Skip to main content Accessibility help
×
Hostname: page-component-5d59c44645-mhl4m Total loading time: 0 Render date: 2024-02-24T14:11:31.276Z Has data issue: false hasContentIssue false

9 - Neuroleptic treatment and tardive dyskinesia

from Part II - Clinical aspects of tardive dyskinesia

Published online by Cambridge University Press:  09 October 2009

Ramzy Yassa
Affiliation:
Douglas Hospital, Quebec
N. P. V. Nair
Affiliation:
Douglas Hospital, Quebec
Dilip V. Jeste
Affiliation:
University of California, San Diego
Get access

Summary

Any reasonable, informed clinician will accept the overwhelming epidemiologic evidence implicating neuroleptic drugs in the causation of tardive dyskinesia, with the caveat that not every case that looks like tardive dyskinesia is neuroleptic-related. Spontaneous dyskinesia (Marsden, 1985; Casey, 1987) and dyskinesias induced by drugs other than neuroleptics, such as antihistamines, antidepressants, and metoclopramide, often are indistinguishable from tardive dyskinesia. As Marsden (1985) pointed out, the causative relationship implies either that neuroleptics induce tardive dyskinesia in individuals who otherwise would not develop it or that neuroleptics precipitate tardive dyskinesia in patients who already carry the substrate for development of tardive dyskinesia.

Patients exposed to neuroleptics differ regarding variables such as age at first neuroleptic exposure, time since the start of neuroleptic treatment, duration of neuroleptic treatment (i.e., actual time on neuroleptics), number and duration of neuroleptic-free intervals, number of neuroleptics used, amount of neuroleptic (i.e., total quantity delivered), average neuroleptic dosage, and maximum neuroleptic dosage. Other areas of interest include comparisons of exposures to high- and low-potency neuroleptics, the number of neuroleptics simultaneously prescribed, the route of administration (depot vs. oral), and different schedules, such as a dose once daily versus twice daily (BID), or doses as needed (PRN) (oral and/or intramuscular). Only adequate knowledge of the pathogenesis of tardive dyskinesia will enable us to decide which of these drug variables are of particular relevance to tardive dyskinesia.

Type
Chapter
Information
Neuroleptic-induced Movement Disorders
A Comprehensive Survey
, pp. 104 - 116
Publisher: Cambridge University Press
Print publication year: 1996

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 coreplatform@cambridge.org 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
×