BRAIN NEURO TREATMENT AND RESEARCH FOR CEREBRAL PALSY
Definition of cerebral palsy
The term cerebral palsy (CP) was originally coined more than a century ago and loosely translates as "brain paralysis." However, a precise definition has remained elusive because cerebral palsy is not a single diagnosis but an "umbrella" term describing nonprogressive brain lesions involving motor or postural abnormalities that are noted during early development. cerebral palsy has been described as follows:
A group of disorders of the development of movement and posture causing activity limitations that are attributed to non-progressive disturbances that occurred in the developing fetal or infant brain. The motor disorders of cerebral palsy are often accompanied by disturbances of sensation, cognition, communication, perception, and/or behavior and/or a seizure disorder.
Age of onset
The brain lesions of cerebral palsy occur from the fetal or neonatal period to up to age 3 years. Insults to the brain after age 3 years through adulthood may manifest clinically as similar or identical to CP, but, by definition, these lesions are not CP. Although the lesion to the developing brain occurs prior to age 3 years, the diagnosis ofcerebral palsy may not be made until after that time. Some authorities advocate not making a definitive diagnosis in some cases until age 5 years or later. This approach allows the clinical picture to be clear and potentially allows exclusion of progressive diseases . In addition, some children have been diagnosed with cerebral palsy at an early age, only to have the symptoms resolve later .
CP is restricted to lesions of the brain only; diseases specific to the peripheral nerves of the spinal cord (eg, spinal muscular atrophy, myelomeningocele) or to the muscles (eg, muscular dystrophies), although causing early motor abnormalities, are not considered CP cerebral palsy.
Approximately 30-50% of patients with cerebral palsy have mental retardation, depending on the type of CP. However, because of oromotor, fine motor, and gross motor difficulties, communication in cerebral palsy patients may be impaired and expression of intellectual capacity may be limited. However, if cerebral palsy is approached in a multidisciplinary manner, with physical, occupational, and nutritional therapy to maximize rehabilitative efforts, patients can be more fully integrated academically and socially.
Approximately 15-60% of children withcerebral palsy have epilepsy, and epilepsy is more frequent in patients with spastic quadriplegia or mental retardation.
Etiology and risk factors
The etiology of cerebral palsy is not well understood, and brain lesions are thought to be associated with prenatal, perinatal, or postnatal events of varying causes. Risk factors for cerebral palsy are multifactorial and can include preterm birth, multiple gestation, intrauterine growth restriction, male sex, low Apgar scores, intrauterine infections, maternal thyroid abnormalities, prenatal strokes, birth asphyxia, maternal methyl mercury exposure, and maternal iodine deficiency.
Classification and types
CP cerebral palsy is classified according to resting tone and what limbs are involved (called topographic predominance). Spastic CP, due to cortex/pyramidal tract lesions, is the most common type and accounts for approximately 80% of cases . Spasticcerebral palsy is characterized by spasticity (velocity-dependent increase in tone), hyperreflexia, clonus, and an upgoing Babinski reflex. Extrapyramidal or dyskineticcerebral palsy is characterized more by abnormal involuntary movements.
Typical types of CP
* Spastic hemiplegia -cerebral palsy predominantly affecting one side of the body, with upper extremity spasticity more than lower extremity spasticity (eg, right side involved with right arm more so than right leg)
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