CEREBRAL PALSY

CEREBRAL PALSY
Is a disorder of movement and posture that result from
non-progressive lesion or injury of the immature brain

Alterations:
Muscle tone
DTR
primitive reflexes
Postural reactions

HALLMARK of CP

- ABNORMAL PATTERNS OF MOVEMENT
RELATED ANATOMY
NEURAL DEVELOPMENT

From Embryo:

3 primary layers

Ectoderm
Mesoderm
Endoderm
RELATED ANATOMY
EARLY DEVELOPMENT

ETIOLOGY
Premature infants
Multifactorial

In children with N birth weight :

80% of disabilities are a result of factors occurring
before birth

20% are attributed to factors occurring around the
birth or in the immediate post birth period (first 4
weeks of life)

ETIOLOGY
In children with low birth weight:

Uncertainty remains as to when the brain damage
occurred

Any prenatal, perinatal or postnatal condition
anoxia
Hemorrhage

Infants born between 32 and 42 weeks gestation

ETIOLOGY
Prenatal Perinatal Postnatal
Maternal infection
Rubella
Cytomegalovirus infection
Herpes simplex
Toxoplasmosis
Maternal diabetes
Rh incompatibility
Toxemia
Maternal malnutrition
Maternal thyroid disorders
Maternal seizure
Maternal irradiation
Abnormal placental attachment
Congenital anomalies of the
brain
Coagulation factor
abnormalities
Factor V Leiden mutation
Antiphospholipid antibodies
Prematurity
Obstetric complications
Mechanical birth trauma
Breech delivery
Forceps delivery
Twin or multiple births
Prolapsed umbilical cord or
umbilical cord flow
abnormalities
Low birth weight (<1750g)
Small for gestational age (SGA)
Low Apgar score (<4 at 5 min)
Placenta previa
Abruption placentae

Neonatal infection (meningitis,
encephalitis)
Environmental toxins
Trauma
Kernicterus
Brain tumor
Anoxia
Cerebrovascular accident
Neonatal hypoglycemia
Acidosis
ETIOLOGY
Abnormal development of the brain
Anoxia
Intracranial bleeding
Excessive neonatal asphyxia (hypoxic ischemic
neonatal encephalopathy)
Trauma
Hypoglycemia
Infections

EPIDEMIOLOGY
Leading cause of disability in childhood

The reported incidence varies but is approximately 2-3
per 1000 live births (Molnar 2004)

All races are affected by this disorder

The spastic subtype is the most common, affecting
about 75% - 80% of the children with CP

M>F (1.33:1)

PATHOPHYSIOLOGY
Several neuropathic lesions have been
identified:
Hemorrhagic below the lining of the ventricles
(subependymal or interventricular)

PATHOPHYSIOLOGY
Hypoxia causing encephalopathy

Can also occur in full-term infant

PATHOPHYSIOLOGY
Hypoxic-ischemic injury- known to disrupt the normal metabolic processes,
starving the cells of oxygen









Decreased perfusion resulting from systemic hypotension and poor autoregulation of cerebral
blood flow

Emboli- block distal perfusion and thrombosis

Clot formation from polycythemia or a hypercoagulable state

PATHOPHYSIOLOGY
Periventricular Leukomalacia
DIAGNOSIS
CT-Scan especially for children under 2 years
old
MRI is more effective > 2 years
Blood pH - To diagnose a patient with
asphyxia, or decreased oxygen supply
DIFFERENTIAL DIAGNOSIS
Condition Cerebral Palsy Similarities Differences
Global Developmental Delay GDD is an umbrella term for
symptoms not yet
considered as CP or other
syndromes. GDD patients
present with delayed motor
function, which is similar
from CP patients

Spina Bifida Both cases present with
learning disabilities,
deformities such as talipes
equinus foot, abnormal
reflexes and spasticity
Symptoms of Spina bifida
depend on the level of the
spinal cord, and these
patients would seldom
present with behavior
problems
Autism Both cases would present
with delayed motor
development
Patients with autism would
present more with behavior
problem, while CP patients
would present more with
motor problems.

SIGNS AND SYMPTOMS
(5 Major Findings)

Delayed motor development
Ab(N) tone
Ab(N) Posture
Ab(N) reflex
Ab(N) motor performance

CLINICAL PRESENTATION
Classification:

Nature of neuromuscular abnormality
Body parts involved
Etiology

Neurologic Classification:

Categories

1. Spastic (pyramidal) CP
2. Dyskinetic (extrapyramidal) CP
3. Mixed types

CLINICAL PRESENTATION
Spastic types

Most common (75%)
Manifest signs of UMN lesions:

1. Hyperreflexia
2. Clonus
3. Persistent primitive reflexes
CLINICAL PRESENTATION
Body parts involved:

CLINICAL PRESENTATION
Dyskinetic types

1. Athetosis slow , writhing, involuntary
movements




CLINICAL PRESENTATION
2. Chorea abrupt, irregular, jerky movements

CLINICAL PRESENTATION
3. Choreoathethoid

CLINICAL PRESENTATION
4. Dystonia- slow, rhythmic

CLINICAL PRESENTATION
5. Ataxic- unsteadiness, uncoordinated

CLINICAL PRESENTATION
MIXED TYPE

Spastic- dyskinetic 10-15%
Spastic- ataxic 5-10%
Rigid spastic rare

CLINICAL PRESENTATION
Clinical Signs:

Early Signs with Predictive value:

1. Tone abnormalities of trunk, neck and
limbs
2. Weak cry and suck
3. Need for tube feeding
4. Decreased activity level > 1 day


CLINICAL PRESENTATION
Tone abnormalities

Hypotonia earliest stage
Hypertonia spastic and rigid type

CLINICAL PRESENTATION
Opisthotonic

resistance when pulled to sit
hip extensor tightness
earliest sign of spasticity

Fluctuating tone dyskinesias

CLINICAL PRESENTATION
Reflex Abnormalities

Hyperreflexia, clonus
Adductor catch most common

Persistent primitive reflexes:
Spastic Tonic labyrinthine,
positive supportive reaction, grasp
Dyskinesia Moro, Tonic Neck

CLINICAL PRESENTATION
Postural abnormalities

Increased Flexor Pattern
Spasticity
Acquired Hemiparesis:

CLINICAL PRESENTATION
Delayed Motor Development

Related to degree of neuromuscular
dysfunction

Delay in sitting common sign

PROGNOSIS

1. Based on the type of CP

BEST prognosis spastic hemiplegia/ ataxic

POOR prognosis quadriplegia, flaccid/rigid

PROGNOSIS
2. Based on the onset of sitting

GOOD if px can sit by 2 years old

FAIR px can sit between 2-4 years old (50%
chance of ambulation)

POOR if px cannot sit by years old

PROGNOSIS
3. Based on primitive reflexes

GOOD - if at 1 yr. is (+) parachute and no primitive
reflex

FAIR if at 1 yr. there is (+) parachute and 1
primitive reflexed

POOR if at 1 yr. there is (+) parachute and 2
primitive reflexed
PROGNOSIS
4. RETARDATION / INTELLIGENCE RATIO

The severity of retardation is inversely
proportional to the childs prognosis for
ambulation
PROGNOSIS
5. ACCORDING TO SPEECH

GOOD can speak a word by 2 yrs. Old

FAIR can utter a recognizable sound at 2 yrs.
Old

POOR no words/ sound at 3 years old
PROGNOSIS
6. UPPER EXTRIMITY PROGNOSIS

No handedness / dominance by 2 yrs. Old

No concept of midline by 2 yrs. Old

No lateralization by 2 yrs. old
PHARMACOLOGICAL MANAGEMENT
The following are a list of the most frequently
used anti-spasmodic drugs used to treat
cerebral palsy:

Baclofen (Lioresal)
Dantrium (Dantrolene)
Botox (Botulinum toxin)
Flexeril (Cyclobenzadrine)

Anti-seizure Medications for Cerebral Palsy

Depakene (Valproic Acid)
Valium (Diazepam)
Dilantin (Phenytoin)
Epival (Divalproex)
Klonopin, Rivotril (Clonazepam)
Zarontin (Ethosuximide)

PHYSICAL THERAPY
MODALITIES



THERAPEUTIC EXERCISES

PHYSICAL THERAPY
Phelps
PHYSICAL THERAPY
Deaver
PHYSICAL THERAPY
Doman and Delacato - a series of set patterns
repeated many times during the day,
attempting to train cerebral dominance and
normalization of function

PHYSICAL THERAPY
Rood - Emphasizes sensory and motor systems
equally, activating muscles through sensory
receptors

PHYSICAL THERAPY
Bobath (most widely used) -
neurodevelopmental treatment to normalize
tone
PHYSICAL THERAPY
Vojta-European method - activates postural
development and equilibrium reactions to guide
normal development


PHYSICAL THERAPY
Conductive education - based on theory that
difficulties with motor dysfunction are problems of
learning