A Clinician’s Guide to the Pathophysiology of Traumatic Brain Injury

Traumatic brain injury induces a complex pathophysiological cascade of cellular events. Central components of this response include increases in cerebral glucose uptake, reductions in cerebral blood flow, indiscriminate excitatory neurotransmitter release, ionic disequilibrium, and intracellular cal...

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Main Authors: Andranik Madikians, Christopher C Giza
Format: Article
Language:English
Published: Thieme Medical and Scientific Publishers Pvt. Ltd. 2006-06-01
Series:The Indian Journal of Neurotrauma
Subjects:
Online Access:http://www.ijntonline.com/June06/abstracts/03.PDF
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author Andranik Madikians
Christopher C Giza
author_facet Andranik Madikians
Christopher C Giza
author_sort Andranik Madikians
collection DOAJ
description Traumatic brain injury induces a complex pathophysiological cascade of cellular events. Central components of this response include increases in cerebral glucose uptake, reductions in cerebral blood flow, indiscriminate excitatory neurotransmitter release, ionic disequilibrium, and intracellular calcium accumulation. Acute glutamate release and nonspecific neuronal depolarization induce threatening perturbations in neuronal function. Restoration of homeostasis requires significant increases in glucose metabolism; however, there is often a concomitant reduction in cerebral blood flow, resulting in an uncoupling of supply and demand. Understanding the nature and timing of these processes provides the practicing clinician with a mechanistic rationale for acute physiological monitoring, aggressive interventions to address and minimize secondary injuries, implementation of advanced neuroimaging techniques, and careful monitoring return to normal activity in head injured patients.
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spelling doaj.art-619adb0ea4d747619b288ac6c8d033ce2023-12-02T05:20:06ZengThieme Medical and Scientific Publishers Pvt. Ltd.The Indian Journal of Neurotrauma0973-05082006-06-0131917A Clinician’s Guide to the Pathophysiology of Traumatic Brain InjuryAndranik MadikiansChristopher C GizaTraumatic brain injury induces a complex pathophysiological cascade of cellular events. Central components of this response include increases in cerebral glucose uptake, reductions in cerebral blood flow, indiscriminate excitatory neurotransmitter release, ionic disequilibrium, and intracellular calcium accumulation. Acute glutamate release and nonspecific neuronal depolarization induce threatening perturbations in neuronal function. Restoration of homeostasis requires significant increases in glucose metabolism; however, there is often a concomitant reduction in cerebral blood flow, resulting in an uncoupling of supply and demand. Understanding the nature and timing of these processes provides the practicing clinician with a mechanistic rationale for acute physiological monitoring, aggressive interventions to address and minimize secondary injuries, implementation of advanced neuroimaging techniques, and careful monitoring return to normal activity in head injured patients.http://www.ijntonline.com/June06/abstracts/03.PDFcerebral blood flowglucose metabolismglutamatemonitoringpositron emission tomography (PET)
spellingShingle Andranik Madikians
Christopher C Giza
A Clinician’s Guide to the Pathophysiology of Traumatic Brain Injury
The Indian Journal of Neurotrauma
cerebral blood flow
glucose metabolism
glutamate
monitoring
positron emission tomography (PET)
title A Clinician’s Guide to the Pathophysiology of Traumatic Brain Injury
title_full A Clinician’s Guide to the Pathophysiology of Traumatic Brain Injury
title_fullStr A Clinician’s Guide to the Pathophysiology of Traumatic Brain Injury
title_full_unstemmed A Clinician’s Guide to the Pathophysiology of Traumatic Brain Injury
title_short A Clinician’s Guide to the Pathophysiology of Traumatic Brain Injury
title_sort clinician s guide to the pathophysiology of traumatic brain injury
topic cerebral blood flow
glucose metabolism
glutamate
monitoring
positron emission tomography (PET)
url http://www.ijntonline.com/June06/abstracts/03.PDF
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