Affective, neurocognitive and psychosocial disorders associated with traumatic brain injury and post-traumatic epilepsy

Research output: Contribution to journalReview ArticleResearchpeer-review

Abstract

Survivors of traumatic brain injury (TBI) often develop chronic neurological, neurocognitive, psychological, and psychosocial deficits that can have a profound impact on an individual's wellbeing and quality of life. TBI is also a common cause of acquired epilepsy, which is itself associated with significant behavioral morbidity. This review considers the clinical and preclinical evidence that post-traumatic epilepsy (PTE) acts as a ‘second-hit’ insult to worsen chronic behavioral outcomes for brain-injured patients, across the domains of emotional, cognitive, and psychosocial functioning. Surprisingly, few well-designed studies have specifically examined the relationship between seizures and behavioral outcomes after TBI. The complex mechanisms underlying these comorbidities remain incompletely understood, although many of the biological processes that precipitate seizure occurrence and epileptogenesis may also contribute to the development of chronic behavioral deficits. Further, the relationship between PTE and behavioral dysfunction is increasingly recognized to be a bidirectional one, whereby premorbid conditions are a risk factor for PTE. Clinical studies in this arena are often challenged by the confounding effects of anti-seizure medications, while preclinical studies have rarely examined an adequately extended time course to fully capture the time course of epilepsy development after a TBI. To drive the field forward towards improved treatment strategies, it is imperative that both seizures and neurobehavioral outcomes are assessed in parallel after TBI, both in patient populations and preclinical models.

Original languageEnglish
Pages (from-to)27-41
Number of pages15
JournalNeurobiology of Disease
Volume123
DOIs
Publication statusPublished - 1 Mar 2019

Keywords

  • Anxiety
  • Co-morbidity
  • Cognition
  • Depression
  • Epilepsy
  • Seizure
  • Social behavior
  • Traumatic brain injury

Cite this

@article{ba2523e32b164d4ba8da59dd383f2fd1,
title = "Affective, neurocognitive and psychosocial disorders associated with traumatic brain injury and post-traumatic epilepsy",
abstract = "Survivors of traumatic brain injury (TBI) often develop chronic neurological, neurocognitive, psychological, and psychosocial deficits that can have a profound impact on an individual's wellbeing and quality of life. TBI is also a common cause of acquired epilepsy, which is itself associated with significant behavioral morbidity. This review considers the clinical and preclinical evidence that post-traumatic epilepsy (PTE) acts as a ‘second-hit’ insult to worsen chronic behavioral outcomes for brain-injured patients, across the domains of emotional, cognitive, and psychosocial functioning. Surprisingly, few well-designed studies have specifically examined the relationship between seizures and behavioral outcomes after TBI. The complex mechanisms underlying these comorbidities remain incompletely understood, although many of the biological processes that precipitate seizure occurrence and epileptogenesis may also contribute to the development of chronic behavioral deficits. Further, the relationship between PTE and behavioral dysfunction is increasingly recognized to be a bidirectional one, whereby premorbid conditions are a risk factor for PTE. Clinical studies in this arena are often challenged by the confounding effects of anti-seizure medications, while preclinical studies have rarely examined an adequately extended time course to fully capture the time course of epilepsy development after a TBI. To drive the field forward towards improved treatment strategies, it is imperative that both seizures and neurobehavioral outcomes are assessed in parallel after TBI, both in patient populations and preclinical models.",
keywords = "Anxiety, Co-morbidity, Cognition, Depression, Epilepsy, Seizure, Social behavior, Traumatic brain injury",
author = "Semple, {Bridgette D.} and Akram Zamani and Genevieve Rayner and Shultz, {Sandy R.} and Jones, {Nigel C.}",
year = "2019",
month = "3",
day = "1",
doi = "10.1016/j.nbd.2018.07.018",
language = "English",
volume = "123",
pages = "27--41",
journal = "Neurobiology of Disease",
issn = "0969-9961",
publisher = "Elsevier",

}

Affective, neurocognitive and psychosocial disorders associated with traumatic brain injury and post-traumatic epilepsy. / Semple, Bridgette D.; Zamani, Akram; Rayner, Genevieve; Shultz, Sandy R.; Jones, Nigel C.

In: Neurobiology of Disease, Vol. 123, 01.03.2019, p. 27-41.

Research output: Contribution to journalReview ArticleResearchpeer-review

TY - JOUR

T1 - Affective, neurocognitive and psychosocial disorders associated with traumatic brain injury and post-traumatic epilepsy

AU - Semple, Bridgette D.

AU - Zamani, Akram

AU - Rayner, Genevieve

AU - Shultz, Sandy R.

AU - Jones, Nigel C.

PY - 2019/3/1

Y1 - 2019/3/1

N2 - Survivors of traumatic brain injury (TBI) often develop chronic neurological, neurocognitive, psychological, and psychosocial deficits that can have a profound impact on an individual's wellbeing and quality of life. TBI is also a common cause of acquired epilepsy, which is itself associated with significant behavioral morbidity. This review considers the clinical and preclinical evidence that post-traumatic epilepsy (PTE) acts as a ‘second-hit’ insult to worsen chronic behavioral outcomes for brain-injured patients, across the domains of emotional, cognitive, and psychosocial functioning. Surprisingly, few well-designed studies have specifically examined the relationship between seizures and behavioral outcomes after TBI. The complex mechanisms underlying these comorbidities remain incompletely understood, although many of the biological processes that precipitate seizure occurrence and epileptogenesis may also contribute to the development of chronic behavioral deficits. Further, the relationship between PTE and behavioral dysfunction is increasingly recognized to be a bidirectional one, whereby premorbid conditions are a risk factor for PTE. Clinical studies in this arena are often challenged by the confounding effects of anti-seizure medications, while preclinical studies have rarely examined an adequately extended time course to fully capture the time course of epilepsy development after a TBI. To drive the field forward towards improved treatment strategies, it is imperative that both seizures and neurobehavioral outcomes are assessed in parallel after TBI, both in patient populations and preclinical models.

AB - Survivors of traumatic brain injury (TBI) often develop chronic neurological, neurocognitive, psychological, and psychosocial deficits that can have a profound impact on an individual's wellbeing and quality of life. TBI is also a common cause of acquired epilepsy, which is itself associated with significant behavioral morbidity. This review considers the clinical and preclinical evidence that post-traumatic epilepsy (PTE) acts as a ‘second-hit’ insult to worsen chronic behavioral outcomes for brain-injured patients, across the domains of emotional, cognitive, and psychosocial functioning. Surprisingly, few well-designed studies have specifically examined the relationship between seizures and behavioral outcomes after TBI. The complex mechanisms underlying these comorbidities remain incompletely understood, although many of the biological processes that precipitate seizure occurrence and epileptogenesis may also contribute to the development of chronic behavioral deficits. Further, the relationship between PTE and behavioral dysfunction is increasingly recognized to be a bidirectional one, whereby premorbid conditions are a risk factor for PTE. Clinical studies in this arena are often challenged by the confounding effects of anti-seizure medications, while preclinical studies have rarely examined an adequately extended time course to fully capture the time course of epilepsy development after a TBI. To drive the field forward towards improved treatment strategies, it is imperative that both seizures and neurobehavioral outcomes are assessed in parallel after TBI, both in patient populations and preclinical models.

KW - Anxiety

KW - Co-morbidity

KW - Cognition

KW - Depression

KW - Epilepsy

KW - Seizure

KW - Social behavior

KW - Traumatic brain injury

UR - http://www.scopus.com/inward/record.url?scp=85051808081&partnerID=8YFLogxK

U2 - 10.1016/j.nbd.2018.07.018

DO - 10.1016/j.nbd.2018.07.018

M3 - Review Article

VL - 123

SP - 27

EP - 41

JO - Neurobiology of Disease

JF - Neurobiology of Disease

SN - 0969-9961

ER -