Chapter

Traumatic Brain Injury and Posttraumatic Epilepsy

David A. Prince, Isabel Parada and Kevin D. Graber

in Jasper's Basic Mechanisms of the Epilepsies

Fourth edition

Published on behalf of ©Jeffrey L. Noebels, Massimo Avoli, Michael A. Rogawski, Richard W. Olsen, and Antonio V. Delgado-Escueta

Published in print July 2012 | ISBN: 9780199746545
Published online April 2013 | e-ISBN: 9780199322817 | DOI: http://dx.doi.org/10.1093/med/9780199746545.003.0024

Series: Contemporary Neurology Series

Traumatic Brain Injury and Posttraumatic Epilepsy

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The epidemiology of posttraumatic epilepsy (PTE) has been extensively analyzed and reviewed in a number of studies of both civilian and military brain injuries1,2 (reviewed in ref. 3). Several conclusions from this research are relevant to considerations of the potential mechanisms and prophylaxis of PTE. Results clearly show that the incidence of PTE is related to the severity of injury, and is therefore significantly higher in the military during wartime than in the civilian population, ranging up to 53% with penetrating wounds1,2 (reviewed in ref. 3). Both the increased incidence at older ages and the potential development of PTE by the large number of individuals who have survived severe concussive injury during recent conflicts suggest that the size of the affected population will increase in coming years, emphasizing the need for understanding the underlying pathophysiological processes and the development of prophylactic strategies.4,5 Although initial seizures in those who develop epilepsy most commonly have a focal origin in neocortex, both partial neocortical and temporal lobe epilepsy can follow traumatic brain injury (TBI) in humans.6 One remarkable feature of PTE is the variable, often very prolonged latency from injury to epilepsy, which can range from weeks to years.1,2,6 This provides a possible window for prophylactic intervention once more information regarding the underlying pathophysiological processes and strategies for modifying them is available. However, the long latency also represents a potential therapeutic problem, particularly in the absence of reliable biomarkers of epileptogenesis in progress. This chapter will focus on examples of aberrant excitatory and inhibitory processes in injured epileptogenic cortex and potential approaches to prevention of epileptogenesis that are focused on these pathophysiological mechanisms. Some of the challenges for the development of prophylactic therapies are also discussed. Readers are referred to a number of reviews and papers published very recently that deal with various aspects of the basic mechanisms, pathogenesis, and potential prophylaxis of PTE and complement the areas covered in this chapter.6–18

Chapter.  9974 words.  Illustrated.

Subjects: Neurology

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