Atypical neuroleptic

from Wikipedia, the free encyclopedia

Atypical neuroleptics ( syn. Atypical antipsychotics , or atypicals for short ) are a heterogeneous group of drugs that are used to treat schizophrenia and other psychoses . "Typical antipsychotics" such as chlorpromazine or haloperidol have been used for this purpose since the 1950s (first generation of antipsychotics). From the 1990s, however, various neuroleptics based on different mechanisms of action were developed for the same indications . In order to clearly differentiate this group of antipsychotics of the “second” generation from those of the “first”, the term atypical neuroleptics is used for them.

The term atypical neuroleptic originated with the introduction of clozapine in the treatment of schizophrenia . The new substances are said to cause the typical side effects of neuroleptics less frequently, in particular less frequent extrapyramidal motor disorders (EPMS) and tardive dyskinesia . On the other hand, there are other, sometimes serious, side effects of the new substances. Whether the atypicals, some of which are very expensive, represent real progress is a matter of dispute.

properties

Extrapyramidal motor disorders

Textbooks in psychiatry and pharmacology name the lower EPMS rate (EPMS stands for extrapyramidal motor disorders ) as a characteristic common feature of the atypicals. However, there are no limit values ​​or quantified findings. In general, EPMS and dyskinesia should be largely absent in atypical nerve "in doses that are already antipsychotically effective". However, there are studies available for individual atypicals in which these substances showed a Parkinsonoid incidence comparable to “typical” neuroleptics (for example risperidone vs. flupentixol ). In addition, the first neuroleptics (e.g. chlorpromazine ) produced little EPMS.

Effect on negative symptoms

Atypicals are on the positive effect with equally good symptoms better efficacy against the so-called negative symptoms of psychosis include than the classical neuroleptics. Authors such as Möller or Benkert / Hippius take contradicting views on this. The test instruments used (especially rating scales) do not allow a clear delimitation and no etiological assignment of the negative symptoms. Symptoms such as withdrawal or depressed mood could in individual cases arbitrarily be considered primary (expression of the illness) or secondary (consequence of the personal situation, clinical environment, etc.). Significant progress has not yet been demonstrated.

Molecular pharmacological properties

In addition to the antagonistic effect of classic neuroleptics on dopamine receptors of subtype D 2 , most atypical neuroleptics show a pronounced antagonistic effect on serotonin receptors of type 5-HT 2A . The ratio of the affinity of a neuroleptic for 5-HT 2A receptors to its affinity for D 2 receptors, also known as the Meltzer index , is used to predict atypical neuroleptic properties. The clinical improvement (especially the negative symptoms) and the lower EPMS rate should be based on the inhibition of 5-HT 2A receptors together with the antidopaminergic effect. Other molecular pharmacological properties, such as the partial agonism of aripiprazole and amisulpride on dopamine receptors, can also be used to explain atypical neuroleptic properties. A special role of the dopamine D 4 receptor is also discussed.

Medicinal substances

The following substances are classified as atypicals:

The classification of sulpiride is handled inconsistently, since the term atypical only became popular after the introduction of sulpiride and played no role in its evaluation in practice. The analog substance amisulpride , however, is generally classified as an atypical. The two benzamides differ pharmacologically from the other neuroleptics, both from the older and the newer representatives.

See also

literature

Web links

Commons : Atypical Neuroleptic  - Collection of images, videos, and audio files

Individual evidence

  1. ^ NIMH online: Mental health Medications. 17th September 2009
  2. ^ HC Margolese, G. Chouinard, TT Kolivakis, L. Beauclair, R. Miller: Tardive dyskinesia in the era of typical and atypical antipsychotics. . In: Can J Psychiatry . 50, No. 9, August 2005, pp. 541-547. PMID 16262110 .
  3. ↑ A. ucok, W. Gaebel: Side effects of atypical antipsychotics: a letter overview . In: World Psychiatry . 7, No. 1, February 2008, pp. 58-62. PMID 18458771 . PMC 2327229 (free full text).
  4. ↑ J. Scherer, P. Dobmeier, K. Kuhn, W. Schmaus: Frequency of rigor with flupentixoldecanoate and risperidone depending on the dosage . In: Psychiatr Prax . 31 Suppl. 1, November 2004, pp. 167-169. doi : 10.1055 / s-2004-828461 . PMID 15570542 .
  5. ^ Bangen, Hans: History of the drug therapy of schizophrenia. Berlin 1992, ISBN 3-927408-82-4
  6. ↑ K. Salimi, LF Jarskog, JA Lieberman: Antipsychotic drugs for first-episode schizophrenia: a comparative review . In: CNS Drugs . 23, No. 10, October 2009, pp. 837-55. doi : 10.2165 / 11314280-000000000-00000 . PMID 19739694 .
  7. ^ HY Meltzer: Clinical studies on the mechanism of action of clozapine: the dopamine-serotonin hypothesis of schizophrenia . In: Psychopharmacology (Berl.) . 99 Suppl., 1989, pp. 18-27. PMID 2682729 .