Question

In: Anatomy and Physiology

PATHOLOGY 5-3 CEREBRAL PALSY Pathology Etiology Speed of onset Signs and symptoms  Consciousness  Cognition, language, and...

PATHOLOGY 5-3 CEREBRAL PALSY

Pathology

Etiology

Speed of onset

Signs and symptoms

 Consciousness

 Cognition, language, and memory

 Sensory

 Autonomic

 Motor

 Cranial nerves

 Vision

 Associated disorders

Region affected

Demographics

 Prevalence

Prognosis

Solutions

Expert Solution

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.


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