WEEK 13: CEREBRAL PALSY

Justine Ramos, PTRP, MSPT || November 2023

CCPT211
Miriam Aurea T. Gonzales (3rd year-1st semester)

DEFINITION 3. Cord prolapse

- Cerebral palsy describes a group of permanent disorders
of the development of movement and posture, causing Other Neonatal Causes
activity limitations that are attributed to nonprogressive 1. Hypoxic-ischemic encephalopathy
disturbances that occurred in the developing fetal or 2. Neonatal stroke, usually of the middle cerebral artery
infant brain. 3. Severe hypoglycemia
- The motor disorders of CP are often accompanied by 4. Untreated jaundice
disturbances of sensation, perception, cognition, 5. Severe neonatal infection
communication and behavior as well as seizures and
secondary musculoskeletal problems 5.6 Risk Factors During Labor
- Can occur in utero (prenatal period), near time of Likely Causes of Perinatal Asphyxia
delivery (perinatal period), or within the first 3 years of 1. Prolapsed cord
life (postnatal period) 2. Massive intrapartum hemorrhage
- 3. Prolonged or traumatic delivery due to cephalopelvic
disproportion or abnormal presentation
ETIOLOGY 4. Large baby with shoulder dystocia
1. Spastic Diplegic CP - premature birth 5. Maternal shock from a variety of causes
2. Hemiplegic CP - result of a focal, or sometimes
multifocal, lesion, most frequently caused by perinatal Events Associated with Causal Factors
stroke or congenital malformation. 1. Prolonged second-stage labor
3. Quadriplegic CP - diffuse bilateral insult to the brain, 2. Emergency Cesarean section
such as severe anoxicI or ischemic brain injury. 3. Premature separation placenta
4. Athetoid CP - is most often caused by 4. Abnormal fetal position
hyperbilirubinemia
5. Dystonia and associated dystonic subtypes of CP - In Preterm, Can Include:
basal ganglia and thalamic damage 1. Meconium-stained fluid
2. Tight nuchal cord
Risk factors
Risk Factors Present Before Pregnancy Risk Factors at Birth and Newborn Period
Maternal Factors 1. Decreased birth weight
1. Delayed onset of menstruation 2. Decreased age at birth (length of gestation is the
2. Irregular menstruation strongest determinant)
3. Long intermenstrual intervals 3. Poor intrauterine growth in moderately preterm but not
4. Unusually short or long interval between pregnancies in the very preterm infant
5. Low social class in children with normal birth weight 4. Low placental weight
6. Parity of three or more in preterm infants 5. Low Apgar scores (scores of 0 to 3 at 5 minutes have an
7. Relationship with previous fetal deaths 81- fold increased risk of cerebral palsy)
6. Neonatal seizures
Medical Conditions 7. Sepsis
1. Intellectual disability 8. Respiratory disease
2. Seizures
3. Thyroid disease Postneonatally Acquired CP
Metabolic Encephalopathy
Paternal and Sibling Factors 1. Storage disorders
1. Advanced paternal age (seen more frequently in those 2. Intermedullary metabolism disorders
with athetoid dystonic cerebral palsy) 3. Metabolic disorders
2. Motor deficit in sibling 4. Miscellaneous disorders
5. Toxicity such as alcohol
Prenatal Causes of CP
1. Vascular events such as a middle cerebral artery infarct Infections
2. Maternal infections during the first and second 1. Meningitis
trimesters such as 2. Septicemia
a. Rubella 3. Malaria (in developing countries)
b. cytomegalovirus, and
c. toxoplasmosis Injuries
3. Less common: metabolic disorders, maternal ingestion 1. Cerebrovascular accident
of toxins, and rare genetic syndromes 2. Following surgery for congenital malformations
3. Near-drowning
Risk Factors During Pregnancy 4. Trauma
1. Preeclampsia in term infants but not in preterm infants 5. Motor vehicle accident
2. Multiple pregnancies associated with: 6. Child abuse such as shaken baby syndrome
3. Preterm delivery
4. Poor intrauterine growth Risk Factors for Preterm Infants
5. Birth defects 1. Patent ductus arteriosus
6. Intrapartum complications 2. Hypotension
3. Blood transfusion
Perinatal Causes of CP 4. Prolonged ventilation
Problems During Labor and Delivery 5. Pneumothorax
1. Obstructed labor 6. Sepsis
2. Antepartum hemorrhage 7. Hyponatremia
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[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.
8. Total parenteral nutrition 4. CP is the second most common neurologic impairment
9. Seizures in childhood.
10. Parenchymal damage with appreciable ventricular 5. CP is the leading cause of childhood disability with an
dilatation incidence of two to three per 1,000 births.

From PMR:
PATHOPHYSIOLOGY
NATURAL HISTORY (1843)
® the term cerebral palsy (CP) (originally "cerebral
paresis") was first used by English orthopedic surgeon
William Little in a series of lectures entitled "Deformities
of the Human Frame."
® As a result, CP was known for many years as "Little's
disease."

ANATOMY (COLEWAN)

CEREBRUM
® "big brain"
® CEREBRAL CORTEX
® part of cerebrum
® gray matter
® signals for voluntary movements originate here

A. Left Hemisphere
a. Language
b. Math
c. Analytical

B. Right Hemisphere (hardest to rehabilitate)

a. Arts
b. Judgement/ Insight
c. Memorization
d. Visuospatial Perception

LAYERS OF THE CORTEX

Layer 1 - molecular layer
Layer 2 - granular layer (external)
Layer 3 - granular layer (Internal)
Layer 4 - pyramidal layer (external)
Layer 5- pyramidal layer (internal)
Layer 6 - multiform layer

Frontal Lobe
A. Area 4
è precentral gyrus/ primary motor area
è contralateral manifestation
è DAMAGE: weakness, flaccidity, paresis
B. Area 6
è motor association/ premotor area
è memory tank for motor function
è DAMAGE: spasticity
EPIDEMIOLOGY
1. CP is the most common motor disability of childhood
2. Reported incidence of CP is 1 to 2.3 per 1000 live births.
3. Special Populations: (per 1000 live births)
a. 15 (twins)
b. 80 (triplets)
c. 43 (quadruplets)
d. 40 to 150 (premature/ very low birth weight)

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[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.

Athetoid CP - Pathology
Rh incompatibility or ABO incompatibility -> death of red blood
cells -> release of bilirubin -> hyperbilirubinemia -> kernicterus
(bilirubin
encephalopathy)
All are Rh + and mother is Rh - = the mother’s body would attack
the fetus/ as foreign body -> destruction RBC- 120 days life (2
components: Heme (iron); Globin (O2) -> spleen graveyard ->
cannot store bilirubin -> back to blood -> hyperbilirubinemia >
Basal ganglia -> Bilirubin encephalopathy (kernicterus)
FRONTAL LOBE
C. Area 4 Normal: 2-5mg/dl
7- hyper
16- Toxicity
*jaundice- normal until 14 days (hyperbilirubinemia)
Triad of Kernicterus:
1. Hearing loss (sensorineural- perception)
2. Athetosis
3. Loss of upward gaze (Parinaud's phenomenon)-
Oculomotor Nerve- IO/SO

Spastic CP
1. Intraventricular Hemorrhage
è Between Ventricle
2. Impaired Autoregulation of Cerebral Blood Flow
è Fluctuations in Arterial Blood Pressure
3. Germinal Matrix (watershed Areas) Capillary beds are
fragile (Prenatal)
4. Rupture of capillaries around germinal matrix <-
Pressure <- Venous Obstruction
5. Hemorrhage/ Intraventricular Bleeding
6. Necrosis of White matter (Periventricular)
è Faster process in brain (Axons)
è PVL (Spastic Hemiplegia)
è White spots Quadriplegia
1) Prenatal: Impaired Dev’t brain 1. GP (Athetosis) + Putamen (dystonia)= Lentiform
2) Perinatal: Hypoxia 2. Putamen + GP + Caudate nucleus= Corpus striatum
3) Postnatal: Oligodedrocytes (chorea)
4) Cytokines 3. Subthalamic Nucleus (Ballismus)
7. Affectation layers of cortex (Pyramidal layers)
è 6 layers Direct pathway
è Area 4 (flaccidity/ no movement) - Overactivity: athetosis
è Area 6: Spastic - Underactivity: Bradykinesia
8. Projection tracts Indirect pathway
9. Corticospinal tract - Overactivity: akinesia/ rigidity
è D/t fibers of CST medial (LE) homunculus - Underactivity: Ballismus

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[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.
Ataxic CP - Pathology
Cerebellum
1. Paleocerebellum (Anterior Lobe)
è regulation of muscle tone
è maintenance of gait
è propulsive movements (running, swimming)
2. Neocerebellum (Posterior Lobe)
è coordination of movement
3. Archicerebellum (Flocculonodular lobe)
è balance, spatial reaction
CLASSIFICATION AND CLINICAL MANIFESTATIONS
® Current methods try to incorporate a functional basis for
classification. CP may manifest itself differently as the
child ages. The modified neurologic classification system
divides patients into the following categories:
o Spastic (pyramidal) CP (75%)
o Dyskinetic (extrapyramidal) CP
o Mixed type (combination) CP
SPASTIC TYPES OF CP (75%)
® Children with spastic CP exhibit significant upper motor
neuron (UMN) signs, such as muscle spasticity and
hyperreflexia/clonus.
® Extensor Babinski response (abnormal at >2 years old)
may be present in addition to other persistent primitive
reflexes.
® The spastic group is divided into five subtypes that are
named by the part(s) of the body involved.
® Intraventricular Hemorrhage and Periventricular
Leukomalacia
® Spasticity occurs in approximately 75% of all children
with CP.
® It is the most common neurologic abnormality seen in
children with CP.
® Spasticity - hypertonia in which resistance to passive
movement increases with increasing velocity of
movement."
® The most widely used scale for assessing spasticity is the
Modified Ashworth Scale (MAS).
Distinguishing Features
1. Bunny hop/ Knee walking- Normally when crawling
reciprocal, both knees will move
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2. Combat crawl- FA is moving while LE is pulled
3. Mermaid crawl- d/t windswept deformity- (but most
common in Quadriplegic) pt will move sideways and pull
self
4. Bottom Shuffling- uses gluteal area and hands only
move
5. W sitting – Television Sitting; IR both LE
6. Adductors spasticity – scissoring; most common
7. Toe walking- PF spasticity
8. Cortical thumb- thumb is inside fist; most common in
Hemiplegia
9. Hand fisting- Adducted thumb
10. Strabismus- visual impairment;
a. Esotropia- internal LR6 MRCN3
b. Exotropia- External- MRCN4- problem and LR6
pull
Spastic Diplegia
Definition ® Diplegia is the most common form of
spastic CP.
® ISCHEMIA due to hypoperfusion of the
germinal matrix of the periventricular
region of the premature fetus
® A white matter infarct in the
periventricular areas caused by hypoxia
can lead to spastic diplegic CP.
[Periventricular Leukomalacia]
® Smaller lesions result in diplegic
® LE>UE
® Infants clinically present with a history of
early hypotonia followed by development
of spasticity. Developmental delays,
commonly in the area of gross motor
function, are also noted.
® History of intraventricular hemorrhage is
also typical, especially at 28 to 32 weeks
of gestation.
® MRI may show periventricular
leukomalacia or posthemorrhagic
porencephaly.
Will they ® Often require assistive devices such as a
walk? posterior walker, or lofstrand crutches,
scooter or wheelchair (for long-distance
mobility)
Associated 1. Disproportionate involvement of the legs,
findings although upper extremity motor
perceptual dysfunction also seen
2. Developmental delay in gross motor
skills
3. Ocular findings include strabismus in
50% of the cases (visual deficits in 63%)
4. Mild cognitive impairment (30%) or no
mental retardation
5. Seizures occur in 25%
6. UMN findings in the lower extremities
7. Initial period of hypotonicity; later these
patients develop increased tone in the
lower extremities
Presentation 1. Normal cognition but may have some
social and emotional difficulties
2. increased lumbar spine lordosis
3. anterior pelvic tilt (more evident when
standing)
4. bilateral hip internal rotation
5. bilateral knee flexion- because of
spasticity could also be extension
6. in-toeing
7. equinovalgus
8. Spasticity of Adductors- Scissoring
9. Diplegic gait pattern includes classic
scissoring gait with toe walking.
[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.
10. Mild coordination problems result in the
UEs with UMN findings in the LEs.
Gait deficits - equinus (most common/ like toe
walking) and crouched gait (Excesive flexion
of hips and knees and ankle DF)
Spastic Hemiplegia
Definition 1. Upper and lower extremity on the same
side of the body are affected (UE>LE,
distal>proximal)
2. Most cases congenital (some acquired
10%-30%)
3. Focal perinatal injury
4. Highest incidence of CT/MRI
abnormalities in distribution o MCA
5. Infarction in a vascular distribution
(usually MCA) result in focal and
multifocal ischemic brain necrosis
6. Focal cortical infarcts involving both the
gray and white matter – typically related
to middle cerebral artery strokes
7. Cervical-subcortical lesions, brain
malformations, and nonprogressive
postnatal injuries have also been
identified as the main causes.
8. Children with hemiplegia tend to achieve
all gross and fine motor milestones but
not within the typical time frame. (has
better prognosis than other types of CP)
9. Cognitive function is typically normal but
tend to have social and emotional deficits
10. Require minimal equipment or self-
care/school accommodations
11. Standardized Assessments (video-based)
a. Shriners Hospital for Children
Upper Extremity Evaluation
(SHUEE)
b. Assisting Hand Assessment
(AHA)
Will they Ambulation usually achieved by 2 years of age
walk? (unless severe retardation is associated)
Associated 1. Most common presentation: Failure
findings to use the involved hand (i.e.,
preferential hand used prior to year
of age)
2. Arm > leg
3. Speech is preserved children have
the ability to switch dominance of
hemisphere up until approximately
age 6
4. Asymmetric crawl seen
5. Refractory error; may have
hemianopsia
6. Initial seizures may occur as late as 5
years of age
7. Mild mental retardation or no
retardation
8. Cortical sensory deficit
Why Hemiplegia UE>LE ?
® Lateral- homunculus
® Artery- MCA
o UE
Presentation 1. Hypotonia (1st indicator) then becomes
spastic
2. Hemiparesis- weakness on one side
3. Hemineglect- (L) affected there is
neglect/ the side would not be used by
the pt- Spatial affectation
4. Cranial Nerve affectation
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5. Hand immobility/ hand dominance
affectation
6. Typical arm posture- flexor and extensor
synergies- all is flexed; Ex: UE= flexor
synergy; LE- extensor synergy
a. SH protraction
b. Elbow flexion
c. Wrist flexion
d. Ulnar Deviation
7. Circumducted gait (Not sufficient hip and
knee flexion- circling motion) / tip toeing
(volting gait)
8. Sensory (68%) + visual deficits (32%)
(IMPORTANT SENSORY AX)
9. Good ambulatory prognosis
If MCA ® then (L) is affected- decussation of
brain- pyramidal tract
Spastic Quadriplegia
Definition ® Volitional muscle control of all four
extremities is severely impaired often
accompanied by neck and trunk
involvement
® Extensive lesions affecting the basal
ganglia or occipital area often lead to
visual impairments (strabismus) and
seizures
® Cognition can vary from normal to
severely impaired and is unique to each
child with quadriplegia (severe case CP
mental retardation, breathing, All
extremities)
® Gross and fine motor abilities vary
widely for children with quadriplegia,
from being ambulatory for household
distances with an assistive device to
being dependent for all care.
® MRI in the preterm child shows a
periventricular leukomalacia.
Will they walk ® One-fourth are independent in
ambulation, modified ADL
® One-half require assisted ambulation,
assisted ADL
® One-fourth are completely disabled
Associated 1. Strabismus
findings 2. LEG>ARMS; asymmetry not unusual
3. Mental retardation can be significant
4. Oromotor dysfunction, pseudobulbar
involvement present risk of aspiration
5. Feeding difficultiesmay need G-tube
6. UMN signs in all limbs
7. One-half have seizures
8. Must be monitored for hip dislocation
and scoliosis
9. Initial period of hypotonia which
eventually develops into extensor
spasticity
[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.

10. The more persistent the tone, the hyperbilirubinemia causing bilirubin
poorer the prognosis. deposition in the basal ganglia).
11. Opisthotonus and precocious head ® May be due to hemolysis secondary to Rh
raising can be an early manifestation of or ABO blood type incompatibility or
extensor hypertonicity hematoma breakdown
12. All extremities are involved. ® Diffuse anoxia resulting in hypoxia of the
13. Pattern of truncal hypotonia with basal ganglia and thalamus
appendicular hypertonia or total body WILL THEY ® One-half of children attain walking, most
hypertonia exists WALK? of them after 3 years of age
14. Often a history of difficult deliverv of ® UE function is adequate for ADLs
with evidence of perinatal asphyxia ® One-half of children are nonambulatory,
15. Approximately 50% have a prenatal dependent in ADLs
origin, 30% perinatal, and 20% ASSOCIATED 1. Athetosis-slow writhing, involuntary
postnatal. FINDINGS movements especially in the distal
16. Seizures occur in 50% of affected extremities
children. 2. Seizures in 25%
Presentation 1. Persistent primitive reflexes 3. Sensorineural deafness (high incidence)
2. Opisthotonos posturing- Like 4. Paralysis of upward gaze
decrebrate- Everything is extended 5. These children are generally hypotonic at
except for wrist- stiff body birth
3. Oromotor dysfunction (feeding 6. Classic movement patterns emerge
problems) some time between 1 and 3 years of
4. Drooling/ Sialorrhea age
5. Speech problem 7. The child develops involuntary
6. Deformities: movements first in the hands and fingers.
a. Wind swept deformity- IR 8. Abnormal movements are usually evident
one side in all extremities by 18 months to 3
b. Frog leg deformity/ Pitted years of age
Frog deformity- Hip FABER c 9. Pseudobulbar signs are present with:
ankle DF/PF Drooling, Oromotor dyskinesias,
c. Straphanger deformity- Dysarthria Muscle tone is normal during
i. Scap retraction sleep
ii. SH ABER 10. DTR is normal to slightly increase
iii. FA supination Tension athetosis when moving the limb
iv. Elbow FLX increases tone
v. Wrist FLX 11. Children have normal intelligence 78% of
vi. Finger FLX the time Nonambulatory patients are at
d. Birdwing deformity risk for hip dysplasia and scoliosis
i. Scap retraction 12. The UE >LE
ii. SH ABER
iii. FA Pronation Athetosis
iv. Elbow FLX Definition ® Bizarre, purposeless, involuntary
v. Wrist FLX
movements that are slow and writhing
vi. Finger FLX
® Abnormal in timing, direction, and
spatial characteristics
® Usually large motions of the more
proximal joints. (but more distal)
® Rare as a primary movement disorder
and is most often found in is
combination with chorea. (often mixed
with Spastic-athetoid and Chorea
Athetosis)
® Athetosis is most commonly a
secondary movement disorder in
DYSKINETIC CP conjunction with spasticity.
Dyskinetic CP ® In one extremity= one part would have
DEFINITION Dyskinetic disorders are characterized by spasticity and one could have athetosis
abnormal extrapyramidal movement patterns ® Spastic- Inc. muscle tone velocity
(Dyskinetic movements are defined previously dependent; Athetoisis- Extrapyramidal-
in the modified neurological classification no spasticity/ fluctuating muscle tone
system) increased or decreased- allows limbs to
® Dyskinesia and movement disorders move
result in generally uncontrolled and
involuntary movement Hallmark/ 1. Onset is 5 - 10 years
® Common abnormalities found in imaging features 2. Does not progress
include deep gray matter lesions and, to a 3. Does not cause contractures (from
lesser extent, periventricular white fluctuating muscle tone)
matter lesions. 4. Mental status usually normal
5. Fine > gross motor involvement (Distal
ETIOLOGY ® In the past, most cases were associated > proximal)
with kernicterus (neonatal

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[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.
Clinical 1. Mobile spasm - clawing of fingers/toes
manifestations (inc- period of spasm; relaxation-
decreased)
2. FA Pronation supination
3. Athetoid dance (movements is
manifested in weight bearing
activities)- outward and upward d/t
conflict of cross extension withdrawal
and grasp reflex
4. Fleeting irregular localized
contractions or tonic spasm or dystonia
can occur when triggers occur.
a. Excitement
b. Feeling of falling/ instability
c. Exerting too much effort-
intention effort
5. Reduced
a. Sleeping
b. Fever
c. Prone-lying
d. Drowsy/ fatigued
6. Asymmetric posturing
7. Hand spooning - wrist and finger
extension
8. Individuals with athetosis typically
initiate and attempt control of
movement with the jaw and head. (w/
drooling)
9. Facial grimacing- movement of facial
muscles
10. Tongue thrusting- to swallow better
11. Explosive speech- “airy”
Types of Athetoid CP
Pure Athetoid
1. Subluxation: shoulder (support ligaments- fluctuating),
mandible, hips
2. Proximal > distal
3. Fluctuating muscle tone (low - mid)
Choreoathetoid
1. Most common mixed dyskinetic type
2. Tone: low – high
3. Subluxation: same as pure athetoid
4. Site of lesion: Lentiform
Spastic Athetoid
1. Most common mixed type of cp
2. Distal > proximal - associated movements
3. Distal < proximal – spasticity
4. Delayed or absent: Parachute, Right reaction,
Equilibrium reaction
5. Tone: normal - high
Athetoid with Dystonia
1. muscle spasm with fluctuating tone/ rhythmicß
2. Rare
3. Tone: very low - very high
Chorea
® Abrupt, irregular, jerky movements
Types:
1. Huntington's Chorea
è hereditary disorder (older population)
è autosomal dominant affecting the short arm of
chromosome 4
è affects ages 20 – 30
è Due to loss of most of cell bodies of:
i. Ach (Dementia)
ii. Gaba (does r respond to any
medication)
iii. P substance
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2. Syndenham's Chorea (St. Vitus Dance)
è most common acquired in children
è autoimmune, self limiting (good prognosis)
è cause: gr. A Beta hemolytic Streptoccocus
infection
è cardinal feature: rheumatic heart diseases
3. Hemichorea
è one side of body is affected
Others
1. Dystonia
è a slow motion with a torsional element that
may involve one limb or the entire body and in
which the pattern itself may change over time
2. Rigidity
è is much less common and is felt as resistance to
both active and passive movement and is not
velocity dependent.
3. Tremor
è a rhythmic movement of small magnitude,
usually of the smaller joints, rarely occurs a an
isolated disorder in CP but rather in
combination with athetosis or ataxia.
4. Ballismus
è the most rare movement disorder and involves
random motion in large, fast patterns usually of
a single limb
Ataxia
® Uncoordinated movements often associated with
nystagmus, dysmetria, and wide-based gait:
1. Classic movement patterns emerge sometime between
and 3 years of age. Severely affected or children have
persistent hypotonia. Movement patterns typically
increase with stress or purposeful activity. During sleep,
muscle tone is normal, and involuntary movement stops
2. Pseudobulbar involvement presents with dysarthria,
dysphasia, drooling, and oromotor dyskinesias. These
children have normal intelligence 78% of the time.
3. There is a high incidence of sensorineural hearing loss
which has been associated with hyperbilirubinemia and
neonatal jaundice.
Hypotonia
® can be permanent but is more often transient in the
evolution of athetosis or spasticity
® might not represent a specific type of CP
® Hypotonia is typically correlated with congenital
abnormality, such as lissencephaly.
® A common mixed tone pattern is seen in some children
with quadriplegia, with spasticity evident in the LEs and
severe hypotonia in the trunk and neck.
Associated Impairments
1. Sensory Impairments
a. two-point discrimination, proprioception, and
stereognosis
b. most common in children with hemiparesis
2. Visual Impairments
a. Strabismus
b. Diplegia - refractive errors, strabismus,
abnormal saccadic movements, reduced visual
acuity
c. Hemiplegia - altered visual field
d. Quadriplegia - ocular abnormalities,
oculomotor dysfunction, reduced visual acuity
3. Hearing Impairment
a. Sensorineural hearing loss is most commonly
associated with congenita toxoplasmosis,
[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.
rubella, cytomegalovirus, and herpes (TORCH) 5. Upper extremity
infections, bacterial meningitis, hypoxia, and 1) Spasticity and muscle imbalances
ototoxic drugs. 2) Elbow - flexion contractures
b. Kernicterus was a relatively common cause in 3) Forearm - pronation deformities
athetoid CP. 4) Wrist - flexion, typically with ulnar deviation
4. Cognitive Impairment 5) Finger - flexion and swan neck deformitie
a. common in CP
b. patients with more severe neuromuscular
COMMON GAIT DEVIATIONS IN CP
impairments are at greater risk
5. Emotional and Behavioral Impairments Location Impairment Potential Effects
a. Attention deficit disorder, passivity, HIP Increased adductor tone -Scissoring
immaturity, anger, sadness, impulsivity, -difficulty advancing leg
emotional lability, low self-esteem, and anxiety. in swing phase
6. Epilepsy Increased iliopsoas tone -Anterior pelvic tilt
a. more common in children with more severe CP -increased lumbar
and in children with quadriparesis and lordosis
hemiparesis versus diparesis -crouched gait
7. Oromotor Impairments -> Nutritional Disorders Increased femoral -In-toeing
a. associated with more severe CP anteversion -false genu valgus
1) weak suck -compensatory external
2) poor coordination of the swallowing tibial
mechanism torsion
3) tongue thrusting Abductor weakness Trendelenburg's gait
4) tonic bite reflex may all lead to feeding
difficulties
5) increased risk for aspiration.
6) Speech disorders and are most seen in spastic Knee Decreased hamstring range Crouched gait
quadriparesis or athetosis of motion
8. Respiratory Disorders Hamstring/quadriceps Stiff-knee gait
a. Impaired control of respiratory muscles cocontraction
b. ineffective cough
c. aspiration due to impaired swallowing Ankle Increased gastrocsoleus -Toe walking
d. gastroesophageal reflux tone or -genu recurvatum; -
e. seizures all increase the risk for chronically contracture difficulty clearing foot
increased airway secretions. during swing
Internal tibial torsion -In-toeing
-ineffective pushoff
External tibial torsion -Out-toeing
-ineffective pushoff
Varus Increased ankle
supination in stance or
swing
Valgus -Increased pronation in
stance or swing
-mid-foot break

5.2 Gait Deviations and Their Underlying Causes

Problem Primary Cause(s)
Pelvis
Anterior pelvic tilt Hip flexion contracture/hip extensor
weakness
Increased rotation Decreased push-off from gastrocnemius
Musculoskeletal Disorders (gastroc)
1. Foot/Ankle -hip stiffness
1) Equinus deformity (mc) -hip flexor weakness
2) Equinovarus (hemiparetic CP) Drop of pelvis on Hip abductor weakness
3) Equinovalgus (spastic diparesis & swing side
quadriparesis) Hip
2. Knee Decreased flexion -Hamstring (HS) or gluteus muscle
1) Knee flexion contracture contractors
2) Genu valgus -Weak plantarflexors during push-off
3. Hip -Weak hip flexors
1) Acquired hip dysplasia often to leads to Decreased Hip flexor contracture; knee flexion
progressive subluxation and possible extension (stance) contracture
dislocation Increased Weak adductor muscle: abductor
2) Windswept deformity abduction contracture
4. Spine Increased Adductor contracture/increased tone
1) Kyphosis adduction
2) Lordosis Increased internal -Femoral anteversion
3) Scoliosis rotation

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[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.

-increased tone and/or contracture of 3. Crouched gait pattern

internal rotators; compensation for è knees and hips flexed throughout the gait
external tibial rotation pattern
Increased external -Retroversion of femur è overactive hamstrings in stance phase,
rotation -increased tone or contracture of quadriceps weakness, and triceps surae
external rotators weakness
-compensation for internal è Tight hip flexors
tibial torsion è Tight hamstrings
Knee è Weak quadriceps
increased flexion -Knee flexion contracture: hamstring è Excessive dorsiflexion in both diplegics and
at initial contact tone quadriplegics
-toe strike due to plantarflexor tone
Decreased flexion -Weak hamstrings 4. Jump Knee
at initial contact weak quadriceps è anterior pelvic tilt, hip flexion, knee flexion,
Genu recurvatum -Increased gastroc tone and ankle equinus
in midstance -weak gastric è overactivity of the hamstring in late swing and
-weak hamstrings early stance phases and strong quadriceps
Crouch (stance hip -Knee joint contracture contraction during late stance phase.
and knee flexion) -HS contracture
-hip flexor contracture 5. Stiff knee gait
-poor balance è increased knee extension throughout swing
-severe planovalgus feet phase
-ankle equinus è overactivity of the rectus Femoris
Stiff knee gait -Increased rectus femoris tone
-knee stiffness quadriceps contracture: 6. Recurvatum gait
poor push-off from gastroc è knee extension in early stance progressing to
hyperextension in mid- and late stance phases
Jump knee (knee Overactivity of HS
of gait
flex in early stance)
è overactivity and/or contracture of the
Foot
gastrocnemius.
Equinus at initial Gastroc/soleus contracture
contact gastroc overactivity
Quadriplegic gait
weak dorsiflexors
è Even though functional community ambulation
Decreased push-off -Weak gastroc/soleus
throughout life is not a realistic goal for children with
power -severe planovalgus feet
this type of CP, encouraging ambulation is very
Intoeina (internal -Internal tibial torsion important.
foot proaression) -varus feet
Out-toing (external -External tibial torsion Athetotic gait
toot progression) -severe muscle weakness è Orthopedic and physical therapy treatments usually
-poor balance have little effect on athetotic movements.
Common Gait Deviations Ataxic gait
Hemiplegic gait è General unsteadiness, widened base, irregularity of
• Type 1 - drop foot in swing phase of gait, but has normal steps with interjoint incoordination, prolonged stance
dorsiflexion PROM duration, increased double-limb support duration, slow
• Type 2 - plantarflexion throughout the gait cycle, full speed, and large body sways.
extension or recurvatum of. knee in stance phase
• Type 3 - decreased knee motion, especially during swing SPECIAL TESTS:
phase, due to quadriceps/hamstring co-contraction
• Type 4 - additional restricted motion of the hip due to DIFFERENTIAL DX
hyperactivity of the iliopsoas and hip adductors
DIAGNOSIS
Weak hip flexion and ankle dorsiflexion
Overactive posterior tibialis 1. GROSS MOTOR FUNCTION CLASSIFICATION SYSTEM FOR CP
Hip hiking or hip circumduction ® Gross motor function classification system (GMFCS) is a
Supinated foot in stance phase functionally based system to standardize gross motor
UE posturing function in the CP child.

Diplegic gait ® Level 1: Walks without restrictions; limitations in more

(Gait pattern:Scissoring gait: Hips flexed and adducted, Knees
flexed with valgus, and Ankles in equinus (toe walking)
1. Equinus gait pattern
è ankle in plantarflexion throughout stance
phase with hips and knees extended;
gastrocnemius spasticity
2. Planovalgus
è equinus of the hindfoot and pronation of the
forefoot and midfoot;
è primarily caused by plantarflexor muscle
weakness
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advanced gross motor skills
® Level 2: Walks without assistive devices; limitations
walking outdoors and in the community
® Level 3: Walks with assistive mobility devices;
limitations walking outdoors and in the in communitY
Level 4: Self-mobility with limitations; transported or
use power mobility outdoors and in the community
® Level 5: Self-mobility severely limited even with use of
assistive devices
GMFCS
Level 1: Walks Without Restriction, Limitations in
High-Level Skills
[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.
1. Walks independently by age 2 years without devices
2. Walks as preferred mobility by age 4
3. Difficulty with speed, coordination, and balance for high-
level tasks
Level 2: Walks Without Devices, Limitations Walking
Outdoors
1. Sits with hand support by age 2
2. Crawls reciprocally or walks with device as preferred
mobility by age 4
3. Uses hands to get up from the floor or a chair by age 6
4. Walks without devices indoors by age 6
Level 3: Walks With Devices, Limitations Walking
Outdoors
1. Sits with support by age 2
2. Cruises by age 4, walks with device short distances
3. Does stairs with help by age 6
4. Walks indoors with a device by age 12
Level 4: Limited Mobility, Power Mobility Outdoors
1. Rolls by age 2 years
2. Sits with hand support by age 4
3. May walk short distances indoors with device, poor
balance
4. Preferred independent mobility is a wheelchair by age
12
Level 5: Very Limited Self-Mobility, Even With Assistive
Technology
1. Needs help to roll by age 2
2. Does not attain independent mobility by age 12
3. With high-level assistive technology, may learn to use
power mobility
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Criteria
Levine (POSTER) Criteria
1. Posturing/abnormal movements
2. Oropharyngeal problems
3. Strabismus
4. Tone
5. Evolutional maldevelopment
6. Reflexes
*Abnormalities in four of these six categories strongly point to the
diagnosis of CP
Diagnosis cont.
1. Infants may be diagnosed earlier than 2 years of age.
2. Milder cases of CP may not be diagnosed until 4 to 5
years of age.
3. Cranial ultrasound is often used for the high-risk
preterm infant.
4. In term infants, computed tomography (CT) is
recommended.
5. Magnetic resonance imaging (MRI) is often preferred.
6. A neurologic examination alone is insufficiently sensitive
or specific enough, thus, the quality of an infant's
"general movements" (GMs) have been used by doctors
and researchers to evaluate brain function.
Walking Prognosis
1. This is usually the most frequent question asked by the
parent of a newly diagnosed CP child. Several factors are
relevant. The best indicator of how the child will do is
how the child is doing.
2. Sitting: Alexander (2010) has shown that if independent
sitting occurs by age 2, prognosis for ambulation is good.
3. Crawl: Badell felt that ability to crawl on hands and
knees by 1.5 to 2.5 years is a good prognostic sign.
4. Primitive reflexes: Persistence of three or more
primitive reflexes at 18 to 24 months is a poor
prognostic sign (Table 10-28).
Prognosis also depends on the type of CP (Table 10-25).
PROGNOSIS
1. GMs can be predictive of later CP and are the best
expression of functional motor development.
2. GMs are analogous to later functional motor milestones
and may also predict severity.
3. Cognitive abilities linked with the severity of CP and to
be predictive of many outcomes.
4. The causes of mortality related commonly to the
respiratory and circulatory systems, certain cancers, and
neurologic complications.
5. The GMFCS level is highly predictive of adult motor
function.
6. Molnar's Prognostication Index (for Ambulation)
a. 2 y/o and above
b. Best prognosis - spastic hemiplegia or ataxic
c. Poor prognosis - quadriplegic; flaccid/rigid
d.
[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.
7. Bleck's Ambulation Status (>2 yrs)

From PMR:
1. About 90% of children with CP survive to adulthood.
Immobility and severe or profound retardation reduce
life expectancy.
2. Positive factors for independent living include regular
schooling, completion of secondary school, independent
mobility and ability to travel beyond the house, good
hand skills, living in a small community, and having
spasticity as the motor dysfunction:
a. Mental retardation, seizures, and wheelchair
dependency are factors that reduce the
likelihood of independent living.
3. Positive prognostic indicators for employment include
mild physical involvement, good family support,
vocational training, and good employment contracts.
Outcome Measures
1. Movement Assessment in Infants (MAI)
è Sensitive for infants at 4 months of age
2. Developmental Assessment of Young Children and the
Hammersmith Infant Neurological Evaluation
è highly predictive of CP in infants less than 12
months of age
3. Bayley Motor Scale
è sensitive at 1 year of age
MANAGEMENT
PHARMACOLOGIC
SURGICAL
1. Selective posterior rhizotomy:
® SPR is designed to decrease the excitatory sensory
input to the motor neuron, thereby decreasing
spasticity.
® The procedure consists of a laminectomy to expose
the cauda equina.
® The dorsal roots are electrically stimulated, and
various criteria are used for determining which
parts of the root contain more fibers involved with
abnormal reflexes.
® These rootlets are subsequently severed.
® This technique allows for decreased tone without
significant sensation loss.
2. Intrathecal baclofen pump placement:
® Also see section "Spasticity" in Chapter 12, in
Associated Topics in Physical Medicine and
Rehabilitation.
® A programmable pump delivers baclofen directly
to the intrathecal space of the spinal cord
(equivalent to chemically adjustable rhizotomy).
® Allows for much lower doses of baclofen to be
used, minimizing side effects
® Required to be refilled on a regular basis

1. Nerve/Motor Point Blocks-are indicated for treatment

spasticity affecting specific muscle groups. They
commonly done to decrease hip adductor, hamstring,
and gastrocnemius

EXPECTED EFFECTS OF SPECIFIC NERVE BLOCKS IN THE LOWER

EXTREMITIES
1. Obturator nerve blocks (anterior and posterior
branches): Reduce adductor tone, Diminish scissor gait,
and Promote passive abduction as a means of protecting
hip joint integrity
2. Sciatic branch blocks to the medial hamstrings
(semimembranosus and semitendinosus): Lessen crouch
gait and internal rotation deformities
3. Tibial blocks (and in recent past, tibial branch blocks
the heads of the gastrocnemius): Diminish plantar
flexion tone and allow better tolerance of AFOs
4. Femoral nerve blocks: Diminish spastic recurvatum

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[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.
PHYSICAL THERAPY
1. Therapeutic Exercise, Strengthening, and Stretching
2. Neurodevelopmental Treatment (Bobath)
3. Therapeutic Handling
4. Sensory Integration (Ayres)
5. Modified Constraint-induced Movement Therapy
6. Electrical Stimulation (NMES/ FES)
7. Aquatics
8. Hippotherapy
9. Treadmill Training/Robotic Gait Training
10. Adaptive Equipment
a. Seating and positioning
b. Standers
c. Ambulation Aids
11. Lower Extremity Orthoses

PT Evaluation
1. The first step in the evaluation for suspected CP is a
comprehensive history, including a detailed account of
potential risk factors and family history and thorough
history of developmental milestones.
2. Following a detailed history, a thorough physical
examination should be performed.
3. A careful neurologic exam is an essential piece of the
evaluation
4. Assessment of Movement
5. Assessment of Postural Control
6. Assessment of Postural Tone
7. Musculoskeletal Assessment
a. Goniometric Measurements
b. Evaluation of Spine
c. Thoracic Movement
d. Discrepancy in Leg Length

Bracing
1. Tone-reducing ankle-foot orthoses (TRAFOs) aid in gait
by in controlling the equinus or equinovarus deformity:
a. Designed to decrease abnormal reflexes
b. Full-length foot plate extends past the toe to
discourage toe flexion.
c. Metatarsal support discourages stimulation to
a particularly reflexogenic area of the foot.
d. They are most effective during gait, but use
during rest helps prevent contractures.
2. Knee ankle-foot orthoses (KAFOs):
a. KAFOs add direct control over knee flexion and
extension as well as varus and valgus but add
bulk and weight.
3. Hip-knee ankle-foot orthoses (HKAFOs):
4. HKAFOs add direct control over hip position. KAFO and
HKAFO braces do not significantly improve gait, but they
do decrease deformity.

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[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.

ASSESSMENT
Hypertonicity
1. Modified Ashworth Scale
2. Muscle Stretch Reflex

Hypotonicity (common in Ataxic)

1. Tone Ax

Weakness
1. FMT

Tightness, Contracture and Deformities (not main problem)

1. Range of Motion
2. Leg Length Measurement
3. Special Tests
4. Postural Analysis
Others:
Balance a. Sitting Ax for children with Neuromotor
1. Titing and Saving Reactions PBS Dysfuction
b. Functional Reach test
Functional Outcome Measures (Levitt) c. Lateral Reach test
1. GMFM-88 i. FOR UE
2. Pediatric Balance Scale 1. QUEST
2. Assisting Hand Ax
3. Melbourne Ax of unilateral
limb function
4. Manual Ability Classification
system

Neurologic Evaluation
1. Sensory
2. Pathologic Reflex
3. Primitive reflex

Others:
1. Reach, Grasp, and release
2. Gait

GMFM 88
SCORING
SCORING KEY
0 = does not initiate
1 : initiates
2 partially completes
3 = completes
9 (or leave blank) = not tested (NT) [used for the GMAE-2
scoring*]

A: LYING & ROLLING

SUPINE: NORMAL AGE: 3 MONTHS

1) SUP: ROLLS TO PR OVER R SIDE.
2) SUP: ROLLS TO PR OVER L SIDE..

*AX: FOLLOW TOY; COMPLETION IMPORTANT!

PRONE: NORMAL AGE: 4 MONTHS

1) PR ON FOREARMS: WEIGHT ON R FORFARM FULLY
EXTENDS OPPOSITE ARM FORWARD...
2) PR ON FOREARMS: WEIGHT ON L FOREARM, FULLY
EXTENDS OPPOSITE ARM FORWARD .
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[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.
Bobath
B: SITTING 1. Distal Key Points
1) SIT ON MAT: TOUCHES TOY PLACED 45° BEHIND a. Thumb (extension and abduction)
CHILD'S R SIDE, RETURNS TO START b. Big Toe (dorsiflexion)
2) SIT ON MAT: TOUCHES TOY PLACED L 45° BEHIND 2. Proximal Key Point
CHILD'S L SIDE, RETURNS TO START. a. Head (flexion/ extension)
3) SIT ON BENCH: MAINTAINS, ARMS AND FEET FREE, 10 b. Shoulder (external rotation and abduction)
SECONDS…. c. Hip (FABER)

*BACK TO MIDLINE W/O FALLING / SUPPORT FROM OTHER HAND *Slow Stretch only to not facilitate spasticity

C: CRAWLING & KNEELING Cortical thumb: Rub thenar eminence/ bring out thumb in
1) 4 POINT: CRAWLS UP 4 STEPS ON HANDS AND Extension and Abduction
KNEES/FEET .............
2) 4 POINT: CRAWLS BACKWARDS DOWN 4 STEPS ON Dystonia:
HANDS AND KNEESFEET 1. Rigid
CHECK IF RECIPROCAL AND DON’T FORGET TO STABILIZE PELVIS 2. Head Extension: more px in head flx
3) HIGH KN: ATTAINS HALF KN O RKNEE USING ARMS,
MAINTAINS, ARMS FREE, 10 SECONDS Inhibit extensor synergy in LE
4) HIGH KN: ATTAINS HALF KNEE USING ARMS, 1. Sit in a bolster
MAINTAINS, ARMS FREE, 10 SECONDS ...... 2. Cross sitting
*PX START QUADRUPED UP AND LOOK AND HALF KNEEL 3. Prone on a bolster

D: STANDING Inhibit flexor synergy in UE

1) HIGH KN: ATTAINS STD THROUGH HALF KN ON R 1. Reach objects
KNEE WITHOUT USING ARMS........ 2. Put hands forward and backward extended
2) HIGH KN: ATTAINS STD THROUGH HALF KN ON L
KNEE, WITHOUT USING ARMS),
3) STD: PICKS UP OBJECT FROM FLOOR, ARMS FREE,
RETURNS TO STAND

E: WALKING, RUNNING & JUMPING

1) STD: WALKS FORWARD 10 STEPS, STOPS, TURNS 180°,
RETURNS (20 STEPS IN TOTAL)
2) STD ON R FOOT: HOPS ON R FOOT 10 TIMES VITHIN A
60cm (24") CIRCLE....
3) STD ON L FOOT: HOPS ON L FOOT 10 TIMES WITHIN A
60cm (24") CIRCLE........

Inhibits Extensor tone

(Legs in 90-90)

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[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.

Brunnstrom
1. Reflexes
a. STNR
b. ATNR
c. Soques
d. Ramistes

*Cerebral cortex affected

STNR: FLX Head= FLX UE and EXT LE

ATNR: Same side rot head= EXT and skull side FLX
Soque’s= SH ABD above 90 degrees= Abd and Extension of fingers
Raimeste’s = resist Abd unaffected

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[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.

Rising on to knees, forearms and knees

® Encourage the child's rising onto knees instead of your
lifting the child each time.

1. Place one leg in creeping position and hold firmly or fix

the foot against a heavy box, tip the child's opposite hip
and pelvis up and back with slight touch and wait for
active rise knees, first on to the one that is fixed.
2. The other leg creeps forward on to its knee.
3. Carry this out without giving the child a tip-up at his hip,
if he can manage alone as shown in Fig. 9.31.
4. Use instruction *Knee forward and get up!' Rising onto
forcarms, and later, hands are usually activated as well.

Includes Facilitatory and inhibitory= roods *How to teach kneeling

® Ataxic CP 1. Put one side in IR and ABD slightly
o Hypotonia 2. Give stimuli
o Weakness 3. If unstable LE ask px to reach chair
§ FAST STROKING
§ JOINT POUNDING ELBOW/SH

*FACILITATES RECIPROCAL CRAWL

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[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.
3. for better muscle activation and avoidance of
stimulating spasticity.

Unstable weight bearing through the arms. Use

joint compression through the top of the shoulder or the upper
arm with straight elbow to develop stability on hands in prone, in
sitting or standing positions (Fig. 9.33a,b).

1. A low table is used for training, arm-propping support.

2. Keep the arms in straight alignment with the line of
pressure through shoulder or elbow.
3. Have child's weight through posterior 'heels' of the
hands to avoid finger flexion.
4. Arms are placed on a surface below the child, so the
weight of his body adds to the joint compression,
5. for example, child may enjoy being held upside down for
'standing or walking on hands' with his elbow splints,
for similar effects.
6. Use variety of floor textures to increase tactile
experience.

1. When a child is actively able to commence or complete

rising up on to knees and forearms, but is weak, manual
resistance used reinforce his efforts.
2. Apply manual resistance at the pelvis in a diagonal
direction (Fig, 9.35)

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[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.

-
Physiotherapy suggestions for rolling and
roll-and-rise

Trunk stabilization

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[CCPT] 1.13 Cerebral Palsy – Gonzales, Miriam Aurea T.
Figure 9.161 (a-c) Counterpoising exercises for walking and
climbing stairs as well as for putting on and off socks, shoes and
trouses, and for washing and play activities.

PRINCIPLES OF TX:
1. Maintain each key point of control long enough to be
able for the child to adjust postural
2. Stability of equipments (well inflated vesti ball, leg rolls)
because the softer the equipment, the more unstable it is
for the px
3. Incorporation of play
4. Motor demands
a. Don’t use small objects because fine motor are
affected in cp athetoid than gross motor
function
b. Use heavy weight toys in order for the px to
feel the joint position (precaution exerting too
much effort
c. Side lying: best position to promote midline
orientation
5. Voice pattern
a. Modify your voice pattern (low voice tone)
b. In giving instruction, it should be simple ct.
Clear
c. Low tone - in order to create a calming effect
on them because athetoids are unstable
6. Intermittent jt. Compression - it should be sustained to
promote stability

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