Cerebral Palsy

CP
 *Definition of CP:-
It’s A non progressive permanent impairment of
neuromuscular system leading to disorder of motion, tone, co-
ordination and posture due to brain insult or injury during the
period of early brain growth( generally under 3yrs age). It may
be associated with other evidence of brain damage as epilepsy,
mental retardation ,visual, auditory and or speech impairment.
*Prevalence :-
the estimated prevalence of CP is 100 -600/100.000 of
population.
* Causes of CP :-
1- Prenatal :- ( from last menstrual period till end of labour )
the most common cause 70%:
a- Hereditary ( genetic) e.g. congenital cerebellar
ataxia.
b- Environmental ( acquired) due to :-
- Intrauterine infections: rubella, CMV, mumps, hepatitis,
toxoplasmosis, and syphilis (TORCH).
- toxemia of pregnancy.
- Placental I insufficiency or infraction.
- Fetal anoxia e.g. premature separation of the placenta,
maternal anemia, hypotension.
- Prematurity.
- Maternal malnutrition and vitamin deficiencies.
- Maternal chronic disease as DM or renal failure.
- Pelvic irradiation in the first 3 months of pregnancy.
- In vitro fertilization.
2- Perinatal risk factor( From birth till the 7th day of life in term neonate and 28th days
of life in premature):-
- Hypoxic ischemic encephalopathy (HIE).
- Trauma and hemorrhage occurring in malposition, cephalo pelvic disproportion,
high forceps, breech presentation and delivery by vacuum extraction.
- Premature rupture of membranes.
- Kernicterus
- Infection : Perinatal herpes simplex , neonatal sepsis with meningitis.
3- Postnatal risk factors: ( after perinatal period till age 3yrs)
- Intracranial infection: meningitis, encephalitis.
- Skull fracture with hemorrhage.
- Lead encephalopathy.
- Vascular: Thrombosis, embolism.
- Severe dehydration.
Pathology and pathogenesis:-
Regardless the etiology , the brain damage due to anoxia
and hemorrhage . There may be diffuse atrophy of cortex , loss
of neurons with gliosis, disruption of interconnecting pathways
or delay in brain maturation.
 Classification Of CP
** CP can be classified according to various criteria:-
a- Anatomic site o brain lesion.
b- Clinical picture.
c- Topographic involvement of the extremities.
d- The degree of tonicity.
e- The severity of involvement.
f- The etiology.
1- according to anatomic site f brain lesion.
a- Pyramidal.
b- Extrapyramidal.
c- Cerebellar.
2- According to the clinical picture:
A- Spastic (70% of cases):-
- Increased tone (clasp- knife).
- Deep tendon reflexes are markedly increased ,
usually with sustained ankle clonus.
- Positive Babinski sign.
- Persistence of primitive reflexes as Moro, tonic
neck releflex.
- Abnormal tone leads to contractures most
commonly at hips, knees and ankles.
B- Dyskinesia ( 15% of cases):
There is abnormal movement and change in tone( increased
or decreased)
- Rigidity:- Constant increase in tone. Deep reflexes may be
normal or increased, no clonus , no Babinski sign, and persistent
primitive reflexes.
- Dystonia : sustained contractions of muscle groups that
lead to prolonged , often twisted, posturing of the face , limbs
and trunk.
- Chorea: Quick random movements that may involve any
skeletal muscle groups,pt with chorea have difficulty sustained
position or muscle contraction.
 - Athetosis : Slow, twisting movements, usually around the
long axis of limb and more prominent distally. NB( choreo-
athetosis).
- Tremors: Rhythmic alternating movements.
C- Ataxia ( 5% of cases):
-Means disturbance in balance and equilibrium, often with
hypotonia, incoordination of movement and intension tremers.
D- Mixed ( 10% of cases):
-e.g. spasticity and ataxia may coexist ( as ataxic diplegia).
3- Classification according to the topographic involvement: this for
spastic type:-:
A- Quadriplegia: subdivided into:
- Tetraplegia : Hyper tonicity is equal in the four limbs.
- Cerebral diplegia : hyper tonicity in the lower limbs is more
than its degree in the upper limbs.
- Double hemiplegia: : hyper tonicity is more in the upper
limbs and more in one side than other.
B- Hemiplegia : : one side is involved .
c- Paraplegia : both lower limbs are involved.
d- Triplegia : both lower limbs and one upper limb.
e- Monoplegia: one limb only is involved.
4- Classification according to severity of involvement:-
a- Mild : The child able to move ,to use his arms and
speak well enough, he does not need special care.
b- Moderate : the involvement o handicapping the
pt. in movements, self-help or communication but not
sufficient to disable him entirely. Such pts. need special
care.
c- Severe : there is total involvement and the pt. is
incapacitated being bed ridden or restricted to a wheel
chair.
 Early Diagnosis of CP

** The diagnosis of CP could be suspected with:

A- History of risk factors:-
- TORCH infection : Rubella, toxoplasmosis in the first trimester.
- Low birth wt., Low Apgar score.
- Neonatal jaundice , convulsions or cyanotic attacks in infancy.
- Severe illness including meningitis.
- Head injury associated with loss of consciousness.
B- Developmental observation:
- Delay motor development.
- Any infant who is right or left handed before 2yrs is at risk of
having hemiplegia.

-
 - Any infant who is not active as suspected, who moves one limb
less than other, or keeps his hand clenched after the age of
3months is suspected to have CP.
-Persistent toe walking can be a sign of spasticity .
- Early neck support ( due to hypertonia) is an early
sign of spasticity.
C- Persistence of the primitive reflexes:
- Moro reflex; Palmar grasp reflex; Asymmetric tonic
neck reflex.
d- Absence of the reflexes:
- Parachute reflex; Labyrinthine rightining reflex.
-
• Associated manifestations that may be present with CP:-:-One or
more of the following:-
1- Mental handicap (55% have I.Q.< 70).
2- Epilepsy in about 1/3 have fits.
3-Visual defects in 25-50% o cases; Hearing defect especially
kernicterus; Speech defects; Microcephaly; Learning disorder;
language disorder ( delay speech or dysarthria); Sensory handicaps.
4- Psychological disorders: emotional instability; autistic like
features; sleep disorders
5- Teeth problem: as dental caries and enamel hypoplasia.
6- Malnutrition and bowel disturbances as constipation.
 Management of CP
***The is best a accomplished by the cooperation of ,
pediatrician, physiotherapist, orthopedist, social worker, surgeon
and Psychiatrist with family:-
1- The role of Pediatrician:-
- To take care of the pt. throughout infancy and childhood.
- Supervising his notional status.
- To prescribe drugs need by CP Pt.
- To explain with the help of social workers and the
psychiatrist the nature of the disease to the family.
2- The role of Physiotherapist:
Through passive stretching and exercises will assist
producing muscle relaxation, prevention of contracture and
deformities o the joint.
 3- Durgs used in the management of CP:
- Dantorlene: muscle relaxant in spastic and athetoid children.
- Levodopa: of benefit in the athetoid CP Pt.
- Diazepam : Can be used as muscle relaxant and as sedative.
- IM botulinum toxin A.
- Intrathecal baclofen.
4- Orthopedic surgery :
- Must be employed to improve function by increasing the strength
of motion. Correct deformities, provide stability or for cosmetic reason.
5- Speech therapy :
- Is intended to obtain intelligible speech to facilitate
communication with others.
*Prognosis of CP:-
- 25% good .
- 75% bad due to severe motor handicap with normal mentality ( in 15%) or severe
mental retardation (60%).
- The earlier the treatment the better prognosis. Early treatment gives the child the
opportunity to require more skills in the motor field with a good pattern of movements.
* Prevention of CP:-
-Immunization of all females against rubella.
- Maternal screening against toxoplasmosis early in pregnancy.
- Proper prevention and management of eclampsia and placental insufficiency.
- Improvement of neonatal care.
- Prevention of kernicterus by proper prevention and management of Rh
incompatibility and unconjugated hyperbilirubinemia.
- Early diagnosis and treatment of meningitis.