GM1 damage;
antibodies macrophage BP fluctuations
● Pain: Myalgia
10
 ● Risk of Pneumonia
● Prolonged Hospitalizations and immobility: DVT,
skin breakdown, contracture
● Relapse if tx is inadequate
MEDICAL DIAGNOSIS
● “See UE Neuropathies for Medical Diagnosis”
● Required Clinical features for the diagnosis is
Progressive Weakness in both arms and legs,
and areflexia
● Lumbar puncture is routinely performed in the
workup of patients presenting with rapidly
progressive weakness
● Characteristic Finding: Elevated CSF Protein
with normal WBC count
● Electrodiagnostic Testing is the most useful
confirmatory test for GBS
DIFFERENTIAL DIAGNOSIS
Polyneuropathy - Develops slowly
- Bilaterally and
symmetrically
1st s/sx:
● Sensory impairment in
distal LE, pain is present
and diminished DTRs
● Motor weakness d/t
underlying metabolic
conditions
PROGNOSIS
● Prognosis is good, little to no residual deficits,
10-23% would recover with assisted ventilation
and 7% - 22% will have residual deficits, 1% or
more will have an abscess during the first 6
months from onset
● The primary methods of managing GBS have
helped to improve mortality rates, which can
exceed 5%. Factors that predict a poor outcome
include onset at an older age, a protracted time
before recovery begins, and the need for
artificial respiration. An important objective
evaluation finding that predicts a poor outcome
is significantly reduced evoked motor potential
amplitude, which correlates with the presence of
axonal degeneration.
if anyone in the immediate family has the
disease.
● Other causes of neuropathies, such as diabetes,
may cause symptoms similar to
Charcot-Marie-Tooth disease.
● These other conditions can also cause the
symptoms of Charcot-Marie-Tooth disease to
become worse.
● Medications such as the chemotherapy drugs
vincristine (Marqibo), paclitaxel (Abraxane) and
others can make symptoms worse.
PATHOMECHANICS / PATHOPHYSIOLOGY
The peripheral nerves are a network of nerves that run
from the brain and spinal cord (the central nervous
system).
They carry impulses to and from the rest of the body,
such as the limbs and organs, and are responsible for
the body's senses and movements.
A peripheral nerve is similar to an electrical cable, and is
made up of 2 parts:
● The axon – which transmits electrical
information between your brain and limbs,
similar to the wiring in an electrical cable
● The myelin sheath – which is wrapped around
the axon to protect it and ensure the electrical
signal is not broken, similar to the insulation
around electrical cable
In some types of CMT, faulty genes cause the myelin
sheath to break down.
Without protection, the axons become damaged, which
affects the transmission of messages between the brain
and the muscles and senses. This leads to muscle
weakness and numbness.
In other types of CMT, the axons are directly affected
and do not transmit electrical signals at the normal
strength.
CLASSIFICATION
HSMN type - Autosomal dominant
1 - Affects the child
HSMN type ● Axonal type
2 ● Autosomal dominant
● LATE onset affects more than 30
y/o; adult

CHARCOT-MARIE TOOTH DISEASE (CMTD) HSMN type - Either autosomal dominant or

3 recessive that affects the myelin
DEFINITION sheath and is the MOST SEVERE
● Also known as “hereditary sensory motor TYPE
neuropathy” - Early onset
● Segmental demyelination affecting PNS
● Has glove and stocking paresthesia HSMN type ● REFSUM DISEASE
4 ● Autosomal recessive; over
EPIDEMIOLOGY accumulation of phytanic acid,
plasma and tissue
● Affects individuals in the 1st - 2nd decades of life
● Males > Females HSMN type - FRIEDREICH ATAXIA
5 - Spinocerebellar tract, corticospinal
ETIOLOGY tract, DML affectation
● Charcot-Marie-Tooth disease (CMT) is caused - Spastic paresis
by mutations (faults) in genes that cause the
peripheral nerves to become damaged. HSMN type ● Optic neuropathy
6 ● Autosomal dominant
RISK FACTORS
HSMN type ● RETINITIS PIGMENTOSA
● Charcot-Marie-Tooth disease is hereditary, so 7 ● Peroneal muscular atrophy and
one is at a higher risk of developing the disorder
11
 retinitis pigmentosa Nerve biopsy CMT1 A: diffuse Onion bulbs (but
well-formed may be absent)
onion-bulb Focality of
CLINICAL PRESENTATION
formation abnormalities
Triad of Symptoms:
Inflammatory
- Sensory loss
infiltrates
- Ataxia
Edema
- Motor loss

● Affects large myelinated fibers PROGNOSIS

● Most common foot deformity: Pes Cavus ● A small percentage of people experience severe
weakness or other problems which, in very rare
COMPLICATIONS cases, can be life-threatening. In most affected
● CMT is not a fatal disease. Most people with it individuals, however, Charcot-Marie-Tooth
live to a normal age and remain active. In rare disease does not affect life expectancy.
cases, it may affect the muscles you need to ● CMT is a slowly progressive disorder that is
breathe. Because this can be especially currently considered incurable. However, the
dangerous at night, you may need a nighttime CMT Association has launched a research
breathing assistive device. initiative called the Strategy to Accelerate
● More common complications are: Research (STAR) to look for more effective
○ Injuries from falls therapies and possibly a cure for the most
○ Worsening of the disease that certain common forms of CMT.
medicines can cause ● If unmanaged, contracture formation resulting
○ Injuries or infections of the feet that go from weakness will create further gait
unnoticed because of lack of pain and abnormalities, with clients reporting an
temperature sensation increased number of falls.
● In the upper extremities, clients may develop
MEDICAL DIAGNOSIS problems with writing and handling objects.
● “See UE Neuropathies for Medical Diagnosis” Individuals with CMT should be cautioned that
some medications have been reported to cause
DIFFERENTIAL DIAGNOSIS an exacerbation of CMT.
● A database of the drugs that should be avoided
is maintained by the CMT Association. Among
CMT CIDP the identified medications are several anticancer
drugs, including vincristine, cisplatin,carboplatin,
Family Often positive Negative and taxoids
History (need to evaluate
at-risk family DIABETIC NEUROPATHIES
members)
DEFINITION
Age at onset Early Any age ● Most common causes of neuropathy
● Complication of DM
Disease Slowly Progressive or ● Causes significant morbidity and mortality in
Course progressive relapsing diabetic patients and leads to more
(rarely sudden hospitalizations for diabetic patients than any
worsening) other complication
● Diabetic Neuropathy can affect motor, sensory,
Skeletal Present in all Rarely present cranial, and autonomic nerves in the nerve root.
deformities cases (early onset) plexus, or peripheral nerve.
Muscle group Distal > Proximal Distal and
EPIDEMIOLOGY
involvement proximal
● The prevalence of DN is greater (54%) in type 1
Nerve Diffuse and Non-homogene diabetes (insulin-dependent diabetes mellitus)
conduction homogeneous ous conduction than the prevalence of DN in type 2 diabetes
abnormalities slowing, no slowing: (noninsulin-dependent diabetes mellitus), which
conduction block asymmetries, is 30%.
conduction ● The most reliable estimates from clinical studies
blocks, report that DN, although present in individuals
excessive with diabetes lasting longer than 25 years, is
temporal present in 7% of people within 1 year of
dispersion diagnosis with diabetes

CSF Proteins Normal or Increased to a ETIOLOGY

moderately variable extent, ● DN is likely caused by the chronic metabolic
elevated (usually sometimes disturbances that affect nerve cells and
less than normal Schwann cells in diabetes. For years,
100mg/dl) hyperglycemia was considered the sole cause of
Oligoclonal these secondary complications of diabetes.
bands may be ● Although consequences of hyperglycemia
formed include elevated levels of sorbitol and fructose,
which coincides with deficiencies of
12
 sodium-potassium and adenosine triphosphate CLINICAL PRESENTATION
that alter the function of peripheral nerves, ● Weakness and sensory disturbance of the distal
chronic hyperglycemia leads to abnormalities in extremities in asymmetrical pattern,
microcirculation, creating endothelia capillary ● Wasting muscles of feet and hands,
changes and local ischemia that affect the ● Glove and stocking distribution of sensory
nerve. impairments,
● OH,
RISK FACTORS ● Weakness
● Although hyperglycemia is not directly attributed ● Urinary impairments and significant pain
to damaging nerve fibers causing DN, it is a
contributing factor. Conversely, some people COMPLICATIONS
develop neuropathies even when glycemic ● Foot Ulceration is a major complication in
control is good. A clear relationship does exist patients with PN, especially with DM. There is
between duration of diabetes and development an increased risk of foot ulcer and a greater risk
of DN. After the onset of the neuropathy, control for amputation
of hyperglycemia is known to enhance the ● Autonomic Dysfunction in patients with
possibility of regeneration of fibers. autonomic neuropathy
○ GI system
PATHOMECHANICS / PATHOPHYSIOLOGY ○ Cardiovascular changes
● In diabetic Neuropathy, there is endoneurial and ○ Thermoregulation abnormalities
epineural lymphocyte infiltration that disrupts ○ Erectile Dysfunction
signal conduction, the microvascular ischemia
affecting the peripheral nerve is due to impaired MEDICAL DIAGNOSIS
endogenous fibrinolysis ◊ “See UE Neuropathies for Medical Diagnosis”
● The vascular changes are mediated by the
polyol pathway-- sorbitol and aldose reluctance DIFFERENTIAL DIAGNOSIS
deposit glucose in the tissue that are insulin
independent.
● Accumulation of sobritol produces osmotic Alcohol Abuse Inherited Neuropathy
stress on the cell membrane while at the same
time decreasing nitric oxide and vasodilation Neurotoxic Medications Chronic Inflammatory
● The net result is microvascular disease due to Demyelinating
vasoconstriction, thickening o the capillary Neuropathy
basement membrane, endothelial hyperplasia
and a resulting decrease in oxygen tension and Renal Disease and Spinal Cord Tumors
hypoxia Related Uremic
Neuropathy
CLASSIFICATION
Vitamin B12 Deficiency Vasculitis

Distal Symmetrical The most common type

Sensorimotor of Diabetic Neuropathy
Polyneuropathy and affects at least half of
those with long standing
diabetes
Proximal Neuropathy aka Diabetic Amyotrophy
typically seen in older
patients with type 2
diabetes. It classically
presents acutely or
subacutely with severe
pain that is unilateral or
bilateral
Focal Mononeuropathies Occur in older individuals
with diabete and are
usually acute in onset
and associated with pain.
CN III, VI, VII are most
commonly affected
Autonomic Neuropathy significant cause of
morbidity and even
mortality in persons with
diabetes. this can affect
the cardiovascular,
gastrointestinal,
genitourinary, and
thermoregulatory systems
PROGNOSIS
● DN is a slowly progressive metabolic disorder
that affects many body systems. Estimates are
that more than 50% of nontraumatic
amputations in the United States occur in people
with diabetes. The presence of autonomic
involvement is associated with an increased
mortality risk.
TOXIC NEUROPATHIES
DEFINITION
● Results from exposure to a variety of organic
and inorganic toxins, medications, and heavy
metals.
● They are resolved with appropriate treatment.
● Commonly prescribed therapeutic drugs.
environmental pollutants, industrial solvents, and
other workplace chemicals can be neurotoxic.
● Peripheral Neuropathy is one of the most
common responses of the peripheral nerve to
chemical attack.
EPIDEMIOLOGY
● Most toxic exposures (including heavy metals,
organophosphates, and biologics) are small
scale, or from suicidal or homicidal incidents.
● A large proportion of neuropathies have an
unknown etiology, and 24% of all peripheral
neuropathies are attributed to drugs or toxins.

13

ETIOLOGY
● According to the WHO, 5.1 % of the global
burden of disease and injury is attributable to
alcohol.
● Some herbal medicine products commercially
available have been shown to contain heavy
metals such as lead, mercury, and arsenic.
● Using these herbal products may lead to heavy
metal toxicity and secondary peripheral
neuropathy.
RISK FACTORS
◊ Toxic Exposure through occupations; household
products
◊ Therapeutic drugs that can cause neuropathies.
PATHOMECHANICS / PATHOPHYSIOLOGY
● Most toxins produce distal axonal degeneration
in the longer peripheral nerve
● Several toxic agents damage the neuron directly
or induce primary demyelination
● Nucleoside reverse transcriptase inhibitors
deplete peripheral nerve mitochondrial DNA,
and DNA polymerase activity.
● Typically Present with a glove and stocking
distribution of sensory loss followed by
weakness in the same distribution.
● Presentation may be protracted and insidious as
is common with nutritional or endocrine
etiologies
● Can also cause pain
● Gastrointestinal Complaints
● Mees Lines in the fingernails
COMPLICATIONS
● Can range from subtle to severe and
life-threatening
● Can lead to sensory, motor loss
● Affected brain functioning
● Paralysis
MEDICAL DIAGNOSIS
● See UE PNI Medical Diagnosis
● Standard workup of peripheral neuropathies
include hemoglobin A1C, fasting glucose, TSH,
BUN, creatinine, vitamin B1, vitamin B6, and
vitamin B12. Heavy metal screening should be
performed if a toxin is suspected. However, this
is usually not helpful unless obtained
immediately after an exposure.

DIFFERENTIAL DIAGNOSIS
CLASSIFICATION ● Acute Inflammatory Demyelinating
Polyradiculoneuropathy
● Amyotrophic Lateral Sclerosis
Drugs ● Chemotherapeutic agents – ● Chronic Inflammatory Demyelinating
Associated cisplatin, oxaliplatin, Polyradiculoneuropathy
with Peripheral taxanes, vinca alkaloids, ● Diabetic Neuropathy
Neuropathies bortezomib, suramin, ● Myasthenia Gravis
misonidazole ● Lambert-Eaton Myasthenic Syndrome (LEMS)
● TNF-alpha inhibitors ● Leprosy Neuropathy
(einfliximab, etanercept) ● Metabolic Neuropathy
● Antiretroviral agents ● Nutritional Neuropathy
(zalcitabine, didanosine, ● Paraneoplastic Autonomic Neuropathy
stavudine) ● Uremic Neuropathy
● Cardiac medications ● Vitamin B-12 Associated Neurological Diseases
(amiodarone, perhexiline,
statins) PROGNOSIS
● Thalidomide
● Recovery is based on removal from the toxin
● Antibiotics (metronidazole,
and the degree of involvement. If only segmental
dapsone, podophyllin
demyelination occurs, recovery will occur in
fluoroquinolones, isoniazid,
weeks to months, but if axonal degeneration is
nitrofurantoin)
present, recovery will take months to years.
● Disulfiram
● Pyridoxine excess
LEPROSY
● Colchicine
● Phenytoin, Lithium
DEFINITION
● Chloroquine,
hydroxychloroquine ● Known as Paucibacillary (PB) or tuberculoid,
Hansen’s disease Multibacillary (MB) or
Organic - Aliphatic, aromatic, cyclic, lepromatous, Hansen’s Disease Borderline or
Solvents and halogenated dimorphous, Hansen’s disease
hydrocarbons; alcohols, ● Chronic infectious disease caused by
ethers, esters, ketones, and Mycobacterium leprae
glycols ● Mainly affects the skin, peripheral nerves,
mucous surface of upper respiratory tract and
Heavy Metals ● Arsenic, thallium, lead, eyes
mercury, gold via EPIDEMIOLOGY
environmental exposure ● All ages are affected (from early infancy to old
(e.g. occupation, living age)
conditions, or consumption)
ETIOLOGY
Alcohol ● Infection caused by slow-growing bacteria called
Mycobacterium leprae. These bacteria grow
very slowly and it may take up to 20 years to
CLINICAL PRESENTATION develop signs of the infection.

14

RISK FACTORS
● Children are more susceptible to Hansen’s
disease than adults.
● Also, people in close contact with infected
individuals for long periods of time are at an
increased risk of becoming infected.
PATHOMECHANICS / PATHOPHYSIOLOGY
● The entry route of M. leprae into the human
body is also not definitively known. The skin and
the upper respiratory tract are most likely;
however, recent research increasingly favours
the respiratory route
● Two exit routes of M. leprae from the human
body often described are the skin and the nasal
mucosa. Lepromatous cases show large
numbers of organisms deep in the dermis, but
whether they reach the skin surface in sufficient
numbers is doubtful
CLASSIFICATION
Tuberculoid Have limited disease and relatively
few bacteria in the skin and nerves
Characterized by a few flat or slightly
raised skin lesions of various sizes
that are typically pale or slightly red,
dry, hairless, and numb to touch
(anesthetic)
Lepromatous Have widespread disease and large
numbers of bacteria
Characterized by a much more
generalized disease, diffuse
involvement of the skin, thickening of
many peripheral nerves, and at times
involvement of other organs, such as
eyes, nose, testicles, and bone
CLINICAL PRESENTATION
● Discolored patches of skin that is flat and looks
faded
● Growth and nodules of the skin, dry skin
● Painless ulcers of feet
● Painless swelling/lumps of the face or earlobes
● Loss of eyebrows and eyelashes (by the nerve
damage)
● Numbness of the affected area of the skin
● Weakness or paralysis in the hands and feet
● Enlarged nerves especially around elbows and
knees and neck
● Eye problems (by disease in the mucous
membrane)
● Stuffy nose
● Nosebleed
COMPLICATIONS
● Eye involvement and deformities of the face,
hands, and feet.
○ Deformities of the face can result from
destruction of the partition in the nose
that divides the nostrils (nasal septum)
and other facial tissues.
● In advanced disease, persons with lepromatous
leprosy may lose their eyebrows and eyelashes,
and the eyelids may become paralyzed so that
individuals cannot blink or close their eyes
properly.
● The earlobes may enlarge or become wrinkled.
● Deformities of the hands and feet may result
from muscle paralysis and repeated trauma that
is not felt due to sensory loss.
MEDICAL DIAGNOSIS
● Hansen’s disease can be recognized by the
appearance of patches of skin that may look
lighter or darker than the normal skin.
● Sometimes the affected skin areas may be
reddish.
● Loss of feeling in these skin patches is common.
● May not feel a light touch or a prick with a
needle.
● To confirm the diagnosis, the doctor will take a
sample of skin or nerve (through a skin or nerve
biopsy) to look for the bacteria under the
microscope and may also do tests to rule out
other skin diseases.
DIFFERENTIAL DIAGNOSIS
● Tuberculosis (lupus vulgaris, tuberculosis
verrucosa cutis, erythema induratum of Bazin),
● “Lepromatoid” atypical mycobacterial infection
(e.g., mycobacterium chelonae),
● Leishmaniasis skin infections (lupoid, recidive,
disseminatum, mucocutaneous, diffuse
cutaneous anergic and postkalazar),
● Syphilis (secondary, late secondary, and
tertiary),
● Chromoblastomycosis,
● South American blastomycosis,
● African histoplasmosis, and blastomycosis
keloidalis (Lobo’s disease).
PROGNOSIS
● Untreated, leprosy can cause progressive and
permanent damage to the skin, nerves, limbs,
and eyes.
● Untreated, it can cause paralysis, crippling of
hands and feet, shortening of toes and fingers,
chronic non healing ulcers at the bottom of the
feet, blindness, nose disfigurements
CRPS
DEFINITION
● Complex regional pain syndrome (CRPS) is a
broad term describing excessive and prolonged
pain and inflammation that follows an injury to
an arm or leg. CRPS has acute (recent,
short-term) and chronic (lasting greater than six
months) forms. CRPS used to be known as
reflex sympathetic dystrophy (RSD) and
causalgia.
● Previously known as reflex sympathetic
dystrophy or RSD
EPIDEMIOLOGY
● Affects approximately 26 out of every 100,000
people
● F>M
● Affects people of all ages, including children as
young as three years old, and adults as old as
75 years, most prevalent in mid-thirties
ETIOLOGY
15
 ● Complex regional pain syndrome can develop
Dystonia
after different types of injuries, such as
o UMN lesions
Burning and Ongoing
o CVA
Spontaneous Pain Neuropathic Pain
o Sprains and strains
Disproportionate in the Spontaneous
o Surgeries
intensity to the inciting Triggered by movement,
o Fractures
event loud noises, or strong
o Contusions
emotions
o Crush injuries
Deep, unpleasant,
o Nerve lesions
sensitive, dull
o Stroke

RISK FACTORS
● Stressful life CLINICAL PRESENTATION
● Psychological Factors impact the severity of
symptoms in CRPS
Stage Signs and Symptoms
● Genetic Predisposition
Stage I: Acute Begins 10 days post injury;
PATHOMECHANICS / PATHOPHYSIOLOGY
inflammation: lasts 3-6 months
● CRPS is now regarded as a systemic condition Denervation and
that involves both central and peripheral sympathetic Pain: more severe than
components of the neuraxis and interactions hypoactivity expected, burning, aching.
between the immune and nervous systems. No Increased with position,
one knows for sure what causes the cascade of physical condition, or
neurogenic responses that leads to CRPS. emotional disturbances
◊ Laboratory studies of blood and tissue samples
appear normal; although there is some evidence Hyperalgesia, Allodynia,
of elevated systemic levels of inflammatory increased sensitivity
markers and catecholamines (mediators in
sympathetic hyperactivity) Edema: soft and localized
◊ An injury at one somatic level initiates Vasomotor / Thermal
sympathetic efferent activity that affects many Changes: warmer
segmental levels. CRPS is thought to represent Skin: Hyperthermia, dryness
a reflex neurogenic inflammation. Other: increased hair and
◊ Facilitation of the sympathetic nervous system nail growth
(SNS) and its neurotransmitters and
catecholamines activates primary afferent Stage II: Dystrophic: Occurs 3-6 Months after
nociceptors to create the sensation of pain. Paradoxic onset of pain, lasts about 6
◊ Deterioration of the SNS function is common. Sympathetic months
Excess release of substance P from terminal Hyperactivity Pain: worsens, constant
sensory nerves is part of the overreaction of the burning and aching
neurogenic inflammatory process. Allodynia, Hyperalgesia,
◊ Thermal dysfunctions are related to either the hyperpathia almost always
inhibition of SNS vasoconstriction or facilitation present
of the SNS causing excessive vasoconstriction. Edema: becomes thicker
Clinical studies have shown abnormal SNS and more fibrotic causing
reflexes that indicate CNS dysfunction exists as joint stiffness
well Vasomotor/ Thermal
changes: Neither warm, nor
CLASSIFICATION cold
Skin: thin, glossy, cool, and
Type I Type II sweaty, ridged nails
Other: x-rays reveal disuse
Formerly “reflex Formerly “Causalgia” osteoporosis, cystic and
Sympathetic Dystrophy Occurs after injury to a subchondral bone erosion
(RSD)” major peripheral nerve
Occurs after trauma
remote from the affected Stage III: Atrophic Begins about 6-12 months
extremity, with or without after onset; may last for
minor nerve damage years or may resolve and
reoccur
Allodynia and Hypersensitivity of the Pain: spreads proximally,
hyperalgesia skin to light mechanical occasionally to entire skin
stimulation surface or plateaus; joint
stiffness progresses
Weakness of all muscles, Inability to initiate Edema: continues to harden
inability to move the movement of the Vasomotor/ Thermal
extremity. Stiffness, extremity changes: sympathetic
tremor Stiffness nervous system regulation is
Tremor decreased on affected

16

extremity, affected limb is
cooler
Skin: thin, shiny, cyanotic,
and dry. Fingertips and toes
on involved extremity are
atrophic, Fascia is thickened;
contractures may occur.
COMPLICATIONS
● Sensory Impairments
● Motor Symptoms
● Abnormal Vasomotor Patterns
● Hypersensitivity and abnormal Sweating
● Nail Bed Changes
MEDICAL DIAGNOSIS
● In the absence of a specific biomarker, the
diagnosis of CRPS is based primarily on the
clinical examination and history. Proposed
diagnostic criteria for CRPS requires at least
one symptom in each of the four subgroups, and
one sign in at least two of the four subgroups. A
combination of diagnostic tests aimed at
assessing secondary changes (radiographic
examinations, thermographic studies, sudomotor
function tests, NCV or somatosensory evoked
potentials, and laser Doppler flowmetry) may aid
in establishing a diagnosis. Because of the
evolutionary nature of CRPS, a correct
diagnosis may be delayed, especially in
children.
DIFFERENTIAL DIAGNOSIS
Neuropathic - Peripheral polyneuropathy
Pain Syndromes - Nerve entrapment
- Radiculopathy
- Post-herpetic neuralgia
- Deafferentation pain
post-CVA
- Plexopathy
- MND
Vascular ● Thrombosis
Disease ● Acrocyanosis
● Atherosclerosis
● Raynaud’s Phenomenon
● Erythromelalgia
Inflammation - Erysipelas
- Inflammation-not
otherwise specified
- Bursitis
- Seronegative arthritis
- Rheumatologic diseases
Myofascial Pain ● Overuse
Syndrome ● Disuse
● Tennis elbow
● Repetitive strain injury
● Fibromyalgia
Psychiatric - Somatoform pain
Problems disorders
- Munchhausen syndrome
PROGNOSIS
● In many cases, the pain continues for years or,
less frequently, it may remit, then recur after
another injury. Spontaneous remission is
unusual; only modest improvements have been
reported with most current therapies
● In some cases, malingering for secondary gain
has been documented. Outcome measures for
CRPS I typically concentrate on impairments,
leaving measurement of disability, which is the
most relevant to function, with few assessments
● Physical therapy is indicated, particularly as part
of a program of pain control. Although the goal is
to maintain function so that the individual can
perform normal activities, a vigorous approach is
not indicated.
● Current research is aimed at understanding
physiologic processes and finding the most
effective interventions.
GENERAL HEALTHCARE MANAGEMENT
MEDICAL MANAGEMENT
Braces or splints. These devices keep the affected
limb, fingers, hand or foot in the proper position to
improve muscle function.
Electrical stimulator. Stimulators can activate muscle
served by an injured nerve while the nerve regrows.
However, this treatment may not be effective for
everyone.
Physical therapy. Therapy involves specific movements
or exercises to keep your affected muscles and joints
active. Physical therapy can prevent stiffness and help
restore function and feeling.
Exercise. Exercise can help improve muscle strength,
maintain range of motion and reduce muscle cramps.
SURGICAL MANAGEMENT
Carpal Tunnel - Surgical release of the
Syndrome transverse carpal ligament
is indicated when symptoms
have lasted longer than 1
year and there is both motor
and sensory NCV
involvement, or denervation
is evidenced by fibrillation
potentials on EMG.
- Flexor tenosynovectomy
with transverse carpal
ligament division
- Endoscopic release of the
ligament,
- Neurolysis of the median
nerve is performed through
limited incisions and requires
minimal exposure and
manipulation of the nerve.
Thoracic Procedures:
Outlet ● Scalenotomy
Syndrome ● Scalenectomy
● Clavicle resection
● Pectoralis minor release
● First rib resection
● Cervical rib resection
Approaches:
17
 ● Axillary
● Supraclavicular
● Combined axillary and
supraclavicular
● Posterior
● Subclavicular
● Transclavicular
Surgical Decompression - is performed to relieve the
compression on the affected nerve
Peripheral Nerve Graft - To repair a damaged nerve,
surgeon removes a small part of the sural nerve in leg
and implants this nerve at the site of the repair.
Sometimes surgeons can borrow another working nerve
to make an injured nerve work (nerve transfer).
PHARMACOLOGICAL MANAGEMENT
Medications Associated with Peripheral Neuropathy
Opioid Analgesics
Anticonvulsants
Nerve Blocks
OTHER HEALTHCARE MANAGEMENT
Neurologists/ Doctors trained in
Neurosurgeons diagnosing and treating
peripheral nerve injuries
Orthopedic Surgeons Responsible for repairing
damaged bones,
muscles, and ligaments
Rehabilitation Specialists Responsible for restoring
(PT, OT) function after injury
Anesthesiologists Responsible for
alleviating pain during
surgery
Prosthetist/ Orthotist Responsible for the
prescription of orthosis/
prosthesis after
amputation (if needed)
PHYSICAL THERAPY, EXAMINATION, EVALUATION,
AND DIAGNOSIS
POINTS OF EMPHASIS ON EXAMINATION
Identify the mechanism of Trauma,
injury Entrapment,Compression
, Traction, Dislocation,
Fracture
Onset of symptoms Early, Middle, or Late
Pt’s lifestyle Active or Sedentary
Sensation Decreased or Absent on
one or both sides
Neurological Assessment Decreased or Absent on
one or both sides
Pathological Reflexes (+) indicating UMNL or
LMNL
ROM Decreased ROM in
affected limb
MMT Decreased muscle
strength on affected limb
MBT Significant difference in
MBT as to quadriceps
and gastrocnemius
muscles
LLD
Postural Assessment Watch out for
compensatory strategies
Balance & Tolerance Decreased balance and
tolerance
Gait Impaired gait
Functional Assessment Impaired as to self-care
and mobility
Special Tests
PT PROBLEM LIST
1. Pain
2. Decreased sensation
3. Muscle weakness
4. Decreased ROM
5. Abnormal posture
6. Gait deviation
7. Decreased prehension
8. Poor balance and tolerance
9. Decreased endurance
10. Impaired ADLs
PT DIAGNOSIS
● Neuromuscular Pattern 5F: Impaired Peripheral
Nerve Integrity and Muscle Performance
Associated Peripheral Nerve Injury
● Neuromuscular Pattern 5G: Impaired Motor
Function and Sensory Integrity Associated with
Acute or Chronic Polyneuropathies
PT PROGNOSIS
● For Axonotmesis, muscle fiber innervated by
the axon would depend on the nerve cell body
as a source of nourishment or trophic control
○ When axons would degenerate, the
muscle fibers would rapidly atrophy, so
new accents can erupt from the
proximal end of the damaged axons
● For Neurotmesis, recovery is less likely without
surgical intervention because the proximal end
of the endoneurium is not approximated to the
distal endoneurium
● Even with surgical interventions, prognosis for
recovery is poor in Neurotmesis cases
● Once the axon has a distal contact either with a
muscle or sensory receptor, remyelination would
begin
● Functional recovery after complete injury is
much better in children than in adults
● Recovery of larger, more heavily myelinated
fibers is poorer than smaller ones
18
 ● There’s also poor prognosis in those with
unsuccessful surgical intervention, those with
the presence of infection, inadequate
physiotherapy or PT care, as well as with nerves
that have been completely severed.
● In diabetic polyneuropathy, there is a high risk
for recurrence.
PHYSICAL THERAPY PLAN OF CARE
a. UE
b. LE
c. CN
d. GBS
e. CMTD
f. Diabetic Neuropathies
g. Toxic Neuropathies
h. Leprosy
i. CRPS
PT LONG AND SHORT TERM GOALS
STG:
● Reduce pain
○ Pt will present a decrease of pain from
_/10 to _/10 in VAPS to be able to do
functional activities s any restrictions
● Improve Sensation
○ Pt will demonstrate an improvement in
sensation to be able to identify cold, hot,
touch, vibrations and pain to prevent
from any further skin injuries.
● Promote Mobility
○ Pt will demonstrate an improvement in
mobility to improve transfer techniques
and to do functional activities
● Improve muscle strength
○ Pt will present an increase in muscle
strength in (specific muscles) from _/5 to
_/5 in MMT to promote muscle activation
and improve muscle performance to
prevent atrophy
● Increase ROM
○ Pt will demonstrate an improvement in
ROM on (specific joints) to prevent
contractures
● Promote pt education
○ Such as skin inspection
○ Promote independence in ADLs
○ Assess if pt needs an assistive or
orthotic device
○ Ensure pt education on the course of
the injury or status of the injury
● Improve muscular endurance
○ Pt will demonstrate an improvement in
muscular endurance to be able to do
improve muscle performance and
prevent atrophy
● Abnormal Posture
○ Pt will demonstrate a decrease in
postural deviation to improve posture
and prevent further injuries
● Gait deviation
○ Pt will demonstrate a decrease in gait
deviations to improve gait pattern and
ambulation on an even surface c an
assistive device
● Decreased Prehension
○ Pt will present an improvement in
prehension to improve performance in
ADLs
● Poor balance and tolerance
○ Pt will present an improvement in
balance and tolerance from a grade of _
to _ to improve stability to prevent risk of
falls
● Impaired ADLs
○ Pt will demonstrate an increase in
functional independence to improve
ADL performance
LTG
- Pt will present no pain in (specific area) c a
grade of 0/10 in VAPS and be able to do
functional activities s any restrictions 2 to pain
- Pt will gain normal sensation as to pain, touch,
cold, hot and vibration and decrease the risk of
having skin injuries
- Pt will be able regain mobility and able to
perform transfer techniques s any difficulty
- Pt will regain full muscular strength c a grade of
5/5 for better muscle performance and ADL
performance
- Pt will be able to regain full ROM both active and
passive in (specific joints) to maintain joint
mobility and structure and prevent contractures
- Pt will demonstrate a great improvement in
muscular endurance to delay the onset of
fatigue and for a better performance when doing
functional activities
- Pt will demonstrate a great improvement in
postures and able to do functional activities s
any limitations
- Pt will demonstrate an improvement in gait and
ambulate on an even and uneven surface s any
assistant device
- Pt will be able perform better prehension skills to
promote functional independence
- Pt will present an improvement in balance c a
grade of N for both static and dynamic, and in
tolerance c a grade of G to maintain equilibrium
s any assistance and prevent the risk of falls for
better ambulation
- Pt will be able to perform full independence
when doing ADLs
PT INTERVENTIONS
● HMP, TENS, IFC, Cold compress to decrease
pain
● Use of multiple types of textures or contact for
sensory stimulation (cotton, rough material,
sandpaper, velcro) and stroke around the pt.’s
skin or have the patient manipulate starting with
least irritating texture for 10 mins.; progress to a
more irritating but tolerable stimulus
● Nerve Gliding / Nerve Mobilization
● ES and PREs with graded elastic band
● Stretching exercises
● Splinting
● Postural training in front of mirror for intrinsic
feedback
● Stretching tight muscles and strengthening of
weak muscles
● Gait training on parallel bars, even and uneven
surfaces, ascending and descending stairs to
improve gait cycle and increase endurance
● Hand exercises using therapy putty in utilization
for hand and finger strengthening and resistance
to help develop a strong grip
● Static balance control (sitting, kneeling,
standing) on a firm surface with perturbations
19
 ● Progress activities by working on soft surfaces
(foam, grass, sand), narrowing BOS, moving
arms, or closing eyes
● Wobble board on bilat. LE to one-leg stance for
15 SH
● Ergobike and stationary bicycle for 30 mins.
progress to 45 mins. to increase
cardiopulmonary endurance
● ADL training program of regular exercise that
includes cardiopulmonary, resistance, flexibility,
and neuromotor exercise to improve and
maintain physical fitness
REFERENCES
Books:
Frontera, W. R., & DeLisa, J. A. (2010). DeLisa's
Physical medicine & rehabilitation: Principles and
practice. Philadelphia: Lippincott Williams & Wilkins
Health.
Braddom, R. L., Chan, L., & Harrast, M. A. (2011).
Physical medicine and rehabilitation. Philadelphia, PA:
Saunders/Elsevier.
Magee, David J. (2002). Orthopedic physical
assessment. Philadelphia :Saunders,
Dyck, P., Thomas, P.K. (2005). Peripheral Neuropathy.
Philadelphia, Pennsylvania: Saunders/Elsevier
Websites:
Centers for Disease Control and Prevention (nd).
Guillain-Barre Syndrome. Accessed April 26, 2021.
Retrieved from
https://www.cdc.gov/campylobacter/guillain-barre.html
National Health Service (nd). Charcot-Marie-Tooth
Disease. Accessed April 27, 2021. Retrieved from
https://www.nhs.uk/conditions/charcot-marie-tooth-disea
se/diagnosis/
NCH Healthcare System (nd). Charcot-Marie-Tooth
Disease. Accessed April 27, 2021. Retrieved from
https://www.nchmd.org/education/mayo-health-library/de
tails/CON-20155112
Centers for Disease Control and Prevention (nd).
Hansen’s Disease. Accessed April 27, 2021. Retrieved
from https://www.cdc.gov/leprosy/treatment/index.html
Iowa Department of Public Health (nd). Hansen’s
Disease. Accessed April 27, 2021. Retrieved from
https://idph.iowa.gov/cade/disease-information/hansens-
disease#:~:text=Risk%20Factors,increased%20risk%20
of%20becoming%20infected.
National Organization for Rare Disorders (nd). Leprosy.
Accessed April 27, 2021. Retrieved from
https://rarediseases.org/rare-diseases/leprosy/#:~:text=L
eprosy%20has%20traditionally%20been%20classified,a
nd%20large%20numbers%20of%20bacteria.
Bhat, R. M., & Prakash, C. (2012). Leprosy: an overview
of pathophysiology. Interdisciplinary perspectives on
infectious diseases, 2012, 181089.
https://doi.org/10.1155/2012/181089
Neal. S.L., Fields, K.B. (2010 Jan 15). Peripheral Nerve
Entrapment and Injury in the Upper Extremity. American
Family Physician.
https://www.aafp.org/afp/2010/0115/p147.html#comment
ing
Dahlin, L. B., & Wiberg, M. (2017). Nerve injuries of the
upper extremity and hand. EFORT open reviews, 2(5),
158–170. https://doi.org/10.1302/2058-5241.2.160071
Cedar Sinai (nd). Cranial Neuropathies. Accessed April
28, 2021. Retrieved from
https://www.cedars-sinai.org/health-library/diseases-and-
conditions/c/cranial-neuropathies.html#:~:text=The%20c
auses%20of%20cranial%20neuropathies,face%2C%20o
r%20changes%20in%20vision.
Cadavid, D. (2010). Handbook of Clinical Neurology.
Accessed April 28, 2021. Retrieved from
https://www.sciencedirect.com/topics/medicine-and-denti
stry/cranial-neuropathy
Thatte, M. R., Hiremath, A., Goklani, M. S., Patel, N. R.,
& Takwale, A. B. (2019). Peripheral Nerve Injury to the
Lower Limb: Repair and Secondary Reconstruction.
Indian journal of plastic surgery : official publication of
the Association of Plastic Surgeons of India, 52(1),
93–99. https://doi.org/10.1055/s-0039-1687921
Issack, P. S., & Helfet, D. L. (2009). Sciatic nerve injury
associated with acetabular fractures. HSS journal : the
musculoskeletal journal of Hospital for Special Surgery,
5(1), 12–18. https://doi.org/10.1007/s11420-008-9099-y
Pareyson, D. (2004). Differential diagnosis of
Charcot-Marie-Tooth disease and related neuropathies.
Neurological Sciences, 25, 72- 82.
Thatte, M. R., Hiremath, A., Goklani, M. S., Patel, N. R.,
& Takwale, A. B. (2019). Peripheral Nerve Injury to the
Lower Limb: Repair and Secondary Reconstruction.
Indian journal of plastic surgery : official publication of
the Association of Plastic Surgeons of India, 52(1),
93–99. https://doi.org/10.1055/s-0039-1687921
Barker, K.D.D., Vacek, C.J. (2015). Peripheral
Neuropathies Associated with Drugs and Toxins.
https://now.aapmr.org/peripheral-neuropathies-associate
d-with-drugs-and-toxins/
Krishna D Bharwani, MD, Maaike Dirckx, MD PhD,
Frank JPM Huygen, MD PhD FIPP FFPMCAI (hon),
Complex regional pain syndrome: diagnosis and
treatment, BJA Education, Volume 17, Issue 8, August
2017, Pages 262–268,
https://doi.org/10.1093/bjaed/mkx007
Rutchik, J.S. (2017 December 6). Toxic Neuropathy
Differential Diagnosis. Accessed May 1, 2021. Retrieved
from
https://emedicine.medscape.com/article/1175276-differe
ntial
20
PHARMACOLOGICAL MANAGEMENT SUMMARY

Medications Functions Side Effects PT Implications

Nerve Blocks Blocks transmissions of peripheral nerves to
allow certain surgical procedures of the hand,
foot, shoulder, and so forth.
Can be classified as minor when only one
distinct nerve is blocked or major when
several peripheral nerves are involved
Prolonged administration can produce use extra caution to protect the involved limb when the block
localized muscle pain and necrosis is in effect and should report any muscle pain or signs of
Pt’s ability to feel and move the affected area infection following the use of continuous peripheral nerve
will be decreased blocks

PT PLAN OF CARE SUMMARY

PROBLEM GOAL INTERVENTION

Pain ● Pt will present no pain in (specific area) c a grade of ● HMP
0/10 in VAPS and be able to do functional activities s ● TENS
any restrictions 2 to pain after x PTR sessions ● IFC
● Cold Compress

Decreased or Altered ● Pt will gain normal sensation as to pain, touch, cold, hot ● Use of multiple types of textures or contact for sensory stimulation (cotton, rough
Sensation and vibration and decrease the risk of having skin material, sandpaper, velcro) and stroke around the pt.’s skin or have the patient
injuries after x PTR sessions manipulate starting with least irritating texture for 10 mins.; progress to a more
irritating but tolerable stimulus
● Nerve Gliding/ Nerve Mobilization
Muscle Weakness ● Pt will regain full muscular strength c a grade of 5/5 for ● PREs with graded Elastic Bands
better muscle performance and ADL performance after ● Strengthening Exercises
x PTR sessions

Decreased ROM ● Pt will be able to regain full ROM both active and ● Stretching Exercises
passive in (specific joints) to maintain joint mobility and ● ROM Exercises
structure and prevent contractures

Abnormal Posture ● Pt will demonstrate a great improvement in postures ● Postural training in front of mirror for intrinsic feedback
and able to do functional activities s any limitations

Gait Deviation ● Pt will demonstrate an improvement in gait and ● Gait training on parallel bars, even and uneven surfaces, ascending and descending
ambulate on an even and uneven surface s any stairs to improve gait cycle and increase endurance
assistant device ● Splinting / Assistive Devices

21
Decreased Prehension ● Pt will be able perform better prehension skills to
promote functional independence
Poor Balance and Tolerance ● Pt will present an improvement in balance c a grade of
N for both static and dynamic, and in tolerance c a
grade of G to maintain equilibrium s any assistance and
prevent the risk of falls for better ambulation
Decreased Endurance ● Pt will demonstrate a great improvement in muscular
endurance to delay the onset of fatigue and for a better
performance when doing functional activities
Impaired ADLS ● Pt will be able to perform full independence when doing
ADLs
HOME EXERCISE PROGRAM
● Hot Moist Packs or Cold Compress to painful area to decrease symptoms of pain
● Stretching Exercises to relieve impingement of affected nerve
● Nerve Gliding Techniques to mobilize affected nerve to reduce tingling or abnormal
sensations and impingement
● Strengthening exercises to be able to return to independent ADLs of the muscles
affected by the nerve injury
● Postural Exercises to maintain or improve posture
● Hand exercises using therapy putty in utilization for hand and finger strengthening and
resistance to help develop a strong grip
● Static balance control (sitting, kneeling, standing) on a firm surface with perturbations
● Progress activities by working on soft surfaces (foam, grass, sand), narrowing BOS,
moving arms, or closing eyes
● Wobble board on bilat. LE to one-leg stance for 15 SH
● Ergobike and stationary bicycle for 30 mins. progress to 45 mins. to increase
cardiopulmonary endurance
● ADL training program of regular exercise that includes cardiopulmonary, resistance,
flexibility, and neuromotor exercise to improve and maintain physical fitness
● Splinting / Immobilizations
PRECAUTIONS
● Promote Immobilization of affected area or body part through splints to prevent
exacerbation of pain and other symptoms
● Avoid strenuous activities to prevent nerve injuries
● Take Care of skin to avoid skin injuries and irritation
● Avoid stress and fatigue, rest is needed to recover the body
22
 NEUROMUSCULAR CONDITIONS REVA COMPILATION
VELEZ COLLEGE PHYSICAL THERAPY BATCH 2022

◊ Failure of transmission at many neuromuscular

NEUROMUSCULAR JUNCTION junctions results in weakness of muscle
contraction.
DISORDERS
CLASSIFICATION
WHAT'S INSIDE
1.) Myasthenia Gravis Clinical Subtypes
2.) Lambert-Eaton Myasthenic Syndrome ◊ Ocular MG (OMG). Myasthenic weakness that
3.) Neuromyotonia remains restricted to the ocular muscles for
4.) Botulism more than 2 years
5.) Tetanus
◊ Generalized MG (GMG). This can be further
subclassified in early-onset (EOMG) and
MYASTHENIA GRAVIS late-onset (LOMG) disease, with the cutoff age
usually set at age 40. EOMG patients are more
GENERAL MEDICAL BACKGROUND often women, typically presenting anti-AChR
antibodies and thymus hyperplasia, while LOMG
DEFINITION patients are more frequently male and have
MuSK antibodies in addition to anti-AChR
◊ Myasthenia gravis (MG) is the most common of antibodies.
the disorders of neuromuscular transmission. It ◊ MuSK-antibody myasthenia gravis
is characterized by fluctuating weakness and (MuSK-MG). MuSK antibodies have been
fatigability of skeletal muscles. reported in up to 50% of seronegative
autoimmune MG cases as well as in OMG.
EPIDEMIOLOGY MuSK-MG occurs predominantly in women from
adolescence through middle age
◊ MG is not rare, having a prevalence as high as ◊ Seronegative MG is defined by the absence of
2–7 in 10,000. both anti-AChR and anti-MuSK antibodies
◊ It affects individuals in all age groups, but peaks (“double-seronegative MG”).
of incidence occur in women in their twenties ◊ Thymoma-associated MG. Thymic pathology
and thirties and in men in their fifties and sixties. (thymic lymphofollicular hyperplasia and
◊ Overall, women are affected more frequently thymoma) occurs in 80–90% of MG patients and
than men, in a ratio of ~3:2. is typically milder in seronegative MG
◊ Transient neonatal myasthenia gravis
ETIOLOGY
(TNMG) occurs in approximately 15% of infants
◊ Mainly due to an autoimmune response against born to mothers with autoimmune MG, as the
ACh receptors on the postsynaptic membrane anti-AChR antibodies get transferred across the
and takes place at the site of the neuromuscular placenta.
junction and motor end plate ◊ Juvenile myasthenia gravis (JMG) is defined
◊ How the autoimmune response is initiated and as the onset of immune-mediated MG before
maintained in MG is not completely understood, age 18.
but the thymus appears to play a role in this
◊ Congenital myasthenic syndromes (CMS) are
process.
caused by genetic (mostly autosomal recessive)
RISK FACTORS abnormalities of the NMT.
◊ Lambert-Eaton myasthenic syndrome
◊ Thymic disorders such as hyperthyroidism, (LEMS). LEMS is a rare autoimmune disorder
thymic tumor, or thyrotoxicosis resulting from impaired release of ACh by the
◊ Diabetes presynaptic terminal of the NM junction and in
◊ Immune disorders such as rheumatoid arthritis the autonomic ganglia.
◊ or lupus
◊ Exacerbations may occur before the menstrual Myasthenia Gravis Foundation of America Clinical
◊ period or shortly after pregnancy. Classification
◊ Chronic infections of any kind can exacerbate
MG.
◊ 5% percent to 7% appear to have a familial I Any ocular weakness
association.
II Mild weakness. May also have ocular
PATHOMECHANICS / PATHOPHYSIOLOGY muscle weakness of any severity.
◊ In MG, the fundamental defect is a decrease in IIA Predominantly affecting limb, axial
the number of available AChRs at the muscles, or both. May also have lesser
postsynaptic muscle membrane. involvement of oropharyngeal, respiratory
◊ In addition, the postsynaptic folds are flattened, muscles or both
or “simplified.” These changes result in
decreased efficiency of neuromuscular IIB Predominantly affecting oropharyngeal ,
transmission. Therefore, although ACh is respiratory muscles or both. May also have
released normally, it produces small end-plate lesser or equal involvement of limb, axial
potentials that may fail to trigger muscle action muscles, or both
potentials.

III Moderate weakness affecting other than
ocular muscles. May also have ocular
muscle weakness of any severity
III A Predominantly affecting limb, axial
muscles, or both. May also have lesser
involvement of oropharyngeal, respiratory
muscles or both
III B Predominantly affecting oropharyngeal ,
respiratory muscles or both. May also have
lesser or equal involvement of limb, axial
muscles, or both
IV Severe weakness affecting other than
ocular muscles. May also have ocular
muscle weakness of any severity
IV A Predominantly affecting limb, axial
muscles, or both. May also have lesser
involvement of oropharyngeal, respiratory
muscles or both
IV B Predominantly affecting oropharyngeal ,
respiratory muscles or both. May also have
lesser or equal involvement of limb, axial
muscles, or both
V Defined by intubation, with or without
mechanical ventilation, except when
employed during routine post-operative
management
CLINICAL PRESENTATION
◊ Cardinal feature: fluctuating weakness that is
fatigable, worsening with repetitive activities and
improving with rest and is worsened by
exposure to heat, infection, and stress.
◊ The distribution of muscle weakness often has a
characteristic pattern. The cranial muscles,
particularly the eyelids and extraocular muscles,
are typically involved early in the course of MG;
diplopia and ptosis are common initial
complaints.
◊ Facial weakness: “snarling” expression when the
patient attempts to smile. This is termed as the
“myasthenic snarl”. Weakness in chewing is
most noticeable after prolonged effort, as in
chewing meat.
◊ Speech may have a nasal timbre caused by
weakness of the palate or a dysarthric “mushy”
quality due to tongue weakness.
◊ Difficulty in swallowing may occur as a result of
weakness of the palate, tongue, or pharynx,
giving rise to nasal regurgitation or aspiration of
liquids or food.
◊ Bulbar weakness is especially prominent and
becomes generalized, affecting the limb muscles
as well.
◊ If weakness remains restricted to the extraocular
muscles for 3 years, it is likely that it will not
become generalized, and these patients are said
to have ocular MG.
◊ The limb weakness in MG is often proximal and
may be asymmetric.
◊ Present DTRs
◊ If weakness of respiration becomes so severe
as to require respiratory assistance, the patient
is said to be in crisis.
◊ Neck extensor and flexor muscles are commonly
affected. The weight of the head may overcome
the extensors, producing a “dropped head
syndrome.”
COMPLICATIONS
◊ Myasthenic Crisis
o a medical emergency requiring attention
to life-endangering weakening of the
respiratory muscles and requires
ventilatory assistance.
o Treatment of a crisis occurs in the ICU
because the client requires careful,
immediate control of medications for
survival.
◊ Associated Disorders
o Disorders of the thymus: thymoma,
hyperplasia
o Other Autoimmune disorders:
Hashimoto’s Thyroiditis, Graves’
disease, rheumatoid arthritis, lupus
erythematosus, skin disorders, family
history of autoimmune disorders
o Disorders or circumstances that may
exacerbate MG: hyperthyroidism or
hypothyroidism, occult infection, medical
treatment for other conditions
o Disorders that may interfere with
therapy: tuberculosis, diabetes, peptic
ulcer, GI bleeding, renal disease,
hypertension, asthma, osteoporosis,
obesity
MEDICAL DIAGNOSIS
◊ History Taking
o Diplopia, Ptosis, dysarthria, dysphagia,
dyspnea
o Weakness in characteristic distribution:
proximal limbs, neck extensors,
generalized
o Fluctuation and fatigue: worse with
repeated activity; improved by rest
o Effects of previous treatments
◊ Physical Examination
o Ptosis, diplopia
o Motor power survey: quantitative muscle
testing of muscle strength
o Forward arm abduction time (5 min)
o VItal capacity measurement
o Absence of other neurologic signs
◊ Laboratory Testing
o Anti-AChr radioimmunoassay: ~85%
positive in generalized MG, 50% in
ocular MG; definite diagnosis if positive;
negative result does not exclude MG;
~40% of AChr antibody- negative
patients with generalized MG have
anti-MuSK antibodies
o Repetitive Nerve Stimulation: decrement
of >15% at 3 Hz; highly probable
2
 o Single- fiber EMG: blocking and jitter, ◊ Intravenous Immunoglobulin
with normal fiber density; confirmatory o Intravenous Immunoglobulin (IVIG) is a
but not specific therapy treatment for patients with
◊ Edrophonium (Tensilon) Test antibody deficiencies. It is prepared from
o Used to demonstrate improvement in a pool of immunoglobulins (antibodies)
the myasthenic muscles by inhibiting from the plasma of thousands of healthy
acetylcholinesterase (AChE), an donors.
enzyme required for ACh uptake.
o Muscle strength and endurance are SURGICAL MANAGEMENT
measured before and after ◊ Surgical Removal of Thymoma
administration of the drug.
◊ Muscle Biopsy o To avoid the possibility of a local tumor
o Simplification of the postsynaptic spread
membrane with loss of junctional folds ◊ Thymectomy
and receptors o operation to remove the thymus
◊ For ocular or cranial MG o offers the possibility of long-term benefit,
o Exclude intracranial lesions by CT or and in some cases diminishing or
MRI eliminating the need for continuing
medical treatment.
DIFFERENTIAL DIAGNOSIS
PHARMACOLOGICAL MANAGEMENT
◊ Anticholinesterase Medications
Area Myasthenia Lambert-Eaton o Pyridostigmine
Gravis Myasthenic ▪ Improve muscle strength in MG
Syndrome patients
◊ Glucocorticoids (Prednisone)
Location Postsynaptic Presynaptic o Improve in myasthenic weakness
◊ Other Immunosuppressive Drugs
Onset F>M M > F (>40
years) o Mycophenolate Mofetil
▪ Long-term treatment of
Etiologic Thymus Small Cell myasthenic patients
Association disorders Carcinoma of o Azathioprine
the lung o Calcineurin Inhibitors (Cyclosporine and
Tacrolimus)
Effect on Rest Improved with Exacerbated o Rituximab (Rituxan)
Rest with Rest ▪ Particularly effective in MuSK
antibody-positive MG
Reflexes Normal Depressed or o High-Dose Cyclophosphamide
absent ▪ Long-lasting benefit by
“rebooting” the immune system
Autonomic Absent Present ▪ Reserved for refractory patients
Disturbances ◊ In myasthenia gravis, avoid these following
drugs as they exacerbate the weakness felt by
the patients.
o Antibiotics
PROGNOSIS o Non-Depolarizing Muscle Relaxants for
Surgery
o Beta-Blocking Agents
◊ Although it has become evident that the natural
o Local Anesthetics and Related Agents
course of MG is general improvement in 57%
o Botulinum Toxin
and remission in 13% after the first 2 years,
o Quinine derivatives
severe weakness can be accompanied by high
o Magnesium
mortality.
o Penicillamine
◊ Only 20% of patients remain unchanged, and
mortality from the disease is 5%–9%. Only 4%
of the patients who survive the first 2 years OTHER HEALTHCARE MANAGEMENT
become worse. Of those who will develop ◊ SLP
generalized myasthenia, virtually, all do so by
o Dysarthria and dysphagia
two to three years.
◊ OT
o Functional skill rehabilitation
GENERAL HEALTHCARE MANAGEMENT ◊ Psychologists
o Possible psychosocial issues
MEDICAL MANAGEMENT ◊ Physician
o Diagnosis and prescribing of
◊ Plasmapheresis medications
o Plasma, which contains the pathogenic ◊ Pharmacist
antibodies, is mechanically separated o Giving of medications
from the blood cells, which are returned
to the patient.
3
PHYSICAL THERAPY, EXAMINATION, EVALUATION, ▪ Pt is asked to gaze upward for
AND DIAGNOSIS an extended period of time,
without lifting the head.
POINTS OF EMPHASIS ON EXAMINATION ▪ (+) show drooping of upper
◊ History Taking eyelids
▪ (-) do not show any drooping
o Thymus surgeries o Gorelick’s Test
o Reduction in patient’s AChR antibody ▪ Passive opening of left eyelid
levels leads to a decrease in opening
◊ Chief Complaint of the right eyelid
o Muscle weakness that is fatigable and o Ice Pack Test
▪ An ice pack is applied to the
worse with repetitive activities and affected upper eyelid for 2-5
improving with rest and is worsened by minutes. A positive test is the
exposure to heat, infection, and stress improvement of ptosis by >
◊ Cognition 2mm or more.
o Normal ◊ Outcome Measures
◊ Vision o Quantitative Myasthenia Gravis Score
o May be impaired d/t diplopia and ptosis ▪ A 13-item scale used to quantify
affecting the visual axis disease severity in myasthenia
◊ Pain gravis (MG).
▪ Scores range from 0 (no
o May or may not have pain myasthenic findings) to 39
(maximal myasthenic deficits)
◊ Aerobic Capacity, Endurance and Respiration o Myasthenia Muscle Score
o Impaired d/t severe muscle weakness ▪ Maximal subscore values
and fatigue ranging from 10 to 15, and the
o Presence of Dyspnea and Hoarse Voice total scores ranging from 0 to
◊ Sensation 100, with lower scores indicating
o Normal greater disease severity.
◊ DTRs o Oculobulbar Facial Score
o Present ▪ This measure was developed
specifically to quantify the signs
◊ Cranial Nerve Integrity and symptoms affecting the
o CN III, IV, VI (extraocular muscle extraocular, facial, and
affectation) respiratory muscles in MG,
o CN VII (rule out other conditions) specifically considering patients
o CN IX (pharyngeal muscles) with musculoskeletal MG.
◊ Observation ▪ The total score ranges from 0 to
o Presence of Diplopia, Ptosis, Nasal 21, and higher scores indicate
worse oculo-bulbar and
Speech
respiratory function.
o Impaired Chewing Ability
o Myasthenia Gravis Impairment Index
o Difficulty in performing facial
▪ The scale has 22
expressions patient-reported items (2-week
◊ MMT recall time) and 6 examination
o Presents with proximal limb weakness items that reflect severity and
and facial weakness fatigability of ocular, bulbar, and
◊ ROM limb/generalized impairments.
o LOM 2° to muscle weakness The total scores range between
◊ Posture 0 and 84, but it can also be
o Impaired 2° to proximal muscle scored as an ocular (0–23) and
weakness a generalized (0–61) score,
o Poor head control 2° to weakness of where higher scores indicate
neck flexors greater disease severity.
◊ Coordination ◊ Measures of Disability and Health Related QoL
o Impaired coordination 2° to muscle in MG
weakness o Myasthenia Gravis Disability Scale
◊ Gait, Locomotion and Balance ▪ measure specifically developed
o Impaired 2° to muscle weakness and to quantify disability in patients
fatigue with MG.
◊ Wheelchair Skills and Assistive Devices o MG QoL-60
o Patients may use assistive devices if ▪ A measure of 60 items—each
MG is severe scored in a Likert scale from 0
◊ Functional Assessment to 4—resulting in a total score
o Impaired functional independence 2° ranging from 0 to 240; higher
muscle weakness and fatigue scores indicate worse HRQoL.
◊ Special Tests o MG QoL- 15 and 15 Revised
o Simpson’s Test ▪ A simplified version of MG
QoL-60

4
 ▪ Items are scored in a Likert
(swimming,
scale from 0 to 4 and the total
walking and
sum score ranges from 0 to 60,
jogging)
where higher scores indicate
worse HRQoL
LOM 2° muscle Pt will present c Stretching
weakness an improvement Exercises to
PT PROBLEM LIST
in ROM to affected using
◊ Difficulty in breathing 2° weak respiratory facilitate PNF Techniques
musculature movement in (HR, AC or
preparation for HR-AC)
◊ Decreased aerobic capacity 2° fatigue
ADLs musculature for
◊ Limitation of motion 2° muscle weakness 10 reps x 2 sets
◊ Muscle weakness
PROM
◊ Fatigability
exercises then
◊ Visual Changes (Double vision, difficulty progressed to
maintaining gaze, drooping eyelids) AAROM or
◊ Speech, feeding problems and psychosocial AROM
issues exercises
depending on
◊ Impaired posture 2° muscle weakness pt’s tolerance
◊ Impaired balance and coordination 2° muscle for 10 reps x 2
weakness sets
◊ Impaired gait 2° LE muscle weakness
◊ Impaired functional capacity (dressing, eating, Muscle Pt will present c Light
bathing, transfers, ambulation) 2° muscle weakness increased Resistance
weakness muscle strength Strengthening
in preparation Exercises using
for gait and free weights,
PT DIAGNOSIS
other functional therabands,
◊ Pattern 5A: Primary Prevention/Risk Reduction activities dumbbells
for Loss of Balance and Falling depending on
the pt’s
◊ Pattern 5B: Impaired Neuromotor Development tolerance

FES (50 ms
PT PROGNOSIS pulse duration,
◊ Rehabilitation alone or in combination with other 1:2 pulse
forms of treatment can relieve or reduce interval, 50 Hz
symptoms for some people with MG. frequency) to
large muscle
PHYSICAL THERAPY PLAN OF CARE groups of UE
and LE for 20
mins
Problem List Goals Interventions

Difficulty in Pt will present c Diaphragmatic

breathing 2° an Increase Strengthening
weak respiratory muscle strength Exercises to Fatigability Pt. will present c Cold packs
musculature of weak increase a decrease in applied to the
respiratory diaphragm fatigue in order affected
musculature in strength to improve extremities x 10
order to tolerance to mins
facilitate proper ADLs and
breathing and functional Low to
avoid activities Moderate
respiratory Intensity
complications Aerobic
Exercises
Decreased Pt will present c Pursed Lip and (swimming,
aerobic capacity increased Abdominal walking and
2° fatigue aerobic capacity Breathing jogging)
to promote Exercises (5
proper breathing reps x 2 sets) Pursed Lip and
and to decrease Abdominal
fatigue Low to Breathing
Moderate Exercises (5
Intensity reps x 2 sets)
Aerobic
Exercises

5
Visual changes Pt. will be able Exercise as tolerated by
to adapt/ Instruction using the pt.
compensate c more Audio or
the visual Proprioceptive
changes Cues than
especially in visual cues Pt. will present c Dual task
exercise and in an improvement exercises
ADLs Proper in coordination (alternately
Therapist in preparation raising UE and
Positioning for ADLs and LE, L and R) x
when functional 10 reps x 2 sets
discussing/ activities
teaching the pt
the exercise for Impaired gait Pt. will present c Ambulation
the pt. to see an improved Training for 15
the therapist gait pattern in mins c therapist
order to walk supervision
Speech, feeding Pt. will be able Swallowing properly and highlighting the
problems and to increase Exercises for 10 safely to quality of
psychosocial pharyngeal reps x 2 sets promote carry movement
issues muscle strength over to safe
and increase Pt. education on ambulation at Low to
motivation for proper nutrition home. Moderate
participation in and water intake Intensity
exercise. Aerobic
Family and pt. Exercises
education on (swimming,
good social walking and
support to jogging)
increase pt’s
motivation Stretching and
Strengthening to
Impaired Pt. will show an Postural major muscle
posture improvement in correction in groups of the LE
posture in order front of mirror c for 10 reps x 2
to facilitate verbal and sets
increase in tactile cues
breathing and
proper body Strengthening Impaired Pt. will present c Low to
alignment the weak functional an increase in Moderate
postural capacity functional Intensity
muscles for 10 independence Aerobic
reps x 2 sets and Exercises
depending on performance of (swimming,
the pt’s posture ADLs to walking and
facilitate carry jogging)
Gentle over at home
Stretching to and in the Functional
tight postural community. Simulation
muscles for 10 Training of pt’s
reps x 2 sets ADLs
highlighting the
Impaired Pt will present c Reaching quality of
balance and an improvement exercises in all movement
coordination in balance to directions while
reduce risk of on a seated
falls and in position for 7
Home Exercise Programs
preparation for reps x 2 sets
1. Low to Moderate Intensity Aerobic Exercises
gait training and
depending on the pt’s time and tolerance
other functional Standing
2. AROM exercises to all motions x 7 reps x 2 sets
activities Reaching
to maintain joint integrity and flexibility
Exercises while
3. Postural correction in front of the mirror x 10
feet together in
mins everyday
all directions x
10 reps x 2 sets
Patient Education
and progressed
1. Avoid high intensity exercises.
to feet apart,
2. Patient and family awareness of the condition
feet in tandem,
and the symptoms
eyes closed and
3. Families must have high levels of support to the
farther distance
patient.
6
 4. Perform in the best time of day (most active time
of the day).
5. PACE
○ Plan daily activities
○ Adapt home modifications, adequate
rest, assistive equipment and ask for
help if needed
○ Conserve energy, have routine
check-ups and exercise in cool
temperatures
○ Emotional stability is needed, exercise
in moderation and eliminate
unnecessary tasks
6. Fall Prevention and Proper Falling Techniques

Precautions
1. In muscle strengthening, start with proximal
muscles then work your way distally. Progress to
heavier weights if pt has acclimated but still
within the pt’s tolerance.
2. High intensity aerobic exercise is discouraged
and avoided because it may aggravate the
fatigability of the pt and exacerbate mm
weakness.
3. Be cautious of time of day, intensity and duration
of exercise.
4. Do not exercise in the presence of
exacerbations.

REFERENCES
Books:
Jayam Trouth, A., Dabi, A., Solieman, N., Kurukumbi,
M., & Kalyanam, J. (2012). Myasthenia gravis: a review.
Autoimmune diseases, 2012, 874680.
https://doi.org/10.1155/2012/874680

Jameson, J. L., & Loscalzo, J. (2015). Harrison's

Principles of Internal Medicine (19th edition.). New York:
McGraw Hill Education

Heldal, Anne & Eide, Geir & Romi, Fredrik & Owe, Jone
& Gilhus, Nils. (2014). Repeated Acetylcholine Receptor
Antibody-Concentrations and Association to Clinical
Myasthenia Gravis Development. PloS one. 9. e114060.
10.1371/journal.pone.0114060.

Websites:
Jianu Catalin, Jianu Silviana and Barsan Claudia (May
24th 2019). Clinical Presentation of Myasthenia Gravis,
Thymus, Nima Rezaei, IntechOpen, DOI:
10.5772/intechopen.86566. Available from:
https://www.intechopen.com/books/thymus/clinical-prese
ntation-of-myasthenia-gravis

7
 LAMBERT-EATON MYASTHENIC SYNDROME
GENERAL MEDICAL BACKGROUND
DEFINITION
◊ Lambert-Eaton Myasthenic Syndrome (LEMS) is
an autoimmune disorder characterized by
muscle weakness and fatigue especially of the
proximal muscles because of a defect release of
acetylcholine quanta or vesicle from presynaptic
terminals
EPIDEMIOLOGY
◊ No accurate epidemiological data
ETIOLOGY
◊ LEMS pt. are often associated with neoplasm,
most commonly small cell carcinoma of the lung
◊ It is also associated with carcinoma of the
breast, prostate, stomach, rectum and
lymphomas
RISK FACTORS
◊ Small cell carcinoma
◊ Smokers
PATHOMECHANICS / PATHOPHYSIOLOGY
◊ Calcium plays an important role in the release of
acetylcholine from its vesicle to its presynaptic
membrane of neuromuscular junction
◊ In LEMS, the antibodies are created against the
voltage gated calcium channels that negate the
release of acetylcholine in the presynaptic
terminal. This blocks the normal flow of calcium
thereby preventing the release of acetylcholine
from its vesicle.
◊ There is little to no acetylcholine entering the
synaptic cleft therefore there will be minimal to
no muscle contraction
◊ In contrast to MG, continuous or repeated
contractions will result in improvement of
strength which is termed post-tetanic
potentiation (aka postexercise or post activation
facilitation). It occurs due to an increased influx
of calcium in the presynaptic membrane by
repetitive muscle contractions. This calcium
buildup facilitates the release of acetylcholine by
binding c multiple vesicles, in time, the excess
calcium is cleared off by mitochondria (thus the
effect is temporary)
◊ Basic defect is the small number in acetylcholine
quanta being released from the motor nerve
terminal & the response to nerve impulse due to
the loss of voltage gated calcium channels and
presynaptic motor nerve terminal
CLINICAL PRESENTATION
◊ Weakness
o First symptoms noticed by the pt is
difficulty in walking due to proximal leg
weakness , but also occasionally due to
ataxia.
o Muscle weakness in LEMS is usually
associated with a high level of disability
o Weakness would progress from
proximal to distal muscle groups and in
the cranial direction
o UE are gradually involved with the
oculobulbar region affected at last
◊ Ocular, Bulbar, and Respiratory Sx
o Unusual, although they are well
recognized in LEMS pt.
o Bulbar involvement is rare and may
present as ptosis, diplopia, dysphagia
and ophthalmoplegia but are very mild
o Respiratory failures are also extremely
rare and occurs very late into the
disease course and is associated with
increase mortality
o Respiratory muscles are often spared
and weakness is exacerbated by heat
and exhaustion
o Facial and bulbar muscles are not often
involved
◊ Autonomic Symptoms and Dysfunction
o Autonomic symptoms such as dry
mouth, constipation, impotence, and
bladder urgency
o Autonomic dysfunction are also
common such as blurry vision, dry
mouth, OH, impaired sweating, and
constipation
MEDICAL DIAGNOSIS
◊ Electrophysiological testing can reliably confirm
the diagnosis of LEMS
◊ Nerve conduction studies the latency and
conduction velocities are normal while CMAP is
reduced
◊ Repetitive Nerve Stimulation
o The study of choice to detect LEMS
o There will be an initial decrement in the
CMAP similar to MG
o On brief exercise, there’ll be a steady rise in
CMAP (seen for up to 30 secs)
o CMAP shows small amplitudes, but normal
latency & conduction velocities
o If repeated impulses are administered, it is
normal for CMAP amplitudes to become
smaller as the acetylcholine in the motor
endplate is depleted
o In LEMS, the ↓ is larger than normally
observed
o Eventually, the stored acetylcholine is made
available & the amplitude would ↑ again. In
LEMS, this remains insufficient to reach a
level sufficient for the transmission of an
impulse from nerve to muscle all can be
attributed bc of the insufficient calcium in the
nerve terminal, a similar pattern like MG
o In LEMS, in response to exercising the
muscle though, the CMAP amplitude
increases greatly over 200%, often even
much more.
o Also occurs in the administration of rapid
bursts of electrical stimuli ~20 impulses/sec
for 10 secs. This is attributed to the influx of
calcium in response to these stimuli.
◊ Single Fiber EMG
o More sensitive, · but requires exceptional
technical prowess.
o It will exhibit increased jitter signifying a
pathology at the neuromuscular junction.
o Unable to differentiate between MG & LEMS
o EMG confirmed cases of LEMS, most pt.’s
will demonstrate antibodies of voltage gated
calcium channel on serological testing
8
 o Typical findings in neurophysiology -
notable reduced CMAP with a dramatic
increase after maximum voluntary
contraction
◊ Serology
o Creatinine kinase - usually normal
o thyroid function test - may assist in
reaffirming the diagnosis
o Anti-voltage gated calcium channels
antibodies - can be detected in pts
serum in over 90% of LEMS cases and
is extremely specific
◊ Imaging
o CT/MRI scan to screen for tumors
especially lung carcinomas
unconfirmed diagnosis of LEMS
o Positron Emission Tomography (PET)
Scan may also be performed to search
for an occult tumor, particularly of the
lungs
DIFFERENTIAL DIAGNOSIS
MG LEMS
often associated with often associated with
thymoma and small cell lung carcinoma
hyperthyroidism
facial and bulbar facial and bulbar
weakness are common weakness are unusual
◊ Potassium channel blockers
o Guanidine and aminopyridine increase
intracellular calcium levels by inhibiting
mitochondrial activity
◊ Acetylcholinesterase inhibitors
o Pyridostigmine prevents the destruction
of the acetylcholine, allowing
acetylcholine to accumulate in the
synaptic cleft which leads to the
prolonged and repeated stimulation of
postsynaptic acetylcholine receptors.
o 3.4-Diaminopyridine (3,4 DAP) is the
first line of treatment for LEMS which
in
blocks the presynaptic potassium
channels, increasing the opening time of
the available voltage-gated calcium
channels. A reasonable starting dose is
10 mg 4x daily which can further
increase to 20 mg 4x daily if required.
However, pt. should be warned that they
may experience perioral and peripheral
paresthesia and is contraindicated in
epilepsy.
◊ Chemotherapy
o Targets the associated tumor
◊ Immunotherapy
o Effective in the early stages of LEMS.
Immunosuppression by corticosteroid
therapy may also benefit some pt.

DTRs are preserved decreased or absent PHYSICAL THERAPY, EXAMINATION, EVALUATION,

DTRs and may be normal AND DIAGNOSIS
after exercise
POINTS OF EMPHASIS ON EXAMINATION
(-) autonomic sx (+) autonomic sx ◊ History Taking
orchanges orchanges
o Surgical removal of lung tumor
Decrement response to Nerve stimulation at o Chief Complaint: muscle weakness that
repetitive nerve higher rates or following is fatigable and worse with repetitive
stimulation exercise, there would be activities and improving with rest and is
incremental response worsened by exposure to heat.
occurring in LEMS ◊ Pain
o May or may not have pain
Tx includes Tx involves ◊ Aerobic Capacity, Endurance and Respiration
anticholinesterase plasmapheresis & o Impaired d/t severe muscle weakness
agents, immunosuppression and fatigue
immunosuppressive o Presence of Dyspnea and Hoarse Voice
drugs, plasmapheresis,
◊ Sensation
and intravenous
immunoglobulin o Normal
◊ DTRs
o Absent or diminished
◊ Cranial Nerve Integrity
PROGNOSIS
◊ Prognosis of LEMS would vary, symptoms may o CN III, IV, VI (extraocular muscle may
improve with treatment of an underlying tumor be affected in some cases but not often
and with suppressing the immune system but involved)
not all people respond well to treatment. o CN VII (rule out other conditions)
o CN IX (pharyngeal muscles may be
GENERAL HEALTHCARE MANAGEMENT affected)
◊ Observation
MEDICAL MANAGEMENT o Difficulty in walking
◊ MMT
◊ There is no cure yet for LEMS and medical o Presents with proximal limb weakness
management is strictly symptomatic. and would progress to distal
◊ In some cases, it may be necessary for the ◊ ROM
surgical removal of the tumor if there are any. o LOM 2° to muscle weakness
◊ Posture
PHARMACOLOGICAL MANAGEMENT
9
 o Impaired 2° to proximal muscle
weakness
FES (50 ms
o Poor head control 2° to weakness of
pulse duration,
neck
1:2 pulse
◊ Coordination
interval, 50 Hz
o Impaired coordination 2° to muscle
frequency) to
weakness
large muscle
◊ Gait, Locomotion and Balance
groups of UE
o Impaired 2° to muscle weakness and
and LE for 20
fatigue
mins
◊ Wheelchair Skills and Assistive Devices
o Pt. may need/use assistive devices if
Fatigability Pt. will present c Cold packs
LEMS is severe
a decrease in applied to the
◊ Functional Assessment
fatigue in order affected
o Impaired functional independence 2°
to improve extremities x 10
muscle weakness and fatigue
tolerance to mins
◊ Special Tests ADLs and
o (+) Lambert sign functional Low to
activities moderate
PT DIAGNOSIS intensity aerobic
exercises
◊ Pattern 5A: Primary Prevention/Risk Reduction
(swimming,
for Loss of Balance and Falling walking and
◊ Pattern 5B: Impaired Neuromotor Development jogging) for 20
mins
PT PROGNOSIS
◊ Rehabilitation treatment is symptomatic and Pursed lip and
aims to maintain maximum functional abdominal
independence. However, for PT management at breathing
present, there are no clinical trials that have exercises (5
evaluated the effect of physiotherapy in the reps x 2 sets)
management of LEMS.

PHYSICAL THERAPY PLAN OF CARE Psychosocial Pt. will be able Family and pt.
issues to increase education on
Problem List Goals Interventions motivation for good social
participation in support to
Decreased Pt will present c Pursed lip and exercise. increase pt’s
aerobic capacity increased abdominal motivation
and endurance aerobic capacity breathing
2° fatigue and endurance exercises (5 Impaired Pt. will show an Postural
to promote reps x 2 sets) posture improvement in correction in
proper breathing posture in order front of mirror c
and to decrease Low to to facilitate verbal and
fatigue moderate increase in tactile cues
intensity aerobic breathing and
exercises proper body Strengthening
(swimming, alignment the weak
walking and postural
jogging) for 20 muscles for 10
mins reps x 2 sets
depending on
LOM 2° muscle Pt will present c Stretching the pt’s posture
weakness an increase in exercises on the
ROM to affected Gentle
facilitate musculature for stretching to
movement in 10 reps c 15 SH tight postural
preparation for x 2 sets muscles for 10
ADLs and other reps c 10 SH x
exercises 2 sets

Muscle Pt will present c Light resistance Impaired Pt will present c Reaching

weakness increased strengthening balance and an improvement exercises in all
muscle strength exercises using coordination in balance to directions while
in preparation free weights, reduce risk of on a seated
for gait and therabands, falls and in position for 7
other functional dumbbells preparation for reps x 2 sets
activities depending on gait training and
the pt’s other functional Standing
tolerance activities Reaching

10
 Exercises while depending on
feet together in pt’s tolerance
all directions x for 10 reps x 2
10 reps x 2 sets sets
and progressed
to feet apart,
feet in tandem,
Home Exercise Programs
eyes closed and
1. Low to Moderate Intensity Aerobic Exercises
farther distance
depending on the pt’s time and tolerance
as tolerated by
2. AROM exercises on all proximal joints x 10 reps
the pt.
x 2 sets to maintain joint integrity and flexibility
3. Self-stretching on proximal musculature x10
reps c 15 SH x 2 sets to increase ROM.
Pt. will present c Dual task
Patient Education
an improvement exercises
1. Avoid high intensity exercises.
in coordination (alternately
2. Patient and family awareness on the
in preparation raising UE and
exacerbation of the symptoms
for ADLs and LE, L and R) x
3. Perform in the best time of day (most active time
functional 10 reps x 2 sets
of the day and less heat).
activities
4. PACE
○ Plan daily activities
Impaired gait Pt. will present c Ambulation
○ Adapt home modifications, adequate
an improved training for 15
rest, assistive equipment and ask for
gait pattern in mins c therapist
help if needed
order to walk supervision
○ Conserve energy, have routine
properly and highlighting the
check-ups
safely to quality of
○ Exercise in cool temperatures,
promote carry movement
emotional stability is needed, exercise in
over to safe
moderation and eliminate unnecessary
ambulation at Low to
tasks
home and Moderate
reduce the risk Intensity
Precautions
of falls Aerobic
1. High intensity aerobic exercise is discouraged
Exercises
and avoided because it may aggravate the
(swimming,
fatigability of the pt and exacerbate mm
walking and
weakness.
jogging)
2. Be cautious of time of day, intensity and duration
of exercise.
Stretching and
3. Avoid exercise under the heat.
strengthening to
4. Do not exercise in the presence of
major muscle
exacerbations.
groups of the LE
for 10 reps x 2
REFERENCES
sets
Anwar A, Saleem S, Ahmed MF, Ashraf S, Ashraf S.
Recent Advances and Therapeutic Options in
Impaired Pt. will present c Low to
Lambert-Eaton Myasthenic Syndrome. Cureus.
functional an increase in Moderate
2019;11(8):e5450. Published 2019 Aug 21.
capacity functional Intensity
doi:10.7759/cureus.5450
independence Aerobic
and Exercises
Hill M. The neuromuscular junction disorders. J Neurol
performance of (swimming,
Neurosurg Psychiatry. 2003;74 Suppl 2(Suppl
ADLs to walking and
2):ii32-ii37. doi:10.1136/jnnp.74.suppl_2.ii32
facilitate carry jogging)
over at home
and in the Functional
community. Simulation
Training of pt’s
ADLs
highlighting the
quality of
movement

Prevent Pt. will prevent PROM

immobility 2° to immobility to exercises then
weakness and prevent progressed to
fatigue secondary AAROM or
complications AROM
like contracture exercises

11
 NEUROMYOTONIA improve the yield to 87% but are not widely
available.10
GENERAL MEDICAL BACKGROUND ◊ The classical EMG findings are of spontaneous
doublet, triplet or multiple discharges from motor
DEFINITION nerves.
◊ Fasciculation and fibrillation potentials are also
◊ also known as “Isaac Syndrome” found and some patients may have evidence of
◊ Neuromyotonia is a very rare condition of a mild peripheral neuropathy.
spontaneous, continuous muscle activity of
peripheral nerve origin. DIFFERENTIAL DIAGNOSIS
◊ It is characterized clinically by:
● muscle twitching at rest (visible ◊ Autoimmune neuromyotonia probably
myokymia), represents the severe end of the clinical and
● cramps that can be triggered by electrophysiological spectrum of autoimmune
voluntary or induced muscle contraction, peripheral nerve hyperexcitability, and is only
● impaired muscle relaxation one of a number of disorders that can present
(pseudomyotonia). with clinically-visible myokymic muscle twitching.
◊ Often, patients also have symptoms of ◊ The stiff-man syndrome is a similar condition of
excessive sweating and more rarely mild continuous motor unit activity, where abnormal
muscular weakness, and paraesthesia excitability of spinal interneuronal networks and
descending control over the anterior horn cell is
EPIDEMIOLOGY thought to be the underlying pathophysiology
◊ Acquired neuromyotonia is a rare disorder
Sign Isaac Stiff-man
affecting males and females but is slightly more
Syndrome Syndrome
common among men.
◊ Disease onset is usually between the ages of 15
Age 5-50 y.o. 30-40
and 60 years but has also been reported in
y.o.(Middle age)
childhood.
Onset Subacute, Slow
ETIOLOGY sometimes slow
◊ Most cases are idiopathic, though about 15%
are associated with thymoma, and a small Course Progressive, Progresive
proportion with SCLC. sometimes with
remissions
RISK FACTORS
◊ Thymoma Main focus of Muscle of the Muscle of the
◊ SCLC the disease extremities neck, trunk
sometimes face
PATHOMECHANICS / PATHOPHYSIOLOGY muscle
◊ In acquired neuromyotonia, autoantibodies
cause down regulation of voltage gated Labored Sometimes Often
potassium channels (VGKCs) expressed on the breathing
peripheral nerve terminal.
◊ This reduction in VGKCs prolongs depolarisation Muscle changes Often under Hard
of the nerve terminal, increasing the amount of tension
ACh released from the nerve terminal resulting
in nerve hyperexcitability. Fasciculation Nearly always Absent

Contractures In distal regions, Serous in the

CLINICAL PRESENTATION predominantly muscles of the
◊ The neuronal hyperexcitability results in skeletal flexor occiput, spine
muscle overactivity, which manifests as: (right up to
● muscle twitching or myokymia (which is fracture)
often confused with fasciculation),
● cramps PROGNOSIS
● muscle stiffness
◊ Many patients gain significant symptomatic relief
● muscle hypertrophy (in chronic cases)
from drugs that down regulate voltage gated
◊ Increased sweating, presumably caused by
sodium channels.
continuous muscle activity, is also a common
complaint.
GENERAL HEALTHCARE MANAGEMENT
MEDICAL DIAGNOSIS
MEDICAL MANAGEMENT
◊ In common with MG and LEMS, diagnosis of
neuromyotonia is based on positive titres of
◊ Plasma exchange can provide short term relief;
anti-VGKC antibodies and characteristic findings
the response to IVIg is generally less striking
on neurophysiology.
◊ However, the immunoprecipitation assay used
PHARMACOLOGICAL MANAGEMENT
by most laboratories only detects antibodies in
about 50% of cases; more sensitive tests can

12
 ◊ The symptoms of peripheral nerve
◊ Gait, Locomotion and Balance
hyperexcitability often respond well to
● Imapired gait 2° hypertonicity
anticonvulsants such:
● carbamazepine
◊ Functional Assessment
● phenytoin
● Impaired functional skills as to self-care,
● lamotrigine
and locomotion
- all of which primarily reduce neuronal repetitive
firing through interaction
◊ Fatigue Severity Scale
◊ Resistant cases may benefit from long term
● Pt. presenst c fatigue 2° continuous
immunosuppression with prednisolone and
muscle fiber activity
azathioprine, though not all patients respond to
this.
PT PROBLEM LIST
PHYSICAL THERAPY, EXAMINATION, EVALUATION, 1. Pain 2° to muscle cramps
AND DIAGNOSIS 2. Hypertonicity of muscles
3. LOM 2° pain caused by muscle cramps
4. Muscle fatigue 2° continuous muscle fiber
POINTS OF EMPHASIS ON EXAMINATION
activity
SUBJECTIVE EXAMINATION
5. Muscle Hypertrophy
◊ History Taking 6. Decrease muscle strength 2° to muscle fatigue
◊ Chief Complaint 7. Impaired posture 2° hypertonicity
8. Imapired gait 2° hypertonicity
● Pain 2° to muscle cramps 9. Impaired functional capacity as to self-care, and
● Muscle Stiffness locomotion
● Pseudomyotonia
● Hyperhidrosis (Increase in sweating)
PT DIAGNOSIS
● Muscle weakness
● Fatigue ◊ Pattern 5B: Impaired Neuromotor Development

OBJECTIVE EXAMINATION PT PROGNOSIS

Ocular Inspection ◊ The role of physical therapy in this condition is
◊ Hypertrophy either of the calves, forearm and supportive care for secondary impairments since
hand muscles. the mainstay management for this condition is
◊ Difficulty walking through pharmacological intervention. Although
there are no clinical studies that proved the
Cardiopulmonary Assessment efficacy of rehabilitation in this condition
◊ Vital Signs however, prevention of secondary complications
● WNL must be addressed.
◊ Aerobic Capacity, Endurance and Respiration
● Unimpaired PHYSICAL THERAPY PLAN OF CARE

Neurological Assessment
Problem List Goals Interventions
◊ Cognition
● Unimpaired Pain 2° to Pt. will present HMP x 20 mins.
◊ Communication muscle cramps decrease in pain to decrease
● Unimpaired to facilitate pain sensation
◊ Sensation ROM of affected and elicit
● Unimpaired extremity muscle
◊ DTRs relaxation
● Areflexia 2° muscle hypertonicity
- (due to muscle stiffness, DTR is Hypertonicity of Pt. will present Effleurage x10
hard to elicit) muscles decrease in mins to facilitate
muscle tonicity muscle
◊ Cranial Nerve Integrity Muscle fatigue to improve relaxation on
● Unimpaired tolerance to overactive
◊ Coordination Muscle ADLs and muscles.
● Impaired coordination 2° hypertonicity hypertrophy functional
activities,
Integumentary Assessment; facilitate posture
◊ Palpation and gait and
● Hypertonia decrease
hypertrophy
Musculoskeletal Assessment
◊ ROM Once pain is minimized:
● LOM 2° pain caused by muscle cramps
LOM 2° pain Pt. will present AAROM to all
◊ MMT caused by increase in jnts without
● Muscle weakness 2° fatigue muscle cramps ROM to causing fatigue
facilitate for x10reps x2
◊ Posture movement and sets to facilitate
● Impaired posture 2° hypertonicity
13
 ● Avoid exercising during exacerbations or if can’t
performance of increase of
be tolerated
ADLs range of motion
● Avoid putting ice pack when experiencing
and prevent
muscle cramps. It can exacerbate symptoms
formation of
contractures
REFERENCES
Once muscle hypertonicity is minimized:
Books:
● Maddison PNeuromyotoniaPractical Neurology
Decrease Pt. will present Strengthening
2002;2:225-229.
muscle strength increase in exercise x 5
● Hill M. The neuromuscular junction disorders. J
2° to muscle muscle strength reps x 4 sets c
Neurol Neurosurg Psychiatry. 2003;74 Suppl
fatigue to improve rest periods in
2(Suppl 2):ii32-ii37.
performance in between to
doi:10.1136/jnnp.74.suppl_2.ii32
ADLs facilitate
increase in
Researches:
muscle strength
● Tharani, G., Kamatchi, K., & Yuvarani, G.
(2021). A 60-year-old man with isaacs
Impaired Pt. will present Postural
mertens-syndrome a rare entity. Bangladesh
posture improvement in correction in
Journal of Medical Science, 20(3), 691-693.
posture to front of mirror c
https://doi.org/10.3329/bjms.v20i3.52819
prevent verbal and
developing tactile cues
deformities

Impaired gait Pt. will present c Ambulation

an improved Training for 15
gait pattern in mins c
order to supervision to
facilitate safely improve gait
ambulation pattern and
prevent
compensatory
gait pattern

Impaired
functional
capacity as to
self care and
locomotion

Home Exercise Programs

● HMP x10 mins on muscle cramps
● AAROM exercises x10 reps x2 sets to facilitate
increase of ROM and prevent formation of
contractures
● Strengthening exercise x 5 reps x 4 sets c rest
periods in between to facilitate increase in
muscle strength
● Postural correction in front of the mirror x 10
mins everyday

Patient Education
● Nature of the condition
● Role of physical therapist and impact of exercise
towards the condition.
● PACE
- Plan daily activities
- Adapt home modifications, adequate
rest, and ask for help if needed
- Conserve energy, have routine
check-ups and exercise in cool
temperatures
- Emotional stability is needed, exercise
in moderation and eliminate
unnecessary tasks

Precautions
● Avoid moderate to high intensity exercises that
can cause fatigue

14
BOTULISM
GENERAL MEDICAL BACKGROUND
DEFINITION
◊ Botulism is a very serious food borne illness,
often fatal, and characterized by neuroparalytic
signs and symptoms. Early observations found
an association with consumption of sausages,
and thus the name botulism (derived from
botulus, Latin for sausage) was given to the
disease.
◊ According to CDC, it is a rare but serious illness
caused by a toxin that attacks the body’s nerves
EPIDEMIOLOGY
◊ Botulism occurs worldwide, but the number of
cases reported varies among countries and
regions.
No universal surveillance system to capture
worldwide botulism incidence. However, 30
countries currently participate through an
established surveillance system that includes
standardized case definitions similar to those
used in the United States and Canada.
ETIOLOGY
◊ Botulism is caused by a bacterium called
Clostridium botulinum, producing deadly protein
toxins that can cause paralysis or death.
◊ Bergey's Manual of Systematic Bacteriology lists
four groups of C. botulinum, distinguished on the
basis of their cultural and physiologic
characteristics. These are commonly referred to
as groups I, II, III, and IV
◊ The phenotypic and genetic features of the
organisms are sufficiently distinct from one
group to another to warrant separate species
names
◊ Seven serologically distinct confirmed serotypes
of botulinum toxin (A through G) have been
confirmed. botulinum toxin is produced by four
recognized species of clostridia: Clostridium
botulinum, Clostridium argentinense, Clostridium
baratii, and Clostridium butyricum. certain
strains may produce more than one serotype. all
are anaerobic gram-positive organisms that form
subterminal spores.
◊ Food-borne botulism is caused by consumption
of foods contaminated with botulinum toxin; no
confirmed host-specific factors are involved in
the disease
◊ Wound botulism is caused by contamination of
wounds with C. botulinum spores, subsequent
spore germination, and toxin production in the
anaerobic production in the anaerobic milieu of
an abscess or a wound.
◊ Infant botulism results from absorption of toxin
produced in situ by toxigenic clostridia colonizing
the intestine of children ≤ 1 year of age.
Colonization is thought to occur because the
normal bowel microbia is not yet fully
established.
◊ Adult intestinal botulism has a pathology similar
to that of infant botulism but occurs in adults;
typically, patients have some anatomic or
functional bowel abnormality or have recently
used antibiotics that may help toxigenic
clostridia compete more successfully against
normal bowel microbia.
RISK FACTORS
◊ Consumption of canned foods that are outdated
or have containers that are damaged
◊ Consumption of foods that will be stored for long
periods at room temperature
◊ Feeding of honey to infants younger than 1 year
old
◊ Travel history to Alaska and Canada
◊ Use of black tar heroin
◊ Injection of BTH intramuscularly or
subcutaneously
PATHOMECHANICS / PATHOPHYSIOLOGY
◊ The botulism toxin molecule is produced by the
Clostridium bacterium as a single large protein
that is inactive. Proteins are the end product of
genetic information. When the bacterium
releases this protein, it comes into contact with
enzymes that have been released by the
bacterium or by the tissues of the body as part
of their normal secretory activity. These
enzymes break the large molecule into two
evenly sized pieces or chains - a “heavy” chain
or a “light” chain. The toxin is absorbed by the
cells lining the stomach wall and intestines.
◊ The toxin passes into the bloodstream and
diffuses into body tissues. The only portion of
the body into which the toxin cannot spread is
the CNS since the toxin molecule is too large to
penetrate the BBB. The toxin shape provides a
particular attraction to the membrane nerve
endings of the PNS. This temporary contact with
the receptor on the nerve cell surface causes
the nerve cell membrane to turn inward and
surround the botulinum toxin. This engulfment
process is called receptor-mediated endocytosis
and brings the toxin molecule into the nerve cell.
Once inside the cell, the toxin molecule
interrupts the normal functioning of the SNARE
protein complex. A portion of the toxin molecule
called the light chain is released into the cell
cytoplasm and breaks apart SNAP-25, which is
a protein that is already part of the membrane of
the nerve cell and is necessary for the release of
acetylcholine. If the SNAP-25 is broken apart,
the vesicle containing the acetylcholine is not
attached to the membrane and no message is
sent to the muscle to contract.
CLASSIFICATION
◊ Food-borne Botulism - where individuals
ingest the toxins in food. This type can vary from
a mild illness, to one that can be fatal within 24
hours. People of both genders and all ages are
susceptible to this type of infection.
◊ Wound Botulism - occurs when soil gets into
an open wound. Is the form most analogous to
tetanus. It occurs when the neurotoxin produced
by C. botulinum growing in a wound is
disseminated throughout the body and poisons
the nerve endings causing paralysis. This form
of botulism is extremely rare.
◊ Infant Botulism - is considered the most
common and may be one cause of sudden
infant death. Most infants are less than 6 months
of age when they are infected. Contaminated
15
 honey, which has been used to sweeten milk or ◊ Poor feeding
pacifiers, is the most common source of the ◊ Increasing weakness
infection. The honey is often contaminated with ◊ Bulbar palsy which are indicated by
wind-borne forms of the botulism organism. expressionless face, feeble cry, ptosis, and
◊ Adult Intestinal Colonization Botulism - is impaired gag, suck and swallow reflexes
difficult to confirm because it is poorly ◊ Poor head control
understood but the cases are often caused by C. ◊ Generalized weakness
baratii type F and the involvement of both C. ◊ Hypotonia
botulinum type A and C and C. butyricum type ◊ Respiratory failure often ensues
E. ◊ Cranial nerve deficits
◊ Iatrogenic Botulism - wherein paralysis occurs
after injection of licensed botulinum toxin COMPLICATIONS
products for treatment of conditions involving ◊ Respiratory failure
hypertonicity of large muscle groups.
◊ Inhalation Botulism - does not occur naturally ◊ Death
wherein one report from Germany resulted from
possible inhalational exposure to botulinum toxin MEDICAL DIAGNOSIS
in a laboratory incident ◊ Mouse bioassay - the patient’s serum or fecal
◊ Intentional Botulism - wherein botulinum toxin matter 9stool) is tested and cultured to detect
has been “weaponized” by governments and Clostridium botulinum organisms. The patient’s
terrorist organizations serum is injected into mice, and the subsequent
symptoms are analyzed. It can detect as little as
CLINICAL PRESENTATION 0.03 ng of toxin. The mouse bioassay is the only
diagnostic method currently used for detection
◊ Bilateral descending flaccid paralysis and identification of botulinum toxin.
◊ Cranial nerve deficits: ◊ Sensitive enzyme-linked immosorbent assays
o Diplopia ◊ Laboratory findings - presence of C. Botulinum
o Dysphonia in stool samples of the patients whose sample
o Ptosis were cultured (Food-borne Botulism);
o Ophthalmoplegia identification of botulism neurotoxin in the
o Facial paralysis patient’s serum or by isolation of C. botulinum
o Impaired gag reflex from wound specimens (Wound Botulism);
o Pupillary reflexes may be depressed detection of botulism neurotoxin in the feces
o Fixed or dilated pupils isolating the toxigenic organism
◊ Autonomic symptoms: ◊ CT Scan - to provide pictures of all parts of the
o Dizziness body in cross section; negative results which
o Dry mouth mean that the scan is normal for the patient,
o Sore throat may be part of a series of results that suggest
◊ Constipation the possibility of botulism
◊ Urinary retention ◊ Spinal tap (lumbar puncture) - fluid is removed
◊ Paralyzed diaphragm and accessory breathing from the spinal column and tested for any signs
muscles of infection; a negative results c CSF fluid is
◊ DTRs may disappear suggestive of botulism
◊ EMG (electromyogram) - measures the electrical
Food-borne Botulism: activity of a muscle or a group of muscles; this
◊ Preceded by GI upset, vomiting, and will distinguish botulism from myasthenia gravis;
constipation most results for botulism patient will result in a
◊ Diarrhea is less common normal reading
◊ May also have autonomic dysfunction resulting
in dry mouth, blurred vision, orthostatic DIFFERENTIAL DIAGNOSIS
hypotension, constipation, and urinary retention
◊ Dysphagia
◊ Diplopia Condition Features that Distinguish
◊ Dysarthria Each Condition from
◊ Extremity weakness Botulism
◊ Blurred vision
◊ Dyspnea Guillain-Barre Usually an ascending paralysis,
◊ Paresthesia Syndrome (GBS) although Miller Fisher variant
◊ GI symptoms (particularly Miller may be descending and may
◊ Nausea Fisher variant) have pronounced cranial nerve
◊ Abdominal cramps involvement; abnormal CSF
protein 1-6 weeks after illness
*several of these symptoms can be quite onset; EMG shows abnormal
variable, but usually Pts present with several of nerve conduction velocity;
these symptoms rather than with a single cranial facilitation with repetitive nerve
nerve abnormality stimulation does not occur (as
with botulism); history of
Infant Botulism antecedent diarrheal illness
◊ Initial constipation (3 or more days without a (suggestive of Campylobacter
bowel movement) infection)
◊ Lethargy
16
Myasthenia gravis Dramatic improvement with
edrophonium chloride
(although some botulism
patients may exhibit partial
improvement following
administration of edrophonium
chloride); EMG shows
decrease in muscle action
potentials with repetitive nerve
stimulation
Tick paralysis Ascending paralysis;
paresthesias; careful
examination reveals presence
of tick attached to skin;
recovery occurs within 24
hours after tick removal; EMG
shows abnormal nerve
conduction velocity and
unresponsiveness to repetitive
stimulation
Lambert-Eaton Commonly associated with
syndrome carcinoma (often oat cell
carcinoma of lung); although
EMG findings are similar to
those in botulism, repetitive
nerve stimulation shows much
greater augmentation of
muscle action potentials,
particularly at 20-50 Hz;
increased strength with
sustained contraction; DTRs
often absent; ataxia may be
present
Stroke or CNS Paralysis usually asymmetric;
mass lesion brain imaging (CT or MR)
usually abnormal; sensory
deficits common; altered
mental status may be present
Poliomyelitis Febrile illness; CSF shows
pleocytosis and increased
protein; altered mental status
may be present; paralysis often
asymmetric
Paralytic shellfish History of shellfish (e.g., clams,
poisoning or mussels) or puffer fish
ingestion of puffer ingestion within several hours
fish before symptom onset;
paresthesias of mouth, face,
lips, extremities commonly
occur
Belladona toxicity History of recent exposure to
belladona-like alkaloids; fever;
tachycardia; altered mental
status
Aminoglycoside History of recent exposure to
toxicity aminoglycoside antibiotics;
more likely occur in the setting
of renal insufficiency; most
commonly seen with neomycin;
most commonly associated
with other neurotransmitter
blocking agents such as
succinycholine and paralytics
Carbon monoxide Altered mental status may
toxicity occur; cherry-colored skin
Hypermagnesemia History of use of cathartics or
antacids may be present,
elevated serum magnesium
level
Organophosphate Fever, excessive salivation,
toxicity altered mental status,
paresthesias, miosis
.
PROGNOSIS
◊ According to CDC, the development of antitoxin
and modern medical care means that people
with botulism have a much lower chance of
dying than in the past, when about 50 in every
100 people with botulism died. Today, fewer than
5 of every 100 people with botulism die.
◊ Even with antitoxin therapy and intensive
medical and nursing care, some people with
botulism die from respiratory failure. Others die
from infections or other problems caused by
being paralyzed for weeks or months (CDC).
◊ Patients who survive botulism may have fatigue
and shortness of breath for years afterward and
may need long-term therapy to help them
recover (CDC).
◊ Untreated botulism can lead to death because of
airway obstruction from pharyngeal muscle
paralysis and inadequate tidal volume resulting
from paralysis of diaphragmatic and accessory
respiratory muscles.
◊ Immediate hospitalization is needed in order that
respiratory failure can be detected and managed
appropriately and promptly to prevent further
complications and especially death.
GENERAL HEALTHCARE MANAGEMENT
MEDICAL MANAGEMENT
◊ Intubation - a tube is inserted through the nose
or mouth into the trachea to provide an airway
for oxygen
◊ Mechanical ventilation - where a machine is
used to assist breathing
◊ Gastric lavage - where the stomach contents are
pumped out to clear toxin that has not yet been
absorbed by the bloodstream
◊ Antitoxin therapy -to neutralize toxins to prevent
further damage to the nerves, given for either
food-borne or wound botulism because it is not
generally used in cases of infant botulism
◊ BabyBig or VIG-IV - is a solution made from
human antibody proteins which will reduce the
time an infant will need to be in the hospital
◊ Botulism Antitoxin heptavalent - an
equine-derived heptavalent product
enzymatically de-speciated for treatment of all
forms of adult botulism and infant cases not
involving serotypes A and B
SURGICAL MANAGEMENT
◊ Debriding - to surgically remove the skin of the
affected area in wound botulism
PHARMACOLOGICAL MANAGEMENT
17
 ◊ Penicillin G - recommended in the treatment of ◊ DTR
o Areflexive triceps, biceps, patellar, &
wound botulism and is said to increase
achilles tendon reflexes
circulating botulinum toxin from lysis of bacterial
◊ Cranial Nerve Assessment
cells
o Impaired CN 2 (depressed pupillary light
◊ Metronidazole -recommended in the treatment
reflex)
of wound botulism and is said to increase
o Impaired CN 3 (depressed pupillary
circulating botulinum toxin from lysis of bacterial
reflexes, opthalmoplegia, fixed & dilated
cells
pupils)
o Impaired CN 4 (diplopia)
MEDICATIONS FUNCTIONS o Impaired CN 6 (opthalmoplegia)
o Impaired CN 7 (ptosis, facial paralysis)
Penicillin G This recommended in the o Impaired CN 9 (impaired gag reflex)
treatment of wound o Impaired CN 10 (dysphonia, dysarthria)
botulism and is said to ◊ ROM
increase circulating o ↓ AROM of bilat. UE & LE 2° weakness
botulinum toxin from lysis ◊ MMT
of bacterial cells o ↓ strength of major muscle groups of
bilat↓. UE & LE 2° weakness
Metronidazole This is recommended in ◊ MBT
the treatment of wound o Atrophy of diaphragm
botulism and is said to o Atrophy on bilat. biceps, quadriceps &
increase circulating gastrocnemius 2° ↓ physical activity
botulinum toxin from lysis owing to weakness
of bacterial cells ◊ FMT (for infants)
o Poor head control
◊ Fine motor skills
OTHER HEALTHCARE MANAGEMENT o Poor 2° weakness
◊ SLP ◊ Coordination Assessment
◊ OT o Impaired coordination 2° weakness
◊ RT ◊ Balance & Tolerance Assessment
◊ Nurse practitioner o Impaired static & dynamic balance
◊ Optometrist during sitting, standing & walking 2° LE
◊ Ophthalmologist weakness
o Impaired tolerance during standing &
PHYSICAL THERAPY, EXAMINATION, EVALUATION, walking 2° LE weakness
AND DIAGNOSIS ◊ Gait Assessment
o Impaired gait 2° LE weakness
POINTS OF EMPHASIS ON EXAMINATION ◊ Functional Assessment
o ↓ ability to perform functional ADLs
◊ History ◊ Other Tests
o Consumption of canned foods that are o House-Brackmann Facial Paralysis
outdated or have containers that are Scale
damaged ▪ Dysfunction on the muscles of
o Consumption of foods that will be stored the forehead, eyes, and mouth
for long periods at room temperature (could be mild, moderate, or
o Consumption of honey (for infants severe depending on the
younger than 1 year old) condition’s severity)
o Recent travel in Alaska and Canada o Braden Scale
o Use of black tar heroin ▪ Risk for pressure sores (when
o Injection of BTH intramuscularly or in-patient or bedridden)
subcutaneously o Well’s DVT Scale
◊ Chief Complaint ▪ Risk for DVT (when in-patient or
o Weakness bedridden)
o Paresthesia
o Lethargy PT PROBLEM LIST
◊ Cognition
◊ Weakness
o Unimpaired (to r/o other conditions)
◊ Communication ◊ Paresthesia
o Impaired speech ◊ Lethargy
◊ Vital Signs ◊ ↓CEM 2° paralyzed diaphragm
o WNL (BP may ↓ as the condition ◊ ↓ aerobic capacity
progresses) ◊ Blurred vision
◊ Chest Expansion Measurement ◊ Ptosis
o ↓CEM 2° paralyzed diaphragm ◊ Hypotonia
◊ Aerobic Capacity ◊ Facial paralysis
o Impaired 2° paralyzed diaphragm ◊ Risk for pressure sores
◊ Visual and Hearing Skills ◊ Risk for DVT
o Blurred vision ◊ LOM as to AROM of bilat. UE & LE 2°
◊ Integumentary Assessment weakness
o Hypotonia ◊ ↓ strength of major muscle groups of bilat ↓ UE
& LE 2° weakness
18
 ◊ Atrophy of diaphragm
↓ aerobic Pt. will -Arm ergometer
◊ Atrophy on bilat. biceps, quadriceps &
capacity demonstrate ↑ 10-15 mins in
gastrocnemius 2° ↓ physical activity owing to
aerobic capacity to sitting position
weakness
be able to tolerate within Pt.’s
◊ Poor head control 2° ↓ muscle tone
longer exercises tolerance
◊ Poor fine motor skills 2° weakness
and functional
◊ Impaired coordination 2° weakness
activities. -PBWSTT 10
◊ Impaired static & dynamic balance during sitting,
mins beginning
standing & walking 2° LE weakness
c 1.5 m/s
◊ Impaired tolerance during standing & walking 2°
LE weakness
Blurred vision Pt. will be able to -Compensatory
◊ Impaired gait 2° LE weakness
know how to strategies:
◊ ↓ ability to perform functional ADLs
manage blurred >Verbal cues
vision for better >Tactile cues
PT DIAGNOSIS
performance of
◊ Pattern 5A: Primary Prevention/Risk Reduction exercises and -Pt. education
for Loss of Balance and Falling functional >Safety
◊ Pattern 5B: Impaired Neuromotor Development activities. performance of
exercises and
PT PROGNOSIS functional
activities
◊ Untreated botulism can lead to death because of
airway obstruction from pharyngeal muscle >Referral to
paralysis and inadequate tidal volume resulting optometrist or
from paralysis of diaphragmatic and accessory opthalmologist
respiratory muscles.
◊ Immediate hospitalization is needed in order that Ptosis Pt. will be able to -Patching of the
respiratory failure can be detected and managed know how to unaffected eye
appropriately and promptly to prevent further manage ptosis for during the PTR
complications and especially death. better session
performance of
PHYSICAL THERAPY PLAN OF CARE exercises and -Pt. education
functional as to patching
Problems Goals Interventions activities. the affected eye
at home for
Weakness Pt. will manifest ↓ -FES to large protection
weakness to be muscle groups
able to perform of bilat. UE & LE Hypotonia Pt. will -Rood’s
exercises and 20 mins demonstrate ↑ Facilitatory
functional activities muscle tone for Technique quick
properly. -Biofeedback to better icing x3 reps to
large muscle performance of each extremity
groups of bilat. exercises and while Pts is
UE & LE 20 functional holding a red
mins activities. teether

-Rood’s
Paresthesia Pt. will -Conventional facilitatory
demonstrate TENS 80 Hz 15 Technique light
improved mins moving touch
sensation to be x3-5 reps to
able to receive -Effleurage 10 each extremity
tactile cues mins while Pt. is
properly all looking up at
throughout the hanging toys.
exercises and
functional Facial Pt. will manifest -FES to facial
activities. paralysis improved muscle muscles 10
tone of the face mins
↓ CEM Pt. will -Incentive for better social
demonstrate ↑ spirometry 10 interaction as to -Facial massage
CEM to be able to mins facial expressions. 10 mins
endure the
exercises and -Diaphragmatic -Facial
functional breathing expressions in
activities. exercises 10 front of a mirror
mins 10 mins c verbal
supine-lying & tactile cues
position

19
Risk for Pt. will -Bed mobility ↓ strength of Pt. wil manifest ↑ -PREs x3 sets
pressure demonstrate ↓ risk exercises 10 major muscle strength of large x10 reps c the
sores for pressure sores mins: groups of bilat muscle groups of use of
for better >Side to side ↓ UE & LE, bilat. UE & LE for yellow-colored
performance of movement atrophy on better TheraBand to
exercises and >Upward and bilat. biceps, performance of bilat. UE & LE
functional downward quadriceps & functional
activities. movement gastrocs activities. -Open-chain
>Supine-lying exercises c
position to long 1lb-dumbbell for
sitting position UE and
>Supine-lying 1lb-weight cuff
position to for LE x3 sets
prone-lying x10 reps
position
>Supine-lying Atrophy of Pt. will -Diaphragmatic
position to diaphragm demonstrate breathing
side-lying delayed atrophy of exercises 10
position the diaphragm to mins
be able to endure supine-lying
-Pressure-relievi the exercises and position
ng exercises 10 functional
mins: activities. -Sandbag
>Supine-lying breathing 10
position weight mins c a 5-lb
shifting in all sandbag on the
directions c the abdomen
use of bilat.
elbows Poor head Pt. will be able to -Head control
>Sitting position control develop head activities 10
weight shifting control for stability mins prone-lying
in all directions all throughout the position on a
c the use of exercises and wedge while
bilat. hands. functional following red
activities. toys above the
-Pt. education: visual field
>Proper
nutrition -Pull-to-sit
>Regular activities on a
position change mat 10 mins
>Regular skin while following a
inspection rattle above the
>Skin care visual field

Risk for DVT Pt. will -Ankle pumps Poor fine Pt. will -Gross
demonstrate ↓ risk x3 sets x10 reps motor skills demonstrate prehension
for DVT for better improved fine activities 10
performance of -Toe wiggles x3 motor skills for mins:
exercises and sets x10 reps better >Transferring
functional performance of small balls
activities. -Pt. education: exercises and >Pulling a 2-in
>Donning and functional ribbon
doffing of activities. >Transferring
compression bottles
bandage
>Regular skin -Fine
inspection prehension
>Skin care activities 10
mins:
LOM as to Pt. will manifest ↑ -PROM >Picking up
AROM of AROM of bilat. UE exercises of needles
bilat. UE & & LE for better bilat. UE & LE >Picking up
LE, lethargy performance of x3 sets x10 reps small beads
strengthening >Turning a key
exercises and -AAROM clockwise and
functional exercises of counterclockwis
activities. bilat. UE & LE e
on a powder
board x3 sets Impaired Pt. will manifest -Tossing a ball
x10 reps coordination improved 10 mins

20
 coordination of prone-lying
bilat. UE & LE for -Kicking a position
better hanging ball >Supine-lying
performance of supine lying position to
exercises and position 10 mins side-lying
functional position
activities.
-Functional
Impaired Pt. will manifest -Static balance training in a
static & improved static & exercises within close
dynamic dynamic balance // 10 mins: environment c
balance during sitting, >Feet together verbal & tactile
during standing & walking >Tandem cues as to:
standing & for stability all stance >Self-feeding
walking throughout the >Single leg >Self-care
exercises and stance >Bathing
functional >Hygiene
activities. -Dynamic >Transfers
balance
exercises within
Home Exercise Program
// bars 10 mins:
1. AROM exercises of bilat. UE & LE x3 set x10
>Feet together c
reps
perturbations
2. Diaphragmatic breathing exercises supine lying
>Tandem
position 10 mins
stance c
perturbations
Patient Education
>Single leg
1. Skin inspection
stance c
2. Skin care
perturbations
3. Donning and doffing of compression bandage
4. Wearing of eye patch over the eye with ptosis
Impaired Pt. will be able to -Standing within
5. Energy conservation techniques
tolerance tolerate standing // bars 10 mins
6. Activity pacing techniques
during and walking for
standing & better -Hall ambulatory
Precautions
walking 2° LE performance of c gait belt 1+
1. Avoid high-intensity exercises
weakness exercises and assist 10 mins
2. Have frequent rest between exercises
functional
3. Stop the exercise when not tolerated
activities.
4. Never force an exercise
Impaired gait Pt. will -Standing up
2° LE demonstrate and down x3 REFERENCES
weakness improved gait on sets x10 reps Books:
even surfaces for while holding ◊ Emeluth, D. Botulism: Deadly Diseases and
at least 200 m in onto a back of a Epidemics. USA: Chelsea House Publishers;
preparation for chair for support 2006.
community ◊ Emeluth, D. Botulism: Deadly Diseases and
reintegration. -PBWSTT 10 Epidemics. Second Edition. New York, NY:
mins beginning Chelsea House Publishers; 2010.
c 1.5 m/s ◊ Kasper, D. L. Harrison’s Principles of Internal
Medicine. Nineteenth Edition. McGraw Hill
-Stepping over Education; 2015.
objects on a ◊ Montecucco, C. Clostridial Neurotoxins.
level surface c a Springer; 1995.
gait belt 10 mins
1+ assist Websites:
◊ CDC. Botulism. USA: 2019.
↓ ability to Pt. will -Bed mobility https://www.cdc.gov/botulism/index.html#:~:text=
perform demonstrate ↑ exercises 10 Botulism%20is%20a%20rare%20but,arms%2C
functional ability to perform mins: %20torso%2C%20and%20legs
ADLs ADLs in >Side to side
preparation for movement
community >Upward and
reintegration. downward
movement
>Supine-lying
position to long
sitting position
>Supine-lying
position to

21
TETANUS ◊ IV drug uses
◊ Uncleaned, open wound
GENERAL MEDICAL BACKGROUND
PATHOMECHANICS / PATHOPHYSIOLOGY
DEFINITION

◊ An acute disease manifested by skeletal muscle

spasm and autonomic nervous system
disturbances caused by a neurotoxin from
Clostridium tetani and is preventable by
vaccination.

◊ As per CDC, “the acute onset of hypertonia or

… painful muscular contractions (usually of the
muscles of the jaw and neck) and generalized
muscle spasms without other apparent medical
cause”

EPIDEMIOLOGY

◊ Rare
◊ Worldwide - present in the environment.
◊ In 2001 an estimated 282,000 died worldwide
from tetanus, mostly in Asia, Africa and South
America.
◊ The incidence of tetanus in the UK decreased
following the introduction of national tetanus
immunisation in 19612.
◊ Between 1984 and 2002, there were 186 cases
of tetanus in England and Wales, of which 74%
occurred in individuals aged over 45 years.
◊ Most cases occur in incompletely vaccinated or
unvaccinated individuals. Vaccination status is
known in 50% of cases reported in the United
States between 1972 and 2009; among these
cases, only 16% of patients had had three or
more doses of tetanus toxoid.
◊ Neonatal tetanus is an important cause of
mortality in many countries in Asia and Africa
due to infection of the baby's umbilical stump.
◊ According to the latest WHO data published in
2018 Tetanus Deaths in the Philippines reached
690 or 0.11% of total deaths. The age adjusted
Death Rate is 0.80 per 100,000 of population.
ETIOLOGY
◊ Infection from neurotoxin released by
Clostridium tetani (an anaerobic, gram-positive,
spore-forming rod whose spores are highly
resilient and can survive readily in the
environment throughout the world.) Very low
concentrations of this highly potent toxin can
result in tetanus (minimum lethal human dose,
2.5 ng/kg).
o Superficial abrasions to the limbs are
the commonest infection sites in adults.
o Deeper infections (e.g., attributable to
open fracture, abortion, or drug
injection) are associated with more
severe disease and worse outcomes.
◊ In neonates, tetanus occurs due to inadequate
umbilical cord care, circumcision, or
ear-piercing.
CLASSIFICATION
◊ Generalized tetanus - attacks muscles
throughout the entire body and is the most
common form; the tetanospamin attacks and
inhibits mostly the motor neurons of the CNS
and later the neurons of the ANS as well.
◊ Local tetanus - occurs before generalized
tetanus but this is a much milder form with a
decreased amount of associated toxin release;
attacks muscles in a specific (local) area of the
body
◊ Cephalic tetanus - is rare and shows a
combination of both generalized and local
tetanus; characterized by facial spasms and
paralysis as a result of involvement of the cranial
nerves.
◊ Neonatal tetanus - an illness occurring in a
child who has the normal ability to suck and cry
in the first 2 days of life but who loses this ability
between days 3 and 28 of life and becomes rigid
and has spasms.
◊ Maternal tetanus - tetanus occurring during
pregnancy or within 6 weeks after the conclusion
of pregnancy (whether with birth, miscarriage, or
abortion)
CLINICAL PRESENTATION
Localized Tetanus:
◊ Isolated, small areas of local muscle spasm

RISK FACTORS ◊ CN involvement in localized cephalic tetanus,

the pharyngeal or laryngeal muscles may
◊ Unvaccinated or incomplete vaccination spasm, with consequent aspiration or airway
◊ Age ≥ 65 years old obstruction, and the prognosis may be poor
◊ DM
◊ History of immunosuppression Generalized tetanus
22
◊ The commonest initial symptoms are trismus
(lockjaw), muscle pain and stiffness, back pain,
and difficulty swallowing.
◊ Neonates typically present with inability to suck
◊ As the disease progresses, very painful muscle
spasm develops.
◊ Laryngeal muscle spasms occur early or even in
isolation which can completely obstruct the
airways.
◊ The few conditions that mimic generalized
tetanus include strychnine poisoning and
dystonic reactions to antidopaminergic drugs.
Abdominal muscle rigidity is characteristically
continuous in tetanus but is episodic in the latter
two conditions.
Tetanus Strychnine poisoning
Hx of injury present Evidence of poisoning

◊ Spasm of the respiratory muscles results in Gradual onset Sudden

respiratory failure. Without ventilatory support,
respiratory failure is the commonest cause of Lockjaw is present No lock jaw; generalized
death in tetanus. convulsions
◊ Spasms strong enough to produce tendon Sustained rigidity between Complete relaxation
avulsions and crush fractures (rare) convulsions between seizures
◊ Autonomic disturbance is maximal during the
Abdominal muscle rigidity Abdominal muscle rigidity is
second week of severe tetanus, and death due is continuous. episodic.
to cardiovascular events becomes the major
risk. Death is delayed for few Death in few hours
◊ Blood pressure is usually labile, with rapid days
fluctuations from high to low accompanied by Not so. Chemical analysis reveal
tachycardia. poisoning
◊ Episodes of bradycardia and heart block can
also occur.
◊ Cephalic tetanus can be confused with other
◊ Autonomic involvement is evidenced by
causes of trismus, such as oropharyngeal
gastrointestinal stasis, sweating, increased infection.
tracheal secretions, and acute (often
high-output) renal failure. ◊ Hypocalcemia and meningoencephalitis are
included in the differential diagnosis of neonatal
COMPLICATIONS tetanus.
Hypocalcemia Meningoencephalitis
◊ Laryngospasms
◊ Fractures Involves extremities more Abnormal tone & nuchal
◊ Hypertension than the trunk; Chvostek's rigidity, but not normal
◊ Nosocomial infections & Trousseau’s sign sensory as in tetanus
◊ Pulmonary embolism
◊ Aspiration pneumonia
◊ Death due to cardiovascular/ pulmonary events Tetanus (Lockjaw) Tetany
◊ Vocal cord paralysis leading to respiratory
distress An infection characterized A medical consisting of
◊ Autonomic dysfunction- leading to hypertension by mm spasms beginning the involuntary mm
◊ Asphyxia in the jaw & progress to the contractions which may
◊ Paralytic ileus rest of the body be caused by other
◊ Joint dislocation Spasms may be so severe diseases that increase
◊ Pressure sores that bone fx may occur the AP frequency of mm
◊ Stress ulcers Other sx: fever, heading, cells or nerves that
◊ Coma trouble swallowing, high innervate them
◊ Nerve palsy blood pressure, fast HR Mainly d/t hypocalcemia
◊ Urine retention
◊ Seizures Chvostek sign
Trousseau’s sign
MEDICAL DIAGNOSIS
◊ Wound culture - Presence C. tetani from a
wound provides supportive evidence for tetanus
PROGNOSIS
diagnosis
◊ Serum anti-tetanus immunoglobulin G level
◊ Rapid development of tetanus is associated with
o Serum levels >0.1 IU/mL are deemed
more severe disease and poorer outcome
protective and do not support the
◊ The incubation period (time from wound to first
diagnosis of tetanus.
symptom) and the period of onset (time from first
◊ Bioassay for serum tetanus toxin
symptom to first generalized spasm) are of
◊ Polymerase chain reaction also has been used
particular significance. Shorter times are
for detection of tetanus toxin, but its sensitivity is
associated with worse outcomes.
unknown.
◊ In neonatal tetanus, the younger the infant is
when symptoms occur, the worse the prognosis.
DIFFERENTIAL DIAGNOSIS

23
 ◊ Children and neonates have a higher incidence laryngeal mm makes endotracheal suctioning
of neurologic sequelae and may be at increased difficult.
risk of learning disabilities, behavioral problems, PHARMACOLOGICAL MANAGEMENT
cerebral palsy, and deafness.
◊ Recovery is generally accepted unless periods ◊ If an individual has contracted tetanus, drugs of
of hypoventilation have been prolonged or other
complications have ensued. choice are penicillin and metronidazole.
◊ Additional drugs include Erythromycin,
Factors Associated with POOR Prognosis in Tetanus tetracycline, chloramphenicol, clindamycin
Adult Tetanus Neonatal Tetanus Medications Dose Indication

Age >70 years Younger age, premature Penicillin 100,000 IU - GABA

Incubation period <7 days birth 200,000 antagonist &
Short time from first symptom Incubation period <6 days IU/kg/day associated c
to admission Delay in hospital convulsions
Puerperal, IV, post surgery, admission
burn entry site Grass used to cut cord
Metronidazole 400 g (rectally) Best tx in
Period of onset <48 h Low birth weight
Heart rate >140 beats/min Fever on admission 500 g (IV) every treating &
SBP >140 mmHg 6 hrs for 7 days preventing
Severe disease or spasms anaerobic
Temperature >38.5°C bacterial dse
◊ Failure to remove toxic pockets may elicit
recurrence
GENERAL HEALTHCARE MANAGEMENT
◊ Anti-toxin should be given in an early attempt to
MEDICAL MANAGEMENT
deactivate any circulating tetanus toxin &
prevent the uptake into the nervous system.
◊ Recovery may take 4-6 weeks. There are two preparations available:
◊ The management of tetanus is categorized into Two Antitoxin Preparation
three steps.
1. The organism in the body needs to be destroyed Human Tetanus Immune Equine Derived
to prevent further release of the toxin. globulin (HTIG) Antitoxin
2. The toxin in the body outside of the CNS needs
to be neutralized. 3,000 - 5,000 IU as a 10,000 - 20,000 IU as a
3. The effects of the toxin in the CNS need to be single IU dose single dose or divided
minimized. doses after testing for
◊ Wound debridement should be done to help hypersensitivity
remove the toxins from the body.
o Entry wound should be cleaned & A portion of should be
debrided of necrotic material in order to injected around the
remove anaerobic foci to prevent further wound
infection.
◊ The general medical management consists of Preparation of choice as Used in low-income
controlling the spasms, preventing other it’s less likely to be countries
infections, control fluid and electrolyte balance, associated c any
and respiratory support. anaphylactoid reactions
◊ The primary way to control muscle spasms is
sedation and muscle relaxants **Intrathecal injections of HTIG (50-1500 IU) prevents
◊ Establish a secure airway early in the severe disease progression & leads to better outcome
tetanus to prevent respiratory complications.
◊ Pt should be given the full primary course of ◊ To control mm spasms, pt. are treated in a calm,
immunization. quiet environment as light and noise can trigger
◊ Tetanus is highly prevented by good wound care spasms; mm relaxants are also given including
and immunization. chlorpromazine, phenobarbital, IV magnesium
sulfide.
◊ In neonates, the use of safe, clean delivery as o The problem is the dose necessary to
well as umbilical cord practices and maternal control spasms also cause respiratory
vaccinations can be essential. depression thus in resource limited
◊ Physical therapy should be started as soon as setting s mechanical ventilators,
spasms have ceased, since tetanus patients controlling spasms & providing
often are left with disability from prolonged adequate ventilation is problematic
muscle wasting and contractures resulting in respiratory failure.
o If c ventilary equipment, severe spasms
SURGICAL MANAGEMENT are best controlled c combination of
◊ Tracheostomy is the usual method to secure sedatives or magnesium in relatively
airways in severe tetanus. Tracheal secretions short acting cardiovascular inert,
and dysphagia occurs d/t pharyngeal nondepolarizing neuromuscular blocking
involvement combined c hyperactivity of
24
 agents that allow titration against spasm o For a person who has received a
intensity. complete primary course but no further
◊ Cardiovascular instability in severe tetanus is boosters, 2 doses at least 4 weeks apart
are recommended.
difficult to treat as rapid fluctuations in BP & HR
occur. It is improved by increasing sedation c IV ◊ WHO standard for prevention of maternal &
magnesium sulfate. neonatal tetanus call for admission of 2 tetanus
toxoid at least 4 weeks apart to previously not
Medications Indication
immunized pregnant women; however in high
Magnesium Sulfate Reduces muscle spasm; risk areas a more intensive approach has been
blocks catecholamine successful with all women of child bearing age
release from nerves, and receiving a primary course.
reduces receptor ◊ Education, safe delivery potential postnatal
responsiveness to practices should also be taught to pregnant
catecholamines women.
◊ Sustaining tetanus prone wounds should be
Beta-blockade Control autonomic
dysfunction immunized when vaccination status is
Labetalol (0.25 to 1 incomplete or unknown or if their last booster
mg/min) was given more than 10 years ago.

Morphine sulfate (0.5 OTHER HEALTHCARE MANAGEMENT

to 1 mg/kg per hour by ◊ SLP
continuous intravenous ◊ OT
infusion) ◊ RT
◊ Nurse practitioner
◊ Optometrist
◊ Prophylaxis of thromboembolism with heparin,
◊ Ophthalmologist
low molecular weight heparin, or other
anticoagulants should be administered early. ◊ Cardiologist
◊ Pulmonologist
◊ Tetanus can be prevented by vaccination
PHYSICAL THERAPY, EXAMINATION, EVALUATION,
through being injected by the tetanus toxoid. AND DIAGNOSIS
o 2 forms of toxoid: adsorbed toxoid &
fluid toxoid POINTS OF EMPHASIS ON EXAMINATION
o has been combined c pertussis &
diphtheria to make DTaP vaccines for
infants: at 2 mos, a series of 4 injections Test Expected Results
on monthly intervals; 4, 6, 15-18 mos,
and a booster shot between 4 to 6 y.o History Infections of Clostridium tetani from:
● Superficial abrasions to the
limbs
DTap Vaccine TDAp Vaccine ● Deeper infections (e.g.,
attributable to open
Diphtheria and tetanus Tetanus and diphtheria fracture, abortion, or drug
toxoid and acellular toxoid and cellular injection)
pertussis pertussis ● In neonates, tetanus occurs
due to inadequate umbilical
Given to infants 6 weeks Given as a one time does cord care, circumcision, or
to 6 years of age to adolescents and adults ear-piercing.
Drug addicts
Animal bites
DT Vaccine Td Vaccine Home births

Diphtheria and tetanus Tetanus and diphtheria Chief Complaint Painful lockjaw, severe muscle
toxoid toxoid rigidity/ spasms, headache

Given to infants 6 weeks Given to children and Cognition Lethargic & irritable
to 6 years who have a adults 7 years and older.
contraindication for Contains smaller doses of Communication Impaired speech & swallowing
pertussis diphtheria owing to pharyngeal involvement
◊ WHO: Tetanus vaccination consists of a primary
course of 3 doses in infancy, boosters at 4-7 and VS ↑ BP & HR, ↓RR owing to infection
12-15 y.o, 1 booster in adulthood. & severe spasms, respectively
◊ US-CDC: There should be an additional dose at CEM ↓ CEM 2° stiffness of respiratory
14-16 mos & booster dose every 10 years. mm
◊ Catch up schedule recommends 3 doses of
Aerobic ↓ aerobic capacity 2° stiffness of
primary course for unimmunized adults, followed
Capacity respiratory mm
by 2 further doses.

25
VIsual Acuity/ Impaired vision. spasm; May be unable
Hearing Skills to walk

Integumentary Skin Normothermic/ Functional Ax Modified to complete

Ax hyperthermic dependence in
performing ADLS owing
Tone Hypertonicity; MAS to weakness & severe
Grade 4 mm spasm.

Risk for DVT Well’s ↑ risk 2° immobilization Other Test Spatula (+) Reflex spasm of the
Test to not trigger spasm Test masseters and bite the
spatula
Risk for Braden’s ↑ risk 2° immobilization
Pressure Sore Scale to not trigger spasm Lab study Moderate peripheral
leukocytosis
Sensory Ax Altered sensation. Loss
of sensation near the
wound. PT PROBLEM LIST
◊ Lockjaw
Reflexes DTR Hyperreflexive ◊ Lethargy
◊ Headache
Cranial Nerve III Ophthalmoplegia, ◊ Impaired speech & swallowing owing to
Ax dilated pupil pharyngeal involvement
◊ ↑ BP & HR, ↓RR owing to infection & severe
IV Diplopia spasms, respectively
◊ ↓ CEM 2° stiffness of respiratory mm
VI Ophthalmoplegia ◊ ↓ aerobic capacity 2° stiffness of respiratory mm
◊ Impaired vision.
VII Ptosis, facial paralysis ◊ Hypertonicity
◊ Risk for DVT
IX Impaired gag reflex ◊ Risk for pressure sore
◊ Altered sensation.
X Dysphonia, dysphagia ◊ Hyperreflexive DTR
◊ Impaired CN III, IV, VI, VII, IX, X
ROM AROM ↓AROM all throughout ◊ LOM as to AROM & PROM all throughout the
the body 2° severe body 2° severe spasticity
spasticity ◊ Generalized weakness owing to immobility &
hypertonicity
PROM ↓PROM all throughout ◊ Atrophy 2° physical inactivity owing to severe
the body 2° severe mm spasms
spasticity ◊ Poor head control owing to stiff neck mm
◊ Poor fine motor skill 2° impaired mobility &
MMT ↓MMT all throughout
severe spasticity
the body 2° impaired
◊ Impaired coordination 2° weakness & severe
mobility & severe
spasm
spasticity
◊ Impaired bal/tol 2° weakness & severe spasm
◊ Impaired posture c opisthotonus
MBT Atrophy 2° physical
◊ Impaired gait 2° weakness & severe spasm
inactivity owing to
◊ Modified to complete dependence in performing
severe mm spasms
ADLS owing to weakness & severe mm spasm
FMT(for infants) Poor head control
PT DIAGNOSIS
owing to stiff neck mm
◊ Pattern 5A: Primary Prevention/Risk Reduction
Fine Motor Poor 2° impaired for Loss of Balance and Falling
Skills mobility & severe ◊ Pattern 5B: Impaired Neuromotor Development
spasticity
PT PROGNOSIS
Coordination Ax Impaired coordination
2° weakness & severe ◊ Rapid development of tetanus is associated with
spasm more severe disease and poorer outcome
◊ The incubation period (time from wound to first
Balance & Impaired bal/tol 2° symptom) and the period of onset (time from first
Tolerance Ax weakness & severe symptom to first generalized spasm) are of
spasm particular significance. Shorter times are
associated with worse outcomes.
Postural Ax Impaired. (+) ◊ In neonatal tetanus, the younger the infant is
Opisthotonus when symptoms occur, the worse the prognosis.
◊ Children and neonates have a higher incidence
Gait Ax Impaired gait 2° of neurologic sequelae and may be at increased
weakness & severe
26
 risk of learning disabilities, behavioral problems,
Facial Pt. will manifest ES to facial
cerebral palsy, and deafness.
paralysis improved muscle muscles x 10
◊ Recovery is generally accepted unless periods
tone of the face mins
of hypoventilation have been prolonged or other
for better social
complications have ensued.
interaction as to Massage x 10
facial mins
Factors Associated with POOR Prognosis in Tetanus expressions.
Facial exercises x
Adult Tetanus Neonatal Tetanus 10 mins facing a
mirror
Age >70 years Younger age, premature (smiling,
Incubation period <7 days birth
frowning, puffing
Short time from first symptom Incubation period <6 days
to admission Delay in hospital face, raising
Puerperal, IV, post surgery, admission eyebrows,
burn entry site Grass used to cut cord scrunching face,
Period of onset <48 h Low birth weight egad, etc)
Heart rate >140 beats/min Fever on admission
SBP >140 mmHg ↓ CEM 2° Pt will present an Diaphragmatic
Severe disease or spasms stiffness of increase in breathing
Temperature >38.5°C respiratory respiratory mm exercise x 5 reps
mm strength to x 2 sets
facilitate proper
PHYSICAL THERAPY PLAN OF CARE breathing and Chest press x 10
◊ Main goal of PT: Prevent muscle rigidity and avoid respiratory reps x 2 sets
spasms complications.
◊ Cardiopulmonary physiotherapy can be used to Shoulder
help in the prevention of respiratory retraction x 10
complications reps x sets

↓ aerobic Pt will present c PLB x 5 reps x 2

Problem Goals Interventions capacity 2° increased aerobic set
List stiffness of capacity to
respiratory normalize Abdominal
Hypertonicity Pt. will exhibit Neutral warmth x mm breathing and to Breathing
decreased or 10 min decrease fatigue Exercises x 5
close to normal during reps x 2 sets
tone to improve Slow rolling x 10 performance of
mobility and allow reps x 2 set ADL. Low to Moderate
active exercises. Intensity Aerobic
Stretching x 15 Exercises
SH x 5 reps (swimming,
walking and
Altered Pt. will Conventional jogging) x 20 min
sensation demonstrate TENS 80 Hz x 15
improved mins LOM as to Pt. will manifest ↑ Gentle stretching
sensation to be AROM & AROM & PROM x 15 SH x 5 reps
able to receive Effleurage x 10 PROM all of bilat. UE & LE per mm group
tactile cues mins throughout in preparation for
essential in the body 2° strengthening PROM using PNF
exercises and Sensory severe exercises and patterns x 5 reps
daily activities re-education spasticity functional x 3 sets on bilat.
exercise x 10 activities. UE & LE
mins
AROM using PNF
Impaired Pt. manage Compensatory patterns x 5 reps
vision impaired vision for techniques by x 3 sets on bilat.
better verbal & tactile UE & LE
performance of cueing.
exercises and Generalized Pt. wil manifest ↑ PREs using 2-lb
functional Pt. safety weakness strength and mm cuff wts x 5 reps
activities. education owing to bulk of large x 3 sets on bilat.
immobility & muscle groups of UE & LE
Home hypertonicity bilat. UE & LE for
modifications by improved OKC exercises c
installing better Atrophy performance of 2-lb cuff wts x 5
lighting and use functional reps x 3 sets
of vibrant color in activities.
labels. CKC exercises c
2-lb cuff wts x 5
reps x 3 sets

27
Poor head Pt. will be able to Supine lying Impaired Neutral warmth x
control develop head while object on posture c 10 min
control for stability the visual field x opisthotonus
during exercises 10 mins Slow rolling x 10
and functional reps x 2 set
activities. Head control
activities while Stretching x 15
prone-lying on a SH x 5 reps
wedge board c
toys placed on Strengthening
the visual field to exercises x 10
lift head x 10 reps x 2 sets
mins
Impaired gait Pt. will If pt is able:
Prone-lying on a demonstrate Gait training in //
medicine ball improved gait on bars while
while slightly even surfaces for wearing bilat
tilting to side x 5 at least 20ft in HKAFO/KAFO x
mins preparation for 5 mins
community
Poor fine Pt. will Gross prehension reintegration.
motor skill demonstrate activities 10 mins: PBWSTT while
improved fine -Transferring wearing bilat
motor skills for small balls HKAFO/KAFO x
better -Pulling a 2-in 10 mins
performance of ribbon beginning c 1.5
exercises and -Transferring m/s
functional bottles
activities. Room ambulation
Fine prehension while wearing
activities 10 mins: bilat
-Picking up sticks HKAFO/KAFO c
-Picking up small 1+ assist x 10
beads mins
-Turning a key
clockwise and Modified to Pt. will Low to Moderate
counterclockwise complete demonstrate Intensity Aerobic
dependence improved Exercises
Impaired Pt. will manifest Finger in performing independence in (swimming,
coordination improved coordination, heel ADLS the ability to walking and
coordination of to shin ex, perform ADLs in jogging)
bilat. UE & LE for finger/toe preparation for
better touching x 10 community Functional
performance of reps each reintegration. Simulation
exercises and Training of pt’s
functional Touching a ADLs highlighting
activities. balloon while the quality of
supine lying x 5 movement
min per UE
Refer to OT for
Kicking a hanging better functional
ball supine lying treatment
position x 5 mins
Risk for DVT Pt. will Ankle pumps x 10
Impaired Pt. will manifest Sitting c demonstrate ↓ risk reps x 2 sets
bal/tol improved balance perturbations x 5 for DVT for better
and tolerance for min performance of Toe wiggles x 10
better exercises and reps x 2 sets
performance of If pt is able: functional
exercises and Standing within // activities. Pt. education:
functional bars while Donning and
activities. wearing doffing of
HKAFO/KAFO x compression
5 mins bandage
Regular skin
SLS within // bars check and care
while wearing
HKAFO/KAFO x Risk for Pt. will Bed mobility
5 mins pressure demonstrate ↓ risk exercises x 10
sores for pressure sores mins

28
 ● Kirwan, C. (2006). Tetanus. Retrieved from
for better
https://www.healthknowledge.org.uk/public-healt
performance of Pressure-relief
h-textbook/disease-causation-diagnostic/2b-epid
exercises and exercises 10
emiology-diseases-phs/infectious-diseases/tetan
functional mins
us
activities. Pt. education:
● Thwaites, L. Tetanus. 2021. Available at
-Proper nutrition
https://www.uptodate.com/contents/tetanus#H27
-Regular position
change
-Regular skin
check and care

Impaired Refer to SLP

speech &
swallowing

Ophthalmopl Refer to Optometrist/ Ophthalmologist

egia, diplopia

Cardio and Refer to Cardiologist and/or

Respiratory Pulmonologist
complication

Home Exercise Program

1. Stretching x 15 SH x 5 reps
2. PROM & AROM exercises using PNF patterns x
10 reps x 2 sets
3. Low to Moderate Intensity Aerobic Exercises
depending on the pt’s time and tolerance

Patient Education
1. Skin inspection and care
2. Donning and doffing of compression bandage
and orthosis
3. Wearing of eye patch over the eye with ptosis
4. Energy conservation techniques
5. Activity pacing techniques
6. Home modifications as appropriate to patient’s
need
7. Take medications only as prescribed by your
physician

Precautions
1. Avoid bright lights and noisy environment as
they may trigger the patient’s spasms
2. Perform exercises/ activities during the peak
dose of medications for easier and quality
performance of task
3. Avoid high-intensity exercises
4. Have frequent rest between exercises
5. Stop the exercise when not tolerated
6. Never force an exercise

REFERENCES

Books:

◊ Heymann DL, editor, Control of Communicable

Disease Manual. 18th ed. American Public
Health Association, 2004.
◊ Salisbury DM, Begg NT. Immunisation against
infectious disease (The green Book). London:
HMSO, 1996. Available at
http://www.dh.gov.uk/assetRoot/04/07/29/84/040
72984.pdf

Websites:

● Center for Disease Control and Prevention.

Tetanus for Clinicians, 2020. Retrieved from
https://www.cdc.gov/tetanus/clinicians.html
29
PHARMACOLOGICAL MANAGEMENT SUMMARY

Medications Functions Side Effects PT Implications

Anticholinesterase Improve muscle strength in myasthenia gravis Diarrhea, Abdominal cramps, Overdose may increase muscle weakness and other side effects.
(Pyrodostigmine) Salivation and Nausea Perform exercises at about 1 to 2 hours after taking meds for peak
performance

Beta-blockers Anti-HTN medication or lowers BP Blunted HR, Dizziness, OH Use RPE to monitor exercise intensity
(Propanolol, [-olol]) Pt. is at risk for falls so always put on a gait belt for safety and be
cautious.
Penicillin G This recommended in the treatment of wound Skin rashes, itching, respiratory May have to alter the time of the rehabilitation session to work around the
botulism and is said to increase circulating difficulty (such as wheezing), GI side effects, especially if GI and similar side effects tend to occur at a
botulinum toxin from lysis of bacterial cells problems specific time of the day.
Metronidazole Best in treating and preventing anaerobic GI distress, allergic reactions, CNS May have to alter the time of the rehabilitation session to work around the
bacterial diseases. symptoms side effects, especially if GI and similar side effects tend to occur at a
specific time of the day.

PT PLAN OF CARE SUMMARY

PROBLEM GOAL INTERVENTION

Difficulty in breathing 2° weak ○ Diaphragmatic strengthening exercises to increase diaphragm
Pt. will present c an Increase muscle strength of weak respiratory musculature
respiratory musculature strength
in order to facilitate proper breathing and avoid respiratory complications
○ Chest press & shoulder retraction x 10 reps x 2 sets

Fatigue ○ Low to Moderate Intensity Aerobic Exercises (swimming, walking and

Altered sensation
Abnormal muscle tone
Pt. will present c increased aerobic capacity to promote proper breathing and to
jogging) x 20 mins
decrease fatigue in performance of activities of daily living.
○ Pursed Lip and Abdominal Breathing Exercises (5 reps x 2 sets)
Pt. will demonstrate improved sensation to be able to receive tactile cues ○ Conventional TENS 80 Hz x 15 mins for pain relief
essential in exercises and daily activities. ○ Effleurage x 10 mins
○ Sensory re-education exercise x 10 mins
Hypotonicity
Pt. will manifest a normal muscle tone for better performance of exercises and
○ Rood’s facilitatory Technique quick icing x 3 reps to each extremity
functional activities.
○ Rood’s facilitatory Technique light moving touch x3-5 reps to each
extremity
Hypertonicity
○ Neutral warmth x 10 mins
○ Slow rolling x 10 reps x 2 set
○ Stretching x 15 SH x 5 reps

30
Decreased ROM
Decreased muscle strength
Impaired posture
Pt. will manifest ↑ AROM & PROM of bilat. UE & LE in preparation for
strengthening exercises and functional activities..
Pt.will be able to regain near normal to normal muscle strength to enable
better performance of ADLs or to promote a stable base of
support when performing activities in standing or something like that.
Pt. will show an improvement in posture in order to facilitate increase in
breathing and proper body alignment
○ Gentle stretching x 15 SH x 5 reps per mm group
○ ROM exercises using PNF patterns x 5 reps x 3 sets
○ Light Resistance Strengthening Exercises using free weights,
therabands, dumbbells beginning from 5 reps x 3 sets then progress
depending on the pt’s tolerance.
○ FES (50 ms pulse duration, 1:2 pulse interval, 50 Hz frequency) to
large muscle groups of UE and LE for 20 mins.
○ Biofeedback to large muscle groups of bilat. UE & LE 20 mins
○ Postural correction in front of mirror c verbal and tactile cues
○ Strengthening the weak postural muscles for 10 reps x 2 sets
depending on the pt’s posture
○ Gentle Stretching to tight postural muscles for 10 reps x 2 sets

Impaired balance and Pt. will present c an improvement in balance and coordination to reduce risk of ○ Reaching exercises in all directions while on a seated position for 7
coordination falls and in preparation for gait training and other functional activities. reps x 2 sets
○ Standing Reaching Exercises while feet together in all directions x 10
reps x 2 sets and progressed to feet apart, feet in tandem, eyes
closed and farther distance as tolerated by the pt.
○ Dual task exercises (alternately raising UE and LE, L and R) x 10
reps x 2 sets

Impaired gait Pt. will present c an improved gait pattern in order to walk properly and safely ○ Ambulation Training for 15 mins c therapist supervision highlighting
to promote carry over to safe ambulation at home. the quality of movement
○ Stretching and Strengthening to major muscle groups of the LE for
10 reps x 2 sets
○ Low to Moderate Intensity Aerobic Exercises (swimming, walking and
jogging) x 20 mins
Impaired functional
Pt. will demonstrate improved independence in the ability to perform ADLs in ○ Low to Moderate Intensity Aerobic Exercises (swimming, walking and
performance of ADLs
preparation for community reintegration. jogging) x 20 mins
○ Functional Simulation Training of pt’s ADLs highlighting the quality of
movement
○ Refer to OT for better functional treatment
HOME EXERCISE PROGRAM PRECAUTIONS
1. Low to Moderate Intensity Aerobic Exercises (swimming, walking and 1. Avoid bright lights and noisy environment as they may trigger the patient’s spasms
jogging) x 20 mins 2. Perform exercises/ activities during the peak dose of medications for easier and quality performance
2. Breathing exercises of task
3. ROM exercises 3. Avoid high-intensity exercises.
4. Strengthening exercises 4. Have frequent rest between exercises.
5. Pressure relief techniques 5. Stop the exercise when not tolerated or with presence of exacerbations.
6. Home and activity modification as needed 6. Never force an exercise when feeling unwell.
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7. Energy conservation technique
8. Proper nutrition

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