Tardive dyskinesia

Classification according to ICD-10
G24.0	Drug-induced dystonia Dyskinesia tarda
ICD-10 online (WHO version 2019)

Tardive dyskinesia (also: -dyskin like . Sien, dt "delayed motor disorder", syn. Tardive dyskinesia and tardive dyskinesia , from the French dyskinesia tardive ) are movement disorders, often in the face area (twitching, smacking and chewing movements) such as akathisia , Grimacing or involuntary movements of the extremities ( hyperkinesis ), which can occur as possible damage after prolonged use of neuroleptics . They are counted among the extrapyramidal hyperkinesias . The tardive dyskinesia are for long-term therapy with psychotropic drugs often irreversible and also respond to antagonists such as beta-blockers not, as they soften only side effects of neuroleptics, but have no effect on dyskinesias. Tardive dyskinesia was first described by George Crane in 1968.

definition

Under the generic term tardive dyskinesia , a distinction can be made between different appearances:

Tardive (orobuccolingual) dyskinesia

One with " tics " that is, grimacing and rhythmic movements in the facial area (face, tongue, mouth), also Anglicized as "fly catchers tongue" (dt. "Fly-catching tongue" ) concomitant symptoms circle. Occasionally, combinations of symptoms from other dyskinesias have been observed; for example rhythmic movements such as pelvic dyskinesia or continuous hand movements ("playing the piano in the air"). The clinical picture is often referred to as "classic tardive dyskinesia" .

Tardive dystonia

This manifests itself with the same symptoms as tardive dyskinesia.

Triggering circumstances

These socially stigmatizing and in some cases irreversible disorders occur preferentially - but not exclusively - with the older, “classic” neuroleptics of the butyrophenone or phenothiazine type . Highly potent substances, high doses and prolonged use of medication pose a particularly high risk for patients to develop such dyskinesias at a later point in time. The manifestation can sometimes take place after a very long period of time after ingestion (years, in extreme cases decades later).

The frequency of tardive dyskinesias, which are difficult to influence therapeutically, is estimated at 15% for conventional, highly potent neuroleptics, the manufacturer of Zyprexa gives only 1% for tardive dyskinesias. The exact data situation is assessed as unclear by independent sources. Only clozapine does not seem to cause tardive dyskinesia, but carries the risk of agranulocytosis .

There are still no reliable long-term studies on the newer, so-called atypical neuroleptics , but it seems probable that these too carry a risk in high, antipsychotically effective doses and longer-term administration. Even with so-called atypical neuroleptics, acute movement disorders occur - albeit less often. Olanzapine causes acute extrapyramidal movement disorders in 19% of patients compared to 45% with haloperidol .

In the case of classical psychoses, the atypical neuroleptics undoubtedly have treatment advantages, but for the above reasons a warning must be given before using them in geriatric patients due to restlessness. Additional risk factors for the development of tardive dyskinesia are: smoking, female gender, brain damage, old age. This means that if one or more risk factors are present, an atypical neuroleptic should be used, or even clozapine if the risk is high.

Damage Mechanism

These side effects can occur because the messenger substances , which are influenced by the neuroleptics for the purpose of relieving psychotic symptoms, also occur in other areas of the nervous system . The impairment of the dopaminergic transmission as a result of receptor blockages in the area of ​​the basal ganglia by neuroleptics is considered to be the cause of such disorders.

Symptoms

The characteristics of tardive dyskinesia often resemble normal movement patterns such as chewing, twisting the corners of the mouth, grasping movements or “playing the piano”, which however are performed involuntarily. In many cases, patients are unaware of these movements.

As a rule, the facial muscles, especially the oral and perioral muscles, are affected in tardive dyskinesia. Dyskinesia of the tongue is characterized by slow and repetitive movements in the oral cavity that bulge the cheeks ("candy sign"). Grimacing, raising your eyebrows, or frowning can also be signs of tardive dyskinesia.

Many patients bend and stretch individual fingers in a similar way to playing the guitar or piano. Dyskinesia of the legs can make it seem like you are pedaling slowly in place. Dyskinesia of the diaphragm results in choppy speech or uncontrollable moans.

For comparison: patients with Parkinson's disease have difficulty moving, patients with tardive dyskinesia have difficulty not moving.

Minimizing risk

The newer so-called atypical neuroleptics differ pharmacologically in part significantly from the older preparations. Apparently, tardive dyskinesias occur less frequently with the newer antipsychotics .

However, the respective risk of dyskinesia cannot yet be adequately assessed for many new developments: On the one hand, the experience does not extend over the same periods of time as with butyrophenones or phenothiazines, on the other hand, many people affected received both older and newer substances, which makes it difficult to identify the triggering agent.

Every single dose of a highly potent, “typically” acting neuroleptic increases the individual risk of tardive dyskinesia.

therapy

The only causal therapy would be to discontinue the triggering drug in good time. However, this is often impractical because the problems are recognized too late.

In the United States there are approaches to the prevention of long-term effects through treatment with concomitant administration of vitamins in high doses.

Tardive dyskinesias that have become manifest usually only react inadequately to treatment attempts. The reason is found primarily in the time lag between the damage caused by the use of neuroleptics: the influence itself can then no longer be eliminated.

Drug therapy options are available in the form of dopamine - agonistic substances that are otherwise used in Parkinson's patients, such as lisuride or pergolide . In addition, “movement-normalizing” substances such as tiapride , tetrabenazine or tizanidine are used .

Physiotherapy plays an important role in the alleviation of subjectively stressful complaints (the disorders that are registered as particularly noticeable by outsiders, however, are often beyond the control of the person concerned: stereotypes such as “trampling” the legs happen automatically and unconsciously).

Botulinum toxin is sometimes used for (temporary) improvement.

etymology

Dyskinesia is derived from the ancient Greek prefix δυς- (which denotes something unfortunate or adverse, according to the prefix “miss-” or “un-” in German ) and the word κίνησις kínēsis “movement”. Dyskinesia literally means movement disorder .

literature

• C. Ganos, A. Muenchau: Spaetdyskinesias - history, definition, differential diagnosis and therapy. In: Current Neurology. 38, 2011, pp. 309-314, doi : 10.1055 / s-0031-1287840 .

Individual evidence

1. ↑ ^{a b} W. Wolfgang Fleischhacker, Alex Hofer, Christian Jagsch, Walter Pirker, Georg Psota: Antipsychotikainduzierte tardive Syndrome . In: neuropsychiatry . tape 30 , no. 3 , September 1, 2016, ISSN  2194-1327 , p. 123-130 , doi : 10.1007 / s40211-016-0189-7 .
2. ↑ Medicinal measures in the event of an accelerated heart rate (sinus tachycardia), which was caused by clozapine. Retrieved November 30, 2019 . 
3. ↑ Hans Bangen: History of the drug therapy of schizophrenia . Berlin 1992, ISBN 3-927408-82-4 , p. 86.
4. ↑ German Society for Neurology : LL 11 2012 Dystonia , PDF
5. ↑ New on the market. New "atypical" neuroleptics: Olanzapine (ZYPREXA) / Sertindole (SERDOLECT). In: arznei-telegramm.de 1997, No. 10. Retrieved on December 29, 2019 . 
6. ↑ B. Müller-Oerlinghausen: Neuroleptics. ( Memento of the original from July 18, 2011 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. , Lecture 2007 (PDF file). 
7. ↑ Karl F. Masuhr: Extrapyramidal Hyperkinesis: A Guide for Clinic and Practice . Page 127. Georg Thieme Verlag, 2000, ISBN 978-3-13-105601-6 ( limited preview in Google book search).
8. ↑ Peter Berlit: Clinical Neurology . Page 124. Springer-Verlag, 2006, ISBN 978-3-540-31176-8 ( limited preview in Google book search).
9. ↑ David R. Hawkins: The prevention of Tardive Dyskinesia with high dosage vitamins: A study of 58,000 patients . In: Journal of Orthomolecular Medicine . tape 1 , no. 1 , 1986, pp. 24–26 (English, orthomolecular.org [PDF; accessed on December 16, 2019]): “A study of the practices of 80 physicians over a 10 year caseload of 58,000 patients treated with anti-psychotic drugs plus high dosage vitamins, reveals a total of only 26 patients developing Tardive Dyskinesia. This is an incidence of less than 0.05%. This is a remarkable finding in view of currently reported rates of 10% to as high as 60%. The data are strongly suggestive that the prescribing of high dosage Vitamins B3, C and B6, along with neuroleptic drugs, provides almost 100% protection against the development of this dread neurological disorder which is reportedly irreversible in 50% of those patients in whom it develops . ”
10. ^ Wilhelm Gemoll: Greek-German school and hand dictionary. Munich / Vienna 1965.

This article is about a health issue. It is not used for self-diagnosis and does not replace a diagnosis by a doctor. Please note the information on health issues !