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The first noted case of athetosis was discovered by W. A. Hammond and described in his book Diseases of the Nervous System in 1871. [9] Hammond was also the person who created the term "athetosis", Greek for "without position". [23] In his initial description of athetosis, the extent of the uncontrolled movement was limited to the fingers and toes.
Athetoid cerebral palsy, or dyskinetic cerebral palsy (sometimes abbreviated ADCP), is a type of cerebral palsy primarily associated with damage, like other forms of CP, to the basal ganglia in the form of lesions that occur during brain development due to bilirubin encephalopathy and hypoxic–ischemic brain injury. [1]
Choreoathetosis (CA) is characterized by hyperkinesia (chorea i.e. rapid involuntary, jerky, often fragmented movements) and hypokinesia (athetosis i.e. slower, constantly changing, writhing or contorting movements).
The class competes using a wheelchair. The classification is one of eight for people with cerebral palsy, and one of four for people with cerebral palsy who use a wheelchair. Athletes in this class have moderate quadriplegia, and difficulty with forward trunk movement. They also may have hypertonia, ataxia and athetosis.
Ataxia (from Greek α- [a negative prefix] + -τάξις [order] = "lack of order") is a neurological sign consisting of lack of voluntary coordination of muscle movements that can include gait abnormality, speech changes, and abnormalities in eye movements, that indicates dysfunction of parts of the nervous system that coordinate movement, such as the cerebellum.
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Spastic cerebral palsy is caused by malformation of or damage to the parts of the brain that control movement. [12] What exactly makes some children susceptible to such brain damage is often unknown but it is believed that cerebral palsy may be the result of causal pathways, or chains of events that cause or increase the likelihood of brain injury. [13]
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