SPINAL CORD INJURY (INCOMPLETE)

Mel, Maya Angelou

Queri, Justine Paolo

Spinal Cord Injury

 result from injury to spinal cord
 disruption of ascending and descending tracts
 traumatic insult to spinal cord that can result in alteration of normal motor,
sensory and autonomic function

Related Anatomy
Spinal Cord – serves as a main connection between the brain and the body. It
allows the brain to send orders and messages to the muscles of the body. These
messages result in our ability to breathe, move and walk. The nerves that go from
the spinal cord to the arms, legs, chest and abdomen are called peripheral nerves.
The spinal cord is located in the spine and protected by vertebrae.
Vertebrae – a solid bony structures that are separated by soft disks that allow the
spine to bend and twist.
 Dorsal root – sensory fibers
 Ventral root – motor fibers
(Dorsal and ventral roots join at intervertebral foramen to form the spinal
nerve)
 Gray Matter – seen as H-shaped pillar with anterior and posterior gray
columns or horns, united by thin gray commisure containing small central
canal.
 White Matter – for purposes of description, may be divided into anterior,
lateral and posterior white columns or funiculi.
Rexed Laminae
Posterior/dorsal horn
 Lamina I:Posteromarginal nucleus
 Lamina II: Substantia Gelatinosa of Rolando
 Laminae III/IV: Nucleus Proprius
 Lamina V: Neck of the dorsal horn
 Lamina VI: Base of the dorsal horn
Intermediate zone
  Lamina VII: Intermediomedial nucleus, Intermediolateral nucleus, Nucleus
dorsalis of Clarke in thoracic and upper lumbar region
 Lamina X: Central gray matter; Grisea Centralis
Anterior/ventral horn
 Lamina VIII: Motor interneurons; Commissural nucleus
 Lamina IX: Lateral (in limb regions) and Medial motor neurons,
also phrenic and spinal accessory nuclei at cervical levels, Onuf's nucleus in
the sacral region
Centrally
 Lamina X: Central Zone, gray matter surrounding the central canal
Ascending Tracts – bundles of ascending fibers serve to link different segments of
the spinal cord, while other ascends from the spinal cord to higher centers and, thus
connect the spinal cord with the brain.
 Exteroreceptive– originates from outside the body such as pain, temperature
and touch
 Proprioceptive – originates from inside the body such as muscle and joint
position.

 Lateral Spinothalamic Tract– pain and temperature pathway

 Anterior Spinothalamic Tract – light touch and pressure pathway
 Dorsal Column-Medial Lemniscus Tract – discriminative touch, vibratory
sense and muscle joint sense

 Fasciculus Gracilis – present throughout the length of the spinal cord and
contains the long ascending fibers from the sacral, lumbar and lower six
thoracic spinal nerves.
 Fasciculus Cuneatus– situated laterally in the upper thoracic and cervical
segments of the spinal cord and is separated from the fasciculus gracilis by a
septum.

Descending Tracts – the motor neurons situated in the anterior gray columns of the
spinal cord send axons to innervate skeletal muscle through the anterior roots of the
spinal nerves.
 Lower Motor Neurons – nervous impulses that descend from the medulla,
pons, midbrain and cerebral cortex, as well as those that enter along sensory
fibers from the posterior roots.
 Upper Motor Neurons – nerve fibers descend in the white matter from
different supraspinal nerve centers are segregated into nerve bundles called
descending tracts.

 Corticospinal Tracts– for voluntary movement thus used in performing rapid

skilled movements
 Reticulospinal Tracts– to hypothalamus for control of sympathetic and sacral
parasympathetic outflow
 Tectospinal Tracts– reflex postural movement concerning sight
 Rubrospinal Tracts– activity of flexor muscle and inhibits extensor muscle
activity
 Vestibulospinal Tract –reciprocal of rubrospinal tracts in association with
maintenance of balance
 Olivospinal Tracts – influence activity of the motor neurons in anterior gray
column
 Intersegmental Tracts – interconnect the neurons of different segmental level
 Descending Autonomic Fibers– control sympathetic and parasympathetic
systems

Corticospinal Tract

Spinothalamic Tract
Dorsal Column Lemniscal

Blood supply of the Spinal Cord

The spinal cord is supplied with blood by three arteries that run in the brain,
and arteries that approach through the sides of the spinal column. The three
longitudinal arteries are called the anterior spinal artery, and the right and
left posterior spinal arteries. These travel in the subarachnoid space and send
branches into spinal cord. They form anastomoses via anterior and
posterior segmental medullary arteries, which enter spinal cord at various points
along its length.
The major contribution to the arterial blood supply of the spinal cord below the
cervical region comes from the posterior and anterior radicular arteries, which run
into the spinal cord alongside the dorsal and ventral nerve roots. These intercostal
and lumbar radicular arteries arise from the aorta, provide major anastomoses and
supplement the blood flow to the spinal cord. In humans the largest of the anterior
radicular arteries is known as the artery of Adamkiewicz, or anterior radicularis
magna artery, which usually arises between L1 and L2, but can arise anywhere from
T9 to L5. Impaired blood flow through these critical radicular arteries, especially
during surgical procedures that involve abrupt disruption of blood flow through the
aorta for example during aortic aneurysm repair, can result in spinal cord infarction
and paraplegia.

Dermatomes
A portion of the skin innervated by sensory axons under a particular
segmental nerve root. This is useful in assessing improvement or deterioration.
Nerve
Dermatome Myotome
Root

C1 Vertex of skull None

 Longuscolli, SCM, Rectus
C2 Temple, Forehead, Occiput
capitis

Neck, Posterior cheek, Temporal area,

C3 Trapezius, Levator scapulae
prolongation forward under mandible

Shoulder area, clavicular area, Upper

C4 Trapezius, Splenius capitis
scapular area

Deltoid area, Anterior aspect of entire arm Supraspinatus, Infraspinatus,

C5
to base of thumb Deltoid, Biceps

Anterior arm, Radial side of hand to Biceps, Supinator, Wrist

C6
thumb and index finger extensors

Lateral arm and forearm to index, middle,

C7 Triceps, Wrist flexors
and ring fingers

Medial arm and forearm to middle, ring, Ulnar deviators, thumb

C8
and pinky fingers extensors, thumb adductors

Medial side of forearm to base of pinky

T1 No weakness noted
finger

L1 Back, Over trochanter and groin None

L2 Back, front of thigh to knee Psoas, Hip adductors

Back, Upper buttock, Anterior thigh and Psoas, Quadriceps, Thigh

L3
knee, Medial lower leg atrophy

Medial buttock, Lateral thigh, Medial leg, Tibialis anterior, Extensor

L4
Dorsum of foot, Big Toe hallucis

Buttock, Posterior and lateral thigh,

Extensor hallucis, Peroneals,
Lateral aspect of leg, Dorsum of foot,
L5 Gluteus medius, Dorsiflexors,
Medial half of sole, First, second, third
Hamstring and calf atrophy
toes

Calf and hamstring, Wasting of

S1 Buttock, Thigh, and Leg posterior gluteals, Peroneals, Plantar
flexors

Calf and hamstring, Wasting of

S2 Buttock, Thigh, and Leg posterior gluteals, Peroneals, Plantar
flexors
Myotomes
Segmental nerve root innervating a muscle, again important in determining
level of injury

Pathopysiology
Secondary injury cascade
Is a term that refers to a series of biochemical processes that occur
after an SCI, and that tend to cause further neuronal damage beyond the
mechanical damage caused at the moment of impact. Ischemia of the gray
matter at the site of injury occurs almost immediately after SCI. This ischemia
appears to result from vasoconstriction ofblood vessels supplying the cord,
and is mediated by the rapidrelease of various vasoactive substances such
as serotonin,thromboxanes, platelet-activating factor, peptideleukotrienes,
and opioid peptides after SCI. Ischemia is followed by the development of
edema at the site of injury.

Epidemiology
 Describes striking the young active and well educated people
 Common in half of the person injured younger than 30 y/o
 Occurs frequently in summer and weekends
 More likely to single and divorced
 More common in educated people
 Male > female (4:1)
 80% male
 85% labor force
 59% single
 60% employed
 20% students
 o Quadriplegia – 55% of cases
o Paraplegia 45% of cases
Incidence:
 48% whiplash injury
 21% falls
 15% acts of violence
 14% sports
Falls – most common cause in age > 40 y/o
Traumatic – common in younger age < 40 y/o

Non-traumatic – 30% of cases

1. Tumor
2. Infection
3. Nutritional deficiency
4. Avascular
5. Rheumatoid Arthritis

Etiology
1. Traumatic
- most frequent cause of injury in adult rehab population
- caused by MVA, falls, stab wounds, penetrating injury, GSW, sports
activities
2. Non-traumatic
- Secondary to disease pathologic influence such as vascular
malformation, vertebra subluxation due to RA, transverse myelitis,
neoplasm, abscess of spinal cord, neurological disease such as MS
and ALS

 Occurs from directed forces produced by movement of head and trunk less
often direct injury to vertebra
o C5-C7 – highest frequency of injury
o T12-L2 – affected in thoracolumbar region (weight bearing)
 in Flexion – anterior cord injury
o Compression
 in Hyperextension – whiplash injury
o Spinal Stenosis
o Osteoarthritis
 in Flexion Rotation – combination of anterior and posterior cord injury
Additional contributing factors:
 1. Shearing
2. Distraction

Classification of SCI
A. Incomplete SCI
- Preservation of some injury or motor function below level of injury
- May result from partial intersection in perianal region
- Result from contusion produced by pressure on the cord from
displaced bone and soft tissue or swelling of spinal cord

Characteristics:
 Perianal sensation
 Rectal sphincter contraction
 Cutaneous sensation in saddle area
 Active contraction of sacrally innervated toe flexors
 Often the first sign that a cervical region is incomplete

Spinal Shock:
 Transient reflex depression of cord function below level of injury
 Initially hypertension due to release of catecholamines
 Followed by hypotension
 Flaccid paralysis
 Bowel and bladder involved
 Symptoms last 24-48 hours

Types of Syndrome:
1. Central Cord Syndrome
- A.K.A walking SCI
- Most common in hyperextension injury to cervical region
- Most common incomplete cord syndrome
- Most frequent injury C5-C6
- Associated with congenital or degenerative narrowing of spinal canal
- hemorrhage and edema to most central aspects of spinal cord
Clinical Features:
 More severe neurological impairment of UE than LE
 Varying degrees of sensory loss below the level of lesion but less
severe than motor deficits
 Recovers the ability to ambulate with residual distal arm
 Complete preservation of sacral tracts normal sexual, bowel and
bladder function
2. Anterior Cord Syndrome
- Pure motor SCI
- Related to flexion injuries of the cervical region
- resultant damage to anterior portion of cord
- (-) vascular supply from anterior spinal artery due to compression,
fracture, dislocation, cervical disc protrusion (anterolateral) lumbar disc
protrusion (posterolateral)
Clinical Features:
 Manifested by complete motor paralysis (via corticospinal tract) and
loss of sense of pain and temperature (via spinothalamic tract)
sensory deficit below the lesion
 Preserved dorsal column function (proprioception, kinesthesia and
vibratory sense)

3. Posterior Cord Syndrome

- Extremely rare symptoms
Clinical Features:
 Loss of epicritic sensation (two point discrimination, graphestesia,
stereognosis)
 Dorsal column pathway damage and posterior spinal artery results
loss of proprioception, kinesthesia and vibratory sense
 Wide base of gait
 Walk with stepping gait similar to tabesdorsalis
 Preserved motor function, sense of pain and temperature

4. Brown Sequard Syndrome

- Hemisection of spinal cord typically caused by stab wounds
- Partially lesion occurs where feature is asymmetrical but true
hemisection is rare
Clinical Features:
- Ipsilateral side:
 Loss of sensation in dermatome segment corresponding level of
lesion
 Loss of motor function ,ipsilateral weakness
 Lateral column damage: decreasereflexes, lack of superficial
reflexes
 Dorsal column damage:loss of vibratory sense,proprioception and
kinesthesia
- Contralateral side
  Damage to spinothalamic tract loss of sense of pain and
temperature
Clinical features of all SCI:
 Spinal shock or concussion of cord
 Motor deficits and sensory loss
 Autonomic dysfunction
 Respiratory impairment
Cauda Equina Injuries
- Complete transaction of long nerve roots below level L1 vertebra
- Characterized by incomplete lesion
- Considered as PNI

Conus Medullaris Lesion

- Lesion of tapered end of spinal cord
- Urinary and fecal infection, present
- Paralysis of pelvic floor muscle
- Sensory impairment which is frequently dissociated in saddle area
- DTR usually preserved but have occasional negative ankle jerk

Cauda Conus Lesion

- More common combination of above symptoms

Major Complications in SCI:

1. Bronchopneumonia and Pulmonary Embolism
2. Diaphoresis
3. Spasticity
4. Renal failure
5. Bowel and bladder dysfunction
6. Sexual dysfunction

Secondary Complications:
1. Pressure Sore
2. Autonomic Dysreflexia
3. Orthostatic Hypotension
4. Heterotrophic
5. Contractures
6. DVT
7. Metabolic
8. Weight Loss
9. Reduced Basal Energy Expenditure
10. Anemia
11. Glucose Intolerance
12. Osteoporosis
13. Hypercalciuria
14. Pain
Differential Diagnosis:
TBI
All injuries of the brain caused by an external force resulting to disability or
even death
CVA
A non-traumatic brain injury, caused by occlusion or rupture of cerebral
blood vessels, that results in sudden neurologic deficit characterized by loss
of motor control, altered sensation, cognitive or language impairment,
disequilibrium, or coma.
MS
A chronic inflammatory and demyelinating disease of CNS that can cause:
paralysis, intention tremor, scanning speech and nystagmus.
Prognosis
1. The degree of pathologic changes imposed by trauma
2. Precaution taken to prevent further damage during rescue
3. Prevention of additional compromise of neural tissue from hypoxia and
hypotension
Incomplete Lesion
- Some progressive of muscle return
- With consistent progression of return of function, further recovery can be
expected at the same rate or slightly lower
Ambulation
C8-T1 exercise assisted; wheelchair
T2 –T14 exercise only; KAFO, forearm crutch, walker
T6 long leg brace for physiologic standing
Above T10 wheelchair ambulation
T10 / young attempt long leg brace; house ambulation
T11-T12 functional indoors; KAFO / AFO with crutch
T12 bilateral long leg braces with crutch
L3-S3 community ambulation; AFO with crutch / cane
L4 short leg brace; AFO
Summary of Relship of Level of Lesion – Functional Goal
C4-C5 dependent in self care, bed mobility and wheelchair
transfer

C6 semi-independent / sliding board transfer

C7-T6 independent in self care; bed mobility and wheel chair

transfer

12 | P a g e
 T6-T12 limited ambulated with long leg braces

L4-S2 community ambulation with short leg braces

C4 Lapboard and stick

Dependent in all transfers
(+) pulmonary problem

C5 Projection hand rim (vertical)

Balance forearm orthosis
Universal cuff
Trapeze bar
Independent in all transfer

C6 Projection hand rim (horizontal / oblique)

Sliding board transfer

C7 Plastic coated rims

Drive
Independent PROM of extremities
Level transfers

C8-T1 Normal hand rims

Non level transfers

Assessment of SCI
Neurologic Level
- with normal function of sensory (grade 2) and motor (grade 5)
Motor Level
- Muscle grade of 3 if proximal level is grade 4 or 5
Sensory Level
- At least grade of 1
- Proximal level must be normal or grade 2
0 – (-) sensation
1 – Impaired
2 – normal
Muscle Grading using Daniel’s Numerical grading (0-5)
- Sensory neurological level is named based on last key dermatome to have a
normal 2/2 sensation
- For grading (B) pain and touch sensation are used but are tested separately

13 | P a g e
 - Motor Index Scale
o sum of motor grades of10 kg muscle myotome
o perfect score is 100 (50 / side)

- Sensory Index Score

o Sure of 28 dermatome
o Perfect score is 112
AMIS (Ambulatory Motor Index Scoring)
- Predicts ambulation capacity in lumbar paraplegia
- Muscle assessed (bilateral) Scale MMT
 Hip Flexors 0 = absent 0
 Hip Abductors 1 = trace 1-2
 Hip Extensors 2 = fair 3
 Knee Flexors 3 = good or normal 4
 Knee Extensors

ASIA (American Spinal Injury Association)

14 | P a g e
 A – Complete: no sensory or motor function preserved in sacral segments S4
– S5
B – Incomplete: sensory, but no motor function in sacral segments
C – Incomplete: motor function preserved below level and power graded < 3
D – Incomplete: motor function preserved below level and power graded 3 or
more
E – Normal: sensory and motor function normal

Spinal Shock :
 Transient reflex depression of cord function below level of injury
 Initially hypertension due to release of catecholamines
 Followed by hypotension
 Flaccid paralysis
 Bowel and bladder involved
 Symptoms last 24-48 hours

Neurogenic shock:
 Triad
 hypotension
 bradycardia
 hypothermia
 More commonly in injuries above T6
 Secondaryto disruption of sympathetic outflow from T1 – L2
 Loss of vasomotor tone – pooling of blood
 Blood pressure will not be restored by fluid infusion alone
 Massive fluid administration may lead to overload and pulmonary edema

Frankel Scale
- no longer used
- distinguish between complete and incomplete SCI
- qualitative describes degree of incompleteness
A- complete (have motor paralysis, sensory loss and autonomic dysfunction)
B- sensory only (some sensory function but complete motor paralysis)
C- motor useless (sensory and motor function but some degree of motor
strength not functioning)
D- motor useful
E- recovery (good motor, sensory and autonomic function but may have
abnormal reflexes

15 | P a g e
Stage of SCI Management

Stages Period Goal

Avoid active / passive movement of
Initial 1-10 days spine
Maintain life support function
Prevent long and short term
complication
Acute 11 days – 3 Early mobilization
mos Training for independent living
Intermediate 3 mos – 3 yrs Community adaptation
Return to work / school
Long term 3 yrs above maintenance of health

Management
Pharmacological Treatment:
 Anti spasticity
 Anti hypertension
 Peripheral nerve block – phenol
 Intrathecal injections
 Diuretics
 Anti coagulants
 Analgesics
Surgical:
 Rhizotomy
 Tenotomy
 Myelotomy
 Myotomy
 Neurectomy

PT Management:
 Breathing exercises
 ROM exercise
 Bed mobility and functional exercise
 Selective strengthening
o Musculature to scapula and shoulder in Quadriplegia
o Musculature to hips and trunk in Paraplegia

16 | P a g e
  Transfers and ambulation
 FES, ES, TENS
 Spirometry
 Selective stretching

Initial Evaluation

General Information
Patient’s initial: K. R.
Age: 26 y/o
Sex: Male
Address: #5 Cattleya Homes Makati City
Civil status: Single
Handedness: ®
Occupation: Hotel employee
Referring unit: Makati Medical Center
Rehab unit: Makati Medical Center
Referring MD: Dr. E.S.
Rehab MD: Dr. A.A.
Date of referral: August 7, 2013
Date of rehab consultation:August 7, 2013
Date of IE: August 7, 2013
Dx: Incomplete SCI L2 level

HPI

28 days PTC while the pt is on his way home, a mugger rushed into him but
he refused to give his this things so the mugger stabbed him in the right lower back
with a ‘Balisong’ ~3 inches deep and went away with his valuables, he fell on the
floor with his knees first then, slowly he fell on his chest. After ~5minutes by-passer
saw him and immediately called for help, after ~20 minutes, an ambulance has
arrived, he was first placed in a blanket then carefully placed on a stretcher and into
the ambulance by the paramedics then they rushed him into the hospital. At the time
of arrival at the hospital, vital signs were taken, and an oxygen cannula and dextrose
where given. He was placed in an ICU for 5 days until he became stable.
Bulbocavernosus test was given to him daily while he was in the ICU, he became (+)
to the given test on the third day. After 2 days from the time he became positive to
bulbocavernosus test, he was transferred to a regular room. The doctor confirmed
that the pt has incomplete spinal cord injury at the level of L2. After 2 days of
observation, he was declared to be stable and allowed by the doctor to go home.

When the pt was neurologically and physically stable, the attending MD

referred him to the rehab center for further evaluation and treatment.

Ancillary Procedures

17 | P a g e
 Findings Date
Fracture of pedicle of L2
X-Ray (spine) July 10, 2013
vertebra
MRI Fracture on L2 vertebra July 13, 2013

Laboratory Exam
(N) value Findings Date
WBC 4.9 x 109/ L 8.0 x 109L
4.3 – 5.4 x 1013/L
(male)
RBC 6.0 x 1013 L
3.8 – 5.2 x 10 July 10, 2013
(female)
38-50 % (male)
Hematocrit 51%
34-46 % (female)

Present Medications

Dosage Frequency Indication

Methylprednisolone 32 mg Qid Anti-inflammatory
Baclofen 10mg Qid Anti-spasticity
Cephalexin 500mg Qid Antibiotic

PMHx

(+) Pulmonary Problem (Asthma)

(+) Thoracolumbar Brace
(-) Hospitalization
(-) Trauma
(-) Htn
(-)DM
(-) Cardiopulmonary Disease

FMx

Father Mother
Cardiac Problem (-) (-)
Respiratory Problem (+) (+)
DM (-) (+)
Htn (-) (-)
Tumor (-) (-)

18 | P a g e
PSEHx

 Active lifestyle
 Type A personality
 (+) Smoker 4 sticks/day; 438 pack years (Since August 2007)
 (+) Alcohol beverage drinker (occasional; beer; 3 bottles)
 Lives in a 2 story house with his parents and sister
 Financially independent
 Diet includes: meat and fruits
 Hobbies: basketball and playing guitar
 Home setup
o 2 flight of stairs with metal handrails on the left side
o 14 steps of stairs
o Pt’s room is in the first floor
 ~5 steps from room to comfort room
 ~10 steps from room to kitchen
 ~8 steps from room to dining room
 ~7 steps from room to living room
o Ceramic tiles
o Circular metal door knob

S:

Pt’s c/0: Hindi ko maigalaw ang kanang binti at paa at walang pakiramdam ang
ibang parte mula sa aking paa hanggang balakang

PT translation: Paralysis of (R) LE and loss of sensation of (L) LE from the feet to
hips

Pt’s goal: to be able to walk again and to return to its pre-morbid status

O:

VS: before during after

BP 110/80 120/90 110/80

RR 13 cpm 15 cpm 14 cpm
PR 72 bpm 80bpm 75 bpm
Temperature 37.8 °C 38.2 °C 38°C

Findings: VS are WNL except temperature is normal

Significance: 2° to SCI

19 | P a g e
OI:

 w/c borne
 Alert, coherent, cooperative
 Oriented in person, place and time
 Mesomorph
 (+) Scar (4 stitches) on (R) lumbar area
 (+) Grade 1 pressure sore on both ischium
 (+) Atrophy on (R) leg
 (+) Swelling on Right distal hand and Right distal foot
 (+) Thoracolumbar Brace
 (-) Contracture
 (-) Catheter

Palpation:

 Normal skin turgor & mobility

 (+) Edema on Right distal foot and Right distal hand
 (+) Fever

A.) Tone A:
-Normotonic on (B) UE and hypertonic on (R) LE

Findings: Grade 1 Spasticity on (R) LE Modified Ashworth Scale

Significance: ᛏ firing of gamma motor neurons

B.) Sensory A:
(See Asia Scale)

C.) MSR / DTR

Legend:

O - Areflexia
+ - Hyporeflexia
++ - Normoreflexia
+++ - Hypereflexia
++++ - Clonus

Findings:Normoreflexive on (B) UE and Hypereflexive on (B) LE

20 | P a g e
 Significance: 2º increase firing of gamma motor neuron

D.) Pathologic Reflex

Positive Response
(+) Babinski Extension of big toe and fanning of
little toes
(+) Chaddocks Extension of big toe and fanning of
little toes
(+) Gordon’s Extension of big toe and fanning of
little toes

Findings: (+) Babinski, Chaddocks, Gordon’s Sign

Significance: 2º to Upper motor neuron lesion

E.) Special Test

Beevor sign movement of the navel towards the

head on flexing the neck

Findings: (+) beevor sign

Significance: 2° to UMNL

F.) Associated reaction

Clonus

Findings: (+) clonus on ankles

Significance: increase firing of gamma motor neuron

ROM

All joints of (B) UE and LE, including the trunk, are WNL, actively and
passively done, pain free and with (N) endfeel, except:

(N)
Active Passive Difference Endfeel
Value
HIP (R) (L) (R) (L) (R) (L) (R) (L)
0- 0- Muscle
Flexion 0-120˚ 0˚ 0-120˚ 120˚ 10˚ Soft
110˚ 120˚ Spasticity
0- Muscle
Extension 0-30˚ 0˚ 0-30˚ 0-30˚ 30˚ 5˚ Spasticity Firm
25˚
Abduction 0-45˚ 0˚ 0- 0-45˚ 0-45˚ 45˚ 5˚ Muscle Firm
40˚
21 | P a g e
 Spasticity

0- Muscle
Adduction 0-30˚ 0˚ 0-30˚ 0-30˚ 30˚ 5˚ Spasticity Firm
25˚
0- Muscle
IR 0-45˚ 0˚ 0-45˚ 0-45˚ 45˚ 5˚ Spasticity Firm
40˚
0- Muscle
ER 0-45˚ 0˚ 0-45˚ 0-45˚ 45˚ 5˚ Spasticity Firm
40˚
KNEE
0- 0- Muscle
Flexion 0-135˚ 0˚ 0-135˚ 135˚ 10˚ Spasticity Soft
125˚ 135˚
125- 135- Muscle
Extension 135-0˚ 0˚ 135-0˚ 135˚ 10˚ Spasticity Firm
0˚ 0˚
ANKLE
0- Muscle
Dorsiflexion 0-20˚ 0˚ 0-20˚ 0-20˚ 20˚ 5˚ Spasticity Firm
15˚
0- Muscle
Plantarflexion 0-50˚ 0˚ 0-50˚ 0-50˚ 50˚ 10˚ Spasticity Firm
40˚
SUBTALAR
Muscle
Inversion 0-5˚ 0˚ 0-5˚ 0-5˚ 0-5˚ 5˚ 0˚ Spasticity Firm

Muscle
Eversion 0-5˚ 0˚ 0-5˚ 0-5˚ 0-5˚ 5˚ 0˚ Spasticity Firm

TARSAL
Muscle
Inversion 0-35˚ 0˚ 30˚ 0-35˚ 0-35˚ 35˚ 5˚ Spasticity Firm

Muscle
Eversion 0-15˚ 0˚ 10˚ 0-15˚ 0-15˚ 15˚ 5˚ Spasticity Firm

TRANSVERS
E TARSAL
Muscle
Inversion 0-20˚ 0˚ 15˚ 0-20˚ 0-20˚ 20˚ 5˚ Spasticity Firm

Muscle
Eversion 0-10˚ 0˚ 10˚ 0-10˚ 0-10˚ 10˚ 0˚ Spasticity Firm

MTP
1st MTP
Flexion 0-45˚ 35˚ 35˚ 0-45˚ 0-45˚ 10˚ 10˚ Muscle Firm

22 | P a g e
 Spasticity
Muscle
Extension 0-70˚ 60˚ 60˚ 0-70˚ 0-70˚ 10˚ 10˚ Spasticity Firm

Muscle
2nd MTP Spasticity
Muscle
Flexion 0-30˚ 25˚ 25˚ 0-30˚ 0-30˚ 5˚ 5˚ Spasticity Firm

Muscle
Extension 0-40˚ 30˚ 30˚ 0-40˚ 0-40˚ 10˚ 10˚ Spasticity Firm

Muscle
3rd MTP Spasticity
Muscle
Flexion 0-20˚ 15˚ 15˚ 0-20˚ 0-20˚ 5˚ 5˚ Spasticity Firm

Muscle
Extension 0-30˚ 25˚ 25˚ 0-30˚ 0-30˚ 5˚ 5˚ Spasticity Firm

4th MTP
0- 0-
Flexion 0-10˚ 0-10˚ 0-10˚ 0˚ 0˚ Firm Firm
10˚ 10˚
Extension 0-20˚ 15˚ 15˚ 0-20˚ 0-20˚ 5˚ 5˚ Firm Firm
th
5 MTP
0- 0-
Flexion 0-10˚ 0-10˚ 0-10˚ 0˚ 0˚ Firm Firm
10˚ 10˚
0- 0-
Extension 0-10˚ 0-10˚ 0-10˚ 0˚ 0˚ Firm Firm
10˚ 10˚
PIP JT
1st PIP
0- Muscle
Flexion 0-90˚ 0˚ 0-90˚ 0-90˚ 90˚ 10˚ Firm
80˚ Spacticity
80- Muscle
Extension 90-0˚ 0˚ 90-0˚ 90-0˚ 90˚ 10˚ Firm
0˚ Spacticity
2nd PIP
0- Muscle
Flexion 0-35˚ 0˚ 0-35˚ 0-35˚ 35˚ 5˚ Firm
30˚ Spacticity
30- Muscle
Extension 35-0˚ 0˚ 35-0˚ 35-0˚ 35˚ 5˚ Firm
0˚ Spacticity
3rd PIP
0- Muscle
Flexion 0-35˚ 0˚ 0-35˚ 0-35˚ 35˚ 5˚ Firm
30˚ Spacticity
30- Muscle
Extension 35-0˚ 0˚ 35-0˚ 35-0˚ 35˚ 5˚ Firm
0˚ Spacticity
4th PIP

23 | P a g e
 0- Muscle
Flexion 0-35˚ 0˚ 0-35˚ 0-35˚ 35˚ 5˚ Firm
30˚ Spacticity
30- Muscle
Extension 35-0˚ 0˚ 35-0˚ 35-0˚ 35˚ 5˚ Firm
0˚ Spacticity
5th PIP
0- Muscle
Flexion 0-35˚ 0˚ 0-35˚ 0-35˚ 35˚ 5˚ Firm
30˚ Spacticity
30- Muscle
Extension 35-0˚ 0˚ 35-0˚ 35-0˚ 35˚ 5˚ Firm
0˚ Spacticity
DIP JT
2nd DIP
0- Muscle
Flexion 0-60˚ 0˚ 0-60˚ 0-60˚ 60˚ 10˚ Firm
50˚ Spacticity
50- Muscle
Extension 60-0˚ 0˚ 60-0˚ 60-0˚ 60˚ 10˚ Firm
0˚ Spacticity

3rd DIP
0- Muscle
Flexion 0-60˚ 0˚ 0-60˚ 0-60˚ 60˚ 10˚ Firm
50˚ Spacticity
50- Muscle
Extension 60-0˚ 0˚ 60-0˚ 60-0˚ 60˚ 10˚ Firm
0˚ Spacticity
4th DIP
0- Muscle
Flexion 0-60˚ 0˚ 0-60˚ 0-60˚ 60˚ 10˚ Firm
50˚ Spacticity
50- Muscle
Extension 60-0˚ 0˚ 60-0˚ 60-0˚ 60˚ 10˚ Firm
0˚ Spacticity
5th DIP
0- Muscle
Flexion 0-60˚ 0˚ 0-60˚ 0-60˚ 60˚ 10˚ Firm
50˚ Spacticity
50- Muscle
Extension 60-0˚ 0˚ 60-0˚ 60-0˚ 60˚ 10˚ Firm
0˚ Spacticity

FIM
Grading:

7 – Complete independence
6 – Modified independence
5 – Supervision
4 – Minimal assistance
3 – Moderate assistance
2 – Maximal assistance / complete dependence
1 – Total assist

A. Self Care D. Locomotion

Feeding 6 Walking 1

24 | P a g e
 Bathing 6 Stairs 1
B. Sphincter Care E. Communication

Bladder control 7 Comprehension

7
Bowel mobility 7 Expression 7

C. Transfer F. Social Cognition

Bed to chair 4 Social interaction 7

Chair to wheelchair 4 Problem solving 7
Toileting 3 Memory 7
Tub/Shower 3

Findings: Pt needs total dependence in locomotion and moderate assistance

in Transfers
Significance: 2º to paralysis of (B) LE

Antrophometric measurement:

Muscle bulk measurement

Lower Extremity
(R) (L) Difference
Suprapatellar ridge 20” 23” 3”
to the bulkiest part
(thigh)
Infrapatellar ridge to 14” 16” 2”
the bulkiest part
(Leg)

Findings: atrophy on the right thigh

Significance: decrease muscle fibers on (R) leg due to disuse

A:
PT Impression: Incomplete Brown-Sequard SCI L2 Level
Rehab Potential: good prognosis d/t early intervention
Rehab Concern: Patient’s spastic condition
Rehab Precaution: loss of sensation in (L) LE, respiratory problem (Asthma),
Autonomic Dysreflexia

Problem List

25 | P a g e
 1. LOM as to movements involving the LE
2. Paralysis on (R) LE
3. Sensory loss on (L) LE
4. Difficulty in performing ADL as to locomotion and transfers
5. Grade 1 Pressure Sore on (B) Ischium
6. Atrophy on (R) LE
7. Spastic (R) LE

LTG (3 Months)

1. To prevent secondary complication as to contracture, tightness and disuse

atrophy
2. To maintain patient’s ability and capabilities in doing ADL
3. Maintain Strength and ROM of UE

STG (1 Month)

1. To increase ROM of all the joints of LE up to 10º to 15º increment

2. To increase muscle strength the LE from ms. Grade 1/5 to 3/5
3. To eliminate Grade 1 Pressure Sore on (B) Sacrum
4. Prevent and retard atrophy
5. Improve sensation of (L) LE

PT Management

1. Gentle Manual Stretch on (B) LE in all planes of motion x 10 repetitions x 5 reps x

10 seconds hold
2. Resistance Exercise on (B) UE in all planes of motion x 10 repetitions x 5 sets x
15 seconds hold
3. HMP on (B) LE x 20 minutes
4. ES on (B) LE x 90 contractions x1 set
5. IRR on (B) Sacrum x 20 minutes
6. Sensory sensitization on (L) LE
7.PRE

HI:

1. Pressure relief on (B) ischium every 30 minutes

2. Educate pt. and family on proper bed positioning of pt.
3. Educate pt on proper transfers and ambulation

______________________

26 | P a g e
Maya Angelou N. Mel
UDM-PT intern Batch 2015

______________________
Justine Paolo C. Queri
UDM-PT intern Batch 2015

Multiple Sclerosis
Almeniana, Unice Jane Louise
Villaroman, Maybelle
Definition:

 It is a chronic inflammatory demyelinating disease of a CNS. It is often

referred to as “Great Crippler of the Young Adults “ (Sullivan)
 It is characterized by the appearance of patches of demyelination on the
white matter of CNS ( Snell )
 It is the most common inflammatory demyelinating disease of the CNS,
affecting areas of the brain and spinal cord but sparing the peripheral nerves (
Goodman and Synder )

Related Anatomy

 Neurons- are excitable cells that are specialized for the reception of stimuli
and the conduction of the nerve impulses
 Neurites- responsible for receiving information and conducting impulses
toward from the cell body
 Axon- single long tubular neurite that conducts impulses away from the cell
body
 Oligodendrocytes- responsible for the formation of the myelin sheath of the
nerve fibers in the CNS
 Schwann cells- responsible for the formation of the myelin sheath of the
nerve fibers in the PNS

27 | P a g e
Epidemiology

 Age of onset: 15-50 y/o (Sullivan)

 Most cases occur between ages of 20-40 y/o
 F>M (2:1)
 White> Black>Asian
 Siblings> parents > others
 5x more prevalent in the temperate climates of North America and Europe,
other than tropical countries

Etiology

 UNKNOWN
 Theories:
1. Infectious Origin

28 | P a g e
 -identification of IGG and oligoclonal bands in the CSF
2. Immune Mediated Pathogenesis
-Active T cells has been found in the blood and CSF of the
patient
3. Slow Virus Theory
-acquired during years of puberty and symptom emerges 12
years later
Virus include: herpes simplex, rubella, and measles

Pathophysiology

 The pathologic hallmark of MS is the PRESENCE of MULTIFOCAL

DEMYELINATED PLAQUES
 GLIOSIS- refers to the proliferation of neurological tissue within the CNS and
results in glial scars(plaques)
 Lymphotoxin- specialized lymphocytes that kill the antigen
 Microglia-cell presenting antigen

Areas common:

 Periventricular areas of cerebrum

 Optic nerve
 Cerebral peduncle
 Brainstem
 Dorsal spinal nerve

Immune Theory for the Basis of MS

ACTION EFFECT
Release cytokines Cause defect in blood brain barrier
T cell attach to HLA receptor, release of Destroy the myelin sheath
INF-Y and TNF
T cell attach to HLS receptor-produce Attack the myelin sheath
macrophages
T cell activates the B cell-antibodies Attack oligodendrocytes

Diagnostic Criteria

(Braddom)

 POSSIBLE MS

29 | P a g e
 1. History of relapsing and remitting signs without poor documentation
2. Only one site of involvement of the CNS by physical examination
3. No other diagnostic result
 PROBABLE MS
1. Two documented attacks with clinical laboratory of imaging evidence at
least one lesion
2. One documented attack with clinical laboratory of 2 lesions
 DEFINITE MS
1. Two attacks separated by at least one month with clinical laboratory; at
least two lesions

(Sullivan)

2 Patterns

1. Two or more episodes of worsening lasting more than 24 hrs. and

separated by no less than 1 month
2. Slow or step-wise progression extending over at least 6 months

Patterns of MS

1. Relapsing –remitting MS (40-60%)

- Most mildest form of MS
a. Near full remission- long period of stability
b. Incomplete remission- involving into chronic progressive
2. Primary progressive MS
- Progressive without remission
- More common in men
- Disease onset 40 y/o
3. Secondary progressive MS
- With initial relapsing –remitting course
- Followed by progression
4. Chronic progressive
- Sudden onset
- Disability within 2-10 yrs.
- Commonly on 40 y/o
5. Benign MS (20-30%)
-little or no permanent functional disability

6. Malignant MS
- Rapid progression leading to significant disability or death
30 | P a g e
Clinical Manifestations

1. Sensory disturbance (complete loss of any single sensation is rare)

a) Tingling paresthesias of numbness
b) Lhermitte’s sign- an electric shock like sensation running down the SC
and LE produced by flexing the neck
c) Trigeminal Neuralgia/ Tic douloureux- characterized by short attacks of
severe pain and results from demyelination of the sensory tracts of the
trigeminal nerve
d) Position/ vibratory sense disturbance
e) Pain from painful reflex , spasms, spasticity or abnormal positioning of
limbs
2. Weakness- usually occurs first in the LE though the UE may be involved
3. Spasticity-presents with typical signs of:
a) Ankle clonus
b) Exaggerated stretch reflexes
c) Spontaneous spasms
d) Reflex radiation
e) A positive babinski sign
4. Fatigue
5. Cerebellar Disorders
a) Dysmetria- an inability to fix the range of movement
b) Dysdiadochokinesia- inability to perform rapidly alternating
movements
c) Ataxia- refers to incoordinated movements
d) Vertigo- a generalized feeling of unsteadiness and to some extent
accompanied by nausea and vomiting
6. Cranial Nerve Involvement (2,5,7,8 most commonly involved)
a) Optic neuritis
b) Nystagmus
c) Scotoma
7. Communication Disorders
a) Dysarthria- slurring and incoordination during phonation with
scanning of syllables and low speech volume
b) Dysphagia-difficulty in swallowing
8. Bladder and bowel disturbances
a) Urinary frequency
b) Urgency
c) Incontinence
d) Retention/hesitancy
9. Cognitive and behavioral disturbances

31 | P a g e
 10. Epilepsy- very rare (only1-2%)

CHARCOT’S TRIAD

 Intention tremor
 Nystagmus
 Scanning speech

Exacerbating Factors

 Infectious agents
 Pregnancy (3-6 mos.)
 Fatigue and heat
 Stress
 Trauma
 Heavy metals
 Diet

Differential Diagnosis

 Postinfectious Encephalomyelitis

Postinfectious encephalomyelitis is a subacute syndrome caused by

autoimmune response to a viral infection. Patients complain of acute or
subacute onset of gait abnormalities, confusion, disorientation, problems with
bladder or bowel control, muscle weakness, and other symptoms.
Abnormalities consistent with demyelinating lesions can be seen on MRI
images. This condition may or may not be reversible. Typically, however, it
presents itself as a monophasic illness, but chronic cases do occur and
require long term treatment.

 Primary CNS Vasculitis

Primary CNS vasculitis may result in syndromes resembling MS. Most

notable symptoms include severe headaches, confusion and sudden stroke
like episodes. High protein levels can be seen in CSF, as well as high
erythrocyte sedimentation rate. Patients may have abnormal angiogram of
cerebral vessels. Antinuclear or anti phospholipid antibodies may be present.

 Lyme Disease

Lyme disease is known to cause intermittent neurologic events. Some of

the most frequent problems include Bell's palsy, nonspecific symptoms of

32 | P a g e
 numbness, fatigue and amnesia. CSF findings may resemble those found in
the MS, and MRI may show a white matter disease. History of tick bites,
rashes and arthralgia should be sought after. Screening for Lyme titer and/or
a Lyme PCR in the CSF or blood should help in diagnosis.

 Systemic Lupus Erythematosus

Systemic lupus erythematosus may cause multiple neurologic pathology

such as optic abnormalities, encephalopathy, transverse myelitis, strokes.
One needs to look for systemic abnormalities, such as elevated antinuclear
antibody, leukopenia, hematuria, elevated erythrocyte sedimentation rate. On
some occasions lupus erythematosus and MS may be found in the same
patient.

 Tropical Spastic Paraparesis

Tropical spastic paraparesis is a retroviral disease caused by HTLV-1

virus. It is uncommon in the continental United States, but may be seen
infrequently in patients who resided for some time around the Caribbean Sea
Basin. The major clinical manifestations are progressive spastic paraparesis
or generalized white matter disease.

 Behçet Syndrome

Behçet syndrome can cause MRI findings that are very similar to MS. However, the
main distinguishing features of this condition are oral and genital ulcers, and uveitis,
as well as possible involvement of lungs, joints, intestines, and heart. This group of
patients may present with either quadriparesis, pseudobulbar palsy, cranial
neuropathy, cerebellar ataxia or cerebral venous thrombosis.

 Sarcoidosis and Sjogren's Syndrome

Sarcoidosis and Sjogren's syndrome may show lesions on MRI that resemble those
found in Multiple Sclerosis. These are autoimmune conditions that affect multiple
organ systems and should not be confused with MS. A chest X-ray may show
granulomatous disease of the lungs, and meningeal enhancement is seen in
patients with CNS involvement. Oligoclonal bands and IgG are raised in CSF of
patients with sarcoidosis. Central nervous system involvement and the course of the
disease may show striking similarity to MS. Angiotensin-converting enzyme

33 | P a g e
determination may be used for further differrential diagnosis. It may be elevated in
either serum or CSF but is not reliably abnormal.

Prognosis

FAVORABLE UNFAVORABLE
AGE Younger, <35 y/o >35 y/o
SYMPTOMS monosymptomatic polysymptomatic
TYPE OF SYMPTOMS sensory Early motor;cerebellar
PATTERN Sudden onset, long Progression, frequency
remission exacerbation
ESTABLISHED MS

TYPE Sensory, Brainstem/ Motor, cerebellar

Cranial nerve affectation
DISABILITY Mild to moderate, Moderate to severe, non-
ambulatory ambulatory

Prognostic Indicators

 Before age of 35 y/o

 Multiple system involvement
 Progressive course at onset
 Male sex
 Age at onset >40 y/o
 Cerebellar involvement

Kurtzke Expanded Disability Status Scale (KEDSS)

(Areas or systems assessed)

1. Pyramidal Functions (0-6)
2. Cerebellar Functions (0-5)
3. Brainstem Functions (0-5)
4. Sensory Functions (0-5)
5. Bowel & bladder functions (0-5)
6. Visual Functions (0-5)
7. Mental Functions (0-5)
8. Other functions (0-1)

KEDSS (Classification)
0 - normal neurologic exam, FS all grade 0 or at least Cerebral Gr. 1
1 - no disability, minimal signs in one FS
1.5 - no disability, minimal signs more than one FS
2.0 - minimal disability one FS
2.5 - minimal disability in 2 FS

34 | P a g e
 3.0 -moderate disability one FS
3.5 - fully ambulatory but with moderate disability in one FS
4.0 - fully ambulatory without aid, self-sufficient, up and about for 12H
despite one FS 4
4.5 - fully ambulatory with aid, up and about much of the day, able to work
a full day, minimal assistance needed despite one FS4
5.0 - ambulatory without aid or rest for about 200 meters; impaired full day
activity, at least one FS5
5.5 - ambulatory without aid or rest for about 100 meters
6.0 - intermittent or unilateral constant assistance (cane, crutch, brace)
needed to walk about 100 meters, more than 2 FS3+
6.5 - constant bilateral assistance to walk 20 meters
7.0 - unable to walk beyond 5 meters even with aid; usually more than 1
FS4
7.5 - unable to take more than a few steps; restricted to wheelchair
8.0 - restricted to bed or chair but is out of bed most of the day; effective
use of arms; retains many self-care activities; FS 4+ in several systems
8.5 - essentially restricted to bed much of the day
9.0 -helpless bed patient, can communicate and eat
9.5 - totally helpless bed patient, unable to communicate and swallow;
almost all systems FS4+
10 - death by MS

Medical Management

Pharmacological Management
1. Steroids
 Used to decrease length & severity of exacerbation
 Not effective in chronic progressive MS
2. Immunosuppressive agents
 Primarily for chronic progressive MS
 Also used for those who are unresponsive to steroids
 Cyclophosphamide, azathioprine, cyclosporine etc.
3. Interferon- particular type of interferon (IFN-beta) used to alter the course
of MS too
4. Pemoline and Amantadine- used as medical treatment of fatigue
6. Antispasticity medication

Rehabilitation Management
1. Skin care
 Keep skin clean & dry

35 | P a g e
  Good diet & drink plenty of fluids
 Inspect the skin
 Always provide pressure relief
 Prevention is the best strategy
2. Cool therapeutic pools
3. Management for:
 Pain- cold modalities
 Spasticity- stretching exercise
 LOM- stretching
 Respiratory problem- breathing exercise
 Paresis- AAROM exercise
 Fatigue- moderate conditioning exercise
 Ataxia- Frenkels exercise

PT Management
 Treated in cool environment
 ROM exercise (AROME/PROME)
 Aerobic exercise
 Ergobike
 Pool therapy
 Swimming
 Frenkels exercise
 PNF (use slow reversal technique)
 Do not give PRE’s

Initial Evaluation
General Information
Patients Initial: O.A.
Age: 25
Sex: Female
Address:
Civil Status: Single
Nationality: Canadian & Filipino
Handedness: Right
Occupation: Encoder
Referring Unit: St. Lukes Medical Center (Neuroward)
Rehab Unit: St. Lukes Medical Center (PT Rehab)
Referring M.D.: Dr. K. J.
Rehab M.D.: Dr. C. H.
Date of Referral: April 10, 2013
Date of PT Consultation: April 11, 2013
Date of IE: April 11, 2013
Dx: Relapsing-remitting MS

36 | P a g e
HPI
Present condition started 8 months PTC the pt. experienced blurring of vision
and fatigue on (B) UE & LE while at work. She ignored it thinking it's only d/t
overwork. As she went home, she also felt paresthesia on (B) UE. She decided to
apply liniment on her upper limbs and took Vit. B complex assuming that it's only a
sign of Vit. B deficiency. The symptom disappeared the next day.

1 month PTC after her morning exercise, she experienced paresthesia, fatigue
on (B) LE and heaviness on (B) LE. She took a nap thinking it was d/t over exercise.
Upon waking up, she experienced difficulty in standing and balancing herself. This
prompted her to seek medical advice. Upon arriving at the hospital with her father,
VS (BP: 130/80 mmHg; RR: 18 cpm; PR: 75 bpm) were checked and ancillary
procedures were performed (see ancillary procedures). Based on her hx of
symptoms and CT scan result, she was diagnosed to have probable relapsing-
remitting MS. Dr. K. J. educate her about her condition, what are the exacerbating
factors to be avoided. She was also prescribed Amantadine to be taken in the
morning to reduce muscle fatigability. The dx make her feel more stressed knowing
that her condition might return and progress. The next day the symptoms
disappeared.

3 days PTC the pt. experienced paraplegia on (B) LE and her (L) central
vision was lost. Because her family is aware about her condition, her father rushed
her to the hospital to seek medical attention. The doctor checked her VS (BP:
130/80 mmHg; RR: 20 cpm; PR: 84 bpm) and ancillary procedures were performed.
Based on the MRI result and the onset of symptoms, she was diagnosed to have
relapsing-remitting MS. The pt's family decided to confined her to the hospital for
further observation of symptoms. An IV line was attached to her (R) hand. The next
day, the doctor notices incoordination of movements.

1 day PTC the symptoms relapsed, but incoordination still persist. While the
paraplegia declines to weakness of (B) LE. After the remission of symptoms, she
was the d/c and referred to PT for further evaluation and treatment

Ancillary Procedures
Diagnostic Procedures Findings
Date
CT scan Lesion on midbrain, pons & cerebellum
March 11, 2013
MRI Gliosis on midbrain, pons & cerebellum April 11, 2011

Laboratory Exams
Examinations Normal Values Findings
Date
CBC

37 | P a g e
RBC 3.80-5.10/103uL Normal
April 08, 2013
WBC 4.0-10.5/103Ul increase
April 08, 2013
IgG increase
April 08, 2013

Present Medications
Name of Drugs Dosage Frequency
Indication
Amantadine 100 mg od; am to
decrease fatigue
Azathioprine 75 mg od
to decrease inflammation

PMHx
 (+) Hospitalization ( St. Lukes Medical Center; March 11, 2013; Probable
relapsing-remitting MS)
 (-) Htn
 (-) DM
 (-) Cardiopulmonary problem
 (-) Allergies
 (-) infection

FMHx
Condition Father Mother
Htn (+) (-)
Pulmonary cond. (-) (+)
DM (-) (-)
Cardiac cond. (-) (-)
MS (-) (-)

PSEHx
 Type B Personality
 Active Lifestyle
 (-) Smoker
 (+) Occasional Alcohol Beverage Drinker ( Brandy; 20 shots )
 working 8 hrs/day; 5 days/week since 2008
 stay in canada for 15 years; and in philippines for 10 years
 Lives in a 2 storey house with his parents & sister
 Diet includes: Fish, meat, fruits
 Financially Stable
 Hobbies: Playing badminton
Home Set-up
1 flight of stair with metal handrails on (R) sides
12 steps of stairs

38 | P a g e
 Pt’s room is located at the 2nd floor
~ 22 steps from room to CR
~ 29 steps from room to kitchen
~ 25 steps from room to dining
~ 17 steps from room to living room
Circular door knobs
Tile type flooring

S:
Pt's c/o: easy fatigability, left central loss of vision and incoordination of
movements
PT Translation: Paraparesis on (B) LE, scotomo on (L) eye and incoordination
of movements
Pt's Goal: To increase muscle strength on (B) LE. To improve coordination.

O:
VS before during after
BP 130/80 mmHg 130/80 mmHg
130/80 mmHg
RR 15 cpm 17 cpm
15 cpm
PR 70 bpm 72 bpm
70 bpm
T° 37.1 oC 37.1 oC
o
37.1 C
Findings: VS are WNL
Significance: For baseline purposes

OI:
 w/c borne
 Alert, coherent, cooperative
 Ectomorph
 (+) Ataxia
 (+) (L) eye patch
 (-) facial myokimia
 (-) charcot's triad
 (-) respiratory distress
 (-) swelling
 (-) dysarthria
 (-) ptosis
 (-) dysphagia
 (-) nystagmus

39 | P a g e
Palpation:
 Normothermic on all exposed body part
 normal skin turgor & mobility
 (-) shoulder subluxation
 (-) tenderness

Neurologic Examinations
Tone A:
Findings: Normotonic on (B) UE & LE
Significance: (-) affectation of B.A 6

Sensory A:
A. Superficial Somatic Sensation
Superficial Pain- Pin
Light Touch- Brush
Thermal Sensation- Hot & cold test tube
Findings: 100% intact sensation on (B) UE & LE
Significance: (-) affectation of B.A 3, 1, 2

B. Deep Somatic Sensation

(+) Deep Pain Pressure
(-) Vibratory Sense
(-) Proprioception
Findings: (-) vibratory & proprioception and 40% intact deep pain pressure
Significance: (+) affectation of B.A 5, 7

C. Cortical / Central Integrative Sensation

(+) Stereognosis
(+) Barognosis
(+) Graphestesia
Findings: intact cortical sensation
Significance: intact thalamocortical system

MSR / DTR
Legend:
++ ++
O Arelexia
+ Hyporeflexia ++ ++
++ normoreflexia
+++
+++ Hyperreflexia +++
+++
++ + ++++ Clonus

Findings: hyperreflexive on (B) LE and normoreflexive on (B) UE

40 | P a g e
Significance: 2o to increase firing of gamma motor neuron

Pathologic Reflex
Findings: (-) Babinski, (-) homan’s sign
Significance: (-) affectation to corticospinal system

Associated Reactions
Findings: (-) associated reaction
Significance: (-) affectation to corticospinal system

Cranial Nerve Testing

Findings: All CN are (N) except CN II
Significance: (+) affectation of brainstem

Coordination A:
Non-Equilibrium Test
finger to nose 3
finger opposition 3
heel on shin 3
Grading:
5 - normal performance
4 - minimal impairment
3 - moderate impairment
2 - severe impairment
1 - activity impossible

Findings: all non-equilibrium test of UE are graded 3/5 & of LE 2/5.

Significance: (+) affectation of cerebellum
Equilibrium test
Grading:
4– able to accomplish activity
3– can complete activity; minor physical contact guarding required
maintaining balance
2– can complete activity; significant (moderate to maximal) contact
guarding required to
maintain balance
1 – activity impossible

Standing on one foot 1

Walk: sideways 1
March in place 1

ROM

41 | P a g e
 All muscle on (B) UE are WNL, actively & passively done, pain free with (N)
end feel, except:

Motion End feel

Normal Active Passive Difference
(R) (L) (R) (L) (R) (L)
Hip
Flexion 0-120o 0-55o 0-55o 0- 0- 65o 65o Soft
120o 120o
Extension 0-30o 0-10o 0-10o 0-30o 0-30o 20o 20o Firm
Abduction 0-45o 0-20o 0-20o 0-45o 0-45o 25o 25o Firm
Adduction 0-30o 0-10o 0-10o 0-30o 0-30o 20o 20o Firm
Internal Rotation 0-45o 0-20o 0-20o 0-45o 0-45o 25o 25o Firm
External 0-45o 0-20o 0-20o 0-45o 0-45o 25o 25o Firm
Rotation
Knee
Flexion 0-135o 0-65o 0-65o 0- 0- 70o 70o Soft
135o 135o
Extension 135-0o 65-0o 65-0o 135- 135- 70o 70o Firm
0o 0o
Ankle
Dorsiflexion 0-20o 0-7o 0-7o 0-20o 0-20o 13o 13o Firm
Plantarflexion 0-50o 0-20o 0-20o 0-50o 0-50o 30o 30o Firm
Tarsal
Inversion 0-35o 0-15o 0-15o 0-35o 0-35o 20o 20o Firm
Eversion 0-15o 0-6o 0-6o 0-15o 0-15o 9o 9o Firm
Transverse
Tarsal
Inversion 0-20o 0-8o 0-8o 0-20o 0-20o 12o 12o Firm
Eversion 0-10o 0-4o 0-4o 0-10o 0-10o 6o 6o Firm
Findings: LOM on (B) LE
Significance: 2o to weakness of (B) LE

MMT:
All muscles of (B) UE are grossly graded 5/5 except:

(B) LE
Hip flexors 2+/5
Hip extensors 2+/5
Hip internal rotators 2+/5
Hip external rotators 2+/5
Hip abductors 2+/5
Hip adductors 2+/5
Knee flexors 2+/5
Knee extensors 2+/5

42 | P a g e
 Ankle plantarflexors 2+/5
Ankle dorsiflexors 2+/5
Ankle invertors 2+/5
Ankle evertors 2+/5

Findings: All muscles of (L) UE are graded 3-/5 and (B) LE are graded 2+/5
Significance: 2o to weakness

Special Test
(+) Lhermitte’s sign
(+) Pendulum test
(-) Sulcus sign

Findings: (+) Lhermitte’s sign, Pendulum test and (-) Sulcus sign
Significance: (+) Lhermitte’s sign 2o to MS

Balance and Tolerance:

Legend:
Balance Tolerance
N (normal) can assume, maintain, weight shift, and challenged >45mins
G (good) can assume, maintain and weight shift 31-
45mins
F (fair) can assume and maintain 16-30mins
P (poor) can assume 1-15mins
O (zero) can neither assume nor maintain 0 mins

Balance Tolerance
Sitting F F
Standing P P

Postural Analysis
Findings: All parameters of posture are WNL
Significance: For baseline purposes

ADL:
Fully dependent partially dependent
independent
Self care
Bathing
/
Toileting /
Eating /
Grooming /
UE dressing /
LE dressing /
Bed Mobility

43 | P a g e
Supine to side-lying /
Supine to long sitting
/
Rolling
/
Ambulation / c mod difficulty

Findings: pt is fully independent in all aspects of ADL except for ambulation and
transfers
Significance: 2o to weakness of (B) LE

A:
PT Impression: 5.5 in kurtzky classification
Rehab Potential: Good prognosis because the pt’s functional ability is not
severely impaired
Rehab Concern: to ↑ muscle strength on (B) LE
Rehab Precaution: Pt. have difficulty in performing task related to standing,
pt. has tendency to
fall, uthoff’s sign, treat pt. early in morning because of
fatigability

Problem list
1. easy fatigability
2. LOM on (B) LE
3. Muscle weakness
4. incoordination
5. ADL such in transfer and locomotion

LTG (3 mos.)
1. To prevent 2o complications such as pressure sore
2. improve the strength and endurance of (B) LE
3. To attain the highest functional ability of the pt. in all aspects of ADL & can
perform
independently without difficulty

STG (2 wks)
1. improve pt. endurance
2. To ↑ muscle strength of (B) LE from 2+/5 to 3-/5 & maintain (B) UE
3. To ↓ spasticity of (L) UE
4. To ↑ ROM of (L) UE & (B) LE by 5o increment
5. To improve coordination

P:
PT Management
1. AAROME on (B) LE x 10 reps x 1 set
2. FES on (B) LE x 90 contractions

44 | P a g e
 3. Gentle manual passive stretching on (B) UE x 7-10 sec hold x 10 reps x 1 set
4. Frenkels exercise
5. AROME on (B) LE
6. Pool therapy
7. Aerobic exercise
8. Cold packs & stretching
9. Ultrasound

HI / WI
1. Self stretching exercise
2. exercise early in the morning
3. pressure relief every 30 minutes

________________________________________
Unice Jane Louise A. Almeniana
( UDM / Batch 2015 )

________________________________________
Maybelle B. Villaroman
( UDM / Batch 2015 )

45 | P a g e
 Parkinson’s Disease
Mangilinan, Felix. DC.
Logmao, lorreine

Definition
 A chronic, progressive disease of the nervous system characterized by the
cardinal features of rigidity, bradykinesia, tremor and postural instability.
 Also known as “paralysis agitans” (Sullivan)
 And was first described as “shaking palsy” by James Parkinson

Related Anatomy
 Basal ganglia (BG)
- collection of masses of gray matter situated within each cerebral
hemisphere
Function:
-motor coordination, rate of movements
Functional Parts:
1. Subthalamic nucleus – glutaminergic and excitatory and have many
connections to the globus pallidus and substantia nigra
2. Substantia nigra – dopaminergic and inhibitory and have many
connections to corpus striatum.

Anatomical Parts:
1.Putamen
2. Caudate nucleus
3. Globus pallidus

Neurotransmitter :
Acetylcholine - secreted in the large pyramidal cells of motor cortex, basal
ganglia (excitatory)
Dopamine – substantia nigra pars compacta (inhibitory)
GABA – SC; BG (inhibitory)
Glutamate –presynaptic terminal; cerebral cortex (excitatory)
Serotonin – median raphe of magnus of BS (inhibitory)
Connections of the corpus striate:
Afferent fibers:
CORTICOSTRIATE FIBERS

46 | P a g e
 -all parts of the cerebral cortex send axons to the caudate nucleus and the
putamen. The largest input is from the sensory-motor cortex. Glutamate is the
neurotransmitter of these fibers.
THALAMOSTRIATE FIBERS
-the intralaminar nuclei of the thalamus send large numbers of axons to the
caudate nucleus and the putmen.
NIGROSTRIATE FIBERS
-neurons in the substantia nigra send axons to the caudate nucleus and the
putamen and liberate dopamine at their terminals as the neurotransmitter.

Efferent fibers:
STRIATOPALLIDAL FIBERS
-these fibers pass from caudate nucleus and putamen to the globus palidus.
They have gamma-aminobutyric acid(GABA) as their neurotransmitter.
STRIATONIGRAL FIBERS
-fibers pass from the caudate nucleus and putamen to the substantia nigra.
Some of the fibers use GABA or acetylcholine as the neurotransmitter while
others use substance P

Epidemiology
 PD is a very common neurodegenerative disease that affects more years of age.
(Sullivan)
 Age of onset: 50-60 y/o (Sullivan); 65 y/the caudate (Braddom)
 There are less than 10 new cases per 100,000 under age 50
 Before 50 y/o – appearance of initial symptoms
 Men > women
 80% damage to BG – diagnosed as Parkinson’s disease

Etiology
 Idiopathic
 Abnormalities of basal ganglia (substantia nigra)
 Affects 6th- 8th decade of life

Theories
A. Accelerated aging– direct result of process of accelerated resulting to the brains
ability to produce dopamine decrease

B. Genetic predisposition – genetic cause is hereditary, primary relatives of PD

patients are 2x more likely to develop the disease, abnormal has been cause,
located in chromosome 4 but remain controversial some PD patients has no
genetic link and is believed to be caused by environment and genetical factor

47 | P a g e
C. Oxidative stress – theory c most important date - association c  activity of
superoxide dismutase which generate or  the activity of Hydrogen peroxide ,
an oxygen radical
-  in radical scavengers such as catalase and glutathione which
breakdown H2O2 into H2O and o2 is seen in PD 1° seen as abnormality in
substantia nigra
- impaired mitochondrial respiratory mechanism manifested as 
mitochondrial complex 1 results in  O2 free radicals
- produces Lewy bodies with parkinsonian like symptoms or acquired
2° Parkinsonism
A. Toxin Exposure
- exposure to chemical such as manganese, carbon disulfide, calcium
monoxide, cyanide and methanol
 Manganese- most common toxin that represent a serious occupational
hazard to many miners
B. Drug Induced/ Pharmacological Parkinsonism
- Reserpine
Neuroleptic
Metochlopromide
Tetrabenzine
Tranquilizers- such as chloropromazine, haloperidol and
thoridapine
C. Infectious Parkinsonism
- Post encephalitis
- Encephalitis Lethargica (Von Economo’s Disease)
D. Metabolic Causes
- Metabolic conditions such as d/o of Calcium metabolism resulting to
BG calcification, hypothyroidism
E. Vascular lesion and tremor
F. trauma
G. Deep well water drinking in Rural areas
H. Increase animal fat consumption

Parkinsom Plus – exhibit sign other than PD

A. Olivopontocerebellar atrophy
B. Progressive supranuclear palsy
C. Shy – drager syndrome
D. Cortical basal ganglionic degeneration
E. Diffuse lewy bodies
F. Huntingtons dse
G. Wilson dse

Pathophysiology
48 | P a g e
 The main input structure of the BG is the striatum.
 Input is received from all parts of the cerebral cortex via CORTICOSTRIATE
projection. The striatum also receives from substancia nigra
 Output is channeled primarily through the globus pallidus and the substantia
nigra to the thalamus and back to the cortex.
 The direct pathway facilitates BG output to the thalamus and motor areas of the
cortex while the indirect pathway provides excitatory to the subthalamic nucleus
 Parts of globus pallidus project to the brainstem and in turn to the motor neurons
in the brainstem and spinal cord.
 Degeneration of dopaminergic neuron that produce dopamine.
 Clinical signs begins to emerge with 30 to 60 percent degenerations of neurons
 Nigral cells loss is estimated at 10 percent per year
 Loss of melanin-containing neurons produces characteristics changes in
depigmentation.
 The disease progress and neuron degenerate they developed characteristic body
cytoplasmic inclusion bodies called lewy bodies
 Lewy bodies are abnormal aggregates protein inside the nerve cell.
 Loss of dopamine result in an overactive indirect pathway that is though to
underlie AKINESIA and RiGIDITY
 Underactive direct pathway is thought to be responsible for bradykinesia.

Clinical features:
 Rigidity
- Hallmark of PD
- It is felt uniformly in both agonist and antagonist muscles and in movements in
both directions.
Two types:
a. Cogwheel rigidity - jerky, ratchet-like resistance to passive movement as
muscles alternately tense and relax
b. Windpipe rigidity - more sustained resistance to passive movements with no
fluctuations

 Bradykinesia

-decrease in amplitude and ROM

Akinesia – absence of movements
- deficits in the preparatory phase of movement control
Hypokinesia- reduced speed and amplitude of movement
 Resting Tremor
- Initial symptom of PD
- An involuntary oscillation of a body part
- Occurs at rest and disappear during sleep
- “pill-rolling” motion of the hand

49 | P a g e
 Postural Instability
- Patient stand with a stoop and his or her arms are flexed
- Protracted shoulder, flexed hips and knees
- Frequently fall

Others:
1. mask fascie = emotionless face
2. Microphagia = small writings
3. Reptilian gaze = blinking
 Meyerson’s sign – inability of the patient to stop blinking upon tapping his
glabella
4. Mincing gait =  base of support, short steps
= patient may break into shuffling run to maintain his balance but unable to
stop.
5. Dysphagia
6. Sialorrhea
7. seborrhea
8. bradyphrenia
9. akithesia

clinical signs:
1. positive phenomenon
A. tremor
- usually resting type
- most common symptom with distal involvement
- 3-6 Hz; 4-7 oscillations/ sec.
B. rigidity
- continuous firing of alpha motor neuron
C. simian or flexed posture(kyphotic)
- striatal hand = wrist flexion, MCP, PIP, DIP extension & ulnar
deviation
-striatal foot – dorsiflexion, inverted and toes extension
2. negative
- bradykinesia
- loss of postural reflexes
- postural instability / freezing phenomenon
= kinesia paradoxical – ability to move rapidly during surge of
emotional energy

Stage Character of Disability

50 | P a g e
 I Minimal or absent; unilateral if present
II Minimal bilateral or midline involvement.
Balance not impaired.
III Impaired righting reflexes. Unsteadiness
when turning or rising from chair. Some
activities are restricted, but patient can
live independently and continue some
forms of employment
IV All symptoms present and severe.
Standing and walking possible only with
assistance
V Confined to bed or wheelchair

Differential diagnosis
Other degenerative movement disorder
 Huntington disease – autosomal dominant inherited disease with the occurring
most often in adult life. Characteristic s/sx: involvement d/o, loss of memory and
intellectual capacity, and facial grimace.
 Chorea – patient exhibits involuntary, quick, jerky, irregular movements that are
nonrepetitive.
 hereditary ataxias – friedrich ataxia is a progressive d/o with the presentation of
limb and gait ataxia with diminished muscle stretch reflexes, joint position sense,
and vibratory appreciation.
 Dystonia – characterized by muscle contraction resulting in twisting, turning and
posturing.
 tourette syndrome – constellation of symptoms including tic d/o and comorbid
neurobehavioral problems.

Prognosis
 tremor- predominat patients tend to progress at a slower pace than those
individuals c gait or postural instability as a primarily complaints.
 Akinesia can portend a more rapidly progressing disease process
 Positive prognosis indicates early tremor, rigidity, and a family Hx of Parkinson
dse
 Negative prognostic indicator include bradykinesia, akinesia, postural instability,
gait dysfunction, cognitive deficits, and late age of onset
 Life expectancy is variable but significantly improve c medical management.

Medical Management
Pharmacological Mgt.

51 | P a g e
 Neuroprotective Therapy
1. Selegiline (MAOs)
- Given to improve metabolism of intracerebral dopamine
- Delays the 1° endpoint at which patients need to start taking levadopa by about 9
months and may slow the overall progression of the disease
 Symptomatic Therapy
Levodopa (L-dopa) - mainstay of symptomatic treatment for PD
- Function: metabolic precursor of dopamine that is able to cross
the blood-brain barrier and raise the level of striatal dopamine in basal
ganglia
- Today, commonly administered with Carbidopa
- Sinemet is the most common carbidopa/ L-dopa medication. 1° benefit is in
alleviating bradykinesia and rigidity with less effect of tremor. It does not appear
to have a direct impact on postural instability.
Adverse Effects:
Disturbances on:
1. G.I (anorexia, nausea, vomiting, constipation)
2. Cognitive (confusion and hallucination)
3. Cardiovascular (hypotension and arrhythmias)
4. Genitourinary ( dysuria)
5. Neuromuscular (motor fluctuations and dyskinesia)
6. Sleep disturbances ( insomnia, deep fragmentation)

- Apomorphine test= remissions of signs in patient with possible PD, positive sign
upon taking L-dopa
 Dopamine Agonist (DA)
- Class of drugs designed to act directy on the postsynaptic dopamine receptors
- Administered along with L_dopa, allowing lower doses to be administered with
prolong effectiveness
- Function: reduce rigidity and bradykinesia, and can also reduce motor
fluctuations
Adverse Effects:
1. Orthostatic lightheadedness
2. Nausea is being most common
 Anticholinergic Agents
- Used in early, untreated PD or as an adjunct for patients on levodopa
- Function: block cholinergic,  tremor and rigidity
have no or little effect on bradykinesia and postural instability
Surgical Mgt.
 Ablative Surgery
Pallidotomy- produce destructive lesion in the sensorimotor
portion of the globus pallidus (GPi)
Effects: contralateral; long lasting

52 | P a g e
 Thalamotomy- produce destructive lesion within ventral immediate
nucleus(VIM) of the thalamus
- reduce long lasting tremor that is unresponsive to drug
treatment and may offer some improvement of rigidity

 Deep Brain Stimulation

- implantation of electrodes into the brain where they block the nerve signals
that cause symptoms
- total suppression of tremor is observed in 1/3 to ½ of patients
- major advantage is its potential to alter tremor without producing an
irreversible brain lesion
 Neural Transplantation
- transplantation of cells capable of surviving and delivering dopamine into the
striatum of patients with advance PD

PT Management
1. (PNF) Bilteral symmetrical D2 flexion
2. rhythmic initiation
3. relaxation exercises
4. stretching exercises
5. (PNF) D1 extension pattern

53 | P a g e
 Initial Evaluation

Gen. Info.:
Pt’s Initial: F.R
Age: 71 y/o
Sex: Male
Address: 666 Bronx St. Manila Polo Club Village, Taguig City
Civil Status: Widowed
Handedness: ®
Occupation: Retired boxer
Referring Unit: Medical City
Rehab Unit: Medical City
Referring M.D.: G. A.
Rehab M.D.: G.O.
Date of Admission: Jan. 1, 2010
Date of Referral: Jan. 1, 2010
Date of Rehab Consultation: Jan. 2, 2010
Date of IE: Jan. 2, 2010
Diagnosis: Idiopathic Parkinson’s disease
Informant: Son/ Reliable

HPI:

Present condition started 20 yrs PTA when the patient loss his consciousness
after taking a right straight punch to his face and received a right uppercut from his
foe. The patient was rushed to the hospital and arrived there approximately 15 mins.

54 | P a g e
The patient regain his consciousness after 25 mins. Then xray and ct scan was
taken. The patient was then under observation for 3 days . after 1 week patient was
discharged and resigned to his job as was advised by the doctor.

15 yrs PTA. When his son noticed that his father’s right hand can perform well
upon doing his household stuff but if it’s on rest. Shakes and he also noticed that the
right hand of his father always do “ pill rolling”. He asked his father to take a nap and
shaking of his hand stops but start to appear again when the patient woke up. After
a year, shaking of his left hand occurs but the patient ignore it thinking it was d/t
aging.

10 yrs. PTA when the patient is experiencing difficulty in moving up from the
bed. And his hand his hand movement started to become slow and the resting
tremor of his hand speeds up. This prompted the patient to consult the doctor. The
attending physician prescribed anti- cholinergic drugs ( cogentin 2mg/ml bid) for the
tremor he had. After taking the medications the resting tremor decreased.

7 yrs PTA. The resting tremor of his hand increases more and his movement
became slower. He went again to his physician and performed MRI ( See ancillary
procedure) and r/o that the patient has possible parkinson’s dse. He performed
adpmorphine test to the patient. The patient was under observation in 1 week, after
a week , he was dx to have a parkinson’s dse and was prescribed to take levodopa
(500mg orally,prn) and also his past meds.

At present, the patient was suffering from rigidity on right UE/LE,bradykinesia

and resting tremor of both hands and was admitted d/t suffering from respiratory
distress because of his kyphotic posture that affects his ADL. And frequently
experiences fall. The patient was referred to PT for rehabilitation and further
evaluation.

Ancillary Procedures:

Diagnostic Findings Date

Procedure

MRI Degeneration of nigrastriatal fiber Jan 1 2010

Lab Exams Normal Value Findings Impression Date

Hematocrit 40- 50% 43 normal Jan 1 2010
LDL 65-180mg/dl 70mg/ dl normal Jan 1 2010
Fasting blood 70 to 99 mg/dl 89 mg/ dl normal Jan 1 2010

55 | P a g e
 glucose
wbc cell count 0-5 WBC 3wbc Normal Jan 1 2010

Present Medication:

Dosage Frequency Indication

Cogentin 6ml/mg Bid  ach

Losartan 50mg Od htn
Levodopa 500mg(orally) Prn Eliminate bradykinesia and rigidity

PMHx:
 (+) Htn (controlled; Losartan (50mg/day) since 1999 )
 (+) Trauma repetitive d/t occupation
 (-) Hospitalization
Highest BP: 150/100 mmHg; Baseline: 130/90mmHg; Lowest BP:
100/80mmHg
 (-) DM
 (-) Cardiopulmonary problem

FMHx:
Father Mother
 Htn (+) (+)
 Pulmonary Disease (-) (+)
 DM (-) (-)
 Cardiac Condition (-) (-)
 PD/ movement d/o (-) (-)

PSEHx:
 Type A Personality
 Sedentary lifestyle
 Lives in 2 storey house with 1 children
 ( - ) Alcohol beverage drinker
 ( - ) Smoker
 Financially stable
 Diet includes: meat, vagetables and espresso
 Hobbies : Watching TV and reading newspapers
 Home set-up
2 flight of stairs with wooden handrails on (B) sides
14 steps of stairs
Pt’s room is located at the 2nd floor
~ 16 steps from room to CR
~ 19 steps from room to kitchen

56 | P a g e
 ~ 24 steps from room to dining
~ 30 steps from room to living room
(Tiles granite)

S:
Pt’s c/c: ” laging nanginginig ang mga kamay niya kapag nakapahinga
ito at, gusto niyang makatayo ng tuwid at makapaglakad ng
diretso at makahinga ng maayos ngunit napipigilan ito ng
matigas nyang katawan,.dahil sa postura nyang medyo kuba at
matigas din mga binti dahilan kung kaya din sya natutumba” As
verbalized by his son.
PT Translation: Patients experiences resting tremor and rigidity on (B) UE/LE
resulting into gait problem 2° to postural instability
Pt’s Goal: to prevent 2° complication on his respiratory distress and to
achieved his well being.

O:
VS: a during
p
BP 130/90 mmHg 150/100 mmHg 140/90
mmHg
RR 10 cpm 12 cpm 16
cpm
PR 75 bpm 97 bpm 80 bpm
T° 37.2°C 37.3°C
Afebrile to touch

Findings: All VS are WNL

Significance: For baseline data

OI:
 Ambulatory c walker
 lethargic
 Mesomorph
 Oriented in time, place and situation
 (+) Respiratory distress
 (+) Seborrhea
 (+) Sialorrhea
 (+) Reptilian gaze
 (+) Resting tremor in both hands
 (+) Postural Deviation (see postural analysis)
 (+) fencinating gait
 (+) contracture on hip and knee
 (+) en bloc
 (+) striatal hand
 (+) tophic skin chnages

57 | P a g e
  (-)Swelling on (B) LE
 (-) masked fascie
 (-) attachments

Palpation:
 Normothermic on all exposed part
 Poor,turgor, mobility and consistency
 (-) Edema on (B) LE
 (-) Tenderness
 (-) Taut band, Trigger points

Neurologic Examination

Tone:
Findings: rigidity on both UE/LE lead pipe
Significance: 2° to extrapyramidal system

Sensory A:

A. Superficial Somatic Sensation

Findings: (+) in light touch, superficial pain and thermal sensation

Significance: (-) affectation on BA 3,1,2
B. Deep Somatic Sensation

Findings: (+) in deep pain pressure, vibratory sense, proprioception, and

kinesthesia
Significance: (-) affectation in BA 5,7

C. Cortical/ Central Integrative Sensation

Findings: (+) stereognosis, barognosis, graphesthesia, bilateral cutaneous tactile

localization and two point discrimination
Significance: intact thalamocortical pathway

® (L)
MSR/DTR:
Legend

58 | P a g e
 0 Areflexia
+ Hyporeflexia ++ ++
++ Normoreflexia +++ +++
+++ Hyperreflexia ++ ++
++++ Clonus ++ ++

+++ +++

Findings: areflexia on both UE/LE

Significance: 20 to  firing of alpha motor neuron

Pathologic Reflex:

Reflex Response
(+) glabellar reflex Blinking of eyes
(-) Babinski
(-) Chaddocks

Findings: (-) Babinski, Chaddodks, hoffmans

Significance: affectation of extrapyramidal

Pathologic Reaction:

Reflex Response
(+) Meyerson’s sign Eyes do not blink
(+) stelwag sign Widening of palpebral fissure

Findings: (+) Meyerson’s sign and stelwag sign

Significance: 20 to affectation of extrapyramidal

Cranial Nerve Testing:

Findings: all cranial nerves are intact

Significance: (-) affectation on Brainstem

Coordination A:
Non-equilibrium test

-Finger to Nose -2
-Finger to therapist finger -2
-Finger to finger -2
-Alternate Nose to finger -2
-Finger opposition -2
-Mass Grasp -2
-Pronation /Supination -2

59 | P a g e
 -Rebound test -2
-Tapping hand -2
-Tapping foot -2
-Pointing to Past Pointing -2
-Alternate heel to knee; heel to toe -2
-Toe to Examiner’s Finger -2
-Heel on shin -2
-Drawing a circle(hand and foot) -2
-Fixation/Position Holding(UE/LE)-2

Equilibrium Test
-Standing; (N) comfortable posture -2
-Standing; (N) comfortable posture with
vision occluded -2
-Standing; Feet tighter -2
-Standing; on one foot -2
-Standing; Forward trunk flexion &
return to neutral -2
-Standing; Lateral Trunk Flexion -2
-Walk; Place heel of one foot in front of toe of the opposite foot -2
-Walk; along a straight line -2
-Walk; place feet on floor markers -2
-Walk; sideways -2
-Walk; backward
-Walk; in a circle, alternate directions -2
-Walk; on heel -2
-Walk; on toes -2
-March in place -2

60 | P a g e
 ROM:
All rom of both UE and LE are wNL and passively done except
Motion Norma Difference End
l value Feel
Active Passive Active Passiv
e
(R) (L) (R) (L)
Shoulder
Flexion 0-1800 0-20° 0-20° 0-150° 0-150° 100° 100° Firm
0
Extensio 0-60 0-20° 0-20° 0-60° 0-60° 40° 40° Firm
n
Abductio 0-1800 0-20° 0-20° 0-170° 0-170° 130° 130° Firm
n
Adductio 180-00 20-0° 20-0° 170-0° 170-0° 130° 130° Firm
n
Internal 0-900 0-20° 0-20° 0-90° 0-90° 70° 70° Firm
Rotation
External 0-700 0-15° 0-15° 0-70° 0-70° 55° 55° Firm
Rotation

Elbow
Flexion 0-1500 0-20° 0-20° 0-150° 0-150° 120° 120° Soft
Extensio 150-00 50-0° 50-0° 150-0° 150-0° 90° 90° Hard
n
Pronation 0-800 0-20° 0-20° 0-80° 0-80° 55° 55° Firm
Supinatio 0-800 0-20° 0-20° 0-80° 0-80° 50° 50° Firm
n
Wrist
Flexion 0-800 0-10° 0-10° 0-80° 0-80° 40° 40° Firm
Extensio 0-700 0-10° 0-10° 0-70° 0-70° 50° 50° Firm
n
Radial 0-200 0-5° 0-5° 0-20° 0-20° 15° 15° Hard
deviation
Ulnar 0-300 0-10° 0-10° 0-30° 0-30° 20° 20° Firm
deviation
MCP
Flexion 0-900 0-5° 0-5° 0-90° 0-90° 85° 85° Firm
(2nd -5th
fingers)
Extensio 0-450 0-5° 0-5° 0-45° 0-45° 40° 40° Firm
n
(2nd- 5th

61 | P a g e
fingers)
PIP
Flexion 0-1000 0-10° 0-10° 0-100° 0-100° 90° 90° Firm
(2nd -5th
fingers)
Extensio 100-00 20-0° 20-0° 100-0° 100-0° 65° 65° Firm
n
(2nd – 5th
fingers)

DIP
Flexion 0-900 0-10° 0-10° 0-90° 0-90° 80° 80° Firm
(2nd – 5th
fingers)
Extensio 0-100 0-5° 0-5° 0-10° 0-10° 5° 5° Firm
n
(2nd – 5th
fingers)
1st CMC
Flexion 0-150 0-5° 0-5° 0-15° 0-15° 10° 10° Firm
Extensio 0-200 0-5° 0-5° 0-20° 0-20° 15° 15° Firm
n
Abductio 0-700 0-10° 0-10° 0-60° 0-60° 50° 50° Firm
n
Adductio 70-00 10-0° 10-0° 60-0° 60-0° 50° 50° Firm
n

Normal Active Passive Difference End Feel

value
(R) (L) (R) (L) Active Passive
Hip
Flexion 0-1200 0-20° 0-20° 0-120° 0- 100° 100° Soft
120°
Extension 0-300 0-10° 0-10° 0-30° 0-30° 20° 20° Firm
Abduction 0-450 0-15 0-15 0-45 0-45 30 30 firm
Adduction 0-300 0-5° 0-5° 0-30° 0-30° 25° 25° Firm
Internal 0-450 0-10° 0-10° 0-45° 0-45° 35° 35° Firm
Rotation
External 0-450 0-10° 0-10° 0-45° 0-45° 35° 35° Firm
Rotation
Knee
Flexion 0-1350 0-20° 0-20° 0-135° 0- 115° 115° Soft

62 | P a g e
 135°
0
Extension 135-0 20-0° 20-0° 135-0° 135- 115° 115° Firm
0°
Ankle
Plantarflexion 0-500 0-10° 0-10° 0-50° 0-50° 40° 40° Firm

Dorsiflexion 0-200 0-5° 0-5° 0-50° 0-50° 45° 45° Firm

Tarsal joint 0-350 0-10° 0-10° 0-35° 0-35° 25° 25° Firm
inversion
Tarsal joint 0-150 0-5° 0-5° 0-35° 0-35° 30° 30° Hard
Eversion
Transverse 0-200 0-5° 0-5° 0-20° 0-20° 15° 15° Firm
tarsal joint
inversion
Transverse 0-100 0-10° 0-10° 0-10° 0-10° 0° 0° Firm
tarsal joint
eversion

Findings: LOM upon AROM on (b) UE and LE as to all planes of motion

Significance: 2° to rigidity

MMT:
All muscles of (B) LE and (L) UE are grossly graded 2/5 :

Muscle Group Grade

Shoulder flexors 2
Shoulder extensors 2
Shoulder abductors 2
Shoulder adductors 2
Shoulder IR 2
Shoulder ER 2
Elbow flexors 2
Elbow extensors 2
Wrist flexors 2
Wrist extensors 2
Wrist adductors 2
Wrist abductors 2
MCP flexors 2
MCP extensors 2
PIP flexors 2
PIP extensors 2
DIP flexors 2
63 | P a g e
 DIP extensors 2
1st CMC flexors 2
1st CMC extensors 2
1st CMC abductors 2
1st CMC adductors 2

Hip flexors 2
Hip extensors 2
Hip internal rotators 2
Hip external rotators 2
Hip abductors 2
Hip adductors 2
Knee flexors 2
Knee extensors 2
Ankle plantarflexors 2
Ankle dorsiflexors 2
Ankle invertors 2
Ankle evertors 2

Findings:
Significance: 2° to UMNL

FACIAL MMT

 Smiling wf
 Frowning wf
 Wrinkling of nose and forehead wf
 Surprised wf
 Pouting wf

Findings: all facial muscle are weak functional

Significance: 2° to affectation of extrapyramidal

Hand Grip Analysis:

BP cuff was inflated to 20 mmHg

® (L) Difference
Trial 1 10mm/hg 4mm/hg 6mm/hg
Trial 2 11mm/hg 5mm/hg 6mm/hg
Trial 3 12mm/hg 6mm/hg 6mm/hg
Total 33mm/hg 15mm/hg 18mm/hg

64 | P a g e
 Average 11mm/hg 5mm/hg 3mm/hg

Findings: LOM upon inflating bf cuff to 20 mm/hg

Significance: 2° to rigidity

Hand Function:
Legend:
3- Performs task normal without difficulty
2- Complete task but clumsy
1- Initiates movements
0- Unable to perform activity

A. Power Grip ® (L)

Cylindrical 1 1
Fist 1 1
Hook 1 1
Spherical 1 1

.B. Precision Grip

Lat. Pinch 1 1
Pulp-to-pulp 1 1
Tip-to-tip 1 1
3 jaw chuck 1 1
5 digit pinch 1 1
Findings: HAND FUNCTIONAL ASSESTMENT GRADED 1/3
Significance: 2° TO rigidity

Balance and Tolerance:

Balance Tolerance
N (normal) can assume, maintain, weight shift, and challenged
>45mins
G (good) can assume, maintain and weight shift 31-
45mins
F (fair) can assume and maintain 16-
30mins
P (poor) can assume 1-15mins
O (zero) can neither assume nor maintain 0 mins

Balance Tolerance
Sitting Good 31-45mins

65 | P a g e
 Standing Good 1-15mins

Postural Analysis:
All parameters of posture are correct except for:

ANTERIOR VIEW
1. Forward protrusion of head
2. Shoulders are level but stooped
3. No protrusion,depression or lateral of the sternum,ribs or cartilage
4. Wrist flex
5. Elbow flex
6. Waist angle is equal but the arm is not equidistant from the waist
7. Arms are flexed
8. Palm of both hands faces inferiorly
9. Knees are flexed

Note: postural analysis was done in standing position

Posterior view
1. Shoulders are level but stooped
2. Spine is flexed anteriorly
3. Waist angle is level
4. Arms are flexed
5. Iliac crest is level
6. Gluteus folds are level
7. Popliteal fossa are level
8. Knees are flex
9. Heel slightly pointed to the ground

Lateral view
1. Earlobe in line anteriorly on the shoulder
2. Shoulder protracted
3. Spinal segment flex
4. Knees are flexed

FIM

Findings: all ADL are fully dependent

Significance: 2° to rigidity

A:
PT Impression: Stage IV parkinson’s disease (hoehn and yahr)
Rehab Potential: poor prognosis
Rehab Concern: to improve the mobility of patient
Rehab Precaution: frequently fall; shuffling gait; maintain levodopa
medication

66 | P a g e
Problem List:
1. LOM in Active motion on both UE/LE
2. 2/5 mmt
3. Kyphotic posture
4. Total assistant in an aspect of ADL
5. Bradykinesia
6. Resting tremor
7. Shuffling small step
8. Difficulty in respiration
9. Rigidity on (B) UE/LE

LTG: (5 mos.)
1. To prevent 2° complication of the conditions such as tightness,contracture,
deformity, pressure sore and edema
2. To maintain the mobility of the patient and improve patient’s endurance
3. To attain the highest functional potential as to eating;walking;speaking;good
posture etc.

STG: (3 weeks)
1. PROM→AAROM
2. MMT from 2/5 to 3/5
3.  muscle fatigue
4. Widen base of support

P:
PT Mgt:
1. PROME→AAROME
2. Stretching exercise
3. (PNF) bilateral symmetrical D2 flexion
4. Jacobson’s relaxation exercise
5. Frenkels exercise

WI:
1. Do stretching exercise taught by the PT
2. Take medication on time
3. Always watch the patient from falling.
4. Maintained good hydration

_________________________
Mangilinan, Felix. DC.
UDM/Batch 2015/Designation

67 | P a g e
_________________________
Logmao, lorreine
UDM/Batch 2015/Designation

Guillain-Barre Syndrome
Kierulf, Vanessa Erika D.G.
Zamora , Josephine

Hx:

1859- Landry: acute flaccid paralysis

1916- Guillain,Barre and strohl: “ radiculoneuritis with hyperalbuminosis of CSF
without cellular reaction”, weakness, loss of DTR and  CSF protein without  of
WBC

DEFINITION
- Aka. Acute infectious neuropathy , Landry paralysis, and inflammatory
radiculopathy
- Define as an acute demyelinating d/o in which macrophages strip myelin from
axon in the PNS (tortora)
- GBS is a demyelinating disease that affects the PNS especially spinal nerve
which characterized by abrupt onset of paralysis (Robbin)
- Type of peripheral neuropathy- a condition involving degeneration of the
nerves exending into the head, body and limbs (Parry)
- a demyelinating disorder with perivascular lympholitic infiltration ( Lindsay)

RELATED ANATOMY

Nervous system- one of the smallest and yet the most complex of the 11 body
system
Overview:
1. Structure of the nervous system

68 | P a g e
 - It is make up the nervous system include the brain, cranial nerve, and
their branches, the spinal cord, spinal nerves and their branches,
ganglia, enteric plexuses and sensory receptors
 Brain
o Consist of 100 billion neuron
 CN 1 I-XII
o Carry impulse to and from the brain
o Emerge from the base of the brain
 Spinal cord
o Connects to the brain through the foremen magnum of skull
o Encircled by the bones of the vertebral column
o Consist of 100 million neuron
 Ganglia
o Small masses of nervous tissue
o Consist primarily of neuron cel bodies that are located outside the
brain and the spinal cord

2. Subdivision of Nervous system

a. CNS – which consist of the brain and spinal cord
b. PNS- that includes all nervous tissue outside the CNS
Nervous tissue

It consists of 2 types of cells:

Neurons-provide most of the unique functions o the nervous system such as
sensing and regulating glandular secretion
Basic parts: dendrites  cell body axon axon terminal

FUNCTIONAL CLASSIFICATION
1. Sensory or afferent neuron
- contain sensory receptor at their distal ends and unipolar in structure
2. Motor or efferent neuron
- convey action potential away from the CNS to effectors in PNS through cranial
or spinal nerves.
- Most motor neurons are unipolar in structure
3. Interneuron or association neuron
- process the incoming sensory information fro the sensory neuron and then elicit
a motor response by activating the appropriate motor neuron.
- Most motor neurons are multipolar in structure

NEUROGLIA- support, nourish and protect the neurons and maintain homeostasis in
the interstitial fluid that bathes hem
 CNS
1) Astrocytes
2) Oligodendrocytes
3) Microglia
69 | P a g e
 4) Ependymal cells

 PNS
- Neuralgia of the PNS completely surrounds axon and cell bodies. The 2
types of glial cells in he PNS are Schwann cell and Satellite cell

SCHWANN CELLS

- Encircle PNS axons. Like oligodendrocytes they form myelin sheath around
the axon however, single oligodendrocytes myelinates a single axon
- It enclose as many as 20 or more unmyelinated axons.
- Participate in axon regeneration, which is more easily accomplished in the
PNS than in the CNS

SATELLITE CELLS

- A flat cells that surround the cell bodies of neuron of PNS ganglia which
regulate the exchanges a of materials between neuronal cell bodies and
interstitial fluid

Myelination

- Axon surrounded by multilayered lipid and protein covering called myelin

sheath are said to be myelinated
- 2 types of neuralgia produce Myelin sheath
a. SCHWANN CELLs (PNS)
b. OLIGODENDROCYTES (CNS)

a) Schwann cells (PNS), is the myelin sheath. The outer nucleated cytoplasmic
layer of the Schwann cell, which encloses the myelin sheath, is the neurolemma
(sheath of Schwann), it is found only around axon is injured, the neurolemma
aids regeneration by forming a regeneration tube that guides and stimulates
regrowth of the axon. Gaps in the myelin sheath, called nodes of Ranvier that
appear at intervals along the axon.

b) Oligodendrocytes (CNS) , an oligodendrocytemyelinates parts of several axons.

Each oligodendrocyte puts forth about 15 broad, vflat processes that spiral
around CNS axons, forming a myelin sheath. A neurolemma in not present,
however, because the obligodendrocyte cell body and nucleus do not envelop
the axon. Nodes of Ranvier are present, but they are fewer in number. Axons in
the CNS display little regrowth after injury. This is thought to be d/t the absence
of a neurolemma, and in part to an inhibitory influence exerted by the
oligodendrocytes on axon regrowth.

70 | P a g e
Spiral Peripheral Nervous System
- Entry and exit from nervous system is achieved by spiral nerve
- Dorsal and ventral root lie in the spinal subarachnoid space and come
together at the IV formen to form spinal nerve
- Dorsal root contains sensory fiber, arising from specialized sensory
receptors in the periphery
- Dorsal root ganglia are collections of sensory cell bodies with axons
extending peripherally as well a central process w/c passes into spinal cord in
the region of the posterior horn of grey matter and makes appropriate central
connection.

Sensation is divided into:

- Pain and temperature

- Simple touch
- Discrimination sensation – propioception, vibration

– Sensation is carried from the periphery by axon with specific characteristic .central
and pathway connections also vary.
– Anterior horn of spinal cord contains cell bodies whose axon passes to periphery to
innervate skeletal muscle- the alpha motor neuron. Smaller cell bodies also project into the
anterior root and innervate the intrafusal muscle fiber of muscle spindle-gamma motor
neuron

Etiology
-unknown
- most common cause campylobacter jejuni

Risk Factor cause GBS:

 Viral infection such as

- Herpes infection
- Varicella-zoster
- Mumps
- Cytomegalovirus
- Estein-Barr virus

 Associated with
- Mycoplasma
- Campylobacter

71 | P a g e
 - Infection
- Immunization with (B)
live & dead vaccine
- Anti-toxin
- Trauma
- Surgery
- Rarely malignant disease

Epidemiology:
 2 out of 100,000 people can experience GBS
 An acute, frequent severe & fulminate polyneuropathy occur 3500 cases per
year in US and Canada
 Usually in autoimmune disease, higher incidence rates have been reported in
males than females
 Occur in all age groups but rare in children; during 1st 2 years of life
 2/3 of its case are viral infection
 5-10% occur within 1-4 weeks of a surgical procedure
 In 1997, sudden occur 500 cases followed in the wake of withdrawal swine flu
 Usually in autoimmune disease, higher incidence rates have been reported in
males than females
 Western people are common to have GBS
 Geographical Variation;
- Majority of incidence rates were between 0.84/100,000/year (Finland)
- 1.91/100,000/year (Italy)
 In North America and Europe, around 5% of patients with GBS have the
Axonal Subtypes
 Central and South America, Japan and China axonal subtypes account for
30-47% of cases
 Miller-Fisher syndrome has been found to account for around 5% of cases of
GBS
 Incubation period is 1-6 weeks

Pathophysiology:
Pathologic feature:
- (B) Antibody and cell mediated reaction to peripheral nerve myelin are involved.

 Anti-bodies to myelin glycoprotein or gangliosides

 Develop T-cell mediated assault on myelin assault on myelin base protein
 Segmental demyelination result with 2 ° axonal damage if process is severe
 Peroventicular demyelination with lymphocyte occur within peripheral nerve & nerve
roots
 Lymphocytes and macrophages release cytotoxic substance-(cytokines) w/c
damage Schwann cell/ myelin

72 | P a g e
  When axon is damage and nerve cell death occur regeneration cannot take
place.

Pathology of GBS
 GBS as Neuropathy
1) AIDP
- In this form of GBS, the immune attack is directed against the myelin,
causing loss of the myelin sheath and leading to a “short circuit” so
that electrical messages cannot travel between the brain and the
periphery of the body. There can be secondary damage to the axons
but sometimes the primary immune-mediated attack is against the
axon itself,causing the electrical cable to degenerate. This is called;
2) Axonal GBS (AMAN) & (AMSAN)
 AMAN
o The attack is limited to motor axon that control muscle activity
 AMAN
o Axonal GBS affects (B) sensory & motor function
3) MFS
- Anti-bodies syndrome attacking the myelin sheath of peripheral
nerve, occasionally axon is the primary target
- GQ1b (resp. in bacterial and viral infection)

Classification of GBS

1. Acute inflammatory demyelinating polyneuropathy (AIDP)

a. Primary damage affects the myelin sheath.
b. Causes acute weakness of limb and breathing muscles.
c. Causes sensory symptoms and signs (numbness, tingling).
2. Acute motor axonal neuropathy (AMAN)
a. Primary damage affects motor axons.
b. Causes acute weakness of limb and breathing muscles.
c. Sensation is normal.
3. Acute motor and sensory axonal neuropathy (AMSAN)
a. Damage affects both motor and sensory axons.
b. Causes acute weakness of limb and breathing muscles.
c. Causes sensory symptoms and signs (numbness, tingling).
4. Miller Fisher syndrome (MFS)
a. Primary site of damage uncertain.
b. Causes acute weakness of eye muscles (ophthalmoplegia)
c. Causes loss of balance and incoordination (ataxia)
d. Causes loss of reflexes (areflexia)
 GBS as disease of immune system (most frequent form of GBS)

73 | P a g e
 - Immune system is designed to fight invaders from outside the body ,
mainly viruses and bacteria, However, for reasons that are only partly
understood, the immune system may turn around and attack the body,
resulting in autoimmune disease.
- Pathologic hallmark of autoimmune disease = inflammation with
lymphocytes
- The immune system attacks the myelin, resulting in demyelination and
inflammation.
o Lymphocyte (inflammatory cell)- immune cell that is responsible for attack

Clinical manifestation:

- Rapidly progressive weakness for a period of 3 to 7 days

- Symmetric involving, first LE the UE & then the respiratory
musculature
- Peripheral paresthesias and numbness of limbs
- Sensory loss is usually but mild
- Tendon reflex is decrease or loss
- Facial nerve diplegia
- Glove and stocking sensory loss

If ANS is affected;
- Postural hypotension
- Constipation and Impotence

Clinical Features:
- Children and young adults recover more better than older
- In adults, it depends on the severity of the paralysis;
o If the progression stops after a week or less; they never lose the
ability to walk and will have returned to normal within a month or
two month
o In some case Pt may become completely paralyzed if there is no
improvement until 2 to 3 months after onset of weakness
- The pace of recovery then slows as damaged axons regenerate, a
much slower and less efficient process. Most recovery occurs within
about 2 to 3 years from the onset of GBS

 Predicted for good recovery defined as being able to walk unassisted within 3
months of the beginning of their illness:

 Relatively preserved muscle responses to electrical stimulation of the

motor nerves

74 | P a g e
  Received plasmapheresis within 4 weeks of beginning of symptoms
 Did not need a respirator to support breathing
 Did not see a doctor until after 7 days of symptoms (implying that their
illness developed more slowly)
 Young age

 Predicted poor recovery:

 Low amplitude (size) of the muscle responses to electrical stimulation of
motor nerves
 Did not receive plasmapheresis within 4 weeks of onset of symptoms
 Needed a ventilator to support breathing
 Saw a doctor within 7 days of onset of symptoms (implying that their
illness came on rapidly)
 Older age

Medical Management:

Diagnostic Procedure

1. Nerve conducting Studies: an electrical stimulus which applied at points

along a nerve and evoked muscle reponse recorded. By applying a
stimulus at various points along a nerve and recording the latecy between
stimulus and muscle reponse the motor conduction velocity of a particular
nerve may be measured.
 (N) human peripheral nerve travel at value of;
1. Legs: 40-50 m/sec.
2. Arm: 50-60 m/sec.

2. EMG: a fine needle is inserted into muscle and the recorded activity
displayed on an oscilloscope. It is a primarily of value in muscle disease
but can also give indirect evidence of neuropathies.
3. Blood and urine tests: A sample of your blood or urine may be sent to a
lab to help find the cause of your symptoms. They may also be used to
make sure organs, such as your liver and kidneys, are working correctly.

4. Lumbar puncture: This procedure is also called a spinal tap. Caregivers

will give you medicine to numb a small area of your lower back. They will
insert a needle and remove fluid from around your spinal cord.

 (N) CSF is 40-80 mg/dl

Immunotherapy

1) Plasmapheresis/ PLASMA EXCHANGE (PLEX): This procedure removes

antibodies from your blood. Some of your blood will be removed through an

75 | P a g e
 IV. The blood is then put in a machine that spins and separates the red
blood cells from the antibodies. The cleaned blood is then put back in your
body through the IV
- PLEX is a safe and effective treatment for severe GBS that can be used
in all age groups. it accelerates the rate of recovery, but does not
reduce mortality or improve the ultimate degree of recovery.
2) INTRANERVOUS IMMUNOGLOBULIN (IVIG): it is administered through a
needle or a plastic cannula that is inserted into a vein, usually in the arm.
- IVIG is safe and effective in the treatment of severe GBS, and is easier
to use and has fewer side effects than PLEX. It can be used in all age
groups, but should be used with caution in the elderly or patients with
risk factors for blood clots.

PT management
Acute condition
1) PROME → AAROME x 10 reps. x 1 set, all planes of motion
- To prevent contracture and minimize the risk of nerve compression &
development of bed sore
2) Positioning of limb
- Reduce risk of nerve compression and help maintain awareness of
joint positioning
3) Splints
- Reduce tendon shortening
4) Gentle Manual Stretching on (B) UE/LE x 15 sec. x 10 reps, all planes of
motion
5) Strengthening exercise
6) PNF technique
7) Pool therapy or use of Parallel bar (Initial Tx for ambulation) → underarm
Cruthces → forearm crutches → canes → then initial strength return

If strength begins to return;

- AAROME → AROmE x 10 reps. x 1 set
- Mat exercise
- Building strength & endurance exercise such as stationary bicycle pedaling
and progressive resistive exercise

76 | P a g e
 Initial Evaluation

Gen. Info.:
Pt’s Initial: B.V
Age: 40 y.o.
Sex: Male
Address: Sta. Ana , Manila
Civil Status: Married
Handedness: ®
Occupation: Businessman
Referring Unit: St. Luke’s Hospital
Rehab Unit: St. Luke’s Hospital
Referring M.D.: DR.V.K.
Rehab M.D.: DR.J.Z.
Date of Admission: August 30,2013
Date of Referral: September 14,2013
Date of Rehab September 14,2013
Consultation:
Date of IE: September 14,2013
Diagnosis: Guillain Barre Syndrome

HPI:
Present condition started 2 weeks PTA, the Pt during the triathlon noticed
unusual paresthesia on his (B) feet while pressing the pedal of his bike; he
immediately stopped and massage it. Tingling sensation lasted up to ~10 mins. This
paresthesia manifests and felt until the pt was admitted to the hospital.
1 week PTA, upon walking, running or upon stepping at stairs; he
experienced fornications and weakness from his feet that radiates into his legs and
thigh which sometimes accompanied by numbness and pain. The Pt also
undergone fever that lasted up for 2 days with severe HA( PS 7/10) so, took bioflu
which helps to lessen the said Sx. 1 Day after experiencing fever, Pt experience
sudden ache on his stomach then he take a nap to ease it up but suddenly upon
waking up, the PT unable to move his leg and cannot pull up his body by the help of
his arm and hand.
2 days PTIE, he was immediately rushed to the hospital and arrive ~ 20 mins.
VS were taken (BP: 130/90 mmHg; RR: 20 cpm; PR: 75 bpm; T: 37 C) and ancillary
procedure were done (see ancillary procedure) then the Pt was Dx to have malaise
indicative of GBS then he was transferred immediately to the ICU when the doctor
noticed sudden difficulty on breathing of the pt.; the doctor administered
acetaminophen with codeine for initial Rx, IV line were inserted and O 2 support was
given. Several days after pt was re-evaluated and was Dx to have GBS. When the pt

77 | P a g e
was neurologically and medically stable, the pt was transferred to a private room and
was referred to PT for further evaluation and Tx.

Ancillary Procedures:

Diagnostic Findings Date

Procedure
NCV Very low CMAP’s on distal stimulation from August 30,2013
peroneal, tibial and median and ulnar motor
nerve of 0-15 % of lower limit of (N)
EMG Prolong distal & F-wave latencies August 30,2013

Lumbar  motor unit of action potential with CSF August 30,2013

puncture amount of 40 mg/Dl

Laboratory exam:

Hematology CBC Normal value Findings Date

Hematocrit 40-50% 45% August 30

Hg Female- 120-160 g/L 200 g/L August 30

Male-135-180 g/L
WBC 4.5-11.0 k/mL 5 k/mL August 30
Basophil 0.0-01 0.0-01
Eosinophil 0.02-0.05 0.03
Neutrophil 0.50-0.70 0.55
Platelet 150-400k/mL 405 k/mL August 30

Present Medication:

Dosage Frequency Indication

NSAID’s 5mg prn For inflammation
Codeine 5 mg prn For depression and pain
Prednisone 2mg/kg 3x a day for infection to dec. inflammation

PMHx:
 (-) Hospitalization
 (-) Htn
78 | P a g e
  (-) cardio-pulmonary problem
 (-) Trauma
 (-) DM
 (-) allergy
 (-) surgery
 (-)meningitis

FMHx:
Father Mother
 Htn (+) (+)
 Pulmonary Disease (-) (-)
 DM (-) (-)
 Cardiac Condition (-) (-)
 Stroke (-) (-)

PSEHx:
 Type B Personality
 Active Lifestyle
 (-) Smoker
 (+) Alcoholic beverage drinker (whiskey; 1 bottle, occasionally)
 Financially stable
 Food preference includes: fatty foods, raw foods, vegetables, and fruits
 Recreational activities: Triathlon
 Lives in 2 storey house with 3 children and wife
 Home set up
2 flight of stairs
15 steps of stairs
Patient’s room located at first floor
20 steps from room to living room
10 steps from room to kitchen
12 steps from room to dining
10 steps from room to cr
Circular door knob
S:
Pt’s c/c: generalized weakness on UE and LE
Pt’s goal: to regain strength and perform ADL’s

O:
VS: a during p
BP 120/90 mmHg 130/80 mmHg
120/80 mmHg
RR 18 cpm 20 cpm 18
cpm
PR 75 bpm 80 bpm 75 bpm
T° afebrile to touch

79 | P a g e
 Findings: All VS are WNL
Significance: For baseline data

OI:

 Bed pass
 Alert, coherent, cooperative
 Mesomorph
 (+) facial drooling on (L) side
 (+) tongue drooling
 (+) attachment
 (+) IV line on ® fingertip
 (+) pulse oximetry
 (-) cathter
 (-) pressure sore on all bony prominence
 (-) atrophy
 (-) dysathria
 (-) respiratory distress
 (-) swelling

Palpation:
 Normothermic on all exposed body parts
 Normal skin turgor, mobility and consistency
 (-) Tenderness

Neurologic Examination

Tone:
Findings: hypotonic on (B) UE/LE
Significance: 20 to LMNL

Sensory A:

a. Superficial somatic sensation

STD used:
 Brush for light touch
 Pin for pain
 Thumb for pressure

Findings: 100% intact sensation on ® UE & LE

Significance: (-) affectation of peripheral sensory nerve
® (L)
MSR/DTR:
Legend

80 | P a g e
 1 Areflexia
+ Hyporeflexia + +
++ Normoreflexia + +
+++ Hyperreflexia + +
++++ Clonus 0 0

0 0
Findings: hyporeflexia on UE and Areflexia on LE
Significance: 20 to  firing of alpha and gamma motor neuron

Cranial Nerve Testing:

Findings: all Cranial nerve are assessed and are normal except for CN VII
Significance: 20 to o affectation of facial nerve

ROM:

All ROM of both ® UE and LE are WNL and passively done except

Actively
Motion Differenc
Normal e End feel
value
Shoulder (R) (L) (R) (L)

Flexion 0-1800 0-900 0-900 900 900 Firm

Extension 0-600 0-500 0-500 100 100 Firm

Abduction 0-1800 0-900 0-900 900 900 Firm

Adduction 180-00 90-00 90-00 900 900 Firm

Internal Rotation 0-900 0-450 0-350 450 550 Firm

External Rotation 0-700 0-550 0-600 150 100 Firm

Elbow

Flexion 0-1500 0-1400 0-1300 100 200 Soft

Extension 150-00 140-00 130-00 100 200 Hard

Pronation 0-800 0-700 0-750 100 50 Firm

Supination 0-800 0-700 0-750 100 50 Firm

81 | P a g e
Wrist

Flexion 0-800 0-750 0-750 50 50 Firm

Extension 0-700 0-650 0-650 50 50 Firm

Radial deviation 0-200 0-150 0-150 50 50 Firm

Ulnar deviation 0-300 0-300 0-300 0 0 Hard

Hip

Flexion 0-1200 0-200 0-200 1000 1000 Soft

Extension 0-300 0-100 0-100 200 200 Hard

Abduction 0-450 0-200 0-200 150 150 Firm

Adduction 0-300 0-250 0-250 50 50 Firm

Internal Rotation 0-450 0-250 0-250 150 150 Firm

External Rotation 0-450 0-250 0-250 150 150 Firm

Knee

Flexion 0-1350 0-200 0-200 1150 1150 Soft

Extension 135-00 20-00 20-00 1150 1150 Hard

Ankle

Plantarflexion 0-500 0-300 0-300 20 20 Firm

Dorsiflexion 0-200 0-180 0-180 2 2 Firm

Findings: LOM on (B) UE/ LE actively, all planes of motion

Significance: 20 to tightness

FACIAL MMT
 Smiling -WF
 Frowning -WF
 Wrinkling of nose and forehead -WF

82 | P a g e
  Surprised -WF
 Pouting -WF

Findings: all Facial MMT on (L) side are weak functional

Significance: 20 to affectaion of CN VII

FMT
Grading
Legend
4- Perform task (N) without difficulty
3- Complete tasks but clumsy
2- Initiate task with difficulty
1- Unable to perform the activity

UE LE
Shoulder shrug 3 Flex hip in sitting 2
Reach up 2 Flexion and extension of knee in 2
sitting
Reach opposite shoulder 3 Wiggle knee and toes 2
Hand on sacrum 3 Extension of knee then dorsiflex 1
ankle
Hand on mouth 3 Heel to opposite knee 1

Pronation and supination c elbow flex 900 3 Supine; hip flexion with knee flexion 1

Closes hand from a full open position 2 Bend hip with hip flex ( stand) 1

Open hand from a full closed position 3 Flex affected knee with hip extension 1

Sit from supine 3 Raises affected foot or the first step 1

Sit to stand 3 Stand on toes 1

Bend on each side and return 3 Stand on heels 1

Rotation on each side and return 3 Moves thigh apart 1

Hip hiking 2 March in place 1

Hand Grip Analysis:

BP cuff was inflated to 20 mmHg

® (L) Difference
Trial 1 60mmHg 50mmHg 10mmHg
Trial 2 40mmHg 45mmHg 5mmHg
Trial 3 45mmHg 40mmHg 5mmHg

83 | P a g e
 Total 145 mmHg 135 mmHg 10 mmHg
Average 45 mmHg 45 mmHg 0 mmHg

Findings: pt has weak (L) hand grip

Significance: for baseline purposes

Hand Function:
Legend:
3- Performs task normal without difficulty
2- Complete task but clumsy
2- Initiates movements
1- Unable to perform activity

B. Power Grip
® (L)
Cylindrical 2 2
Fist 2 2
Hook 3 3
Spherical 2 2

.B. Precision Grip

Lat. Pinch 3 3
Pulp-to-pulp 3 3
Tip-to-tip 3 3
3 jaw chuck 2 2
5 digit pinch 2 2

Special Test:
Test Procedure Significance
(-) Homan The patient knee is in an extended For DVT
position and the examiner forcefully
dorsiflex the patient’s ankle

MBM
UE ® (L) Difference
Arm 10.5 10 .5
Forearm 8.5 8.5 0
LE 0
Suprapatellar 18 18 0
ridge( thigh)
Infrapatellar ridge 14 14 0
(LEG)

84 | P a g e
Findings: Muscle bulk is within normal
Significance: for baseline purposes

Balance and Tolerance:

Legend:
Balance Tolerance
N (normal) can assume, maintain, weight shift, and challenged
>45mins
G (good) can assume, maintain and weight shift 31-
45mins
F (fair) can assume and maintain 16-
30mins
P (poor) can assume 1-15mins
O (zero) can neither assume nor maintain 0 min
Balance Tolerance
Sitting F G
Standing P P

ADL
Fully Dependent Partially Independent
Dependent
Self Care
Bathing  c 1 man
assist
Toileting  c 1 man
assist
Eating  c 1 man
assist
Grooming  c maximal
difficulty

UE dressing  c maximal
difficulty

LE dressing  c maximal
difficulty

Bed Mobility  c 1 man

assist
Supine to Side-  c maximal
lying difficulty
Supine to Long  c maximal
Sitting difficulty

Rolling  c maximal
difficulty

85 | P a g e
Findings: all ADL can perform independently with maximal difficulty except for
bathing, toileting, eating and bed mobility which are partially dependent
with 1 man assist
Significance: 20 to GBS

A:
PT impression: Phase 6 GBS
Rehab Potential: Good d/t early intervention
Rehab Concern:  muscle strength and help to perform ADL’s
Rehab Precaution: avoid strenuous activity and always on guard to the patient

Problem List
1) Malaise
2) LOM on (B) UE and LE
3) Facial asymmetry
4) Balance and tolerance
5) ADL problem

LTG (3 mos)
1. To prevent 2° complication such as atrophy, contracture, P° sore, respiratory
problem such as (pneumonia and atelectasis), cardiac arrhythmias, blood clot
and DVT
2. To maintain strength of unaffected body part and endurance
3. To achieve (N) AROM in all planes of motion
4. ↑ Functional muscle strength to complete task with/without difficulty
5. To correct facial asymmetry
6. To achieve fair balance and tolerance as to standing
7. To attain the highest functional activities as to ADL’s from partially
independent  independent without difficulty

STG (3wks)
1. To ↑ AROM by ~ 5 increments of UE and LE, all planes of motion
2. To ↑ muscle strength of UE in next higher grade of FMT
3. To ↑ functional muscle strength of LE to initiate task with/without difficulty
4. To ↑ Facial muscle strength from weak functional into functional
5. To improve balance and tolerance as to standing and sitting
6. To maximize the functional capability as to ADL

P:
PT Management
1. Es on Sh, hand and elbow flexor, extensor, abductor and adductors; Hip and
knee flexor, extensor, abductor and adductors x 90 contraction x 1 set
2. PROME → AAROME x 10 reps., all planes of motion

86 | P a g e
 3. PRE’s on UE using 5 lbs dumbbell x 10 reps, all plane of motion
4. Gentle manual passive stretching on LE x 15 reps x 5 sec. hold, all planes of
motion
5. Es on Face x 30 contractions 20 mins
6. Facial massage and do Facial Expressions
7. Standing and balance and tolerance for 5 mins
8. Hand grip strength exercise
9. Mat exercise

HI:
1. Do exercise thought by Pt such as facial expressions and proper breathing
2. Frequent Proper bed positioning

_________________________
Kierulf, Vanessa Erika D.G.
UDM/Batch 2015

_________________________
Zamora , Josephine
UDM/Batch 20

Spastic Cerebral Palsy

Resurreccion, Clarizza T.
De Vera, Jeffrey V.
Cerebral Palsy

 A disorder of movement and posture that results from a non progressive

lesion or injury of the immature brain.
 Heterogeneous spectrum of clinical syndromes characterized by alteration in
muscle tone, deep tendon reflexes, primitive reflexes and postural reaction.
 A major disturbance of motor function, usually non-progressive, has been
present since infancy or childhood.

Related Anatomy

Embryonic Period

Germinal Stage

87 | P a g e
  The germinal stage begins with conception, when the sperm and egg
cell unite in one of the two fallopian tubes. The fertilized egg, known as
a zygote, then moves toward the uterus, a journey that can take up to
a week to complete. Cell division begins approximately 24 to 36 hours
after conception.
 Cell division continues at a rapid rate and the cells then develop into
what is known as a blastocyst. The blastocyst is made up of three
layers:

1. The ectoderm (which will become the skin and nervous system)
2. The endoderm (which will become the digestive and respiratory
systems)
3. The mesoderm (which will become the muscle and skeletal
systems).

 Implantation occurs when the cells nestle into the uterine lining and
rupture tiny blood vessels. The connective web of blood vessels and
membranes that forms between them will provide nourishment for the
developing being for the next nine months. Implantation is not always
an automatic and sure-fire process. Researcher’s estimate that
approximately 58 percent of all natural conceptions never become
properly implanted in the uterus, which results in the new life ending
before the mother is ever aware she is pregnant.

Embryonic Stage

 The mass of cells is now know as and embryo. The beginning of the
third week after conception marks the start of the embryonic period, a
time when the mass of cells becomes a distinct human being. The
embryo begins to divide into three layers each of which will become an
important body system. Approximately 22 days after conception, the
neural tube forms. This tube will later develop into the central nervous
system including the spinal cord and brain.
 Around the fourth week, the head begins to form quickly followed by
the eyes, nose, ears, and mouth. The cardiovascular system is where
the earliest activity begins as the blood vessel that will become the
heart start to pulse. During the fifth week, buds that will form the arms
and legs appear.

 By the time the eight week of development has been reached, the
embryo has all of the basic organs and parts except those of the sex

88 | P a g e
 organs. It even has knees and elbows! At this point, the embryo weight
just one gram and is about one inch in length.

Fetal Stage

 Once cell differentiation is mostly complete, the embryo enters the next
stage and becomes known as a fetus. This period of develop begins
during the ninth week and lasts until birth. The early body systems and
structures established in the embryonic stage continue to develop. The
neural tube develops into the brain and spinal cord and neurons form.
Sex organs begin to appear during the third month of gestation. The
fetus continues to grow in both weight and length, although the
majority of the physical growth occurs in the later stages of pregnancy.
 The end of the third month also marks the end of the first trimester of
pregnancy. During the second trimester, or months four through six,
the heartbeat grows stronger and other body systems become further
developed. Fingernails, hair, eyelashes and toenails form. Perhaps
most noticeably, the fetus increases quite dramatically in size,
increasing about six times in size. The brain and central nervous
system also become responsive during the second trimester. Around
28 weeks, the brain starts to mature much faster with activity that
greatly resembles that of a sleeping newborn.
 During period from seven months until birth, the fetus continues to
develop, put on weight, and prepare for life outside the womb. The
lungs begin to expand and contract, preparing the muscles for
breathing.

Placenta Blood Circulation

Fetal Blood Circulation

 The villus capillaries are branches of the umbilical vessels. Fetal blood
comes via the two Aa .umbilicales in the villi and leaves the placenta
through a single navel vein, the vena umbilicalis. Their supply amounts
to approximately 40% of the fetal heart blood volume per minute.The
blood pressure in the arteriaumbilicalisamounts to 50 mmHg and the
blood flows through finer vessels that cross through the chorionic plate
to the capillaries in the villi where the arterial blood pressure falls to 30
mmHg. In the umbilical vein the pressure is 20 mm Hg. The pressure
in the fetal vessels and their villus branches always lies over that of the
intervillous space. This protects the fetal vessels from collapse.

89 | P a g e
Cerebellum

 The cerebellum is the area of the hindbrain that controls motor

movement coordination, balance, and equilibrium and muscle tone.
Like the cerebral cortex, the cerebellum is comprised of white matter
and a thin, outer layer of densely folded gray matter.
 The cerebellum is covered by cortex and consists of two hemispheres,
each of which is divided into lobes:

 The anterior lobe, or paleocerebellum, is the second oldest

part of the cerebellum. It receives proprioceptive input from the
spinal cord and controls the anti-gravity muscles of the body,
thus regulating posture.

 The posterior lobe, or neocerebellum, is the newest part of the

cerebellum. This lobe plays an important role in fine motor
coordination.
 The flocculonodular lobe consists of the flocculi, the most
ancient part of the cerebellum. This lobe is involved in the
maintenance of equilibrium.

Cerebral Cortex

 Forms a complete covering of the cerebral hemisphere

 Like gray matter elsewhere in the CNS,consist of a mixture of nerve
cells,nerve fibers,neuroglia and blood vessels.

Layers of Cerebral Cortex

1. Molecular layer -most superficial layer; it consist mainly of a dense

network of tangentially oriented nerve fibers
2. External granular layer -contains large number of small pyramidal
cells and stellate cells
3. External pyramidal layer -composed of pyramidal cells, whose body
size increases
4. Internal granular layer -layer is composed of closely pack stellate
cells
5. Ganglionic layer -contains very large and medium-size pyramidal
cells
6. Multiform layer -many of the cells are modified pyramidal cells, whose
cell bodies are triangular or ovoid

90 | P a g e
 Cortical Areas

 Primary Motor Area

-occupies the precentralgyrus extending over the superior border into
the paracentral lobule
-function of the primary motor area is to carry out individual
movements of different part of the body
-it is not responsible for the design of the pattern of movement but is
the final station for conversion of the design into execution of the
movement
 Premotor Area
-which is wider superiorly than below and narrows down to be confined
to the anterior part of the precentralgyrus, has no giant cells of Betz
-function of the premotor area is to store programs of motor activity
assembled as the result of past experience
-it is particularly involved in controlling coarse postural movement
through its connections with the basal ganglia

Cerebrospinal Fluid

It is found in the ventricles of the brain. It is clear, colorless fluid. It

serve as a cushion between CNS and the surrounding bones, thus protecting
against mechanical trauma. It provides mechanical buoyancy and support the
brain.

 Formation of CSF

The CSF is formed mainly in the choroid plexus of lateral, third and
fourth ventricle. Choroid plexus have a much folded surface and each fold
consist of a core of vascular connective tissue covered with cuboidal
epithelium of the ependymal. The choroid plexus actively secrete CSF and at
the same time they actively transport nervous system metabolites from the
CSF into blood.

The CSF is produced continuously at a rate of about 0.5 ml/minute and

with a total volume of about 130 ml; this corresponds to a turnover time of
about 5 hours.

 Circulation of CSF

The CSF formed in the choroid plexuses of each lateral ventricle flows
into the third ventricle through two narrow, oval openings, the interventricular

91 | P a g e
 foramina. More CSF is added by the choroid plexus in the roof of the third
ventricle. The fluid then flows through the aqueduct of the midbrain, which
passes through the midbrain, into the fourth ventricle. The choroid plexus of
the fourth ventricle contributes more fluid. CSF enters the subarachnoid
space through three openings in the roof of the fourth ventricle: a median
aperture and the paired lateral apertures, one on each side. CSF then
circulates in the central canal of the spinal cord and in the subarachnoid
space around the surface of the brain and spinal cord.

CSF is gradually reabsorbed into the blood through arachnoid villi,

fingerlike extensions of the arachnoid that project into the dural venous
sinuses, especially the superior sagittal sinus (A cluster of arachnoid villi is
called arachnoid granule). Normally, CSF is reabsorbed as rapidly as it is
formed by the choroid plexuses, at a rate of about 20 mL/hr (480 mL/day).
Because the rates of information and reabsorption are the same, the pressure
of CSF normally constant.

Pathophysiology

 Blood vessels are particularly vulnerable to injury in the watershed shed zone
next to the lateral ventricles in the capillaries of the germinal matrix
 The most common neuroanatomic lesion is damage to germinal matrix zone
in the periventricular region of the premature fetus, usually occurring around
24-48 weeks of gestational age.

Bleeding in this area is often criteria in origin and can occur in different
degrees resulting to hypoxia

a. Grade 1 – intraventricular hemorrhage isolated to the germinal matrix.

b. Grade 2 – intraventricular hemorrhage with normal ventricular size.
c. Grade 3 – intraventricular hemorrhage with ventricular dilatation.
d. Grade 4 – intraventricular hemorrhage parenchymal hemorrhage.

5 Basic types of Volpe Postulate

1. Parasagittal Cerebral Injury

 Involves bilateral cortical and subcortical white matter necrosis of
cerebral cortex.
2. Periventricular Leukomalacia

92 | P a g e
  Bilateralnecrosis of white matter adjacent to external angle of lateral
ventricle
 28-48th week
3. Focal and Multifocal Ischemic Brain Necrosis
 Character by injury to all cellular elements caused by infarction within
the vascular distribution
 MCA is common affected
4. Status Marmoratus
 Neuronal injury within the basal ganglia and thalamus
 Manifested by choreoathetosis
5. Selective Neuronal Necrosis
 Injury observed hypoxic – ischemic encephalopathy
 Includes CA 1 region (summer’s sector), lateral geniculate body
 Long term sequelaeincludes mental retardation and seizures

Epidemiology

 Cerebral Palsy is the leading cause of childhood disability.

 The reported incidence varies but is ~2-3 per 1000 live births.
 Prevalence rate of 5.2 per 1000 neonatal survivors at 12 months of age but
reported resolution in up to half of these children by age 7 years.
 Most recent studies report an overall prevalence rate of 1.5-2.0 per 1000 live
births.

Etiology

 Hallmark is Motor Delay

 Immaturity of brain, fragile brain, vasculature and physical stresses of
prematurity predisposes children to a compromised cerebral blood flow.

Causes:

PRENATAL

 Estrogen or thyroid use

 Rh incompatibility
 Maternal infections (TORCH)
Toxoplasmosis
Rubella
Cytomegalo virus

93 | P a g e
 Herpes simplex/zoster
 Drugs
 Eclampsia
 Asphyxia

PERINATAL

 Excessive maternal sedation

 Severe anoxic or ischemic brain injury during actual delivery itself (cord coil)
 Mechanical difficulties in the placenta
 Abnormalities during birth process
 Intrapartum asphyxia
 Neonatal cardiorespiratory distress
 APGAR score of 3 at 10-15 min. = 10
Taken 1 min. after birth
If the score is low, take after 5min.
 15% risk for CP

0 1 2
Appearance Blue Trunk-pink Pink
Extremities-blue
Pulse Rate No pulse <100bpm >100bpm
Grimace No reaction Grimace Cry
Activity No activity Slight flexion Spontaneous mov’t
Respiration No respiration Slight chest mov’t Spontaneous
breathing

POST-NATAL

 4 weeks after birth – 2y/o

 Anoxia
 Any head trauma or injury
 Infection and tumor
 Ischemia and encepalopathies
 Toxic exposures/poisoning
GP-FPAL
G – GRAVIDA, no. of pregnancy
P – PARIDA, no. of delivery
F – FULL-TERM
P – PREMATURE
A – ABORTED
L – LIVING

94 | P a g e
Classification of Cerebral Palsy

 Neurologicclassification

A. Spastic Type

- d/o tend to be the most commonly occurring.

- ~ 75% of the children affected
- Typically manifest signs of upper motor neuron lesion

Subtypes of Spastic CP

Spastic Monoplegia

 Isolated upper or lower extremity

 Rarely seen
 Often the presentation of a misdiagnosed hemiplegia

Spastic Diplegia

 Also known as Little’s Disease

 History of intraventricular hemorrhages, particularly in the 28-32
week-old infant
 Magnetic resonance (MR) imaging may show periventricular
leukomalacia or posthemorrhageporencephaly
 History of early hypotonia followed by spasticity
 Developmental delays most pronounced in the gross motor
sector
 Diplegic gait pattern, including spastic adductors,
gastrocnemius, and hip flexors

Spastic Triplegia

 Three extremities involved, classically bilateral LE and one UE

 Mild coordination problems in noninvolved limb
 Scissoring and toe walking
 Similar features to the spastic quadriplegic

Spastic Quadriplegia

 All extremities involved

 Individuals with more involvement in the UE than the LE
categorized into double hemiplegia

95 | P a g e
  History of a difficult delivery with evidence of perinatal asphyxia
common
~ 50 % prenatal in origin; 30% perinatal; 20% postnatal
 Spasticity and persistent primitive reflexes
Upper motor neuron signs in all limbs
High incidence of visual impairment
Usually most severely involved children
About half have seizures

Spastic Hemiplegia

 One side of the body involved: arm generally more than leg
 Hypotonia may be first indicator of this type of CP
 Cranial nerves may be involved and generally present as facial
weaknesses
 Upper motor neuron signs in hemiplegic side
Hemiplegic gait pattern
 Sensory deficits on the ipsilateral side in 68%;
Stereognosis, graphesthesia, two point discrimination, and joint
position may also be involved.

B. Dyskinetic Type

Athetosis

 slow, writhing movements of the face and extremities,

particularly affecting the distal musculature.

Dystonia

 rhythmic, twisting distortions and changes in tone involving

primarily the trunk and proximal extremities and causing slow,
uncontrolled movements with a tendency toward fixed postures.

Choreiform Movements

 rapid, irregular, jerky motion most commonly seen in the face

and extremities.

Ballismus

 coarse flailing or flinging motion of the extremities characterized

by a wide amplitude of motion.

Tremor

96 | P a g e
  fine shaking motion of the head and extremities

C. Mixed Type

- most common description of CP showing several patterns

- a combination of spasticity and athetosis

Risk Factors:

 General
- Birth too soon
- Gestation age <32 weeks
- Birth weight <2500 g (low birth weight) to <1000g (extremely low birth weight
- Hypoxia
 Maternal History
- Mental Retardation
- Seizure d/o
- Hyperthyroidism
- 2 or more prior fetal deaths
- Siblings with motor deficits

Early Signs and Symptoms:

 Neonatal period
- Diminished activity
- Suck swallow problem
- Apneic spells
- Hypotonic/Hypertonic
- Temperature instability
- Seizures
 During Gestation
- Twin gestation
- Fetal growth retardation
- 3rd trimester bleeding
- Increase urine protein excretion
- Chorioritis
- Premature placenta separation
- Low placenta weight
 Fetal Factors
- Abnormal fetal presentation
- fetal malformations

97 | P a g e
 - fetal bradychardia
- neonatal seizures
 Infantile Period
- Delayed or abnormal development
- Abnormal tone and posture
- Persistent infantile reflex
- Hand dominance appearing < 1 y/o (hemiparesis)
- Behavioral abnormalities(perseverating cry, increase irritability and
decrease attentiveness)

Differential Diagnosis

Global Developmental Delay

Global Developmental Delay (GDD) is the general term used to describe a

condition that occurs during the developmental period of a child between birth and
18 years. It is usually defined by the child being diagnosed with having a lower
intellectual functioning than what is perceived as ‘normal’. It is usually accompanied
by having significant limitations in communication. It is said to affect about 1-3% of
the population.

Prognosis

- Cerebral Palsy has a normal life expectancy. For example, a two year-old
child with mild palsy has a 99% chance of living to the age of 20, compared
with a patient who has severe disease, where the figure may be as low as
40%.
- If a child is able to sit up unaided at the age of 2, they will eventually be able
to walk. If the child is incapable of sitting upright by the age of 4, there little
chance that he or she may walk.

Gross motor functional classification

Level 1: walks without restriction, limitations in high-level skills

Level 2: walks without devices, limitations walking outdoors

Level 3: walks with devices, limitations walking outdoors

98 | P a g e
Level 4: limited mobility, power mobility outdoors

Level 5: very limited self-mobility, even with assistive technology

Medical Management

 Pharmacological Treatment

 Muscle relaxant
 Neuromuscular blockers

 Surgical Intervention

 Selective dorsal rhizotomy

 Intrathecal baclofen stimulators

 PT Management

 Orthopedic device
 Neurodevelopmental/Bobath treatment
 Therapeutic electrical stimulation
 Biofeedback
 Constraint-induced therapy

REFERENCE:

 Braddom
 Molnar
 Google.com

99 | P a g e
 GENERAL INFORMATION

Patient’s name: J.C.

Age: 2 years and 9 mons.
Sex: male
Address: 368 Pritil,Tondo Manila
Tel.No: 346-7643
Weight: 9.8 kg
Height: 32”
Hand Preference: ®
Referring unit: Jose Reyes Memorial Hospital (Pedia ward)
Rehab unit: Jose Reyes Memorial Hospital
Referring M.D.: Dr. C.J.
Rehab M.D.: Dr. J.R.
Date of Consultation: August 20, 2013
Date of Referral: August 20, 2013
Date of Rehab Consultation: August 21, 2013
Date of I.E.: August 21, 2013
Diagnosis: Gross Motor Delay
Informant/Reliability: Mother/Good

HPI:

12 mos. PTC the mother wondered why her baby is still can’t roll and even
crawls compare to other child. She also noticed that the baby can’t maintain sit erect
whenever held in sitting position and can’t assume a standing position.

7 mos. PTC mother noticed also that her child drool saliva frequently. She
also noticed that he spend long time to empty his bottle milk. So she decided to give
him clusivol multivitamins thinking he has poor appetite.

4 mos. PTC, problems still persist; this prompted the mother to go to a doctor.
Upon evaluation, the doctor diagnose that her child has a motor delay. He
suggested that for a while they should wait. Tiki-tiki plus syrup was prescript for the
baby for his appetite.

1 month PTC while the mother dressed her baby’s leg. This prompted the
mother to take him to the doctor. The mother told the dr. about the delayed motor
milestone and the loss of appetite. Cranial Ultrasound were done (see ancillary
procedure) and laboratory exam. He was dx to have spastic cerebral palsy and was
then referred to PT for further evaluation and treatment.

100 | P a g e
A.MATERNAL Hx

a. Prenatal
 Wanted pregnancy
 Fever (May, 2011)(250mg)
 (+) prenatal check-up
 (-) alcoholism
 (-) smoking
 (-) trauma
 (-) infection
 (-) measles
b. Perinatal
 G2P1,1,0,2
 Labor (3 hrs)
c. Postnatal
 (-) newborn screening
 (-) trauma
 (-) convulsion

B.BIRTH Hx
 Jose Reyes Memorial hospital
 Attending M.D.: Dr. A.C
 Caeserian Delivery (Horizontal Suprapubic Incision)
 7 mons. (3 days incubation)
 APGAR SCORE
Grade/Score 1 trial(1min) 2 trial(5min) 3 trial(10min)
Appearance 0 0 1
Pulse 1 1 1
Grimace 1 0 0
Activity 0 1 1
Respiration 1 1 1

C. NUTRITIONAL Hx
 Breast feeding (1mos-6mos)
 Bottle feeding (6mos-14mos) Nido (8oz)
 Mash food (14mos-present)
 Poor suck & swallow
 Drooling of saliva

D. IMMUNIZATION Hx
VACCINE TIME GIVEN DOSAGE
BCG At birth .05ml
DPT 3mos, 6mos, 9mos .05ml
Hepa B 9mos .05ml

101 | P a g e
 OPV 3 mos, 6mos, 9mos 2 drops
Measles 3 mos, 6 mos, 9mos .5 ml

E. PMHx,
 Motor Delay (National Children Hospital)(October 26, 2012)
 (-) convulsion
 (-) seizure
 (-) disease

F. DEVELOPMENTAL Hx
 Developmental Milestone
Motor Milestone Age Expected Age Achieved
Turns head to Newborn 5 mons
side(Prone)
Head in midline 4 mons 7 mons
Lift head in prone 4 mons 8 mons
Roll to prone 7 mons 9 mons
Maintain sitting 7 mons Not yet achieved
Hold bottles 7 mons 9 mons
Creeps on all fours 10 mons Not yet achieved
Stands momentarily 10 mons Not yet achieved
Bangs two cubes 10 mons 12 mons
Walks alone 14 mons Not yet achieved
Pelvic tilt and rotation 14 mons Not yet achieved
Holds crayon full length 14 mons 16 mons
in palm
Uses spoon over 14 mons 16 mons
overpronation
Arms at low guard 18 mons Not yet achieved
Seats self in chair 18 mons Not yet achieved
Walks backwards 18 mons Not yet achieved
Emerging hand 18 mons 19 mons
dominants `
Begins running 24 mons Not yet achieved
Walks up and down 24 mons Not yet achieved
stairs alone
Jumps on both feets 24 mons Not yet achieved
Findings: delayed motor milestone
Significance: 2° to spastic

 General Behavior
 Pt participate in the treatment but sometimes he can’t do some activities
 Behavior norms of Development
 Difficulty in imitating some activities
 Some motor development are still delayed

102 | P a g e
Ancillary Procedures
Impression Date
Cranial Ultrasound Periventricular June 20, 2013
Leukomalacia
Laboratory Exams:
Normal Value Findings Impression Date
Blood
chemistry
Hematocrit 40-50% 45% Normal June 20, 2013
WBC 5-10k/ml 6k/ml Normal June 20, 2013
Basophil 0.0-0.1 0.0-0-0.1 Normal June 20, 2013
Eosinophil 0.02-0.05 0.02-0.03 Normal June 20, 2013
Neutrophil 0.50-0.75 0.50-0.60 Normal June 20, 2013
Platelet 150-400k/ml 200k/ml Normal June 20, 2013
Hemoglobin 120-126g/L 125g/ml Normal June 20, 2013

Present medications
Name of Drug Dosage Frequency
Indication
Tiki-tiki syrup 2.5ml bid multivitamins

S:
Informant’s c/o: “naninigas ang kanyang mga binti” as verbalized by his mother
PT Translation: spasticity on both LE
Infomant’s goal: to be able to move and use his LE like for ambulation

O:
VS
Normal a during p
RR: 25-50cpm 30cpm 55cpm 35cpm
PR: 120-170bpm 130bpm 150bpm 139bpm
T°: 37°C 37°C 37°C 37°C

OI:

 Mother-borne
 Poorly nourished
 Alert, coherent, cooperative
 Sometimes cry
 Microcephalic
 (+) drooling of saliva
 (+) stiff leg
 (-) postural deviation
 (-) attachment
103 | P a g e
  (-) strabismus
 (-) scissoring feet

PALPATION:
 Normothermic on all exposed body part
 Normal skin turgor, mobility and consistency
 Fontanelle closure: ANT.: 25mon
POST.: 14 mon

NEUROLOGICAL EVAL:
A. Tone A:
Normotonic on both UE and hypertonic on both LE

Finding: Grade 1 spasticity on both LE

Significance: 2° to affectation of BA 6

B. Sensory A:
STD used: Pinch for Pain
Thumb for Pressure

Findings: 100% sensory intact on (B) UE and LE

Significance: Intact B.A. 3, 1, 2

C. Visual A:
VTD used: Colored object like red ball
 Eye muscle tracking – Good
 Introduction of color object

Findings: Pt has normal eye muscle tracking

Significance: 2° to

D. Auditory A:
 clapping of hands Weak
 calling his name Weak

Findings: Pt has slow response

Significance: (+) affectation of B.A 41 and 42

E. DTR:

Legend:

104 | P a g e
 O areflexia
+ hyporeflexia ++ ++
++ normoreflexia ++
++
+++ hyperreflexia +++ +++
++++ clonus +++ +++

Findings: normoreflexive on both UE and hyperreflexive on both LE

Significance: ↑ firing of gamma motor neuron

F. Pathologic Reflex
Reflex Stimulus Response
Babinski Reflex Stroke lat outside edge of (+)
sole of the foot
Hoffman’s Sign Flicker the nails of distals (+)
phalanx of 3rd fingers
Bechterew’s Mendel Sign Stroke lat aspect of (+)
dorsum of the foot over
the cuboid bone

Findings: Pt (+) is Babinski reflex, Hoffman’s sign and Bechterew’s Mendel Sign
Sig. 2° to UMNL
G. Primitive Reflex
Reflex Stimulus Response
Moro Sudden neck extension (+)
ASTNR Head turning to side (-)
Symmetric tonic neck Neck flexion, neck (+)
extension
Tonic Labyrinth Head position in space, (+)
strongest at 45o horizontal
-supine
-prone
Automatic neonatal On vertical support plantar (-)
walking contact and passive tilting
of body forward and side
to side

ROM
All joints of both LE are WNL, passively done pain free with normal end feel, except:

105 | P a g e
 Motion Normal PASSIVE Difference End-feel
R L R L
HIP
Flexion 0-120o 20-90o 20- 30o 20o Firm
100o
Extension 0-30o 0-15o 0-20o 15o 10o Firm
Abduction 0-45o 0-20 o
0-25o 15o 20o Firm
Adduction 0-30o 25-30o 25-30o 0o 0o Firm
IR 0-45o 30-40o 30-40o 5o 5o Firm
ER 0-45o 0-10o 0-10o 35o 35o Firm
KNEE
Flexion 0-135o 30- 30- 25o 20o Firm
110o 115o
Extension 135-0o 110- 115- 25o 20o Hard
30o 30o
ANKLE
Plantarflexion 0-50o 30-40o 30-40o 10o 10o Firm
Dorsiflexion 0-20o 0-10o 0-10o 10o 10o Firm
o o
Tarsal jt. 0-35 0-15 0-15o 20o 20o Firm
Inversion
Tarsal jt 0-15o 10-15o 10-15o 0o 0o Firm
eversion
Transverse 0-20o 0-10o 0-10o 10o 10o Firm
tarsal jt
inversion
Transverse 0-10o 5-10o 5-10o 0o 0o Firm
tarsal jt.
Eversion
Findings: LOM on both LE in all planes of motions
Significance: 2o to Muscle Spasticity

FMT

Legend: FMT Grading Legend: BALANCE Legend: TOLERANCE

1 – No ability 1 – can assume N (normal) - >45 mins
2 – Beginning c difficulty 2 – can assume and G (good) - 30-45
3 – Achieve c abnormal maintain mins
pattern 3 – can assume, maintain F (fair) - 15-30
4 – near normal/normal and weight shift mins
4 – can assume, maintain, P (poor) - 1-15 mins
weight shift and challenged Nil/0 (zero) - 0 min
 Rolling – 2
 Creeping – 2
 Crawling – 2

106 | P a g e
  Head Control – 2
 Trunk Control – 2
Sitting: Kneeling: Standing:
-balance: 2 -balance: 2 -balance: 2
-tolerance: P -tolerance: P -tolerance: P
Findings: Pt. begin c difficulty as to rolling, creeping, head control, trunk control, and
crawling. Pt can assume and maintain sitting, kneeling and standing within 1-15
mins and has a poor tolerance.
Significance: 2° to spastic CP
ADL
Findings: Pt is fully dependent in all aspect of ADL
Significance: 2° to childhood motor delay

A:
PT Impression: Spastic Cerebral Palsy
Rehab Potential: Good because Pt age is favorable in Prognosis
Rehab Concern: Pt has still delayed some motor milestone
Rehab Precaution: Pt. is too young

Problem List:
1. Spasticity on both LE
2. Delayed Motor Milestone
3. Poor Appetite
4. Weakness of both UE
LTG: (3 months)
1. To prevent further complication such as subluxation, contracture and
tightness
2. To maintain the strength of UE
3. To attain the highest functional capability of the patient as to independent.
4. To increase ROM of all joints of both LE 10o motion

STG: (3 wks.)
1. To increase ROM of all joints of both LE 5o motion
2. To increase Muscle Grade of hip and knee flexors and extensors from 1 to
grade2
3. To help the pt. develop normal functions such as rolling, creeping and
crawling
107 | P a g e
Plan:

PT Management:
1. Play therapy
2. Gentle manual passive stretching on both LE x !% sec.hold x 10 reps. X 1 set
all planes of motion
3. PROME on both LE x 10 reps. X 1 set all planes of motion
4. NDT’s as to Bobath
5. Massage
HI:
1. Educate the mother to perform PROME
2. Avoid feeding the pt. solid foods

Resurreccion, Clarizza T.
UDM/Batch 2013

De Vera, Jeffrey V.
UDM/Batch 2013

Cerebral Palsy (dyskinetic)

Jimenez, Ramon Jr., J.
Cabales, Jericho

108 | P a g e
Definitions:
 Group of conditions characterized by motor dysfunction due to non-
progressive brain damage early in life. (Levitt)
 Chronic non-progressive disorder of movement of posture of early onset.
(Garrison)
 Is often associated with other neurologic difficulties, including mental
retardation. (Garrison)
 A collection of syndromes characterized by: (BRADDOM)
 d/o of movement and posture
 caused by non-progressive injury
 immature brain
 Paralysis resulting from non-progressive brain damage.(BRADDOM)
 Heterogeneous spectrum of syndromes characterized by alteration in muscle
tone, deep tendon reflexes, primitive reflexes and postural reaction.
(MOLNAR)
 Abnormalities of motor function used as genetic term defining non-
progressive static disturbances of motor function seen in infant or childhood.
(Harrison)
Hallmark : MOTOR DELAY

TRIADS OF CEREBRAL PALSY:

 Retardation of motor akills
 Persistence of infantile reflexes
 Presence of associated reaction

Cerebral -- Refers to the two halves or hemispheres of the brain, in this case to the
motor area of the brain’s outer layer (called the cerebral cortex), the part of the brain
that directs muscle movements.
Palsy - Refers to the loss or impairment of motor function.

Related Anatomy:

Brain
Central Nervous System
Spinal Cord

109 | P a g e
Developmental of Brain
3 primary vesicle:
 Forebrain vesicle (prosencephalon)
 Midbrain vesicle ( mesencephalon)
 Hindbrain vesicle ( rhombencephalon)

- By the 5th week, the forebrain and hindbrain vesicles divided into two
secondary vesicles.
Forebrain vesicle forms:
 Telencephalon --- it’s primitive cerebral hemispheres
 Diencephalon – which develops optic vesicles
Hindbrain vesicle forms:
 Metencephalon – the future pons and cerebellum.
 Myelencephalon – or medulla oblongata

Lateral Ventricle – the cavity in each cerebral hemisphere

Third Ventricle – cavity of diencephalon
Midbrain Vesicle –forms cerebral aqueduct or aqueduct of Sylvius.
Fourth Ventricle – the cavity of hindbrain

MENINGES OF BRAIN :
1) Dura mater outer
3 extensions of dura mater separate parts of the brain
a) Falx cerebri (FALKS) separates the two hemispheres of the cerebrum
b) Falx cerebelli separates the two hemispheres of the cerebellum
110 | P a g e
 c) Tentorium cerebelli separates the cerebrum from the cerebellum
2) Arachnoid mater middle
3) Pia mater inner

A. Brain Stem
Three structurally and functionally connected regions
1) Medulla Oblongata --it forms the Inferior part of the Brain Stem.
2) Pons -- lies directly Superior to the Medulla and Anterior to the Cerebellum and is
about 2.5 cm.
3) Midbrain – extends from the Pons to the Diencephalon and is about 2.5 cm long.

B. Cerebellum
- the second largest part of the brain , occupies the Inferior and Posterior
aspects of the cranial cavity.
The cerebellum and it’s motor function
 Overall functions:
Postural control
Equilibrium
Control of voluntary movements
 Called as silent area of the brain principally because of electrical excitation of
this structure does not any cause any sensation and rarely any motor
movement.
 Vital control of rapid muscular activities
 Loss of this area of the brain can cause total incoordination
 Helps to sequence the motor activities and also monitors and make corrective
adjustments in the motor activities

Anatomical functional areas of the cerebellum
 Floccunodular lobe- oldest of all portion of the cerebellum, it developed along
with the vestibular system controlling equilibrium.
 Anterior lobe- responsible for muscle tone.
 Posterior lobe- responsible for coordinated movements.

Vermis
 Most cerebellar control functions for the muscle movements of the axial body,
the neck, and the shoulders.
 Each side of the vermis is a large, laterally protruding hemisphere and each
side of the hemisphere is divided into intermediate zone and lateral zone.
- Intermediate zone- concerned with the control of muscular
contactions.
- Lateral zone- remote level for this area joins in the overall planning
of sequential motor movements.

Afferent pathway

111 | P a g e
  Corticopontocerebellar pathway- originate mainly in the motor and premotor
cortex.
1. Olivocerebellar tract- passes from the inferior olive to all parts of the
cerebellum reticular formation
2. Vestibulocerebellar fiber- originates the vestibular apparatus itself and
others from vestibular nuclei nd terminate in the flocculonodular lobe and
fastigial nucleus of cerebellum.
3. Reticulocerebellar fiber- originates in different portions of the reticular
formation..

Efferent pathway
1. Pathway that originates in midline structures of the cerebellum (vermis)
2. Pathway that originates in the intermediate zone of the cerebellar
hemisphere.
3. Pathway begins in the cortex of lateral zone of the cerebellar hemisphere
then passes to the dentate nucleus, then to ventrolateral and
ventronuclei of the thalamus to cerebral cortex.

Major levels of the cerebellum

1. Molecular
2. Purkinje
3. Granular

Other inhibitory cells in the cerebellar cortex

1. Basket cells
2. Stellate cells
3. Golgi cells

C. Diencephalon -- extends from the Brain Stem to the Cerebrum and surrounds
the Third Ventricle; it includes the Thalamus, Hypothalamus, and Epithalamus.

1) THALAMUS is the major relay station for most sensory impulse that reach the
primary sensory areas of the cerebral cortex from the spinal cord and brain stem.
Based on their positions and functions, there are seven major groups
of nuclei on each side of the thalamus
a. The anterior nucleus receives input from the hypothalamus and sends output to
the limbic system
-It functions in emotions and memory.
b. The medial nuclei receive input from the limbic system and basal ganglia and
send output to the cerebral cortex. They function in emotions, learning, memory, and
cognition (thinking and knowing).
c. Nuclei in the lateral group receive input from the limbic system, superior colliculi,
and cerebral cortex and send output to the cerebral cortex.
*lateral dorsal nucleus functions in the expression of emotions.

112 | P a g e
* lateral posterior nucleus and pulvinar nucleus help integrate sensory
information.
d.. Five nuclei are part of the ventral group.
*ventral anterior nucleus receives input from the basal ganglia and sends output to
motor areas of the cerebral cortex; it plays a role in movement control
ventral lateral nucleus receives input from the cerebellum and basal ganglia and
sends output to motor areas of the cerebral cortex; it also plays a role in movement
control.
*ventral posterior nucleus relays impulses for somatic sensations such as touch,
pressure, vibration, itch, tickle, temperature, pain, and proprioception from the face
and body to the Cerebral cortex.
* lateral geniculate nucleus relays visual impulses for sight from the retina to the
primary visual area of the cerebral cortex.*
medial geniculate nucleus relays auditory impulses for hearing from the ear to the
primary auditory area of the cerebral cortex.
e.. Intralaminar nuclei lie within the internal medullary lamina
2) HYPOTHALAMUS controls many body activities and is one of the major
regulators of homeostasis. Sensory impulses related to both somatic and visceral
senses arrive at the hypothalamus, as do impulses from receptors for vision, taste,
and smell. Other receptors within the hypothalamus itself continually monitor osmotic
pressure, glucose level, certain hormone concentrations, and the temperature of
blood.
3) EPITHALAMUS is a small region superior and posterior to the thalamus. It
consists of the Pineal Gland and Habenular Nuclei

D. Cerebrum is the “seat of intelligence.” It provides us with the ability to read, write,
and speak; to make calculations and compose music; and to remember the past,
plan for the future, and imagine things that have never existed before. The cerebrum
consists of an outer cerebral cortex, an internal region of cerebral white matter, and
gray matter nuclei deep within the white matter.

E. Basal Ganglia- A major function of the basal ganglia is to help initiate and
terminate movements of the body. The basal ganglia also suppress unwanted
movements and regulate muscle tone. In addition, the basal ganglia influence many
aspects of cortical function including sensory, limbic, cognitive, and linguistic
functions. Basal ganglia functions and disorders such as Parkinson disease and
schizophrenia
 The basal ganglia is like the cerebellum are another accessory motor system
that functions not by itself but always in close association with the cerebral
cortex and corticospinalsytem.
 They are located laterally to the thalamus occupying a large portion of the
deeper regions of both cerebral hemisphere
 Almost all of the motor and sensory nerve fibers connecting the cerebral
cortex and spinal cord pass between two major masses of the basal ganglia
the caudate nucleus and the putamen.

113 | P a g e
  This mass of nerve is called the internal capsule –the neuronal circuity of the
basal ganglia.
 Motor portions of the basal ganglia to be the caudate nucleus, the putamen
and the globus pallidus.
 The putamen circuit- function of basal ganglia in executing patterns of motor
activity
 One of the most principal roles of the basal ganglia in motor control is to
function in association with the corticospinal system to control complex
patterns of motor activity
 The caudate circuit- role of basal ganglia for cognitive control of sequence of
motor functions.

MOTOR CORTEX

Motor cortex - Anterior to the central cortical Sulcus, occupying approximately the
posterior one third of frontal lobes
Somatosensory cortex – Posterior to the central which feeds the motor cortex many
of the signal that initiate motor activities.
The Motor Cortex three subareas
The Primary Motor Cortex (Area 4)
The Premotor Cortex (Area 6)
Supplementary Motor Area

The Primary Motor Cortex (Area 4)

Lies in the first convolution of the frontal lobes anterior to the central sulcus. It begins
laterally in the sylvian fissure, spreads superiorly to the uppermost portion of the
brain, and then dips deep into the longitudinal fissure
Topographical presentation of the body in the brain (HOMONCULUS)
Face and mouth region near the sylvian fissure
Arm and hand area, in the midportion of the primary motor cortex
Trunk, near the apex of the brain.
Leg and foot areas, in the part of the primary motor cortex that dips into the
longitudinal fissure
*note that more than one half of the entire primary motor cortex is concerned with
controlling the muscles of the hands and muscles of speech.

The Premotor Cortex (area 6)

Lies 1 to 3 cm anterior to the primary motor cortex, extending inferiorly into the
sylvian fissure and superiorly in the longitudinal fissure where it abuts the
supplementary motor area, which has function similar to those of the premotor area.
Topographical organization is roughly the same as the primary motor cortex
Nerve signals cause much more complex “patterns” of movement than the discrete
patterns generated in the primary motor cortex.

114 | P a g e
The premotor cortex, basal ganglia, thalamus and primary motor cortex constitute a
complex overall system for the control of complex patterns of coordinated muscle
activity
Supplementary motor area
It lies mainly in the longitudinal fissure but extends a few cm onto the superior
frontal cortex. Contractions elicited by stimulating this area are often bilateral rather
than unilateral.
This area functions in concert with the pre-motor area to provide body-wide
attitudinal movements of head and eyes, and so forth, as background for the finer
motor control of the arms and hands by the pre-motor area and primary motor
cortex.

Corticospinal (Pyramidal) tract

Originates about 30 percent from the primary motor cortex, 30 percent from
premotor and supplementary motor areas and 40 percent from the somatosensory
areas posterior to the central sulcus.
Betz cells-(a giant pyramidal cells) are about 60 micrometers in diameter and their
fiber transmit nerve impulses to the spinal cord at a velocity of about 70 m/sec, the
most rapid rate of transmission of any signal from the brain to spinal cord.
Red nuclei-serve as an alternative pathway for transmitting cortical signals to the
spinal cord

Blood Supply of the brain

-Four major arteries and their branches supply the brain with blood. The four arteries are
composed of two internal carotid arteries (left and right) and two vertebral arteries that ultimately
join on the underside (inferior surface) of the brain to form the arterial circle of Willis, or the
circulusarteriosus.

115 | P a g e
VERTEBRAL ARTERY
-The vertebral arteries actually join to form a basilar artery. It is this basilar artery that joins
with the two internal carotid arteries and their branches to form the circle of Willis. Each vertebral
artery arises from the first part of the subclavian artery and initially passes into the skull via
foramina in the upper cervical vertebrae and the foramen magnum.

Branches of the vertebral artery

 MENINGEAL BRANCHES
-Supply meninges of the brain
-Small and supply the bone and dura in the posterior cranial fossa
 POSTERIOR SPINAL ARTERY
-Gives blood supply to posterior surface of the spinal cord
-Arises from vertebral artery or the posterior inferior cerebellar artery
-Descends on the posterior surface of the spinal cord close to the posterior roots of the
spinal nerves
 ANTERIOR SPINAL ARTERY
-Formed from a contributory branch from each vertebral artery near its terminal
-Together with reticular artery, it gives blood supply to anterior surface of the spinal cord
 POSTERIOR INFERIOR CEREBELLAR ARTERY
-Largest branch of the cerebellar artery
-Supplies the inferior surface of the vermis, the central nuclei of the cerebellum, and the
undersurface of the cerebellar hemisphere
-Also supplies the medulla oblongata and the choroid plexus of the fourth
ventricle
 MEDULLARY ARTERY
- Responsible for giving blood supply to medulla oblongata
 BASILAR ARTERY
-formed by the union of the two vertebral arteries, ascends in a groove on the anterior
surface

116 | P a g e
 Branches of basilar artery
 PONTINE ARTERY
-Numerous vessel that enter the substance of the pons
-Gives blood supply to pons
 LABYRINTHINE ARTERY
-A long narrow artery that accompanies the facial and the vestibulocochlear nerves into the
internal
acoustic meatus and supplies the internal ear
-Gives blood supply to internal ear
 ANTERIOR INFERIOR CEREBELLAR ARTERY
-Supplies the anterior and inferior parts of the cerebellum
 SUPERIOR CEREBELLAR ARTERY
- Arises close to the termination of the basilar artery
- Supply the superior surface of cerebellum
- Also supplies the pons, pineal gland, and the superior medullary velum
 POSTERIOR CEREBRAL ARTERY
 Joined by the posterior communicating branch of the internal carotid
artery
CORTICAL BRANCH – Supply the internolateral and medial surface of the temporal
lobe and the
lateral and medial surface of the occipital lobe.
CENTRAL BRANCHES – Supply parts of the thalamus and the lentiform nucleus as
well as the midbrain, pineal and the medial geniculate
bodies.
CHOROIDAL BRANCH – Enters the inferior horn of the lateral ventricle and supplies the
choroid
Plexus.
-Also supplies the choroid plexus of the third ventricle

INTERNAL CAROTID ARTERY

-The internal carotids arise from the common carotid arteries and pass into the skull via the carotid
canal in the temporal bone. The internal carotid artery divides into the middle and anterior cerebral
arteries.

Branches of internal carotid artery

 OPTHALMIC ARTERY
-arises as the internal carotid artery emerges from the cavernous sinus
-it enters the orbit through the optic canal below and lateral to the optic nerve
-supplies the eye and other orbital structures, and its terminal branches supply the frontal
area of the scalp,
the ethmoid and the frontal sinuses and the dorsum of the nose
 POSTERIOR COMMUNICATING ARTERY
-small vessel that originates from ICA close to its terminal bifurcation
-runs posterior above the occulomotor nerve to join PCA, thus forming part of the circle of
willis

117 | P a g e
  CHOROIDAL ARTERY
-gives blood supply to choroid plexus
-gives off numerous branches to crus cerebri, lateral geniculate body, optic tract and internal
capsule
 ANTERIOR CEREBRAL ARTERY
-found near at corpus callosum
-smaller terminal branch of ICA
-runs forward and medially superior to optic nerve and enters longitudinal fissure of
cerebrum
 MIDDLE CEREBRAL ARTERY
-largest branch or ICA
CORTICAL BRANCH – supply the entire lateral surface of hemisphere, except for
narrow strip
-supply all motor area except the leg area
CENTRAL BRANCH – supply lentiform and caudate nucleus and internal capsule

The circle of Willis is composed of the right and left internal carotid arteries joined by the
anterior communicating artery. The basilar artery (formed by the fusion of the vertebralarteries)
divides into left and right posterior cerebral arteries that are connected (anastomsed) to the
corresponding left or right internal carotid artery via the respective left or right posterior
communicating artery. A number of arteries that supply the brain originates at the circle of Willis,
including the anterior cerebral arteries that originate from the anterior communicating artery.
The circle of Willis provides multiple paths for oxygenated blood to supply the
brain if any of the principal suppliers of oxygenated blood (i.e., the vertebral and internal carotid
arteries) are constricted by physical pressure, occluded by disease, or interrupted by injury. This
redundancy of blood supply is generally termed collateral circulation.

Arteries supply blood to specific areas of the brain:

 Corpus Striatum and Internal Capsule -supplied by medial and lateral striate central
branches of the MCA; the central branch of the ACA supply the remainders if these
structure.
 Thalamus – supplied by branches of posterior communicating artery, basilar and PCA
 Midbrain- supplied by PCA, superior cerebellar artery, basilar artery
 Pons – supplied by basilar artery, anterior, inferior and superior cerebellar artert
 Medulla Oblongata – supplied by vertebral, anterior and posterior spinal, posterior inferior
cerebellar artery, basilar artery
 Cerebellum – supplied by superior cerebellar, anterior inferior cerebellar and posterior
inferior cerebellar

Veins of specific areas the Brain:

 Midbrain - drained by the veins that open into basal or great cerebral veins
 Pons - drained by veins that open into the basal vein, cerebellar veins or
neighboring venous sinuses

118 | P a g e
  Medulla Oblongata - drained by veins that open into the spinal veins and
neighboring venous sinuses
 Cerebellum - drained by veins that empty into the great cerebral vein or
adjacent venous sinuses

Cerebrospinal Fluid (CSF)

 is a clear, colorless liquid that protects brain and spinal cord against chemical
and physical injuries.
 It also carries oxygen, glucose, and other needed chemical from the blood to
neurons and neuroglia.

Choroid Plexus Lateral Ventricle Foramen of Monro

Fourth Ventricle Sulvius Aqueduct Third Ventricle

Foramen of Subarachnoid
Foramen of Lushka Arachnoid Villi
Magendie Space

119 | P a g e
Ventricle CSF- filled Cavities within the Brain
 Lateral

 Ventricle
- Located in each hemisphere of cerebrum. Anterior to it is separated by a
thin membrane, the septum pellucidum
 Third Ventricle
- Narrow cavity along the middle superior to the hypothalamus and between
® and left halves of thalamus
 Fourth Ventricle
- Lies between the Brainstem and cerebellum

Total volume of CSF is 80-150mL (3-5oz) in adult.

20mL/hr (480mL/day) normal CSF production and reabsorption rate.

Functions of CSF
1) Cushions and protects the CNS from trauma.
2) Provides mechanical buoyancy and support the brain.
3) Serves as a reservoir and assists in the regulation of the content of the skull.
4) Nourishes the CNS
5) Removes metabolites from the CNS
6) Serves as a pathway for pineal secretions to reach the pituitary gland.

CSF Contributes to homestasis in 3 main ways:

1. Mechanical Protection
2. Chemical Protection
3. Circulation

EPIDEMIOLOGY:
 Is the leading cause of childhood disability.(MOLNAR)
 Incidence varies but ~2.3 per 1000 live births. (MOLNAR)
 Prevalence rate of 5.2 per 1000 neonatal survivor at 12 months but reported
resolution in up to half of these children by age of 7 y/o. (MOLNAR)

120 | P a g e
  Recent studies overall prevalence rate of 1.5-2.0 per 1000 live births.
(MOLNAR)
 Incidence varies but is ~ 1-2.3 per 1000 live births.(BRADDOM)
 F=M ratio
 1.09 per 1000 child in Asia

ETIOLOGY:
 Brain injury that leads to CP can occur in prenatal, perinatal or postnatal
period (Braddom)
 Prenatal: Overwhelming evidence suggests that in approximately 70% to
80%, cerebral palsy is prenatal origin.
 PREMATURITY – most common cause of brain injury in children and most
common cause in prenatal.
Strongest Predictors of CP:
1. Presence of congenital anomaly
2. Low Birth Weight
3. Low Placental Weight
4. Abnormal fetal Position

 Intrapartum Period- Infrequent source of CP

Prenatal cause
- Includes: toxoplasmosis, rubella, cytomegalovirus, Herpes simplex.
- Infections
- Intrauterine stroke & genetic malformation
- Fragile brain
- Vasculature maternal MR
- Hyperthyroidism

Perinatal cause
- Anoxic or ischemic brain injury
- Mechanical difficulties of placenta umbilical cord or actual delivery.
Intrapartum asphyxia

Postnatal cause
- CNS infection
- Vascular cause
- Head injury
- Others: anoxia, ischemia inflammation.
Maternal Hx:
1. Economic
- Poverty
- Poor acess to prenatal care
2. Cultural or Behavioral
- Cigarettes smoking
- Alcohol intake
- Drug abuse

121 | P a g e
 - Unmarried status
- Black race
- Short interpregnancy internal
3. Biologic/ genetic
- Hereditary disease
- Low birth weight of previous infant
- Poor maternal nutrition
4. Reproduction
- Prolonged gestation/labor
- Breech presentation
- Uterine bleeding
- Premature rupture of membrane
- Fetal d/o
5. Medical
- Maternal Htn.
- Maternal diabetes
- Cardiopulmonary disease
- Ingestion of illegal drugs
- Inadequate prenatal care
6. Two/ more prior deaths
7. Hyperthyroidism/ seizure d/o of mother

Congenital Acquired

Prenatal Perinatal Postnatal

Anoxia Anoxia Trauma

Maternal anemia shock Respiratory obstruction Skull fracture
Placental disturbances Atelectasis Brain contusion
Rh incompatibility Placenta previa Infections
Maternal Infection Premature separation of Meningitis
Rubella placenta Encephalitis
Toxoplasmosis Over sedation Cerebrovascular accident
Cytomegalovirus Breech delivery Anoxia
Herpesvirus Trauma Shock
Syphilis Cephatopelvic disproportion Poisoning
Trauma Cesarean section Near drowning
Metabolic factors Prematurity < 32 weeks Brain tumor
Brain malformation gestation Coagulopathies
Congenital malformation Birth weight < 2500gm Exposure to toxic
Socioeconomic factor Growth retardation substances
Maternal mental Intracranial hemorrhage Otitis media
retardation Seizures Infection Kernicterus
Hyperthyroidism Bradycardia and hypoxia Progressive
Thyroid used Seizures hydrocephalus

122 | P a g e
Rh incompatibility Hyperbilirubinemia
AIDS transfer to the child Neonatal cardiovascular
during delivery or respiratory distress—
breastfeeding difficulty in breathing of
Ecclampsia hypertensive newborn
pregnant mother APGAR of 3 in 10-15 min
Prolonged labor
Infection of chorion
Placental abruption
Cord prolapsed
Uterine rupture or similar to
birth asphyxia

Grades of Intraventricular Hemorrhage in the Premature brain.

Grade Hemorrhage

1 Isolated to germinal matrix

2 With normal ventricular size
3 With ventricular dilatation
4 With parenchymal hemorrhage

Five basic subtypes of hypoxic ischemic neuropathology

1) Parasagittal cerebral injury
 Principal lesion of the term infant involves bilateral cortical and adjacent
subcortical white matter necrosis of the superior medial and particularly the
posterior aspects of cerebral convexities.
 Most frequent long term consequences of injury to this region are Spastic
Quadriplegia.

2) Periventricular Leukomalacia
 Strongest predictor of Cerebral Palsy in premature neonate.
 Occurs in preterm infant involving bilateral white matter necrosis adjacent to
the external angles of the lateral ventricles affecting the centrum semiovale
and optic and acoustic radiations.
 The long term manifestations include Spastic Diplegia and Spastic
Quadriplegia with visual and cognitive deficits in more severe injury
 Can occur in 28th to 34th week of fetal life.

3) Focal and multifocal ischemic brain necrosis

 Characterized by injury to all cellular elements caused by an infraction within
a vasculature distribution.
 Middle cerebral artery is most common vascular territory affected, with the left
side twice as commonly involved as the right.

123 | P a g e
  The long term neurologic manifestation reflect the location and extent of the
primary lesion and include Spastic Hemiplegia, Spastic Quadriplegia and
seizures.
 Can occur in 34th to 40th weeks of fetal life

4) Status Marmoratus
 Rarest lesion
 Characterized by neuronal injury within the basal ganglia (thalamus, caudate
nucleus, globus pallidus, and putamen)
 Its long term neurologic manifestation is Choreoathetosis .

5) Selective Neuronal necrosis

 Prolong deprivation of oxygen and amino acids.
 Most common variety of injury observed in hypoxic- ischemic
encephalopathy,
 It coexists with one or more of other lesion.
 The long term sequelae include mental retardation and seizures.

Factors associated with prenatal hypoxic-ischemic cerebral injury

 Multiple pregnancy
 Maternal bleeding
 Maternal drug use.

Neurologic Classification:
Spastic (pyramidal ) Cerebral palsy
 Most common occur
 d/t an UMNL, involving the Pyramidal tract
 This group accounts for approximately 75% of children affected.
 It is typically manifest signs of Upper Motor Neuron Lesion involvement

Topographic Subdivisions:
A.Spastic Monoplegia

 Isolated upper or lower extremity involvement

 Rarely seen
 Usually mild clinical presentation
 Often the presentation of a misdiagnosed hemiplegia
B.Spastic Diplegia
 AKA Little’s disease
 History of prematurity common
 History of intraventricular hemorrhages, particularly in the 28- 32 week old
infant.

124 | P a g e
  More complex, multifactorial cause in the term infant ,although in 28% no
identifiable risk factor present
 History of early hypotonia followed by spasticity
 Developmental delay most pronounced in the gross motor sector
 Lower extremity spasticity caused by damage to pyramidal fibers within
internal capsule.
 Mild coordination problems in upper extremities

C.Spastic Triplegia
 Three extremities involved, classically bilateral lower extremities and one
upper extremity
 Spasticity in involved limbs
 Mild coordination problems to involved limbs
 Scissoring and toe walking
 Similar features to the spastic quadriplegic

D.Spastic Quadriplegia
 All extremities involved
 Individuals with more involvement in the upper extremities than the lower
extremities categorized into double hemiplegia
 History of difficult delivery with evidence of perinatal asphyxia common
 Approximately 50% prenatal in origin : 30% perinatal : 20% postnatal.
 Opisthotonic posturing
 Oromotor dysfunction

E.Spastic hemiplegia
 One side of the body involved
 Most cases; congenital (70-90%) ; acquired causes (10-30%) including
vascular, inflammation and traumatic events.
 Asymmetric periventricular leukomalacia may be common caused.
 Hemiparesis usually evident by 4-6 months
 Hypotonia may be first indicator of this type of CP.
 Facial weakness
 Growth retardation
 Spasticity in hemiplegic side
 UMN signs in hemiplegic side
 Hemiplegic gait pattern
2. Dyskinetic (extrapyramidal) Cerebral Palsy
 Characterized by extrapyramidal movement patterns.

125 | P a g e
  These abnormal responses are secondary to abnormal regulation, defects in
postural control, and coordination deficits.
 The movement can be divided into hyperkinetic and dystonic group.
Disorder characterized by extrapyramidal movement patterns. These abnormal
responses are secondary to abnormal regulation of tone, defects in postural tone
and coordination deficits.
Child with extrapyramidal disorder is generally hypotonic at birth.
 Classic movements emerges sometime between 1 to 3 years of age.
 UE are more frequently involved.
 Persistence of hypotonia for the longest time.
 Movement patterns increases with stress or purposeful activity and can
change from hour to hour depending on fatigue and other factors.
 During sleep, the muscle tone is normal and involuntary movement stops.
 The term athetosis is used when moving the limb, increases tone.
 Pseudobulbar involvement
 Intelligence is frequently good
 Hearing loss of a specific high frequency type
 Drive and outgoing personalities
 Articulatory speech difficulties

Dyskinetic movements :
1) Athetosis
 Slow, writhing, involuntary movements particularly in the distal extremities
2) Chorea
 Abrupt , irregular, jerky movements usually occurring in the head, neck
and trunk.
3) Choreoathetoid
 Combination of athetosis and choreiform movements
4) Dystonia
 Slow, rhythmic movements with tone changes generally found in the trunk
and extremities: abnormal posture.
5) Ataxic
 Unsteadiness with uncoordinated movements; often associated with
nystagmus, dysmetria, and wide-based gait.
Topographic Subdivisions of Dyskinetic CP:
A. Athetoid CP
 First become apparent when child is 2-3 years of age.
 Before that age hypotonia is oresent
 Characteristic is writhing, uncontrolled mov’t vary in intensity but increase
when the child is sudden stress, tension, weight bearing, even sudden
changes of light or physically stimulated
 Speech is often severely impaired by oropharyngeal ms involvement

126 | P a g e
 Involvement Quality of Tone Involuntary mov’t
Athetoid c Usually quadriplegia Moderate spasticity Fluctuating tone
Spasticity c head and upper fluctuations range seen more distally
body more involved from normal to high than proximally
then lower body
Athethoid c tonic Quadriplegia only c Fluctuations range Both proximal and
spasm full body distribution from low to very distal.
high. Seen in the form of
The rapid changes excessive
in tone creates a extension or
tonic spasm flexion
Choreoathetoid Quadriplegia only Fluctuations range More proximal
from low to high to than distal.
normal Fluctuation in ms
tone creates mov’t
that may look
intentional but are
often involuntary
Pure Athetoid Usually quadriplegia Fluctuationsrange Fluctuates more
to from low to mid- proximal than
normal distal
Large range
fluctuations c facial
grimacing
Ataxic Usually quadriplegia Fluctuations range Rapid fluctuations
seen in head injury from low to low- seen more distally
normal in form of a tremor,
but c proximal
instability

4. Ataxic CP
 Cerebellar impairment of balance and coordination and is the least
frequently seen clinical type
 Children show hypotonia and delay in achieving motor milestones.
 Gait disturbances and UE fine motor impairment often improve somewhat
as the child matures and learns to compensate for motor delay (Low and
Downey, 1982)
 Nystagmus
 Intellectual impairment appears
 Clumsy

5. Mixed types
 Description from both spastic and dyskinetic classification

127 | P a g e
  Spasticity commonly coexists c athetosis
 A combination of two or more forms

PATHOPHYSIOLOGY:

CLINICAL MANIFESTATION:
Major Findings in Cerebral Palsy
128 | P a g e
  Delayed motor milestone
 Abnormal posture
 Abnormal tone
 Abnormal reflexes
 Abnormal motor performance

Early Signs and Symptoms:

a) Neonatal Period (1-28day)
1) Diminished activity
2) Suck and swallow problem
3) Apneic spell
4) Hypotonic or Hypertonicity
5) Temperature Instability
6) Presence of seizure
b) Infantile Period( 1 mos- 2 yr)
1) Delayed abnormal development
2) Abnormal tone and posture
3) Persistence in primitive reflexes
4) Increase irritability
5) Decrease attentiveness
6) Gestational age : <9 months
7) Birth Weight :
 < 2500 g low birth
 <1500 g very low birth

 May manifest
 Hypoglycemia
 Respiratory distress syndrome
 Hyperbilirubinemia
 Prone to sepsis
 Hemorrhage

DIAGNOSIS:
APGAR Score
- Dr. Virginia Apgar, developed the scoring system to identify babies at risk for
complications or bad outcome from delivery (specifically CP)
- 1st minute being taken then if they got a low score it will repeat then next 5
mins and after 5 mins again.

APGAR Scoring System

0 1 2
Appearance Pale Pink body Blue Pink
extremities
Pulse Absent <100bpm >100bpm

129 | P a g e
 Grimace Absent Grimace Cry active
Activity Limp Some tone Active
Respiration Absent Irregular Regular and Cry

STANDARIZED NORM-REFERENCED ASSESMENT TOOLS

-serve as baseline for measuring developmental progress with therapeutic
intervention

1) BAYLEY SCALES OF INFANT DEVELOPMENT-widely used assessment tool

which includes a mental scale, motor scale & infant behavior record covering an age
span of 2-30 months

2) GESSEL DEVELOPMENTAL SCHEDULES- designed to provide assessment of

developmental skills in 5 areas: adaptive, gross motor, fine motor, language &
personal-social: covers an age span from 1-72 months of age.

3) PEABODY DEVELOPMENTAL MOTOR SCALES- consists of standardized,

norm-referenced gross& fine motor scales: assess skills between the age 1 & 83
months.

4) BRUININKS OSERETSKY TEST OF MOTOR DEFFICIENCY- assesses gross &

fine motor skills in children between of 4.5 & 14.5 years.

DIFFERENTIAL DIAGNOSIS:
1. Angelman Syndrome
- Characterized by severe developmental delay or intellectual disability, severe
speech impairment, gait ataxia and/or tremulousness of limbs, and a unique
behavior c an inappropriate happy demeanor that includes frequent laughing,
smiling, and excitability.
- Developmental delay are first noted at around 6 mos old.
- Unique clinical feat. of AS do no become manifest until after age of 1 yr old
and it take several years before the correct clinical Dx is obvious

2. Cri du chat Syndrome

- Aka Lejeune’s Syndrome, Chromosome 5p depletion Syndrome, 5p minus
syndrome
- Rare genetic disorder d/t a missing part of chromosome 5
- 1:50,000 live birth
- F>M (4:3 ratio0
- characterized by intellectual disability and delayed development, small head
size (microcephaly), low birth weight, and weak muscle tone (hypotonia) in
infancy

3. Prader-willi Syndrome

130 | P a g e
 - Rare genetic disorder in which seven genes are deleted or
unexpressed. Characteristic of PWS is "low muscle tone, short stature,
incomplete sexual development, cognitive disabilities, problem behaviors,
and a chronic feeling of hunger that can lead to excessive eating and life-
threatening obesity.

4. Rett Syndrome
- Originally termed as cerebroatrophic hyperammonemia is a
neurodevelopmental disorder o the grey matter of the brain that almost
exclusively affects females.
- The clinical features include small hands and feet and a deceleration of the
rate of head growth (including microcephaly in some).
- Repetitive stereotyped hand movements, such as wringing and/or
repeatedly putting hands into the mouth, are also noted.

5. Sotos Syndrome
- Rare genetic disorder characterized by excessive physical growth during the
first 2 to 3 years of life.
- Accompanied by autism mild mental retardation, delayed motor, cognitive,
and social development, hypotonia (low muscle tone), and speech
impairments.
- Children with Sotos syndrome tend to be large at birth and are often taller,
heavier, and have larger heads (macrocephaly) than is normal for their age.

PROGNOSIS
 Prolonged hypotonic stage is a precursor of dyskinesia rather than spasticity
 75% of spastic Cerebral Palsy eventually ambulates expect spastic
quadriplegia
 85% with CP Diplegia eventually ambulates
 Hypotonic CP rarely walk
 Independent nsitting by 2y/o can become independent walker with or without
assistive device
 Can’t sit by 4 y/o can’t walk

MOLNAR GRADING
Independent sitting occurs by 2 yrs Good prognosis
Ability to crawl on hands and knees by 1.5-2.5 yrs good prognosis
Persistence of 3 or more primitive reflexes at 18-24 mos is poor prognosis
Ability to transition from supine to prone by 18 mos was shown to be a predictor of
independent ambulation in spastic diplegics
Bleck’s Index
Moro Reflex
Neck Righting
Extensor Thrust

131 | P a g e
ATNR
STNR
Foot Placing (Present till lifetime)
Parachute (Present till lifetime)
Scoring: Grading:
1 point if reflex is abnormal 0 point – Good
0 point if reflex is normal 1 point - Guarded
2-7 points - Poor

Other Condition Associated with CP

1. Intellectual disability
2. Seizure disorder
3. Delayed growth and development
4. Spinal deformities and OA
5. Impaired vision
6. Hearing loss
7. Speech and language disorders
8. Drooling
9. Incontinence
10. Abnormal sensations and perceptions
11. Learning difficulties
12. Infections and long-term illness
13. Contractures
14. Malnutrition
15. Dental problems
16. Inactivity

MEDICAL MANAGEMENT:
A) Laboratory
 Blood and Urine Samples – in evaluating metabolic diseases and some
genetic diseases.
 Routine Test – includes thyroid functioning, lactate and pyruvate, organic and
amino acids.
 Evaluation of cerebrospinal fluid – may assist in determining asphyxia.

B) Diagnostic Procedure
1) Cranial Ultrasound
 Uses high-frequency sound waves to produce pictures of the brains of young
babies.
 It is used for high-risk premature infants because it is the least intrusive of the
imaging techniques
 Not as successful as computed tomography or magnetic resonance imaging
at capturing subtle changes in white matter—the type of brain tissue that is
damaged in CP
 The most commonly used test for premature infant.

132 | P a g e
  It provides useful information about the ventricular system.
 It provides diagnostic information on intraventricular hemorrhage and hypoxic
ischemic injury to the periventricular white matter
 It allows clinician to follow the changes in the brain associated with
periventricular leukomalacia.
2) Computed tomography (CT)
 It has a wide spectrum of uses in this population.
 It is helpful in diagnosing congenital malformation, intracranial hemorrhages,
and periventricular leukomalacia.in the infant.
3) MR imaging studies
 Limited use in the mature infant and are the most beneficial after the chil is 2-
3 weeeks old.
 It is study of choice for following white matter disease because it allows
visualization of myelin on T2 images and visualization of the sulci.
 It is the best diagnostic test
4) Positron-emission tomography (PET)
 Experimental tool used to define flow and glucose metabolism.
 Single photon emission computed tomography (SPECT)
 Is another experimental tool used to document cerebral perfusion.
 Using radioactive tracers, areas of the brain that are njured or hypoperfused
shows a decreased radioactive pattern.
5) P magnetic resonance spectroscopy
 One of the newest techniques for evaluating asphyxia.
6) MR spectroscopy
 Measures phosphorus containing compounds in the brain.
7) Evoked Potentials
 Used to evaluate the brain’s responses to external stimuli
8) Electroencephalogram (EEG)
 Measures electrical activity on the surface of the brain.
 It is useful tool in evaluating severe hypoxic-ischemic injury

Pharmacological Medications for Spasticity

 Botulinum toxin (BT-A), injected locally, has become a standard treatment

for overactive muscles in children with spastic movement disorders such as
CP. BT-A relaxes contracted muscles by keeping nerve cells from over-
activating muscle. The relaxing effect of a BT-A injection lasts approximately
3 months. Undesirable side effects are mild and short-lived, consisting of pain
upon injection and occasionally mild flu-like symptoms. BT-A injections are
most effective when followed by a stretching program including physical
therapy and splinting. BT-A injections work best for children who have some
control over their motor movements and have a limited number of muscles to
treat, none of which is fixed or rigid.
 Intrathecal baclofen therapy uses an implantable pump to deliver baclofen,
a muscle relaxant, into the fluid surrounding the spinal cord. Baclofen
decreases the excitability of nerve cells in the spinal cord, which then reduces
133 | P a g e
 muscle spasticity throughout the body. The pump can be adjusted if muscle
tone is worse at certain times of the day or night. The baclofen pump is most
appropriate for individuals with chronic, severe stiffness or uncontrolled
muscle movement throughout the body
 Baclofen
-GABA-B receptor in Spinal Cord
-25.5-5mg bid, increase 2.5mg dose Q 3 days
-SIDE EFFECTS: confusion, depression, weakness, GI upset, decrease
seizure
threshold.
 Diazepam
-acts on (B) brainstem reticular activating system and Spinal Cord
-1-2 mg bid
-SIDE EFFECTS: lethargy, urinary retention, dependence
-prompt withdrawal causes seizures
 Dantrium
-acts at the level of intra-and extrafusal mm fibers, decrease release of
calcium ions
from Sarcoplasmic Reticulum
-0.5mg/kg/day
-SIDE EFFECTS: weakness, fatigue, lethargy, diarrhea
-Needs to monitor liver and blood count during use.
 Clonidine
-alpha antagonist, originally used to treat HTN
-serendipitously decrease spasticity
-0.05-0.1mg bid
-SIDE EFFECTS: temporary sedation, hypotension
-Transdermal patches- 0.2-0.3mg
 Zanaflex
-replace oral clonidine
-1-2mg od

Surgery

Orthopedic surgery

 often recommended when spasticity and stiffness are severe enough to make
walking and moving about difficult or painful.
 Surgeons can lengthen muscles and tendons that are proportionately too
short, which can improve mobility and lessen pain.
 Tendon surgery may help the symptoms for some children with CP but could
also have negative long-term consequences.
 Orthopedic surgeries may be staggered at times appropriate to a child’s age
and level of motor development.
 Surgery can also correct or greatly improve spinal deformities in people with
CP.

134 | P a g e
  Surgery may not be indicated for all gait abnormalities and the surgeon may
request a quantitative gait analysis before surgery.

Surgery to cut nerves.

Selective Dorsal Rhizotomy (SDR)

 Surgical procedure recommended for cases of severe spasticity when all of

the more conservative treatments – physical therapy, oral medications, and
intrathecal baclofen -- have failed to reduce spasticity or chronic pain.
 A surgeon locates and selectively severs overactivated nerves at the base of
the spinal column.
 SDR is most commonly used to relax muscles and decrease chronic pain in
one or both of the lower or upper limbs.
 It is also sometimes used to correct an overactive bladder.
 Potential side effects include sensory loss, numbness, or uncomfortable
sensations in limb areas once supplied by the severed nerve.

Selective Posterior Rhizotomy

-sectioning a variable percentage of sensory nerve rootlets after L2-S1
laminectomy.
-theoretically, this resulted in decrease peripheral excitatory influence in
anterior horn cell.
-Favorable px selection criteria:
 Lack of dystonia or athetosis
 Preservation of functional strength independent of spasticity
 Presence of selective motor control
 Younger age (3-8y/o)
 Lack of significant joint contracture
 Previous orthopedic procedure

PT Management.

 Electrical Stimulation
 Transcutaneous Nerve Stimulation
 Progressive Resistive Exercises (PRE’s)—for strengthening

THERAPEUTIC APPROACHES:

NEURODEVELOPMENTAL TECHNIQUES:
Phelps
 Used orthopedic approach c conventional techniques from poliomyelitis
treatment regimens
 Emphasize inhibiting abnormal movement
 15 Modalities used for specific types of CP

135 | P a g e
 1. Massage
2. PROM
3. AAROM
4. AROM
5. Resisted motion followed according to child capability
6. Conditioning motion
7. Confused motion or synergistic motion involves resistance to ms group
8. Combined motion
9. Relaxation technique
10. Movement from relaxation
11. Rest
12. Reciprocation
13. Balance
14. Reach and grasp and release
15. Skills of ADL

Principle Crothers
 involve patient in a meaningful program
 Need active movement and stimulation activities to prevent contractures and
encourage participation of severely involved children
 Overprotection by parent discouraged

Progressive pattern movements

 Temple Fay, neurosurgeon in Philadelphia, recommended that the CP be
taught motion according to its development in evolution.
 Regarded ontogenic development as recapitulation of phylogenetic
 Consist of 5 stages
Stage 1 Prone lying
Stage 2 Homolateral Stage
Stage 3 Contralateral Stage
Stage 4 On hands and knees
Stage 5 Walking pattern
Deaver
 emphasized functional ability rather than patterns of movement
 Extensively used bracing
 Functional activities facilitated by intensive training efforts

Doman-Delacato system
 Follows the basic tenets postulated by Fay,
 Children is hung upside down and whirled around to stimulate the vestibular
apparatus
 No longer recommended

Synergistic movement patterns

136 | P a g e
  Signe Brunnstrom (1970), a PT, produces motion by provoking primitive
movement patterns or synergistic movement patterns which are observed in
fetal life or immediately after pyramidal tract damage.
 Most of his therapy has been on adult hemiplegics

Proprioceptive Neuromuscular Facilitations

 Herman Kabat, Margaret Knott and Dorothy Voss
 Method for the inhibition of hyperclonus
 Main feature of this are use of Movement pattern

Neuromotor development
 Eirene Collis, stressed neuromotor development as a basic for assessment
and treatment

Rood-
 Developed the sensorimotor approach
 Overall goal was activate movement and postural response at an automatic
level while following a developmental sequent similar to Bobath
 Used specific sensory stimulation to elicit movement

Bobath
 Developed the approach called “Neurodevelopmental Treatment”
 Advised for CP with early signs

Main goals: Normalize tone, inhibit abnormal primitive reflex patterns, facilitate
automatic reactions and subsequent normal movement

Ayres
 Sensory integration used to enhance development of preschool/school-age
children c learning disabilities
 Based on premise that “disordered sensory integration” accounts for some
aspects of learning disorders.

Vaclav Vojta
 Promulgates reflex rolling and reflex creeping
 Used in Germany but not in USA because it makes the child cry

Rehabilitation Approach in CP patient

1) focused on assets of pt. and not on deficits
2) look for strategies to prevent complications
3) therapies should meet changing needs base on appropriate and regular
assessment
4) consider the whole child
5) support the entire family

137 | P a g e
REFERRENCES:
1. Pediatric Neuropathology – A Text Atlas by D. Armstrong
2. The Help Guide to Cerebral Palsy 2nd Edition by Nadire Berker & Salim
Yarcin
3. De Lisa’s Physical Medicine and Rehabilitation 5th edition vol. 2
4. Handbook of Physical Medicine and Rehabilitation Basis Susan J. Garrison
5. Physical Medicine and Rehabilitation 3rd edition Braddom
6. Nursing care of Children and Families 2nd edition Mott, James and Sperhac
7. Principles of Surgery 5th edition Schwartz, Stiires, Spencer
8. http://www.brainandspinalcord.org/cerebral-palsy/index.htmlhttp://
www.brainandspinalcord.org/cerebral-palsy/index.html
9. http://emedicine.medscape.com/article/975728-overview#a0104
10. http://www.mayoclinic.com/health/cerebral-palsy/DS00302http://
www.mayoclinic.com/health/cerebral-palsy/DS00302
11. http://www.cerebralpalsysource.com/About_CP/index.html

INITIAL EVALUATION

GENERAL INFORMATION
Patient’s Initial: K.M.
Age: 2 yrs and 4 mos
Sex: ♂
Address: 623 Biak-na-Bato, Pandacan Manila
Tel. No.: 916-1279
Weight: 9.2 kg
Height: 74 cm
Hand Preference: ®
Referring Unit: PGH (Pedia OPD )
Rehab Unit: PCPI
Referring M.D.: Dr. K.C.
Rehab M.D.: Dr. A.J.
Date of Consultation: Jan 23, 2013
Date of Rehab Consultation: Jan. 26, 2013
Date of I.E.: Jan 26, 2013
Diagnosis: Delayed Motor Milestone
Informant/Reliability: Mother/Good

138 | P a g e
HPI:
Present condition started 22 mos PTC when the mother noticed that when
carrying her child, the Pt’s head is dropping backward. She just ignored it thinking it
was normal at his age.

18 mos PTC the mother noticed that the Pt do not hold the bottle when she is
giving it. She also noticed that the Pt is having a very long time before he can empty
it. The mother thought that the Pt has poor sucking reflex so she started giving the
Pt tiki-tiki plus syrup to ↑ the appetite, but it didn’t help. The next month the mother
noticed that the Pt. able do some baby talk and still has poor sucking reflex.

14 mos PTC the mother noticed that the when the Pt is lying down he doesn’t
move.. The mother started wondering what’s wrong c her child. The next month they
went to the health center for the measles vaccine the Pt. The mother as the doctor
about what she’ve noticed for the past few months. The doctor done Physical
Examination to rule out delayed motor milestone and was referred to the PT. But
they cannot afford the therapy so the mother just perform massaging the Pt’s ms,
nothing was changed.

11 mos PTC the mother started to introduce semi-solid food to the Pt such as
lugaw. She was having a hard time feeding him and the Pt also choke when eating.
The mother thought that the Pt has a poor appetite so she change the vitamins into
Children’s Clusivol (See Present Medication) to ↑ the appetite of the Pt which didn’t
help.

7 mos PTC the mother noticed that the Pt prefer to use his ® hand when
holding bottle and toys. 3 mos PTC slow rhythmic movement starts to developed on
(B) hands of the Pt. the mother noticed the rhythmic movement when the Pt is
holding his bottle or toys and diminished when sleeping. She just ignored it thinking
it was only due to his condition.

1 week PTC the Pt now able to stand momentarily c difficulty. The mother
noticed that slow rhythmic movement also starts to developed in (B) feet and the
intensity of the movement in (B) hands ↑ which makes the Pt having a hard time
holding things. This prompted her to go to Manila to seek further medical advice.
MRI were done (See Ancillary Procedure). Pt was then diagnosed to have dyskinetic
CP. The Pt was then referred to PT for further evaluation and treatment.

A. MATERNAL Hx
139 | P a g e
a. Prenatal:
 Wanted, planned pregnancy
 Irregular check-up on health center
 RH incompatibility
 (+) Multivitamin capsule intake (500mg, od)
 (+) Iron Sulfate intake (500mg, od)
 (+) TT1 vaccine
 (-) Alcoholism
 (-) Smoking
 (-) X-ray
b. Perinatal:
G3P0301
c. Postnatal:
 (-) Newborn Screening
 (-) Trauma
 (-) Infection
 (-) Seizure

B. BIRTH Hx

 Bicol Regional Hospital

 Attending M.D.: Dr. L.G.
 NSD (Sept. 8, 2010 at 3:07am)
 Complete Breech
 Jaundice 3 days p birth
 Incubation for 2 weeks

 APGAR SCORING

Grade/Score 1 Trial (1min) 2 Trial (5mins) 3 Trial (10mins)

Appearance 1 1 2
Pulse 1 2 2
Grimace 0 1 1
Activity 0 0 0
Respiration 1 1 1

C. NUTRITIONAL Hx (Post Natal)

140 | P a g e
  Breast feeding (1 mos-2 y/o)
 Bottle feeding (2mos-Present) Milo/Bear Brand 2:5 dilution
 AM Feeding (9mos-Present) 8oz/day
 Semi-solid food lugaw (16mos-Present)

 (+) feeding problem (Poor sucking and swallowing)
 Loss of Appetite

D. IMMUNIZATION Hx
 BCG At birth
 DPT 2 mos, 3 mos, 4 mos
 OPV 2 mos, 4 mos, 6 mos
 Hepa-B 9 mos, 10mos, 11 mos
 Measles 14 mos
 Mumps 14 mos

E. PMHx
 (+) Delayed motor milestone (Bicol Health Center, 14mos)
 (-) Convulsion
 (-) Disease
 (-) Infection
 (-) Trauma

F. DEVELOPMENTAL Hx

a. Developmental Milestones

Motor Milestone(s) Age Expected Age Achieved

Turns head to side (Prone) Newborn 6 mos
Head in midline 4 mos 9 mos
Lift head in prone 4 mos 11 mos
Roll to supine 4 mos 15 mos
Utter 1 word 7 mos 14 mos
Roll to prone 7 mos 19 mos
Maintained sitting 7 mos 23 mos
Holds bottle 7 mos 17 mos
Creeps on all four 10 mos 25 mos
Momentarily standing 10 mos 28 mos
Utter 2 words 10 mos 21 mos

141 | P a g e
 Walks alone c high guard 14 mos Not yet Achieved
Piles two cubes 14 mos Not yet Achieved
Hold crayon full length 14 mos Not yet Achieved
palm
Emerging hand dominance 18 mos 15 mos
Arms at low guard 18 mos Not yet Achieved
Seat self in chair 18 mos Not yet Achieved
Walks backward 18 mos Not yet Achieved
Hand dominance 24 mos 18 mos
Begins running 24 mos Not yet Achieved
Walks up and down stair 24 mos Not yet Achieved
alone
Jumps on (B) feet 24 mos Not yet Achieved
Builds 8 cube tower 24 mos Not yet Achieved
Imitate vertical line 24 mos Not yet Achieved

Findings: Pt exhibit a delayed motor milestone

Sig.: 2° to Dyskinetic CP

b. General Behavior
 Pt slight participates c the PT during treatment and has a short attention
span.

c. Behavioral Norms of Development

 The Pt. having a hard time imitating, doing gross and fine motor movement
such as holding bottle and toys.
ANCILLARY PROCEDURES

Diagnostic Procedure(s) Findings Date

MRI Lesion at Globus Pallidus Jan. 23,
2013

Lab. Exam
Normal Value Findings Date
Hemoglobin (g/dl) Male (13.5 - 16.5) 15.5g/dl June 24,2013
Female (12.0 -
15.0)

Hematocrit (%) Male (41 - 50) 46% June 24,2013

Female (36-44)
RBC ( x 106 /ml) Male 4.5-5.5 5.2 x 106 /ml June 24,2013
Female 4.0-4.9
WBC (cells/ml) 4,500 - 10,000 10,000cells/mL June 24,2013

142 | P a g e
 Neutrophils 62% 62% June 24,2013
Basophils 0 - 1 (0 - 0.75%) 0.74% June 24,2013
Eosinophils 0 - 3 (1 - 3%) 2% June 24,2013
Lymphocytes 24 - 44 (25 - 33%) 30% June 24,2013
Monocytes 3 - 6 (3 - 7%) 4% June 24,2013
Platelet count 100,000 to 300,000 June 24,2013
450,000

PRESENT MEDICATIONS

Name of Drug Dosage Frequency Indications

Children Clusivol 2.5mL bid multivitamins
Syrup

S:
Infomant’s c/o: “Nahihirapang makatayo ang anak ko at galaw ng galaw yung mga
kamay at paa nya” as verbalized by mother
PT Translation: Pt has difficulty in standing and manifest involuntary movement of
(B) hands and feet.
PT Goal: To be able to stand s difficulty and manage involuntary movement of (B)
hands and feet.

O:
I. V.S.

Ā ṗ
PR: 95bpm 99bpm
BR: 30cpm 33cpm
T°: 37 C 37 C

Findings: All V.S are WNL

Sig.: For Baseline data

II. O.I.
 Mother-borne
 Poorly nourished
 Alert, coherent, cooperative
 Short attention span
 Normocephalic (See head circumference)
 (+) Sialorrhea

143 | P a g e
  (+) Parinaud Syndrome
 (+) Athetosis on (B) hands and feet
 (-) Scoliosis
 (-) deformity
 (-) Strabismus
 (-) Scar on head

III. PALPATION
 Normothermic in all exposed body part
 Normal skin turgor, mobility and consistency
 (+) Ant. Fontanelle Closure 2 yrs
 (+) Post Fontanelle Closure 2 mos
 (-) Shoulder Subluxation

IV. NEUROLOGICAL EVALUATION

A. Tone A:
Findings: Normotonic on (B) UE and LE
Sig.: For Baseline data

B. Sensory A:
STD used:
 Pinch for Pain
Findings: 100% sensory intact on (B) UE and LE
Sig.: For Baseline Data

C. Visual
VTD: Blue ball for localization and tracking
 Eye ms tracking – Poor
 Introduction of colorful object – Normal
Findings: Pt cannot perform movement of the eye in upward gaze
Sig.: 2° to Kernicterus

D. Auditory
 Calling K.M.’s name Weak
 Banging a tambourine Weak
Findings: Slowness in responding in auditory
Sig.: 2° to Kernicterus

144 | P a g e
E. MSR/DTR
Legend:
0- Areflexia + +
+- Hyporeflexia + + + +
++ - Normoreflexia
+++ - Hyperreflexia + +
++++ - Clonus + +

Findings: Hyporeflexive on (B) UE and LE

Sig.: ↓ firing of alpha motor neuron

F. PATHOLOGIC REFLEX
Reflex Stimulus Response
Babinski Reflex Stroke lat outer edge of (-)
sole of the foot
Hoffman’s Sign Flicker the nails of distal (-)
phalanx of 3rd finger
Bechterew’s-Mendel Sign Stroke lat aspect of (-)
dorsum of the foot over
the cuboid bone
Findings: Pt is (-) in Babinski reflex , Hoffman’s sign and Bechterew’s Mendel Sign
Sig.: 2° to LMNL

F. PRIMITIVE REFLEX

Reflex Stimulus Response Persistence

Foot Placing Move forward the (+) 15 – 18 mos of
Pt age and last life
time
Parachute Suspend Pt in air (+) Birth – 6 mos
Reaction by pelvis and and last Life
move head time
suddenly towards
the floor
Moro Reflex Drop head (-) Birth – 4 mos
backward
ATNR Head turn to one (-) 4 – 6 mos of
side age
Neck Righting Rotation of head (-) Birth – 6 mos
to one side
(Actively or
Passively)
Extensor Thrust Stimulate sole of (-) Birth- 2 mos of

145 | P a g e
 the foot of flexed age
leg
STNR Flexion or (-) 4 – 6 mos of
Extension of head age
Findings: Pt is (+) in Foot placing and parachute reaction.
Sig.: For Baseline Data

V. ROM
All joints of (B) UE and LE are WNL. Actively and Passively done, pain free c
normal end feel.
Findings: All joints are WNL
Sig.: For Baseline Data

VI. FMT
Legend: FMT Grading Legend: BALANCE Legend: TOLERANCE
1 – No ability 1 – Can assume N (normal) - >45 mins.
2 – Beginning ability with 2 – Can assume & maintain G (good) -30-45 mins
difficulty 3 – Can assume, maintain F (fair) -15-30 mins.
3 – Achieved with abnormal & weight shift P (poor) - 1-15 mins
pattern 4 – Can assume, maintain, Nil/ 0 (zero) - 0 mins.
4 – Near normal/ Normal weight shift & challenged

 Rolling – 4
 Creeping – 4
 Crawling – 4

 Head Control – 4
 Trunk Control – 3

Sitting: Kneeling: Standing:

-Balance: 3 -Balance: 2 -Balance: 1
-Tolerance: G -Tolerance: F -Tolerance: P

146 | P a g e
Findings : Pt. achieved c normal pattern as to rolling, creeping, and crawling. While
nearly normal in head control and has difficulty in beginning ability in Trunk control. Pt
sitting balance can weight shift in 30-45 mins, in kneeling balance her can assume and
maintain for 15-30 mins. In standing he can assume and has a poor tolerance
Sig.: 2° to Dyskinetic Cerebral Palsy

VII. Reach Grasp and Release

Legend:
Poor – (-) RGR or (+) Reach (-) Grasp and
Release
Fair – (+)Release and Grasp c difficulty in
Releasing or (+) Reaching c Difficulty in grasping
or Releasing
Good – Complete and (+) RGR

® (L)
Reach + +
Grasp + (Strong) - (Weak)
Release + +
Findings: Pt has stronger Grasp in ® hand and weak grasp in left hand.
Sig.: 2° to dyskinetic cerebral palsy

VIII. ANTHROPOMETRIC MEASUREMENT

A. Head Circumference
19.24”
Findings: Pt’s has normocephalic
Sig.: For Baseline Data

IX. ADL
Findings: All ADL are fully dependent c 1 man assist
Sig.: 2° to dyskinetic Cerebral Palsy

A:
PT Impression: Athetoid Cerebral Palsy
Rehab Potential: Good because of early intervention
Rehab Concern: Pt still cannot stand still
Rehab Precautions: Pt has poor balance in standing and has a delayed protective
reflexes

Problem List:
1. Delayed motor milestone
2. Athetosis on (B) UE and LE

147 | P a g e
 3. Difficulty in sitting, kneeling, and standing in balance and tolerance
4. Muscle weakness in (B) UE and LE
5. Kneeling balance has grade of 2
6. Trunk control grade of 3
7. Difficulty in eating and swallowing
8. Poor RGR on (L) hand and Fair RGR on ® hand
9. Weak eye ms tracking especially in upward gaze
10. Sialorrhea
11. Hearing problem
12. Difficulty in speaking

LTG(3 mos):
1. To prevent 2° complication such as scoliosis, kyphosis, deformity and RLD.
2. To maintain a good posture and normal ROM
3. To Strengthen the RGR on (B) hand.
4. To attain good balance and tolerance as to sitting, kneeling and standing.
5. To attain highest functional level of Pt and to perform partial dependency c 1 man
assist in ADL such as feeding, dressing and ambulation.
6. To lessen athetosis on (B) UE and LE

STG (4 weeks):
1. To improve sitting balance of the Pt from grade 3 to 4.
2. To improve kneeling balance of the Pt from grade 2-3.
3. To ↑ standing balance from grade 1 to 3.
4. To ↑ FMT grade in rolling, creeping and crawling from Grade 3 to 4 and trunk
control from grade 2 to 3.
5. To ↑ RGR of ® hand from Fair to good and RGR of (L) hand from Poor to fair.

P:
PT MANAGEMENT
1. Slow PROME on (B) LE x 10 reps x 1 set x all planes c incorporation of play
therapy
2. Play Therapy
3. Levitt’s technique
4. Phelps method
5. Vestibular ball exercise
6. Vestibular board exercise
7. Standing box

HI:

148 | P a g e
 1. Do exercises taught by PT such as Standing exercises ,walking exercises and
play therapy.
2. Do exercises taught by OT
Note: Please refer Pt to OT
3. Adequate sleep
4. Nutrional diet

_________________________
Jimenez, Ramon Jr., J.
UDM/Batch 2015

__________________________
Cabales, Jericho
UDM/Batch 2015

149 | P a g e
 CEREBROVASCULAR ACCIDENT
(THROMBOTIC)
Nikki Jane T. Credo
Ann Mmay R. Giray

DEFINITION:

 It is an acute of neurological dysfunction due to an abnormality in cerebral circulation

with resultant signs and symptoms that correspond to involvement of focal areas of the
brain(Sullivan).
 I t is a non –traumatic brain injury caused by occlusion or ruptures of cerebral blood
vessels that result in sudden neurologic deficit characterized by loss of motor
control ,altered sensation , cognitive or language impairment , disequilibrium or
coma(Braddom).
 Ancientwriters of history, science and poetry used the word APOPLEXY, meaning a
sudden strike of paralysis, dumbness, or fainting from which the victim frequently to
recover(Braddom)
 It is a clinical syndrome characterized by the sudden development of a persisting focal
neurologic (de Lisa).

RELATED ANATOMY:

In the very early of pregnancy, between the 15th and 28th day, the neural tube
forms and then becomes the brain, spines and vertebral column.
In the developing vertebrate, the neural tube is the embryo's precursor to the central
nervous system, which comprises the brain and spinal cord. The neural

150 | P a g e
 groove gradually deepens as the neural folds become elevated, and ultimately the folds
meet and coalesce in the middle line and convert the groove into a closed tube, the
neural tube or neural canal (which strictly speaking is the center of the neural tube), the
ectodermal wall of which forms the rudiment of the nervous system.
There are four subdivisions of the neural tube that will each eventually develop
into distinct regions of the central nervous system: Theprosencephalon,
the mesencephalon, the rhombencephalon and the spinal cord.

 The prosencephalon further goes on to develop into the telencephalon (the forebrain
or cerebrum) and the diencephalon (the optic vesicles and hypothalamus).
 The mesencephalon develops into the midbrain.
 The rhombencephalon develops into the metencephalon (the pons and cerebellum) and
the myelencephalon (the medulla oblongata).

Lobes of the brain

Brain lobes were originally a purely anatomical classification, but have been shown also
to be related to different brain functions. Thetelencephalon, the largest portion of the
human brain, is divided into lobes, but so is the cerebellum. If not specified, the
expression "lobes of the brain" refers to the telencephalon.
There are four uncontested lobes of the telencephalon:

1. Frontal lobe—conscious thought; damage can result in mood changes

2. Parietal lobe—plays important roles in integrating sensory information from various
senses, and in the manipulation of objects; portions of the parietal lobe are involved
with visuospatial processing
3. Occipital lobe—sense of sight; lesions can produce hallucinations
4. Temporal lobe—senses of smell and sound, as well as processing of complex stimuli
like faces and scenes.

Circle of Willis
Circle of willis or the circulus arteriosus is the main is the main arterial anastomatic trunk
of the brain. Anastomosis occurs when the blood vessels bring blood to one spot from
which it is then redistributed. The circle of willis is a point where the blood carried by the
two internal carotid and the basilar system comes together and them redistributed by
anterior, middle and posterior cerebral arteries.
The anterior cerebral arteries of the two hemisphere are joined together by an
anterior communicating artery. The middle cerebral arteries are linked to the posterior
cerebral arteries by the posterior communicating arteries. This anastomosis or
communication between arteries make collateral circulation, defined as “the flow of
blood through an alternate route” possible. This safety mechanism, allowing the brain
areas to continue receiving adequate blood supply even when there is a blockage
somewhere in an arterial system. The blood streams of the internal carotid system and
the basilar system meet the posterior communicating arteries. If there are no problems
in either system, the pressure of the streams will be equal and they will not mix.
However, if there is a blockage in one of them blood will flow from the intact artery to the
damage one, preventing a cerebral vascular accident.

151 | P a g e
 Broadmann Areas

Sensory Areas

 Primary Somatosensory area (3,1,2)

 Located directly posterior to the central sulcus of each cerebral hemisphere in the
postcental gyrus of each parietal lobe
 Receives nerve impulse to from somatic sensory receptors for touch, proprioception
(joint and muscle position), pain and temperature

 Primary Visual area (17)

 Located on the medial surface of the occipital lobe and occasionally extending around
the lateral surface
 Receives impulses conveying visual information

 Primary Auditory area (41,42)

 Located in superior art of the temporal lobe near the lateral cerebral sulcus
 Interprets the basic characteristics of sound such as pitch and rhythm

 Primary Gustatory area (43)

 Located at the central base of the postcentral gyrus groove the lateral cerebral sulcus in
the parietal lobe
 Receives impulses related to taste

 Primary Olfactory area (28)

 Located in the temporal lobe on the medial aspect

 Receives impulses related to smell

Motor areas

 Primary Motor area (4)

 Located in the precentral gyrus of the frontal lobe

 Controls voluntary contraction of specific muscles or group of muscles

 Broca’s speech areas (44,45)

 Responsible for speech production

 Located in the frontal lobe, usually the left frontal lobe just superior to the lateral
cerebral sulcus

152 | P a g e
 Association areas

 Somatosensory association area (2,7)

 Just posterior to the primary somatosensory areas

 Integrates and interprets sensation
 Determine exact shape and texture of an object without looking at it

 Visual association area (18,19)

 Located at the occipital lobe

 Essential for recognizing and evaluating what is seen

 Auditory association area (22)

 Wernicke’s area
 Interpret the meaning of speech by transmitting words in thoughts
 Located at the inferior and posterior to the auditory areas in temporal cortex; it
determines if a sound is speech, music or noise

 Wernicke’s (posterior language) area (22, 39,40)

 Common integrative area (5,7,39,40)
 Premotor area (6)

 Controls learned skilled movements and serves as a memory bank for such movements

 Frontal eye field (8)

 Controls voluntary movements of the eyes

Homonculus

The homonculus refers to a miniature “person” represented in each half

(hemisphere) of the brain. The feet start at the top in the middle of the head and (in
general) the parts of the body are inverted from there down to the sides. Again in
general, the sizes of the brain area devoted to each region is related to the sensitivity
and degree of control we have over those parts.
EPIDEMIOLOGY:

 Affects approximately 700,000 American adults per year, 500,000 of this cases are new
ones, the remaining 200,000 are recurrent cases.
 Usually a disease of a aged (>=65 y/o), but in 28% of cases individuals of <65 y/o are
afflicted by the said disease.
 The third leading cause of death in US, it follows next to heart disease and cancer.
 One if the most common neurological diseases in the US, wherein patients are admitted
in the hospital due to neurological disorders.

153 | P a g e
 Blacks living in America are more prone than White, Mexican, anad Native Americans
twice, and between males and females there is a 1.25 : 1 incidence of stroke conditions.
 14 percent of stroke survivors will again experience stroke w/in a year, then after
another year these survivors will experience another attack, then after 5 years for the
third time the patient will experience what is called a “complete stroke”.
 It is said that 1. Increased age 2. Hypertension, 3. Heart disease, 4. and Diabetes
lessens the rate of stroke survivors dramarically.

ETIOLOGY:

 Atherosclerosis- is a major contributory factor in cerebrovascular disease. It is

characterized by plaque formation with an accumulation of lipids, fibrin, complex
carbohydrates and calcium deposits on arterial walls that leads to progressive
narrowing of blood vessels. Interruption of blood flow by atherosclerotic plaque occurs
at certain sites of predilection. These generally include bifurcation, constriction, dilation
or angulations of arteries. The most common sites for lesions to occur are at the origin
of the common carotid artery or at its transition into the middle cerebral artery, at the
main bifurcation of the middle cerebral artery and at the junction of the vertebral arteries
with the basilar artery.
 Ischemic stroke- are the results of a thrombus, embolism or conditions that produce
low systematic perfusion pressures. The 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, a thrombus results from platelet adhesion and
aggregation on plaques.

THROMBOTIC STROKE

 Refers to the formation or development of a blood clot within the cerebral arteries of
their branches
 It is the most common type of stroke that occurs, accounting for 40% of the cases
 Occurs most commonly at night during sleeps or during periods of inactivity
 Extensive and severely impaired
 Affects larger vessels in the absence of good collateral channels

PATHOPHYSIOLOGY:

Interruption of blood flow for only a few minutes sets in motion a series of
pathologic events. Complete cerebral circulatory arrest result in reversible cellular
damage with a core area of focal infarction within minutes. The transitional surrounding
the core is termed the ischemic prenumbra and consist of viable metabolic lethargic
cells. Ischemia triggers a number of damaging and potentially reversible events, termed
ischemic cascade. The release of excess neurotransmitter (glutamate and aspartate)
produces a progressive disturbance of energy metabolism and anoxic depolarization.
This result in an inability of brain cells to produce energy, particularly the adenosine

154 | P a g e
 triphosphate (ATP). This followed by excess influx of calcium ion and pump failure of
neuronal membrane. Excess calcium reacts with intracellular phospholipids to form free
radicals. Calcium influx also stimulates the release of nitric oxide and cytokines. Both
mechanisms further damage the brain cells. The extension of the infarction into the
prenumbra area generally takes places over a period of 3 to 4 hours.

Ischemic stroke 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 to the tissue necrosis and widespread rupture of cell membranes with
movement of water from the blood into the brain tissues. The swelling gradually
subsides and generally disappears by 2 to 3 weeks. Significant edema can elevate
intracranial pressure, leading to intracranial hypertension and neurological deterioration
associated with contralateral and caudal shift of the brain structures (brainstem
herniation). Clinical signs of elevating intracranial pressures include decreasing level of
conciousness (stupor and coma), widened pulse pressure, increased heart rate,
irregular respiration (Cheynes-stokes respiration), vomiting, unreacting pupil (cranial
nerve III signs) and 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 internal carotid artery.

CLINICAL MANIFESTATION:
Based on the cause

THROMBOTIC

 Onsets develops within minutes, hours or days

 60% occur during sleep awakening
 Pt. is unware of the problem so that she falls to the ground when standing from sleep
 Has a temporal profile (warning signs)
 TIA (transient ischemic attack) – deficit occurs in less than 2 hours and disappears after
24 hours
 Comes in any form; (most common), weakness, numbness, neuropathies, disturbance
in the level of sensorium hemeplegia.
 Stroke in evolution; There is progression in the development of new neurologic
symptoms.
 Completed stroke- there is no longer development of new neurologic deficit.

SIGNS AND SYPMTOMS:

Any or all of the ff. may be found:

1. Altered level of consciousness

2. Disturbance in postural bone
3. Sensory dysfunction
4. Intellectual impairment
5. Incontinence
6. Disturbance of communication

155 | P a g e
7. Loss of voluntary movement
8. Visual disturbance
9. Perceptual disorder
10. Primitive reflexes
11. Synergy patterns
12. Shoulder, sublaxation and pain
13. Deconditioning

RISK FACTORS:

1. HTN- 20 DM hypercholesterolemia
2. Valvular dse
3. MI (recent)
4. Bacterial endocarditis
5. Alcoholism
6. Smoking
7. Atrial fibrillation
8. Previous TIA

CLINICAL CHARACTERISTICS OF THE COMMON APHASIC SYNDROME

APHASIA FLUENCY EXPRESSION COMPREHENSION REPETITION NAMING

Broca’s Impaired Impaired Mildly impaired Impaired Impaired
Wernicke’s Normal Impaired Impaired Impaired Impaired
Global Impaired Impaired Impaired Impaired Impaired
Transcortical Impaired Moderately Minimally impaired Normal Impaired
motor impaired
Transcortical Normal Minimally Moderately impaired Normal Impaired
sensory impaired
Transcortical Impaired Impaired Impaired Normal Impaired
mixed
Conduction Normal Impaired Normal Impaired Mildly
impaired
Anemia Normal Normal Normal Normal Impaired

STROKE REHABILITATION

“Rehabilitation can commence as early as 72 hours post stroke once patient is

medically stable”
Goals of Treatment (Acute Stroke)

 Changes associated with recovery are monitored

 Tolerance to positions and activity is increased
 Upright and weight bearing status is improved

156 | P a g e
 Risk of secondary impairments and re-occurrence of condition is reduced
 Joint integrity and mobility is maintained
 Awareness of hemiplegic side and motor function are improved
 Trunk control, symmetry and balance are improved
 Strength, power and endurance are increased
 Functional independence in ADL’s and functional mobility are increased
 Aerobic capacity and endurance increased
 Pt. family and caregiver knowledge and awareness of the diagnosis, prognosis,
interventions and goals and outcomes are increased
 Cared is coordinated with patient, family caregivers and other professionals
 Safety of the patient and family, caregivers are improved
 Placement are determined
 Self management of symptoms is improved
 Sense of well being is improved

Goals of Treatment (Post Acute Stroke)

 Prevent or minimized secondary complication

 Compensate for sensory and perceptual loss
 Promote selective movement control and normalization of postural tone
 Improve postural control and balance
 Develop independent functional mobility skills
 Develop independent ADL’s
 Develop functional cardiorespiratory endurance
 Encourage socialization and motivation

NEUROANATOMICAL CLASSIFICATION

1. Internal Carotid Artery (ICA)

 Occlusion occurs most frequently in the first part of the ICA immediately beyond the
carotid bifurcation
 Often asymptomatic
 Ocular infarction; embolic occlusion of either retinal branch or central retinal artery
 Transient monocular blindness (amaurosis fugax)

 ICA nourishes the optic nerve and retina as well as the brain
 Occurs prior to onset of stroke

 Cerebral Infarction

 presentation of complete ICA occlusion variable, from no symptom to severe , massive

infarction on ACA and MCA

 Contralateral motor or sensory symptoms are present

157 | P a g e
2. Middle Carotid Artery (MCA)

 Occlusion occurs at the stem of middle cerebral or at one of the two divisions of the
artery in the sylvian sulcus
 SUPERIOR DIVISION

 most common cost of occlusion of superior division of MCA is an embolus

 Supplies rolandic and prerolandic area
 Sensory and motor defecits on the contralateral face and arm
 Head and eyes deviated toward to side of infarct
 Left side lesion global aphasia then turns to broca’s aphasia
 Right side lesion deficit ion spatial perception, hemineglect, constructional apraxia,
dressing apraxia
 Muscle tone usually decreased initially and gradually increases over days or weeks to
spasticity

 INFERIOR DIVISION

 Lateral temporal and inferior parietal lobes

 With lesion on the other side – superior quadrantoponia or homonymous hemianopsia
 (L) side lesion – Wernicke’s aphasia
 ® side lesion – Left visual neglect

CLINICAL MANIFESTATION OF MCA SYNDROME

Sign and Symptoms Structure involved

Contralateral hemiparesis UE and face Primary motor cortex
(LE spared)
Contralateral hemisensory loss UE and Primary sensory cortex and internal
face (LE spared) capsule
Motor speech impairment: broca’s or Broca’s cortical area in the dominant
nonfluent aphasia with limited vocabulary hemisphere, typically the left hemisphere
and slow hesitant speech
Receptive speech impairment: Wernicke’s cortical area in the dominant
wernicke’s or fluent aphasia with left hemisphere
impaired auditory comprehension and
fluent speech with normal rate and
melody
Global aphasia non fluent speech with Both third frontal convolution and
poor comprehension posterior portion of the superior temporal
gyrus
Perceptual deficits: unilateral neglect, parietal sensory association cortex in
depth perception, spatial relation and non dominant hemisphere, typically the
agnosia right
Limb-kinetic apraxia Premotor or parietal cortex

158 | P a g e
 Contalateral homonymous in
hemianopsia
Loss of conjugate gaze to the opposite
side
Ataxia of contalateral limb (sensory
ataxia)
Pure motor hemiplegia
Optic radiation in internal capsule
Frontal eye fields or their decending
tracts
Parietal lobe
Upper portion of posterior limb of internal
capsule

3. Anterior Cerebral Artery

 If occlusion is at the stem of the ACA proximal to its connection with anterior
communicating artery. It usually well tolerated because adequate collateral circulation
comes from the artery of the opposite side
 If both ACA arise from one stem, major disturbance occurs during the medial aspects of
both cerebral hemisphere resulting Aphasia, Paraplegia, Incontinence and frontal lobe/
personality dysfunction
 Occlusion of one of ACA distal to anterior communicating arteryresults in:

 Contralateral weakness and sensory loss, affecting mainly distal contralateral leg
 Mild or no involvement of UE; head and eyes may be deviated toward side of lesion
acutely
 Urinary incontinence
 May produce trancortical motor aphasia
 Gait apraxia

CLINICAL MANIFESTATION OF ACA SYNDROME

Sign and Symptoms Structure involved

Contralateral hemiparesis in LE (UE is
impaired)
Contralateral hemisensory in LE
Urinary incontinence
Problems with limitation and bimanual
tasks, apraxia
Abulia, slowness, delay, lack of
spontaneity, motor inaction
Contralateral grasp reflex, sucking reflex Uncertain localization
Primary motor area, medial aspect of
cortex, internal capsule
Primary sensory area, medial aspect of
cortex
Posteromedial aspect of superior frontal
gyrus
Corpus callosum
Uncertain localization

4. Posterior Cerebral Artery

159 | P a g e
 Occlusion on PCA can produce a variety of clinical effect because both of the upper
brainstem and the inferior parts of the temporal lobes and the middle parts of the
occipital lobe are supplied by it.
 Visual field cuts
 Prosopagnosia
 Palinopsia
 Alexia
 Transcortical sensory aphasia

CLINICAL MANIFESTATION OF PCA SYNDROME

Sign and Symptoms Structural involved

Peripheral territory
Contralateral homonymus hemianopsia Primary visual cortex
Bilateral homonymous hemianopsia with Calcarine cortex (macular sparring is due
some degree of macular sparring to occipital pole receiving collateral blood
supply from MCA)
Visual agnosia Left occipital lobe
Prosopagnosia Visual association cortex
Dyslexia Dominant calcarine lesion and posterior
part od corpus callosum
Memory detect Lesion of inferomedial portion of
temporal loe bilaterally or on the
dominant side only
Topographic disorientation Non dominant primary visual area
usually bilateral
Central territory
Central post stroke (thalamic) pain Ventral posterolateral nucleus of
spontaneous pain and dysesthesias, thalamus
sensory impairment (all modalities)
Involuntary movements choreoathetosis, Subthalamic nucleus or its pallidal
intention tremor, hemiballismus connection
Contralateral hemiplegia Cerebral peduncle of midbrain
Occulomotor nerve palsy and 3rd nerve and cerebral peduncle of
contralateral hemiplegia midbrain
Paresis of vertical eye movements slight Supranuclear fiber to 3rd cranial nerve
miosis, ptosis and sluggish papillary light
response

5. Vertebrobasilar Artery

160 | P a g e
 Occlusion of the vertebrobasilar system can produce a wide variety of symptoms with
both ipsilateral and contralateral signs because some of the tracts will crossed and
others will not
 Numerous cerebellar and cranial nerve abnormalities are present

CLINICAL MANIFESTATION OF VERTEBROBASILAR SYNDROME

Syndrome Location Cranial nerve affected

Wallenburg’s Lateral medulla V
Weber’s Medial basal midbrain III
Benedikt’s Tegmentum of the midbrain III
Locked-In Bilateral basal pons
Millard – Gubler Lateral pons VI, VII

CHARACTERISTIC Of ® AND (L) HEMIPLEGIA

® Hemiplegia (L) Hemiplegia

(L) Hemisphere ® Hemisphere
Visuomotor perception and memory Visuomotor perceptual impairment
intact
Visual learning Loss of visual memory
Behavior to be learned should be Left-sided neglect
demonstrated step by step encouraging
limitation
Unable to communicate effectively Impulsive or unorganized in activities of
daily living
Vocabulary and auditory span reduced Lack insight into these problems
Caregivers may assume that the patient Safety problems with many falls
comprehends much more than she/he
does
Limit or eliminate words Lack of insight
Able to pick-up ideas of conversation Inability to follow through
through body language, tone of voice
and facial expression
Able to learn mistake Cannot be trusted
Able to synthesize parts of a task Neglect is more common than right
hemiplegic
Will learn from observing others Vision
Cautious and unorganized when Touch
approaching an unfamiliar situation
Give lot of feedback Proprioception
Visuomotor perceptive and visuomotor Hearing
memory provide ways in which learning

161 | P a g e
 may proceed
Right-sided neglect worsens in response
time
Lack of verbal comprehension
Learn from observing others in the
therapy department
Does not learn from mistakes or
observing others
Learning is impaired
Person’s performance may not improve
Often battles with staff or premature
discharge
Visuomotor perceptual impairment
Loss of visual memory
Left-sided neglect improves
Verbal fluency

DIFFERENTIAL DIAGNOSIS:

 Epilepsy/Seizure- characterized by uncontrolled excessive activity of either a part of all

of central nervous system.

3. types of epilepsy:

1. GRAND MAL- characterized by extreme neuronal discharges in all areas of the brain.

Causes: strong emotional stimuli, alkalosis caused by over breathing, drugs, fever, and
loud noises.

2. PETIT MAL- involves the basic thalamocortical brain activating system, the person who
has this kind of epilepsy shows twitch-like contraction of the muscles.
3. FOCAL- affects localized regions of the cerebral cortex or deeper structures of both
cerebrum and brain stem.

 MULTIPLE SCLEROSIS (MS)- chronic inflammatory, demyelinating disease of the

central nervous system.
 Patient who had confusion caused by drugs, alcohol, or metabolic abnormalities.
 Brain tumor or subdural hematoma.
 Encephalitis, labyrinthins, brain abscess, hypoglycemia, migraine, hysterical or
psychogenic symptoms.

PROGNOSIS:

 Recovery from stroke is generally fastest in the 1st weeks after onset.
 Reduction of edema, absorption of damage tissues, and improved local circulation and
cellular metabolism allows intact neurons that were previously inhibited to regain its
function.
 Prolonged recovery with improvements occurring a period of years is especially
apparent in the areas of language and visuospatial function.

162 | P a g e
 Patient with small lacunar strokes demonstrate improved motor recovery over patient
with large hemispheric lesions
 Functional mobility skills are impaired following stroke and vary considerably from
individual to individual.
 Motor and perceptual impairments have the greatest impact on functional performance.

PATTERNS OF RECOVERY OF STROKE:

1. Return of DTR within 48 hours.

2. Gradual continuous progression from flaccidity- spasticity- normal muscle tone.
3. Complete motor paralysis- synergy pattern- voluntary segmental movement.
4. Synergy pattern are mass composite movement.

POOR PROGNOSTIC INDICATION FOR FUNCTIONAL RECOVERY:

1. Prolonged flaccidity
2. Late onset of motion (2-4 weeks)
3. No voluntary hand movement at 4-6 weeks
4. Severe proximal spasticity
5. Late return of DTR

POOR PROGNOSTIC INDICATION FOR NEUROLOGIC RECOVERY:

1. Previous stroke
2. Urinary and bowel incontinence
3. Old age
4. Visuospatial deficits

FATALITY RATE:
Atherothrombic brain infarction - 15%
Cerebral – embolus -16%
Subarchnoid hemorrhage -46%
Intracerebral hemorrhage -82%
Approximate overall rate -22%

MEDICAL MANAGEMENT:

GEN. MEDICAL MANAGEMENT:

163 | P a g e
 Improve cerebral perfusion by reestablishing circulation and oxygenation is delivered via
mask or nasal cannula. Patient in a coma may require intubation or assisted ventilation
and suctioning.
 Maintain adequate blood pressure. Hypertension or extreme hypertension is treated;
anti hypertension agents have the added risk of inducing hypotension and decreasing
cerebral perfusion.
 Maintain sufficient cardiac output (CO), if the causes of stroke are cardiac in origin ,
medical management focuses on control of arrhythmias and cardiac decompensation.
 Restore/maintain fluid and electrolyte balance.
 Maintain blood glucose levels within the normal range.
 Control seizures and infections.
 Control intracranial pressures and herniation using anti edema agents.Ventriculostomy
maybe indicated to monitor and drain cerebrospinal fluid.
 Maintain bladder function, which may include urinary catheter. Catheterization is
typically short- term but may be long- term with the patient in coma.
 Maintain integrity of skin and joints by instituting protective positioning; a turning
schedule every 2 hours; and early physical and occupational therapy.
 Family should be in full support of the patient to avoid psychological effect such as
depression .

PHARMACOLOGICAL INTERVENTION :

 Anticoagulant Therapy – used to improved perfusion and reduced the risk of recurring
clots (embolism and thrombosis); clotting times are monitored as there is an increased
risk of bleeding.
 Ex. Heparin
 Coumadin- 10 mg daily and therafter (usually 2-4 days) adjusted according to
prothrombin time.
 Antiplatelet Therapy- long-term, low dose is used to decrease the risk of the recurrent
stroke: higher doses may be used in place of anticoagulants and may be recommended
for patient with atrial fibrillation.
 Ex. Aspirin – 160-300 mg/day
 Dipyridamole – 400 mg daily
 *or combination of 2, but giving combination can result to headache.
 Diuretics-reduces water content in the brain
 Ex. Furosemide- lasix: adult- initially 0.5-2 tab. Daily, maintenance 0.5-1 tab. Daily
 Children – 2 mg/kg body wt. up to a max of 40 mg daily
 Hyperosmolar agents- if (+) edema or swelling in the brain
 Ex. IV-mannitol
 Vasodilators(papaverine)


NEUROSURGICAL INTERVENTION:

164 | P a g e
 Endarterectomy which is the surgical removal of the lining and plaque of artery.
Internal carotid artery stenosis affect approximately 25% of elderly persons. It is used to
prevent stroke but not to treat acute srtokes.
 Surgery can be used to repair a superficial ruptured aneurysm or AVM, prevent
rebleeding, and evacuate a clot. Larger, deeper intracranial or brainstem vascular
lesions are generally not amendable to surgery.
 Angioplasty a balloon-tipped catheter is place at the base of the aneurysm, isolating it
from the circulation of the artery to which it attached. This can keep the aneurysm from
bursting, or it can prevent re-bleeding of aneurysm that has recently hemorrhage.
 Aneurysm clipping a tiny clamp is placed at the base of the aneurysm, isolating it from
the circulation of the artery to which is attached. This can keep the aneurysm from
bursting, or it can prevent re-bleeding of aneurysm that has recently hemorrhage.

PHYSICAL THERAPY INTERVENTION:

 Proper bed positioning

 ES/FES
 ROM exercises
 PRE’s exercises
 Tilt table
 Parallel bar exercises
 PNF
 NDT’s

 BOBATH – use of specific posture appropriate for tasks, while suppressing synergies
with sensory input and motor feedback.
 BRUNNSTROM – Enhance use of synergies through the use of cutaneous and
proprioceptive stimuli
 ROODS – Modification of muscle tone and voluntary motor activity through the use of
cutaneous sensory stimuli.
 KABAT, KNOT, & VOSS – Uses reflexes and patterning technique for proprioceptive
neuromuscular facilitation.

 CYCLING/ERGOMETER
 ORTHOSIS- e.g ADA (ankle dorsiflexion assist), AFO (ankle-foot orthosis)
 ASSISTIVE DEVICES – e.g standard cane , quad cane

STROKE IN ELDERLY

 Stroke onset in the young more favorable prognosis for long and short survival.
 Effect of age for functional recovery not yet well established.
 Elderly more likely to have other associated medical problems and limited social
supports.

165 | P a g e
 Thus, older adult stroke patients usually require more medical monitoring, longer
recovery time, reduced exercise intensities and more psychological support during
rehabilitation compared to younger stroke patient.

STROKE IN YOUNG ADULT

 Estimated 1/3 of stroke patient are <65 yrs.old.

 25% of strokes affect individuals between 45-65 y/o; where hemorrhagic strole is more
common in the young

OTHER CAUSES OF CEREBRAL INFARCTION:

1. Atherosclerosis (20%)
2. Cardiogenic embolism (CHD and atrial fibrillation)
3. Cerebral vasculitis (10%)
4. Coagulopathy (10%)

 Rehabilitation program must address the issue of employment, sexuality, child care and
parenting.

PEDIATRIC STROKE

 Rare, incidence of 2.5 per 100,000 children per year.

 Clinical presentation usually different
 Manifest with seizure, fever and delayed developmental milestone.
 May be as a result of hereditary conditions, CHD, metabolic d/o, coagulopathy, drugs,
intracerebral vascular abnormalities.
 Prognosis is better than adults but residual deficit are common.
 Focus of rehabilitation: functional restoration and compensation, psychosocialsupport
and attainment of normal developmental skills.

166 | P a g e
 Initial Evaluation
General information
Patients Name: MJ
Age: 70years old
Address: 214 M. Clara ST. Samp. Manila
Sex: Male
Civil Status: Married
Handedness: Right Handedness
Occupation: Retired Police
Referring Unit: USTH
Rehabilitation Unit: USTH (PT Rehab)
Reffering M.D.: Dr. O.A.
Rehabilitation M.D.: Dr.F.U.
Date of Admission: Aug. 14, 2013
Date of Referral: Aug. 17, 2013
Date of PT Consultation: Aug. 17, 2013
Date of IE: Aug. 17, 2013
Diagnosis: ® CVA (L) Hemiparesis (Thrombotic)
Informant/Reliability: Wife/Good

HPI :
Present condition started 1 day PTA when pt. attended their family reunion at
night. As the party goes on the pt. enjoyed eating particularly fatty foods and drink a lot
of alcohol (~ 5 bottles of rhum) together with his relatives. When the party ends, they go
back home and sleep immediately
On the day of admission several hours around 10:00am, when the pt. wakes up
he falls to the floor, he shouted for help because of the numbness at the (L) UE &
LE.His wife checks his BP (180/ 120 mmHg) and gives metoprolol and decided to go to
the hospital.
On the hospital the pt.’s vital signs check and ancillary procedures were done
(see ancillary) & some medicines gave to him like urolynase & catapress. He was
admitted for 3 days for observation and when thept. becomes stable, he was now the
referred to for further evaluation

Ancillary procedure:

167 | P a g e
Diagnostic procedure Findings Date

MRI hypodense on ® MRI Aug. 14, 2013

Laboratory exams
Examination
Normal Value Findings Date
Hct 40-50% 55% Aug. 14,
2013
RBC 135-=180g/L 185% Aug. 14,
2013
WBC 4.5-11k/mL 4.6k/mL Aug.
14, 2013
Basophil 0.0-0.1 0.1 Aug. 14,2013
Eosinophil 0.02- 0.05 0.4 Aug.
14,2013
Neutrophil 0.05-0.07 0.60 Aug. 14,2013

Present Medication
Name of Drugs Frequency Dosage
Indication

Urokynase bid 1.5 million IU (45 mL NaCl)

Thrombolytics
AS\SPIRIN OD 500mg
anticoagulants

Past Medical History:

(+) Htn (controlled, since 2005, Metoprolol,bid)

Baseline: 150/90 mm/Hg

Highest: 165/95 mm/Hg
Lowest: 130/90 mm/Hg

(-) hospitalization
(-) DM
(-) tumor
(-) seizure
(-) pulmonary problem
(-) cardiac condition
(-) TIA

FMHx
Father Mother

168 | P a g e
Htn (+) (+)
DM (-) (-)
Cardiac condition (-) (-)
Pulmonary problem (-) (-)
Seizure (-) (-)

PSEHx

 Type b personality
 Sedentary lifestyle
 Financially stable
 (+) smoker (~ 40 sticks/year)
 (+) alcohol beverage drinker (~8 bottles; rhum, beer; occasionally
 live in a 2 storey house with his wife and son
 diet includes: meat, vegetables, fats
 hobbies includes: reading, watching TV
 home set-up
o a flight of stair with ceramic handrails on (b) sides
o 12 steps of stairs
o Pt.’s room located on 2nd floor
 ~14 steps from room to CR
 ~15 steps from room to dining area
 ~17 steps from room to kitchen
 ~14 steps from room to living room

Patient’s c/c: “hirap dawn yang igalaw ang kaliwang bahagi ng kanyang katawan dahil
sa panghihina “ as verbalized by his wife.
PT tanslation: I Difficulty in moving d/t (m) weakness
Patient’s Goal: to be able to do again his (n) ADL

O
VITAL SIGNS(VS):
before during
after
BP 140/80mmHg 130/80mmHg
120/80mmHg
RR 17cpm 19cpm
17cpm
PR 75bpm 80bpm
75bpm
Temp. afebrile to touch

Significance: for baseline purposes

169 | P a g e
OCULAR INSPECTION (OI):

 Bed bound
 Alert, coherent cooperative
 Oriented in time, place, situation
 Mesomorph
 (+) tongue deviation to the ®
 (+) sialorrhea
 (+) aphasia
 (+) cortical thumb
 (-) respiratoty distress
 (+) atrophy
 (-) pressure sore
 (-) swelling

PALPATION:

 Normothermic in all exposed body parts

 (N) skin turgor & mobility
 (-) tenderness
 (-) (m) spasm
 (-) shoulder subluxation

(-) Crepitus
(-) Subluxation/dislocation
(-) Muscle guarding/Spasm

NEUROLOGIC EXAMINATION

Tone:
Finding: normotonic on ® UE and LE and hypotonic on (L) UE and LE
Significance: Secondary to UMNL

Modified Ashworth Scale

Grade: 3- Considerable increase in muscle tone, passive movement is difficult.

A. Sensory A.

b.1 Superficial Somatic Sensation

STD used: Superficial Pain – pinprick
Light Touch – wisp of cotton
Thermal sensation – hot/cold using test tube

170 | P a g e
Findings: 100% sensory intact on ® side of the body while 30% sensory intact on (L)
side of the body
Significance: Secondary to lesion on B.A. 3,1,2

b.Deep Somatic Sensation

Findings: (+) proprioception, kinesthesia, deep somatic sensation & vibratory sense
Significance: Secondary to lesion on B.A. 5,7

b.3. Cortical/Central Integrative sensation

Findings: (+) stereognosis, graphesthesia, bilat. Cutaneous tactile localization

Significance: intact thalamocortical system

MSR/DTR (Muscle stretch reflex/ Deep Tendon reflex

++ +++
++ +++
++ +++

++ +++

++ +++

Findings: normoreflexia on right UE and LE

hypereflexia on left UE and LE

Significance: secondary to increase firing of gamma motor neuron

Pathologic Reflex

Reflex Response
Babinski fanning of fingers
Hoffman’s flexion of fingers
Chaddocks flexion of wrist and fanning of fingers

Findings: (-) babinski, Hoffman;s and chaddocks

Significance: secondary to UMNL
171 | P a g e
Cranial Nerve Testing

Findings: intact in all CN

Significance: (-) affectation on brainstem

ROM (RANGE OF MOTION)

ROM
All joints of (B) UE and LE are WNL actively and passively done, pain free
c (N) endfeel, except for the following
Motion Normal Active Passive Difference Endfeel
value
(R) (L) (R) (L) Activ Passi
e ve
Shoulder:
Flexion 0-180˚ 0- 0- 0- 0- 80˚ 0 Ms. Flaccidity
13 100 180 180
0˚ ˚ ˚ ˚
Extension 0-60˚ 0- 0- 0- 0- 30˚ 0 Ms. flaccidity
60˚ 30˚ 60˚ 60˚
Abduction 0-180˚ 0- 0- 0- 0- 90˚ 0 Ms. flaccidity
18 0˚ 180 180
0˚ ˚ ˚
Elbow:
Flexion 0-150˚ 0- 0- 0- 0- 85˚ 0 Ms. flaccidity
15 65˚ 150 150
0˚ ˚ ˚
Extension 150-0˚ 15 65- 150 150 85˚ 0 Ms. flaccidity
0- 0˚ -0˚ -0˚
0˚
Pronation 0-80˚ 0- 0- 0- 0- 20˚ 0 Ms. flaccidity
80˚ 60˚ 80˚ 80˚
Supination 0-80˚ 0- 0- 0- 0- 20˚ 0 Ms. flaccidity
80˚ 60˚ 80˚ 80˚
Wrist: Ms. flaccidity
Flexion 0-80˚ 0- 0- 0- 0- 30˚ 0 Ms. flaccidity
80˚ 50˚ 80˚ 80˚
Extension 0-70˚ 0- 0- 0- 0- 30˚ 0 Ms. flaccidity
70˚ 40˚ 70˚ 70˚
Radial 0-20˚ 0- 0- 0- 0- 10˚ 0 Ms. flaccidity
deviation 20˚ 10˚ 20˚ 20˚
Ulnar 0-30˚ 0- 0- 0- 0- 10˚ 0 Ms. flaccidity
deviation 30˚ 20˚ 30˚ 30˚
MCP: Ms. flaccidity
Flexion(2nd- 0-90˚ 0- 0- 0- 0- 30˚ 0 Ms. flaccidity
th
5 ) 90˚ 60˚ 90˚ 90˚

172 | P a g e
Extension(2nd 0-45˚ 0- 0- 0- 0- 15˚ 0 Ms. flaccidity
-5th) 45˚ 30˚ 45˚ 45˚
PIP: Ms. flaccidity
Flexion(2nd- 0-100˚ 0- 0- 0- 0- 60˚ 0 Ms. flaccidity
5th) 10 40˚ 100 100
0˚ ˚ ˚
Extension(2nd 100-0˚ 10 70- 100 100 30˚ 0 Ms. flaccidity
-5th) 0- 0˚ -0˚ -0˚
0˚
DIP: Ms. flaccidity
Flexion(2nd- 0-90˚ 0- 0- 0- 0- 50˚ 0 Ms. flaccidity
5th) 90˚ 40˚ 90 90˚
Extension(2nd 90-0˚ 40- 40- 90- 90- 50˚ 0 Firm
-5th) 0˚ 0˚ 0˚ 0˚
1st CMC:
Flexion 0-15˚ 0- 0- 0- 0- 10˚ 0 Firm
5˚ 5˚ 15˚ 15˚
Extension 0-20˚ 0- 0- 0- 0- 10˚ 0 Firm
10˚ 10˚ 20˚ 20˚
Abduction 0-70˚ 0- 0- 0- 0- 40˚ 0 Firm
30˚ 30˚ 70˚ 70˚
Adduction 70-0˚ 30- 30- 70- 70- 40˚ 0 Firm
0˚ 0˚ 0˚ 0˚

Motion (N) value Active Passive Difference End Feel

(R) (L) (R) (L) Activ Passive
e
Hip:
Flexion 0-120˚ 0- 0- 0- 0- 100˚ 0 Soft
20˚ 20˚ 120˚ 120˚
Extension 0-30˚ 0- 0- 0-30˚ 0-30˚ 20˚ 0 Firm
10˚ 10˚
Abduction 0-45˚ 0- 0- 0-45˚ 0-45˚ 25˚ 0 Firm
20˚ 20˚
Adduction 0-30˚ 0- 0- 0-30˚ 0-30˚ 0 0 Firm
30˚ 30˚
IR 0-45˚ 0- 0- 0-45˚ 0-45˚ 20˚ 0 Firm
25˚ 25˚
ER 0-45˚ 0- 0- 0-45˚ 0-45˚ 25˚ 0 Firm
20˚ 20˚
Knee:
Flexion 0-135˚ 0- 0- 0- 0- 115˚ 0 Soft
20˚ 20˚ 135˚ 135˚
Extension 135-0˚ 20- 20- 135- 135- 115˚ 0 Firm
0˚ 0˚ 0˚ 0˚

173 | P a g e
Ankle:
PF 0-50˚ 0- 0- 0-50˚ 0-50˚ 20˚ 0 Firm
30˚ 30˚
DF 0-20˚ 0- 0- 0-20˚ 0-20˚ 5˚ 0 Firm
15˚ 15˚
Tarsal jt. 0-35˚ 0- 0- 0-35˚ 0-35˚ 20˚ 0 Firm
Inversion 15˚ 15˚
Tarsal jt. 0-15˚ 0- 0- 0-15˚ 0-15˚ 5˚ 0 Hard
Eversion 10˚ 10˚
Transverse 0-20˚ 0- 0- 0-20˚ 0-20˚ 10˚ 0 Firm
tarsal jt. 10˚ 10˚
Inversion
Transverse 0-10˚ 0-5˚ 0-5˚ 0-10˚ 0-10˚ 5˚ 0 Firm
tarsal jt.
Eversion

Facial MMT

 Smiling WF
 Frowning F
 Wrinkling of nose and forehead F
 Surprised F
 Pouting WF

Finding: all (m) of facial expression are graded except for smiling and pouting which
is WF
Significance: secondary to ms. Flaccidity

ADL:
Fully Dependent Partially Dependent Independent
Self-care:
Bathing / c 1 man assist
Toileting / c 1 man assist
Eating c mod. difficulty
Grooming: c mod. difficulty
UE dressing / c 1 man assist
LE dressing / c 1 man assist c mod. difficulty
Bed mobility:
Supine-side lying c mod. difficulty
Supine-long sitting c mod. difficulty
Rolling c mod. difficulty
Transfers:
w/cmat / c 1 man assist

174 | P a g e
 Bedw/c / c 1 man assist
Ambulation Cannot erformed

Findings: All ADL’s can performed independently c mod. Difficulty except for bathing,
toileting, UE/LE dressing, w/c to mat, bed to w/c, ambulation which is partially
dependent c one man assist
Significance: 2˚ flaccidity
A:
PT Impression: Stage 1 in Braddom
Rehab Potential: Good prognosis d/t early intervention.
Rehab Concern: To increase the strength & to return to his normal doings
Rehab Precaution: Pt is hypertensive
Problem List:
1. LOM on (L) UE & LE
2. Facial asymmetry deviated to the ®
3. Tongue deviation
4. Sialorrhea
5. Ms. Weakness on (L) UE& LE
6. ADL problems
Problem list
1.To prevent 2˚ complication as to contracture, pressure sore and atrophy.
2.To prevent onset of respiratory distress and DVT.
3.To increase functional muscle strength of UE and LE without difficulty.
4.To attain the highest functional capabilities of the pt as to ADL.
5.To achieve normal balance and tolerance as to standing.

LTG ( 3mons)
1. To prevent complication such as contracture, pressure sore and atrophy
2. To maintain strength & improves endurance
3. To attain highst highest functional level of the pt. as to ADL from independent c
mod. Difficulty to independent s difficulty

STG( 3weeks)
1. To increase ROM by ~ 10 increment of ® UE & LE
2. To increase ms. Strenght of (L) UE from 3-/5 to 4/5 &® LE from 3+/5 to 4/5
3. To improve ADL to fully independent
P
PT Management:
1. AAROME to AROME on (L) UE & LE x 10 reps x 1 set
2. Facial Massage x 5mins
3. PRE’s on ® UE & LE
4. ES on the face UE/LE x 90 cxn.
5. Tongue exercise ( tongue twister)

Home Instruction:

175 | P a g e
 1. Turning every 2 hours and proper bed positioning
2. Provide support from the family member for motivation
3. Home modification
4. Do exercise taught by the PT.

_________________
Credo, Nikki Jane T.
UDM/Batch 2015

_________________
Giray, Ann Mae
UDM/Batch 2015

POLIOMYELITIS
Blanco Mary Joy P.

 An acute infection caused by a group of enterovirus which attacks the GIT

principally and the nervous system secondarily
 Aka Heine-Medin disease , Acute Anterior Poliomyelitis , Infantile Paralysis
 often called polio or infantile paralysis, is an acute, viral, infectious disease spread
from person to person, primarily via the fecal-oral route
 An acute viral infection in which anterior horn cell of the spinal cord and motor nuclei
of the brain stem are selectively involved.

Related Anatomy :

Respiratory system

Parts of the respiratory system

Lungs

176 | P a g e
 The lungs are the main organs of the respiratory system. In the lungs oxygen is
taken into the body and carbon dioxide is breathed out. The red blood cells are
responsible for picking up the oxygen in the lungs and carrying the oxygen to all the
body cells that need it. The red blood cells drop off the oxygen to the body cells, then
pick up the carbon dioxide which is a waste gas product produced by our cells. The red
blood cells transport the carbon dioxide back to the lungs and we breathe it out when
we exhale.

Trachea

The trachea (TRAY-kee-uh} is sometimes called the windpipe. The trachea filters the
air we breathe and branches into the bronchi.

Bronchi

The bronchi (BRAHN-ky) are two air tubes that branch off of the trachea and carry
air directly into the lungs.

Diaphragm

Breathing starts with a dome-shaped muscle at the bottom of the lungs called the
diaphragm (DY-uh-fram). When you breathe in, the diaphragm contracts. When it
contracts it flattens out and pulls downward. This movement enlarges the space that the
lungs are in. This larger space pulls air into the lungs. When you breathe out, the
diaphragm expands reducing the amount of space for the lungs and forcing air out. The
diaphragm is the main muscle used in breathing.

THE LYMPHATIC SYSTEM

Major lymphatic ducts.

The lymphatic system aids the immune system in removing and destroying waste,
debris, dead blood cells, pathogens, toxins, and cancer cells.

The lymphatic system absorbs fats and fat-soluble vitamins from the digestive system
and delivers these nutrients to the cells of the body where they are used by the cells.

The lymphatic system also removes excess fluid, and waste products from the
interstitial spaces between the cells.

THE TRANSFORMATION

Arterial blood carries oxygen, nutrients, and hormones for the cells. To reach these cells
it leaves the small arteries and flows into the tissues. This fluid is now known as

177 | P a g e
interstitial fluid and it delivers its nourshing products to the cells. Then it leaves the cell
and removes waste products.

After this task is complete, 90% of this fluid returns to the circulatory system as venous
blood.

LYMPH

The remaining 10% of the fluid that stays behind in the tissues as a clear to yellowish
fluid known as lymph.

Unlike blood, which flows throughout the body in a continue loop, lymph flows in only
one direction within its own system. This flow is only upward toward the neck. Here, it
flows into the venous blood stream through the subclavien veins which are located on
either sides of the neck near the collarbones.

After plasma has delivered its nutrients and removed debris, it leaves the cells. 90% of
this fluid returns to the venous circulation through the venules and continues as venous
blood.

The remaining 10% of this fluid becomes lymph which is a watery fluid that contains
waste products. This waste is protein-rich due to the undigested proteins that were
removed from the cells.

LYMPHATIC CIRCULATION

The lymph is moved through the body in its own vessels making a one-way journey
from the interstitial spaces to the subclavian veins at the base of the neck.

Since the lymphatic system does not have a heart to pump it, its upward movement
depends on the motions of the muscle and joint pumps.

As it moves upward toward the neck the lymph passes through lymph nodes which filter
it to remove debris and pathogens.

The cleansed lymph continues to travel in only one direction, which is upward toward
the neck.

At the base of the neck, the cleansed lymph flows into the subclavian veins on either
side of the neck.

THE ORIGIN OF LYMPH

178 | P a g e
Lymph originates as plasma (the fluid portion of blood). The arterial blood, which flows
out of the heart, slows as it moves through a capillary bed. This slowing allows some
plasma to leave the arterioles (small arteries) and flow into the tissues where it
becomes tissue fluid.

Also known as extracellular fluid, this is fluid that flows between the cells but is not into
the cells. This fluid delivers nutrients, oxygen, and hormones to the cells.

As this fluid leaves the cells, it takes with it cellular waste products and protein cells.

Approximately 90% of this tissue fluid flows into the small veins. Here it enters the
venous circulation as plasma and continues in the circulatory system.

The remaining 10% of the fluid that is left behind is known as lymph.

LYMPHATIC CAPILLARIES

In order to leave the tissues, the lymph must enter the lymphatic system through
specialized lymphatic capillaries. Approximately 70% of these are superficial capillaries
located near, or just under, the skin. The remaining 30%, which are known as deep
lymphatic capillaries, surround most of the body’s organs.

Lymphatic capillaries begin as blind-ended tubes that are only a single cell in thickness.
These cells are arranged in a slightly overlapping pattern, much like the shingles on a
roof. Each of these individual cells is fastened to nearby tissues by an anchoring
filament.

LYMPHATIC VESSELS

The lymphatic capillaries gradually join together to form a mesh-like network of tubes
that are located deeper in the body.

As they become larger, and deeper, these structures become lymphatic vessels.

Deeper within the body the lymphatic vessels become progressively larger and are
located near major blood veins.

Like veins, the lymphatic vessels, which are known as lymphangions, have one-way
valves to prevent any backward flow.

Smooth muscles in the walls of the lymphatic vessels cause the angions to contract
sequentially to aid the flow of lymph upward toward the thoracic region. Because of their
shape, these vessels are previously referred to as a string of pearls.

179 | P a g e
LYMPH NODES

Lymph nodes kill pathogens and cancer cells. They also

remove debris and excess fluids. Lymph Notes.com

There are between 600-700 lymph nodes present in the average human body. It is the
role of these nodes to filter the lymph before it can be returned to the circulatory system.
Although these nodes can increase or decrease in size throughout life, any nodes that
has been damaged or destroyed, does not regenerate.

Afferent lymphatic vessels carry unfiltered lymph into the node. Here waste products,
and some of the fluid, are filtered out.

In another section of the node, lymphocytes, which are specialized white blood cells, kill
any pathogens that may be present. This causes the swelling commonly known as
swollen glands.

Lymph nodes also trap and destroy cancer cells to slow the spread of the cancer until
they are overwhelmed by it.

Efferent lymphatic vessels carry the filtered lymph out of the node so that it can continue
its return to the circulatory system.

The Spinal Cord is connected to the brain and is about the diameter of a human finger.
From the brain the spinal cord descends down the middle of the back and is surrounded
and protected by the bony vertebral column. The spinal cord is surrounded by a clear
fluid called Cerebral Spinal Fluid (CSF), that acts as a cushion to protect the delicate
nerve tissues against damage from banging against the inside of the vertebrae.

The anatomy of the spinal cord itself, consists of millions of nerve fibres which transmit
electrical information to and from the limbs, trunk and organs of the body, back to and
from the brain. The nerves which exit the spinal cord in the upper section, the neck,
control breathing and the arms. The nerves which exit the spinal cord in the mid and
lower section of the back, control the trunk and legs, as well as bladder, bowel and
sexual function.

180 | P a g e
The nerves which carry information from the brain to muscles are called Motor
Neurones. The nerves which carry information from the body back to the brain are
called Sensory Neurones. Sensory Neurones carry information to the brain about skin
temperature, touch, pain and joint position.

The brain and spinal cord are referred to as the Central Nervous System, whilst the
nerves connecting the spinal cord to the body are referred to as the Peripheral Nervous
System.

Ascending and Descending Spinal Tracts

The nerves within the spinal cord are grouped together in different bundles called
Ascending and Descending tracts.

Ascending tracts within the spinal cord carry sensory information from the body,
upwards to the brain, such as touch, skin temperature, pain and joint position.

Descending tracts within the spinal cord carry information from the brain downwards to
initiate movement and control body functions.

Spinal Nerves

Nerves called the spinal nerves or nerve roots, branch off the spinal cord and pass out
through a hole in each of the vertebrae called the Foramen. These nerves carry
information from the spinal cord to the rest of the body, and from the body back up to
the brain.

There are four main groups of spinal nerves, which exit different levels of the spinal
cord.

These are in descending order down the vertebral column:

Cervical Nerves "C" : (nerves in the neck) supply movement and feeling to the arms,
neck and upper trunk. Also control breathing.

Thoracic Nerves "T" : (nerves in the upper back) supply the trunk and abdomen.

Lumbar Nerves "L" and Sacral Nerves "S" : (nerves in the lower back) supply the
legs, the bladder, bowel and sexual organs.

Spinal Cord Level Numbering System

The spinal nerves carry information to and from different levels (segments) in the spinal
cord. Both the nerves and the segments in the spinal cord are numbered in a similar
way to the vertebrae. The point at which the spinal cord ends is called the conus
medullaris, and is the terminal end of the spinal cord. It occurs near lumbar nerves L1

181 | P a g e
and L2. After the spinal cord terminates, the spinal nerves continue as a bundle of
nerves called the cauda equina. The upper end of the conus medullaris is usually not
well defined.

There are 31 pairs of spinal nerves which branch off from the spinal cord. In the cervical
region of the spinal cord, the spinal nerves exit above the vertebrae. A change occurs
with the C7 vertebra however, where the C8 spinal nerve exits the vertebra below the
C7 vertebra. Therefore, there is an 8th cervical spinal nerve even though there is no 8th
cervical vertebra. From the 1st thoracic vertebra downwards, all spinal nerves exit
below their equivalent numbered vertebrae.

The spinal nerves which leave the spinal cord are numbered according to the vertebra
at which they exit the spinal column. So, the spinal nerve T4, exits the spinal column
through the foramen in the 4th thoracic vertebra. The spinal nerve L5 leaves the spinal
cord from the conus medullaris, and travels along the cauda equina until it exits the 5th
lumbar vertebra.

The level of the spinal cord segments do not relate exactly to the level of the vertebral
bodies i.e. damage to the bone at a particular level e.g. L5 vertebrae does not
necessarily mean damage to the spinal cord at the same spinal nerve level.

Spinal Cord Nerve Levels

182 | P a g e
 Diagram Showing The Relationship Between Spinal Nerve Roots and Vertebrae

Epidemiology :

 Between the ages of 1-5 years (most common) through no age is immune
 80-90 % of the cases produces of mild illness lasting 1-3 days
 Causes a major illness to paralysis , which maybe mild or severe widespread and
permanent
 Affects children and young adults

Etiology

Poliovirus and enterovirus belonging to picorna group exist in 3 immunoligal

6.Brunhilde- most paralytic

7.Lansing-2nd most paralytogenic and frequent
8.Leon-least frequent type

Predisposing factor :

 Age
 Climate
 Oral surgery

183 | P a g e
 Lactation and pregnancy
 Patent respiratory tract infection
 Fatigue and overexcretion

Pathophysiology :

Poliovirus enters the body through the mouth, infecting the first cells with which it comes
in contact — the pharynx and intestinal mucosa. It gains entry by binding to an
immunoglobulin-like receptor, known as the poliovirus receptor or CD155, on the cell
membrane.The virus then hijacks the host cell's own machinery, and begins to replicate.
Poliovirus divides within gastrointestinal cells for about a week, from where it spreads to
the tonsils (specifically the follicular dendritic cells residing within the tonsilar germinal
centers), the intestinal lymphoid tissue including the M cells of Peyer's patches, and the
deep cervical and mesenteric lymph nodes, where it multiplies abundantly. The virus is
subsequently absorbed into the bloodstream.

Known as viremia, the presence of virus in the bloodstream enables it to be widely

distributed throughout the body. Poliovirus can survive and multiply within the blood and
lymphatics for long periods of time, sometimes as long as 17 weeks. In a small
percentage of cases, it can spread and replicate in other sites, such as brown fat, the
reticuloendothelial tissues, and muscle. This sustained replication causes a major
viremia, and leads to the development of minor influenza-like symptoms. Rarely, this
may progress and the virus may invade the central nervous system, provoking a local
inflammatory response. In most cases, this causes a self-limiting inflammation of the
meninges, the layers of tissue surrounding the brain, which is known as nonparalytic
aseptic meningitis. Penetration of the CNS provides no known benefit to the virus, and
is quite possibly an incidental deviation of a normal gastrointestinal infection. The
mechanisms by which poliovirus spreads to the CNS are poorly understood, but it
appears to be primarily a chance event—largely independent of the age, gender, or
socioeconomic position of the individual.

Paralytic polio

Denervation of skeletal muscle tissue secondary to poliovirus infection can lead to

paralysis.

In around 1% of infections, poliovirus spreads along certain nerve fiber pathways,

preferentially replicating in and destroying motor neurons within the spinal cord, brain
stem, or motor cortex. This leads to the development of paralytic poliomyelitis, the
various forms of which (spinal, bulbar, and bulbospinal) vary only with the amount of
neuronal damage and inflammation that occurs, and the region of the CNS affected.

184 | P a g e
The destruction of neuronal cells produces lesions within the spinal ganglia; these may
also occur in the reticular formation, vestibular nuclei, cerebellar vermis, and deep
cerebellar nuclei.[ Inflammation associated with nerve cell destruction often alters the
color and appearance of the gray matter in the spinal column, causing it to appear
reddish and swollen. Other destructive changes associated with paralytic disease occur
in the forebrain region, specifically the hypothalamus and thalamus. The molecular
mechanisms by which poliovirus causes paralytic disease are poorly understood.

Early symptoms of paralytic polio include high fever, headache, stiffness in the back and
neck, asymmetrical weakness of various muscles, sensitivity to touch, difficulty
swallowing, muscle pain, loss of superficial and deep reflexes, paresthesia (pins and
needles), irritability, constipation, or difficulty urinating. Paralysis generally develops one
to ten days after early symptoms begin, progresses for two to three days, and is usually
complete by the time the fever breaks.

The likelihood of developing paralytic polio increases with age, as does the extent of
paralysis. In children, nonparalytic meningitis is the most likely consequence of CNS
involvement, and paralysis occurs in only one in 1000 cases. In adults, paralysis occurs
in one in 75 cases.In children under five years of age, paralysis of one leg is most
common; in adults, extensive paralysis of the chest and abdomen also affecting all four
limbs — quadriplegia — is more likely.Paralysis rates also vary depending on the
serotype of the infecting poliovirus; the highest rates of paralysis (one in 200) are
associated with poliovirus type 1, the lowest rates (one in 2,000) are associated with
type 2.

Prognosis

Patients with abortive polio infections recover completely. In those who develop only
aseptic meningitis, the symptoms can be expected to persist for two to ten days,
followed by complete recovery. In cases of spinal polio, if the affected nerve cells are
completely destroyed, paralysis will be permanent; cells that are not destroyed, but lose
function temporarily, may recover within four to six weeks after onset. Half the patients
with spinal polio recover fully; one-quarter recover with mild disability, and the remaining
quarter are left with severe disability.The degree of both acute paralysis and residual
paralysis is likely to be proportional to the degree of viremia, and inversely proportional
to the degree of immunity.Spinal polio is rarely fatal.

A child with a deformity of her right leg due to polio

Without respiratory support, consequences of poliomyelitis with respiratory involvement

include suffocation or pneumonia from aspiration of secretions. Overall, 5–10% of
patients with paralytic polio die due to the paralysis of muscles used for breathing. The
mortality rate varies by age: 2–5% of children and up to 15–30% of adults die. Bulbar

185 | P a g e
polio often causes death if respiratory support is not provided;with support, its mortality
rate ranges from 25 to 75%, depending on the age of the patient.When intermittent
positive pressure ventilation is available, the mortality can be reduced to 15%.

Clinical manifestation :

Symptoms

There are three basic patterns of polio infection: subclinical infections, nonparalytic, and
paralytic. About 95% of infections are subclinical infections, which may not have
symptoms.

SUBCLINICAL INFECTION SYMPTOMS

General discomfort or uneasiness (malaise)

Headache

Red throat

Slight fever

Sore throat

Vomiting

People with subclinical polio infection might not have symptoms, or their symptoms may
last 72 hours or less.

Clinical poliomyelitis affects the central nervous system (brain and spinal cord), and is
divided into nonparalytic and paralytic forms. It may occur after recovery from a
subclinical infection.

NONPARALYTIC POLIOMYELITIS

Back pain or backache

Diarrhea

Excessive tiredness, fatigue

Headache

Irritability

Leg pain (calf muscles)

Moderate fever

186 | P a g e
Muscle stiffness

Muscle tenderness and spasm in any area of the body

Neck pain and stiffness

Pain in front part of neck

Pain or stiffness of the back, arms, legs, abdomen

Skin rash or lesion with pain

Vomiting

Symptoms usually last 1 - 2 weeks

PARALYTIC POLIOMYELITIS

Fever 5 - 7 days before other symptoms

Abnormal sensations (but not loss of sensation) in an area

Bloated feeling in abdomen

Breathing difficulty

Constipation

Difficulty beginning to urinate

Drooling

Headache

Irritability or poor temper control

Muscle contractions or muscle spasms in the calf, neck, or back

Muscle pain

Muscle weakness that is only on one side or worse on one side

Comes on quickly

Location depends on where the spinal cord is affected

Worsens into paralysis

Sensitivity to touch; mild touch may be painful

187 | P a g e
Stiff neck and back

Swallowing difficulty

Differential Diagnosis :

 Guillain-Barré syndrome (GBS) may be described as a collection of clinical

syndromes that manifests as an acute inflammatory polyradiculoneuropathy with
resultant weakness and diminished reflexes. With poliomyelitis under control in
developed countries, GBS is now the most important cause of acute flaccid
paralysis.
Although the classic description of GBS is that of a demyelinating neuropathy with
ascending weakness, many clinical variants have been well documented in the medical
literature. Acute inflammatory demyelinating polyradiculoneuropathy is the most widely
recognized form in Western countries, but the variants known as acute motor axonal
neuropathy (AMAN) and acute motor-sensory axonal neuropathy (AMSAN) also are
well recognized.

Based on a clinical spectrum of symptoms and findings, many believe that strictly
defined subgroups of GBS exist. However, these subgroups are not easily
distinguished.

GBS remains a diagnosis made primarily through the assessment of clinical history and
findings . Serum autoantibodies are not measured routinely in the workup of GBS, but
results may be helpful in patients with a questionable diagnosis or a variant of GBS .

Approximately one third of patients require admission to an intensive care unit, primarily
because of respiratory failure. After medical stabilization, patients can be treated on a
general medical/neurologic floor, but continued vigilance remains important in
preventing respiratory, cardiovascular, and other medical complications. Treatment with
intravenous immunoglobulin or plasma exchange may hasten recovery.

The West Nile virus is one of the many members of the genus Flavivirus that are known
to cause human disease. The life cycle of the West Nile virus involves the microbe's
transmission from nonhuman animals to humans by way of Aedes, Culex, or Anopheles
mosquitoes. The West Nile virus can infect horses, birds, dogs, and other mammals.
However, wild birds are apparently the optimal hosts for harboring and replicating the
virus.

The West Nile virus has been reported in Africa, Asia, Europe, the Middle East, and
North America. In 1999, the first cases of West Nile virus disease were reported in New
York City, and the infection has been spreading throughout the North American
188 | P a g e
continent ever since.In 2002, a total of 3,389 cases were reported in the United States.
Approximately 55% of these cases were from the Midwest (Illinois, Michigan, Ohio,
Indiana).

 The West Nile virus causes serious manifestations in approximately 1% of persons

who are infected, with increased morbidity and mortality in individuals older than 50
years. In hospitalized patients in New York City, neurologic sequelae of the West
Nile virus included severe muscle weakness, with approximately 10% of patients
developing a complete flaccid paralysis. One in 150 West Nile virus infections
results in encephalitis or meningitis, and the mortality rate from severe illness is 3-
15%. Individuals older than 75 years are at particular risk.
As the elderly population increases and the distribution of the West Nile virus spreads
nationwide, a growing number of infected individuals may require comprehensive
inpatient rehabilitation to overcome the virus's disabling effects.

PT Management :

Surgical management :

Hip and knee contractures of over 30°

In general, hip and knee contractures exceeding 30° will all require surgery, unless one
or both arms are weak in addition to bilateral lower limb paralysis, making the use of
crutches difficult or impossible. In a young child with fairly recent contractures, the most
important single factor responsible for the deformity is a tight tensor fascia lata and
iliotibial band. In the older child or adult, however, other ligamentous and tendinous
structures play an important part and must be divided as well.

The iliotibial band contracture produces flexion deformities of the hip and knee on the
same side. Souttar’s release involves the soft tissue release on the anterolateral aspect
of the hip joint, whereby the tensor fascia lata and gluteus maximus are released from
their origins, as they contribute to the formation of the iliotibial band. Yount’s release
involves reexcision of the thickened anterolateral fascia lata so that the knee
contracture is better corrected.

The subcutaneous method of division is very satisfactory for less severe contractures,
provided it is done correctly and as extensively as necessary. Care must be taken to
avoid damaging the femoral and popliteal arteries, as well as the common peroneal
nerve. The biceps, however, should always be divided under direct vision because of
the risk of damaging the adjacent lateral popliteal nerve.

189 | P a g e
Tendon transfer to reestablish muscle power

In selecting a tendon to transfer, the muscle should be sufficiently strong to supplement

the power of a paralyzed muscle. The nerve and blood supply of the transferred muscle
should be preserved in order to avoid iatrogenic weakness.

For efficiency, the transferred tendon should be securely attached (with tension) close
to the insertion of a paralyzed tendon and should be routed in a direct line between its
origin and the new insertion. The transferred tendon loses its power by one grade.

The transferred tendon should also be retained in its own sheath, avoiding tunnels in
fascia or bone or an interosseous membrane to avoid adhesions.

The joint across which the muscle acts must be in a satisfactory position; all contracted
structures must be released before the tendon transfer.

When possible, an agonist muscle, with the same range of excursion of its tendon,
should be chosen.

Muscle transplantation to replace a paralyzed muscle

In muscle transplant procedures, unlike in tendon transfer, both the origin and the
insertion of a muscle are detached along with its neurovascular pedicle. This procedure
is not as popular as tendon transfer, because of the difficulty in finding a normal muscle
to transplant, donor-side morbidity, the technical difficulty of the procedure, and the
shortage of microvascular surgeons in developing nations, where residual polio is still
seen.

Stabilization of relaxed or flail joint

Tenodesis, fixation of ligaments, and construction of artificial check ligaments are used
to restrict the range of movement or to eliminate abnormal motion of a joint. With few
exceptions, these procedures have been discarded, as deformity in the opposite
direction may occur, and the tendon or artificial check ligaments may stretch with time.
This technique can still be helpful in skeletally immature patients.

Arthrodesis

Arthrodesis is used to correct a deformity, relieve pain in arthritic joints, and reduce the
number of joints a weak muscle is acting across. Arthrodesis is more popular than
tenodesis. In skeletally immature patients, extra-articular arthrodeses can be performed,
allowing continued growth of the skeleton.

Limb lengthening

190 | P a g e
Often, poliomyelitis is unilateral, causing limb-length inequality, which occasionally
requires limb lengthening. In leg lengthening for patients with poliomyelitis, callus
maturation is slow and patients tend to develop contractures despite physiotherapy,
bracing, or joint fixation. Concomitant and secondary surgery are frequently required to
treat associated problems or residual deformities. Lengthening along an intramedullary
locked nail can significantly shorten the treatment time with relatively few complications.

Joint replacement surgery

In patients with post-polio residual deformities, joint replacement can be indicated. In

one study, pain and knee scores improved following total knee arthroplasty in patients
with a history of poliomyelitis and antigravity quadriceps strength, but there was less
pain relief in patients with less than antigravity quadriceps strength.

Recurrence of instability and progressive functional deterioration are possible in all

knees affected by poliomyelitis that have undergone total knee replacement, but they
appear to occur more commonly in more severely affected knees.

Ilizarov techniques

There are many drawbacks to using conventional approaches for the treatment of
complex foot deformities, such as the increased risk of neurovascular injury, soft tissue
injury, and shortening of the foot. An alternative approach that can eliminate these
problems is the Ilizarov method. Pin-tract problems, contractures, residual deformity,
and recurrence of deformity can complicate the Ilizarov method

Pharmacological Management :

Pyridostigmine is a parasympathomimetic and a reversible, except possibly in stressful

conditions

cholinesterase inhibitor. Since it is a quaternary amine, it is poorly absorbed in the gut

and does not cross theblood–brain barrier

191 | P a g e
192 | P a g e