In: Anatomy and Physiology
PATHOLOGY 5-3 CEREBRAL PALSY
Pathology |
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Etiology |
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Speed of onset |
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Signs and symptoms |
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Consciousness |
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Cognition, language, and memory |
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Sensory |
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Autonomic |
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Motor |
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Cranial nerves |
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Vision |
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Associated disorders |
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Region affected |
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Demographics |
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Prevalence |
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Prognosis |
CEREBRAL
PALSY
Cerebral palsy (CP) is defined as a nonprogressive neuromotor
disorder of cerebral origin. It includes heterogeneous clinical
states of variable etiology and severity ranging from minor
incapacitation to total handicap. Most of the cases have multiple
neurological deficits and variable mental handicap. The term does
not include progressive, degenerative or metabolic disorders of the
nervous system.
It is difficult to estimate the precise magnitude of the problem
since mild cases are likely to be missed. Approximately 1-2 per 100
live births is a reasonable estimate of the incidence.
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. The mechanism of CP in a large proportion of cases
remains unclear and primary neurological aberrations may be
unfolded in future. The importance of role of birth asphyxia has
been questioned by recent data and asphyxia may be manifestation of
the brain damage rather than the primary etiology.
Pathology
A variety of pathological lesions such as cerebral atrophy,
porencephaly, periventricular, leukomalacia, basal ganglia thalamic
and cerebellar lesions may be observed.
Speed of
onset
Most commonly early months of life , gradually appears so diagnosis
may be delayed until age age two years in most of the cases.
Signs and
symptoms
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.
Memory deficits are seen .One of the two has intellectual
disability so consious and cognitive are impaired.
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.
Affected
region.
Cerebral cortex
Prevalance
2-4 per 1000 live births.
Prognosis.
Children affected with cerebral palsy live between 30-70 years
depending upon the severity of the condition.