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.
[9] Some examples of these types of involuntary movements include:[10] In some cases, an individual's legs can be so affected that walking becomes difficult or impossible.
[13] Respiratory irregularity, such as grunting and difficulty breathing, is another symptom associated with tardive dyskinesia, although studies have shown that the rate of people affected is relatively low.
[14] Tardive dyskinesia is often misdiagnosed as a mental illness rather than a neurological disorder,[15] and as a result, people are prescribed neuroleptic drugs, which increase the probability that the person will develop a severe and disabling case, and shortening the typical survival period.
Tardive akathisia involves painful feelings of inner tension and anxiety and a compulsive drive to move the body.
Tardive myoclonus, a rare disorder, presents as brief jerks of muscles in the face, neck, trunk, and extremities.
The Abnormal Involuntary Movement Scale (AIMS) examination is a test used to identify the symptoms of tardive dyskinesia (TD).
[20] However, the time-course of tardive dyskinesia and its increased prevalence in older populations and drug and alcohol users suggest that dopamine supersensitivity is not a complete explanation.
Such individual differences may be due to genetic polymorphisms, which code for D2 receptor binding site affinity, or prior exposure to environmental toxins.
Decreased functional reserve or cognitive dysfunction, associated with aging, intellectual disability, alcohol and drug use, or traumatic head injuries, has also been shown to increase risk of developing the disorder among those treated with neuroleptics.
[24] Other dopamine antagonists and antiemetics can cause tardive dyskinesia, such as metoclopramide and promethazine, used to treat gastrointestinal disorders.
[25] From 2008, there have been reported cases of the anti-psychotic medication aripiprazole, a partial agonist at D2 receptors, leading to tardive dyskinesia.
[27] The available research seems to suggest that the concurrent prophylactic use of a neuroleptic and an antiparkinsonian drug is useless to avoid early extrapyramidal side-effects and may render the person more sensitive to tardive dyskinesia.
[33] Elderly people are also at a heightened risk for developing TD,[10] as are females and those with organic brain injuries or diabetes mellitus and those with the negative symptoms of schizophrenia.
Although further research is needed, studies reported a much lower percentage of individuals developing tardive dyskinesia than the current rate of people for those taking antipsychotic drugs.
[40] Tetrabenazine, which is a dopamine depleting drug, is sometimes used to treat tardive dyskinesia and other movement disorders (e.g. Huntington's chorea).
[10] As of 2018, evidence is insufficient to support the use of benzodiazepines, baclofen, progabide, sodium valproate, gaboxadol, or calcium channel blockers (e.g.
[46][47][48] Tardive dyskinesia most commonly occurs in people with psychiatric conditions who are treated with antipsychotic medications for many years.
"[50] More drastic data was found during a longitudinal study conducted on individuals 45 years of age and older who were taking antipsychotic drugs.
However, some studies express concern that the number of people affected has decreased far less than expected, cautioning against the overestimation of the safety of modern antipsychotics.