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Late-onset dyskinesia, also known as tardive dyskinesia, occurs after long-term treatment with an antipsychotic drug such as haloperidol (Haldol) or amoxapine (Asendin). The symptoms include tremors and writhing movements of the body and limbs, and abnormal movements in the face, mouth, and tongue – including involuntary lip smacking, repetitive pouting of the lips, and tongue protrusions.
Tardive dyskinesia (TD) is an iatrogenic disorder that results in involuntary repetitive body movements, which may include grimacing, sticking out the tongue or smacking the lips, [1] which occurs following treatment with medication.
Since it is difficult to measure extrapyramidal symptoms, rating scales are commonly used to assess the severity of movement disorders. The Simpson-Angus Scale (SAS), Barnes Akathisia Rating Scale (BARS), Abnormal Involuntary Movement Scale (AIMS), and Extrapyramidal Symptom Rating Scale (ESRS) are rating scales frequently used for such assessment and are not weighted for diagnostic purposes ...
Levodopa-induced dyskinesia (LID) is a form of dyskinesia associated with levodopa (l-DOPA), used to treat Parkinson's disease. It often involves hyperkinetic movements, including chorea, dystonia, and athetosis. [1] In the context of Parkinson's disease (PD), dyskinesia is often the result of long-term dopamine therapy.
Studies on diseases that are similar in nature to PD have revealed insights into the causes of movement disorders. Hypnogenic paroxysmal dyskinesia is a form of epilepsy affecting the frontal lobe. Single genes have been identified on chromosomes 15, 20, and 21, which contribute to the pathology of these epilepsy disorders. [4]
Causes [ edit ] Dysdiadochokinesia is a feature of cerebellar ataxia and may be the result of lesions to either the cerebellar hemispheres or the frontal lobe (of the cerebrum ), it can also be a combination of both. [ 3 ]
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