Athetosis

Athetosis
Bilateral athetosis
Classification and external resources
Specialty	neurology
ICD-10	R25.8
ICD-9-CM	781.0
DiseasesDB	16662
MeSH	D001264
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Athetosis is a symptom characterized by slow, involuntary, convoluted, writhing movements of the fingers, hands, toes, and feet and in some cases, arms, legs, neck and tongue. Movements typical of athetosis are sometimes called athetoid movements. Lesions to the brain are most often the direct cause of the symptoms, particularly to the corpus striatum. This symptom does not occur alone and is often accompanied by the symptoms of cerebral palsy, as it is often a result of this disease. Treatments for athetosis are not very effective, and in most cases are simply aimed at the uncontrollable movement, rather than the cause itself.

Athetosis can vary from mild to severe motor dysfunction; it is generally characterized by unbalanced, involuntary movements of muscle tone and a difficulty maintaining a symmetrical posture. The associated motor dysfunction can be restricted to a part of body or present throughout the body, depending on the individual and the severity of the symptom. One of the pronounced signs can be observed in the extremities in particular, as the writhing, convoluted movement of the digits. Athetosis can appear as early as 18 months from birth with first signs including difficulty feeding, hypotonia, spasm, and involuntary writhing movements of the hands, feet, and face, which progressively worsen through adolescence and at times of emotional distress. Athetosis is caused by lesions in several brain areas such as the hippocampus and the motor thalamus, as well as the corpus striatum; therefore children during the developmental age could possibly suffer from cognitive deficits such as speech impairment, hearing loss, and failed or delayed acquirement of sitting balance.

Athetosis is a symptom primarily caused by the marbling, or degeneration of the basal ganglia. This degeneration is most commonly caused by complications at birth or by Huntington's disease, in addition to rare cases in which the damage may also arise later in life due to stroke or trauma. The two complications of particular interest are intranatal asphyxia and neonatal jaundice.

Asphyxia directly causes basal ganglia damage due to lack of oxygen and therefore, insufficient nutrient supply. The lesions caused by asphyxia are most prominent on the caudate nucleus and the putamen. However, a less-studied consequence of the resulting hypoxia is its effect on the concentrations of the neurotransmitter dopamine within the synapses of neurons in the basal ganglia. Hypoxia leads to an increase in the extracellular dopamine levels and therefore, an increase in the activity of the dopaminergic neurons. Furthermore, this increase in extracellular concentration is not caused by an increase in the neurotransmitter synthesis, but instead on inhibiting its reuptake back into the neurons and glial cells. Therefore, there is an increased dopaminergic effect as dopamine remains in the synapse at higher concentrations leading to additional post-synaptic response. As a result, the uncontrollable writhing motions witnessed with athetosis deal with the over-activity of synapses within the basal ganglia.

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