Medback - Cerebral Palsy (Ppt)

8/12/2019 Medback - Cerebral Palsy (Ppt)

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CEREBRAL PALSY


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CEREBRAL PALSY

Is a disorder of movement and posture that result fromnon-progressive lesion or injury of the immature brain

Alterations:

Muscle tone DTR

primitive reflexes

Postural reactions

HALLMARK of CP

- ABNORMAL PATTERNS OF MOVEMENT


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RELATED ANATOMY

NEURAL DEVELOPMENT

From Embryo:

3 primary layers

Ectoderm Mesoderm

Endoderm


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RELATED ANATOMY

EARLY DEVELOPMENT


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ETIOLOGY

Premature infants

Multifactorial

In children with N birth weight:

80% of disabilities are a result of factors occurringbefore birth

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


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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


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ETIOLOGYPrenatal Perinatal Postnatal

Maternal infection

Rubella

Cytomegalovirus infection

Herpes simplex

Toxoplasmosis

Maternal diabetes

Rh incompatibility

Toxemia

Maternal malnutrition

Maternal thyroid disorders

Maternal seizure

Maternal irradiationAbnormal placental attachment

Congenital anomalies of the

brain

Coagulation factor

abnormalities

Factor V Leiden mutationAntiphospholipid 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 (


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ETIOLOGY

Abnormal development of the brain

Anoxia

Intracranial bleeding

Excessive neonatal asphyxia (hypoxic ischemicneonatal encephalopathy)

Trauma

Hypoglycemia

Infections


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EPIDEMIOLOGY

Leading cause of disability in childhood

The reported incidence varies but is approximately 2-3per 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)


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PATHOPHYSIOLOGY

Several neuropathic lesions have been

identified:

Hemorrhagic below the lining of the ventricles

(subependymal or interventricular)


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PATHOPHYSIOLOGY

Hypoxia causing encephalopathy

Can also occur in full-term infant


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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 cerebralblood flow

Emboli- block distal perfusion and thrombosis

Clot formation from polycythemia or a hypercoagulable state


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PATHOPHYSIOLOGY

Periventricular Leukomalacia


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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


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DIFFERENTIAL DIAGNOSIS

ConditionCerebral 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 similarfrom 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.


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SIGNS AND SYMPTOMS

(5 Major Findings)

Delayed motor development

Ab(N) tone

Ab(N) Posture

Ab(N) reflex

Ab(N) motor performance


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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


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Spastic types

Most common (75%)

Manifest signs of UMN lesions:

1. Hyperreflexia

2. Clonus

3. Persistent primitive reflexes


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Body parts involved:


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Dyskinetic types

1. Athetosis

slow , writhing, involuntarymovements


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2. Chorea abrupt, irregular, jerky movements


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3. Choreoathethoid


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4. Dystonia- slow, rhythmic


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5. Ataxic- unsteadiness, uncoordinated


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MIXED TYPE

Spastic- dyskinetic 10-15%

Spastic- ataxic 5-10%

Rigid spastic rare


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Clinical Signs:

Early Signs with Predictive value:

1. Tone abnormalities of trunk, neck andlimbs

2. Weak cry and suck3. Need for tube feeding

4. Decreased activity level > 1 day


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Tone abnormalities

Hypotonia

earliest stage Hypertonia spastic and rigid type


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Opisthotonic

resistance when pulled to sit hip extensor tightness

earliest sign of spasticity

Fluctuating tone dyskinesias


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Postural abnormalities

Increased Flexor Pattern Spasticity

Acquired Hemiparesis:


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Delayed Motor Development

Related to degree of neuromusculardysfunction

Delay in sitting

common sign


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PROGNOSIS

1. Based on the type of CP

BEST prognosis spastic hemiplegia/ ataxic

POOR prognosis quadriplegia, flaccid/rigid


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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


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PROGNOSIS

3. Based on primitive reflexes

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

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

POOR if at 1 yr. there is (+) parachute and 2primitive reflexed


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PROGNOSIS

4. RETARDATION / INTELLIGENCE RATIO

The severity of retardation is inversely

proportional to the childs prognosis for

ambulation


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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


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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


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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)


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Anti-seizure Medications for Cerebral Palsy

Depakene (Valproic Acid)

Valium (Diazepam)

Dilantin (Phenytoin)

Epival (Divalproex)

Klonopin, Rivotril (Clonazepam)

Zarontin (Ethosuximide)


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PHYSICAL THERAPY

Phelps


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PHYSICAL THERAPY

Deaver


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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


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PHYSICAL THERAPY

Rood - Emphasizes sensory and motor systems

equally, activating muscles through sensory

receptors


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PHYSICAL THERAPY

Bobath (most widely used) -

neurodevelopmental treatment to normalize

tone


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PHYSICAL THERAPY

Conductive education - based on theory that

difficulties with motor dysfunction are problems of

learning

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