Skip to main content Accessibility help
×
Hostname: page-component-586b7cd67f-dlnhk Total loading time: 0 Render date: 2024-11-22T23:27:56.713Z Has data issue: false hasContentIssue false

11 - Genetic factors underlying drug-induced tardive dyskinesia

from Part V - Specific psychotropic drugs and disorders

Published online by Cambridge University Press:  20 August 2009

Ronnen H. Segman
Affiliation:
Department of Psychiatry, Hadassah-Hebrew University Medical Center, Jerusalem, Israel
Bernard Lerer
Affiliation:
Department of Psychiatry, Hadassah-Hebrew University Medical Center, Jerusalem, Israel
Bernard Lerer
Affiliation:
Hadassah-Hebrew Medical Center, Jerusalem
Get access

Summary

OVERVIEW

Tardive dyskinesia (TD) affects about one fifth of schizophrenia patients following chronic exposure to dopamine receptor antagonist drugs. Spontaneous dyskinesia has been reported in unmedicated schizophrenia patients and patients with TD have been reported to show distinct clinical features, suggesting a common underlying phenotype that may bear a distinct genetic predisposition. Drug- and patient-related risk factors for the development of TD have received much research attention but appear to predict only a minor part of the variance in the incidence of TD. Genetically determined individual variability in factors affecting drug levels, as well as compensatory responses to chronic dopaminergic antagonism, may account for a major portion of the variance in the incidence of TD. To-date, however, there has been a conspicuous lack of studies exploring a genetic predisposition to TD. Current data stem from sporadic clinical observations and from supportive, albeit indirect, evidence from rodent studies showing strain differences in behavioral and phamacodynamic models for drug-induced TD. Despite the lack of an established genetic contribution or mode of inheritance for vulnerability to develop TD, in recent years a number of groups have ventured to examine directly a possible contribution of specific candidate genes to TD, employing case-control association design in chronically medicated schizophrenia patients. Such studies report direct association of candidate polymorphic genes with drug-induced TD, providing further support for the existence of a genetic contribution and suggesting the likelihood of a polygenic, multifactorial inheritance for such vulnerability.

Type
Chapter
Information
Publisher: Cambridge University Press
Print publication year: 2002

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

Save book to Kindle

To save this book to your Kindle, first ensure [email protected] is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×