Someone has late dyskinesia
Distortion of voluntary movements through involuntary muscle activity. Paroxysmal kinesigen dyskinesias (PKD) are rare dyskinesias that are triggered in those affected by voluntary movements and that are manifested by unilateral or bilateral chorea, chorea athetosis, ballism, or dystonic posture. The syndrome is often familial or hereditary; sporadic cases also occur. PKD can also occur secondary to various diseases or metabolic disorders and disappear again with treatment of these metabolic disorders. It is known to occur in the context of multiple sclerosis, after strokes, early childhood brain damage, substance abuse, diabetes mellitus, hypoparathyroidism, and hyperthyroidism. Tardive dyskinesia (late dyskinesia) Potentially irreversible, late-onset extrapyramidal symptoms of movement disorder, often caused by long-term use of standard antipsychotics. Manifestations include involuntary movements of the mouth, tongue, lips, limbs, and trunk. Repetitive chewing, smacking and swallowing movements are the most common, the tongue can often no longer be held straight out of the mouth (early signs), and head and trunk movements also occur. Treatment can be difficult, and prolonged symptoms often result in non-compliance or discontinuation of antipsychotic treatment. Tardive dyskinesias are more common in smokers than non-smokers. The information on the frequency of this serious side effect of neuroleptics varies widely. For inpatients, the figures fluctuate between 0.5 and 70%. On average, according to meta-analyzes taking classic antipsychotics, around 20% of patients should have or develop tardive dyskinesia, while previously untreated patients with schizophrenia should suffer from tardive dyskinesia in 5% . When antipsychotics are discontinued, patients with tardive dyskinesia should experience relapses more quickly than patients without dyskinesia. The dyskinesias are often masked when the neuroleptic dose is increased and then reappear when the dose is reduced. Some authors establish a connection between tardive dyskinesias and the supersensitivity psychoses, which are controversial in the literature. It is undisputed that significantly fewer dyskinesias are to be expected with atypicals than with classic antipsychotics. Whether clozapine causes tardive dyskinesia at all is controversial. Really reliable comparative figures between atypicals and classic antipsychotics are not yet available. What is certain is that the number of patients with tardive dyskinesia has declined significantly in recent years since the introduction of atypicals. Treatment with atypicals may therefore be preventive. Women, patients with (also accompanying) affective disorders and elderly patients are particularly at risk. Concomitant diseases such as diabetes or brain damage also have a beneficial effect. The late dyskinesias, which sometimes persist, are not only a medical but also a social problem. They contribute significantly to the stigmatization of the mentally ill. Slow dosage increases and slow dose reductions can reduce the risk. Therapy is usually switched to clozapine, sometimes tiapride or nitoman helps, sometimes botulinum toxin treatments are also possible. Dyskinesias are one of themn strongly debilitating and stigmatizing side effects that occur in particular with conventional neuroleptics. Little is known, apparently people who suffer from schizophrenia already have an increased risk of dyskinesia as part of the disease. Some authors had therefore already suspected that the late dyskinesia was not a side effect of the treatment at all, but a symptom of the disease. More recent studies that show a clearly lower risk among atypicals, however, show the opposite. People over the age of 50 are particularly sensitive to this side effect. While an average risk of 5% per year is assumed, this risk in people over 50 years of age is 25%, 34%, and 53% after 1, 2, and 3 years of cumulative use of conventional neuroleptics. In a study in Estonia, of 99 chronic institutionalized schizophrenic patients between the ages of 8-65 years who were treated with conventional neuroleptics (79.8%) or clozapine (20.2%), 61.6% had movement disorders, 31.3% had neuroleptic-induced akathisia , 23.2% had neuroleptic-induced Parkinsonoid and 32.3% neuroleptic-induced late dyskinesia. In a meta-analysis, the annual incidence of late dyskinesia among atypicals was 0% in children and 0.8% (range = 0.0% - 1.5%) among adults, 6.8% in a mixed old population and 5.3% (range = 0.0% - 13.4%) in patients over 54 years of age. In adults, the I.incidence with haloperidol 5.4% (range = 4.1% - 7.4%). Quotation from Leucht et al., NeuroTransmitter 11Â · 2003 page 51 ff .: It was shown that under long-term treatment with conventional neuroleptics the incidence of late dyskinesias (approx. 5% per year) was five times higher than under atypicals ( approx. 1% per year). Extrapolated, this means that after five years of relapse prophylactic treatment, about 25% of the patients treated with typical drugs develop late dyskinesia, while with atypical drugs only about 5% of the patients would suffer from these serious side effects. It is possible that late dyskinesia, which is very disabling, can be successfully treated by bilateral deep brain stimulation in the globus pallidus. In any case, an initial study on the matter was successful.
Margaret G. Woerner, Jose Ma. J. Alvir, Bruce L. Saltz, Jeffrey A. Lieberman, and John M. Kane Prospective Study of Tardive Dyskinesia in the Elderly: Rates and Risk Factors Am J Psychiatry 1998 155: 1521-1528. [Abstract] [Full Text Gervin et al. Spontaneous Abnormal Involuntary Movements in First-Episode Schizophrenia and Schizophreniform Disorder: Baseline Rate in a Group of Patients From an Irish Catchment Area Am. J. Psychiatry 1998; 155: 1202-1206. ABSTRACT | FULL TEXT Sven Janno, M.D., Matti Holi, M.D., Ph.D., Katinka Tuisku, M.D., Ph.D., and Kristian Wahlbeck, M.D., Ph.D. Prevalence of Neuroleptic-Induced Movement Disorders in Chronic Schizophrenia Inpatients Am J Psychiatry 161: 160-163, January 2004,: Christoph U. Correll, M.D., Stefan Leucht, M.D., and John M. Kane, M.D. Lower Reviews and OverviewsRisk for Tardive Dyskinesia Associated With Second-Generation Antipsychotics: A Systematic Review of 1-Year Studies Â © 2004 American Psychiatric Association, Am J Psychiatry 161: 414-425, March 2004Chouinard G., Annable L., Mercier P., Ross-Chouinard A. (1986a): A five-year follow-up study of tardive dyskinesia. Psychopharmacol.Bull. 22, 259-263 Jenner P., Marsden C.D. (1987): Neuroleptic-induced tardive dyskinesia. Acta psychiat. Belg. 87, 566-568, Jeste D.V., Potkin S.G., Sinha S. et al. (1979): Tardive Dyskinesia: reversible and persistent. Arch. Gen. Psychiat. 36, 585-590 Sachdev P.S. (2000): The current status of tardive dyskinesia. Austral.and N.Z. J. Psychiatr. 34 (3), 355-69S.A. Chong, E.C. Tan, C.H. Tan, Mythily, Smoking and tardive dyskinesia: lack of involvement of the CYP1A2 gene, J Psychiatry Neurosci 2003; 28 (3): 185-9.abstract / rÃ © sumÃ © in HTML / full text in PDF Philippe Damier, Stephane Thobois, Tatiana Witjas, Bilateral Deep Brain Stimulation of the Globus pallidus to Treat Tardive Dyskinesia Arch Gen Psychiatry. 2007; 64: 170-176
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