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Kinesia paradoxa can very easily be stimulated by visual and auditory cues, but there is an additional method that does not require any external cues. By having an individual focus all their attention on walking or another movement, they are sometimes able to control akinesia in its early stages.
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.
Four motor symptoms are considered cardinal signs in PD: slowness of movement (bradykinesia), tremor, rigidity, and postural instability. [1] Typical for PD is an initial asymmetric distribution of these symptoms, where in the course of the disease, a gradual progression to bilateral symptoms develops, although some asymmetry usually persists.
Paroxysmal kinesigenic dyskinesia (PKD), also called paroxysmal kinesigenic choreoathetosis (PKC), is a rare hyperkinetic movement disorder of the paroxysmal dyskinesias characterized by attacks of involuntary movements, which are triggered by sudden voluntary movements.
This is characterized by attacks of involuntary movements (dystonia, chorea, or ballism), which are typically triggered by sudden voluntary movements, but can also be triggered by involuntary movements as well (for example, hyperventilating).
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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.
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.