Skip to main content Accessibility help
×
Hostname: page-component-78c5997874-fbnjt Total loading time: 0 Render date: 2024-11-06T09:57:38.540Z Has data issue: false hasContentIssue false

3 - Limbic connectivity: anatomical substrates of behavioural disturbances in epilepsy

Published online by Cambridge University Press:  05 October 2010

Michael Trimble
Affiliation:
Institute of Neurology, London
Bettina Schmitz
Affiliation:
Humboldt-Universität zu Berlin
Get access

Summary

Introduction

Behavioural disturbances associated with epilepsy are due, in part, to a number of important psychological and social factors; however, it is useful to acknowledge that there are neurobiological factors as well. Not only does identification of organic bases for behavioural aberrations help reduce the stigma they invariably engender, but also it provides a rational scientific approach to prevent or reverse a significant cause of disability experienced by persons with epilepsy.

Cognitive and psychiatric disturbances associated with epilepsy may be due to the same underlying pathological process that causes the epileptic condition, and there is evidence that behavioural impairment may be related to the pathophysiological nature of the underlying lesion, its effect on development and its location (Engel et al., 1986; Engel and Shewmon, 1991). With respect to location, mesial temporal and other limbic epileptogenic lesions are most likely to be associated with behavioural disturbances (Engel et al., 1986; Engel and Shewmon, 1991). Temporal lobe epilepsy is the most common form of human epilepsy, and hippocampal sclerosis is the most common human epileptogenic lesion (Engel, 1998). Furthermore, mesial temporal lobe epilepsy with hippocampal sclerosis may be the most refractory to antiepileptic drugs (Engel, 1998). Consequently, limbic system dysfunction is undoubtedly the most important cause of behavioural disturbances associated with epilepsy.

Epileptogenicity itself is known to cause enduring changes in brain function and structure in a number of ways which can result in altered behaviour.

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
×