Contents

Disclaimer

Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always check the product information and clinical procedures with the most up to date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulations. The authors and the publishers do not accept responsibility or legal liability for any errors in the text or for the misuse or misapplication of material in this work. Except where otherwise stated, drug dosages and recommendations are for the non-pregnant adult who is not breastfeeding.

Show Summary Details
Page of

Pathophysiology and causes of seizures 

Pathophysiology and causes of seizures
Chapter:
Pathophysiology and causes of seizures
Author(s):

Thomas P. Bleck

DOI:
10.1093/med/9780199600830.003.0231
Page of

PRINTED FROM OXFORD MEDICINE ONLINE (www.oxfordmedicine.com). © Oxford University Press, 2021. All Rights Reserved. Under the terms of the licence agreement, an individual user may print out a PDF of a single chapter of a title in Oxford Medicine Online for personal use (for details see Privacy Policy and Legal Notice).

date: 28 September 2021

Seizures result from imbalances between excitation and inhibition, and between neuronal synchrony and dyssynchrony. Current models implicate the cerebral cortex in the genesis of seizures, although thalamic mechanisms (particularly the thalamic reticular formation) are involved in the synchronization of cortical neurons. Often, the precipitants of a seizure in the critical care setting are pharmacological. Several mechanisms linked to critical illness can lead to seizures. Failure to remove glutamate and potassium from the extracellular space, functions performed predominantly by astrocytes, occurs in trauma, hypoxia, ischaemia, and hypoglycaemia. Loss of normal inhibition occurs during withdrawal from alcohol and other hypnosedative agents, or in the presence of GABA. Conditions such as cerebral trauma, haemorrhages, abscesses, and neoplasms all produce physical distortions of the adjacent neurons, astrocytes, and the extracellular space. Deposition of iron in the cortex from the breakdown of haemoglobin appears particularly epileptogenic. Although acute metabolic disturbances can commonly produce seizures in critically-ill patients, an underlying and potentially treatable structural lesion must always be considered and excluded.

Access to the complete content on Oxford Medicine Online requires a subscription or purchase. Public users are able to search the site and view the abstracts for each book and chapter without a subscription.

Please subscribe or login to access full text content.

If you have purchased a print title that contains an access token, please see the token for information about how to register your code.

For questions on access or troubleshooting, please check our FAQs, and if you can't find the answer there, please contact us.