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G.ERIC MD4
Cerebral palsy (CP) is defined as a nonprogressive
neuromotor disorder of cerebral origin.
Etiopathogenesis
Factors may operate prenatally, during delivery or in the
postnatal period. Cerebral malformations, perinatal
hypoxia, birth trauma, chorioamnionitis, prothrombotic
factors, acid base imbalance, indirect hyperbilirubinemia,
metabolic disturbances and intrauterine or acquired
infections may operate. Most infants have multiple risk
factors. Prematurity is an important risk factor for spastic
diplegia while term weight babies get quadriparesis or
hemiparesis.
CONT…
A variety of pathological lesions such as cerebral
atrophy, porencephaly, periventricular, leukomalacia,
basal ganglia thalamic and cerebellar lesions may be
observed.
Types of Cerebral Palsy
classified on basis of topographic
distribution, neurologic findings and etiology.
Spastic Cerebral Palsy This is the commonest form (65%) and
is topographically
classified into spastic quadriparesis, diplegia or hemiparesis.
Early diagnostic features of neural damage
include abnormally persistent neonatal reflexes, feeding
difficulties, persistent cortical thumb after 3 months age
and a firm grasp. They have variable
degrees of mental and visual handicaps, seizures and
behavioral problems.
Spastic quadriparesis is more common in term babies and
exhibits signs including opisthotonic posture, pseudobulbar
palsy, feeding difficulties, restricted voluntary
movements and motor deficits.
Spastic diplegia is commoner in preterm babies and is
associated with periventricular leukomalacia. The lower
limbs are more severely affected with extension and
adduction posturing, brisk tendon jerks and contractures
Spastic hemiplegia is usually recognized after 4-6 months
age. Early hand preference, abnormal persistent fisting,
abnormal posture or gait disturbance may be the
presenting
complaint
Hypotonic (Atonic) Cerebral PalsyDespite pyramidal
involvement, these patients are atonic
or hypotonic. Tendon reflexes are normal or brisk and
Babinski response is positive. They are often severely
mentally retarded. In cerebellar involvement, hypotonia
is not associated with exaggerated reflexes. Muscles may
show fiber disproportion and delayed CNS maturation is
common.
Extrapyramldal CP
This form accounts for 30% of cases. The clinical
manifestations
include athetosis, choreiform movements, dystonia,
tremors and rigidity. Arms, leg, neck and trunk may be
involved. Mental retardation and hearing deficits may be
present.
Cerebellar Involvement
This form is seen in less than 5% of the patients. There is
hypotonia and hyporeflexia. Ataxia and intention tremors
appear by the age of 2 yr. Nystagmus is unusual; mental
status may be near normal in some of these patients
Evaluation
Eyes. Nearly half of the patients have strabismus,
paralysis
of gaze, cataracts, coloboma, retrolental fibroplasia,
perceptual and refractive errors.
Ears. Partial or complete loss of hearing is usual in
kernicterus. Brain damage due to rubella may be
followed
by receptive auditory aphasia.
Speech. Aphasia, dysarthria and dyslalia are common
among dyskinetic individuals.
Sensory defects. Astereognosis and spatial disorientation
are seen in one-third of the patients.
Seizures. Spastic patients usually have generalized or
focal
tonic seizures. Seizures are more common in disorders
acquired postnatally. These patients respond poorly to
antiepileptic agents. Electroencephalograms show gross
abnormalities.
Intelligence. About a quarter of the children may have
borderline intelligence (IQ 80-100); and about half of
them
are severely mentally retarded.
Miscellaneous. Inadequate thermoregulation and
problems
of social and emotional adjustment are present in many
cases. These children may have associated dental defects
and are more susceptible to infections
Diagnosis
The diagnosis of cerebral palsy should be suspected in a
child with low birthweight and perinatal insult;
clinically
has an increased tone, feeding difficulties and global
development delay. Abnormalities of tone posture,
involuntary movements and neurological deficits should
be recorded. Evaluation includes perinatal history,
detailed neurological and developmental examination
and
assessment of language and learning disabilities
Dlfferentlal Diagnosis
 Neurodegenerative disorders.
 Hydrocephalus and subdural effusion.
 Brain tumors or space occupying lesions
 Muscle disorders
 Ataxia-telangiectasia
Prevention
Prevention of maternal infection, fetal or perinatal
insults,
good maternal and neonatal care reduces prevalence.
Early diagnosis, prompt adequate management plans
can
reduce the residual neurological and psychosocial
emotional handicaps for the child and his family.
Management
The management plan should be holistic, involve the
family and be directed to severity, type of neurological
deficits and associated problems. Stress on improving
posture, reducing tone, preventing contractures and
early
stimulation is necessary
Tranquilizers are administered for behavior
disturbances and muscle relaxants may be used for
improving
muscle function. Baclofen and tizanidine help to reduce
spasticity. Diazepam may ameliorate spasticity and
athetosis. Dantrolene sodium helps in relaxation of
skeletal
muscles. Dynamic contractures can be managed with
botulinum toxin injection or alternatively nerve block
with
phenol.
Occupational therapy. The beginning is made with simple
movements of self-help in feeding and dressing with
progressive development of more intricate activities like
typing.
Orthopedic support. Tendon, muscle and bony surgeries
may be required. Light weight splints may be required
for tight tendo-Achilles and cortical thumb.
Cp

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Cp

  • 2. Cerebral palsy (CP) is defined as a nonprogressive neuromotor disorder of cerebral origin.
  • 3. Etiopathogenesis Factors may operate prenatally, during delivery or in the postnatal period. Cerebral malformations, perinatal hypoxia, birth trauma, chorioamnionitis, prothrombotic factors, acid base imbalance, indirect hyperbilirubinemia, metabolic disturbances and intrauterine or acquired infections may operate. Most infants have multiple risk factors. Prematurity is an important risk factor for spastic diplegia while term weight babies get quadriparesis or hemiparesis.
  • 4. CONT… A variety of pathological lesions such as cerebral atrophy, porencephaly, periventricular, leukomalacia, basal ganglia thalamic and cerebellar lesions may be observed.
  • 5. Types of Cerebral Palsy classified on basis of topographic distribution, neurologic findings and etiology. Spastic Cerebral Palsy This is the commonest form (65%) and is topographically classified into spastic quadriparesis, diplegia or hemiparesis. Early diagnostic features of neural damage include abnormally persistent neonatal reflexes, feeding difficulties, persistent cortical thumb after 3 months age and a firm grasp. They have variable degrees of mental and visual handicaps, seizures and behavioral problems.
  • 6. Spastic quadriparesis is more common in term babies and exhibits signs including opisthotonic posture, pseudobulbar palsy, feeding difficulties, restricted voluntary movements and motor deficits. Spastic diplegia is commoner in preterm babies and is associated with periventricular leukomalacia. The lower limbs are more severely affected with extension and adduction posturing, brisk tendon jerks and contractures
  • 7. Spastic hemiplegia is usually recognized after 4-6 months age. Early hand preference, abnormal persistent fisting, abnormal posture or gait disturbance may be the presenting complaint
  • 8. Hypotonic (Atonic) Cerebral PalsyDespite pyramidal involvement, these patients are atonic or hypotonic. Tendon reflexes are normal or brisk and Babinski response is positive. They are often severely mentally retarded. In cerebellar involvement, hypotonia is not associated with exaggerated reflexes. Muscles may show fiber disproportion and delayed CNS maturation is common.
  • 9. Extrapyramldal CP This form accounts for 30% of cases. The clinical manifestations include athetosis, choreiform movements, dystonia, tremors and rigidity. Arms, leg, neck and trunk may be involved. Mental retardation and hearing deficits may be present. Cerebellar Involvement This form is seen in less than 5% of the patients. There is hypotonia and hyporeflexia. Ataxia and intention tremors appear by the age of 2 yr. Nystagmus is unusual; mental status may be near normal in some of these patients
  • 10. Evaluation Eyes. Nearly half of the patients have strabismus, paralysis of gaze, cataracts, coloboma, retrolental fibroplasia, perceptual and refractive errors. Ears. Partial or complete loss of hearing is usual in kernicterus. Brain damage due to rubella may be followed by receptive auditory aphasia. Speech. Aphasia, dysarthria and dyslalia are common among dyskinetic individuals.
  • 11. Sensory defects. Astereognosis and spatial disorientation are seen in one-third of the patients. Seizures. Spastic patients usually have generalized or focal tonic seizures. Seizures are more common in disorders acquired postnatally. These patients respond poorly to antiepileptic agents. Electroencephalograms show gross abnormalities.
  • 12. Intelligence. About a quarter of the children may have borderline intelligence (IQ 80-100); and about half of them are severely mentally retarded. Miscellaneous. Inadequate thermoregulation and problems of social and emotional adjustment are present in many cases. These children may have associated dental defects and are more susceptible to infections
  • 13. Diagnosis The diagnosis of cerebral palsy should be suspected in a child with low birthweight and perinatal insult; clinically has an increased tone, feeding difficulties and global development delay. Abnormalities of tone posture, involuntary movements and neurological deficits should be recorded. Evaluation includes perinatal history, detailed neurological and developmental examination and assessment of language and learning disabilities
  • 14. Dlfferentlal Diagnosis  Neurodegenerative disorders.  Hydrocephalus and subdural effusion.  Brain tumors or space occupying lesions  Muscle disorders  Ataxia-telangiectasia
  • 15. Prevention Prevention of maternal infection, fetal or perinatal insults, good maternal and neonatal care reduces prevalence. Early diagnosis, prompt adequate management plans can reduce the residual neurological and psychosocial emotional handicaps for the child and his family.
  • 16. Management The management plan should be holistic, involve the family and be directed to severity, type of neurological deficits and associated problems. Stress on improving posture, reducing tone, preventing contractures and early stimulation is necessary
  • 17. Tranquilizers are administered for behavior disturbances and muscle relaxants may be used for improving muscle function. Baclofen and tizanidine help to reduce spasticity. Diazepam may ameliorate spasticity and athetosis. Dantrolene sodium helps in relaxation of skeletal muscles. Dynamic contractures can be managed with botulinum toxin injection or alternatively nerve block with phenol.
  • 18. Occupational therapy. The beginning is made with simple movements of self-help in feeding and dressing with progressive development of more intricate activities like typing. Orthopedic support. Tendon, muscle and bony surgeries may be required. Light weight splints may be required for tight tendo-Achilles and cortical thumb.