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      The pathophysiology of traumatic brain injury at a glance

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          Abstract

          Traumatic brain injury (TBI) is defined as an impact, penetration or rapid movement of the brain within the skull that results in altered mental state. TBI occurs more than any other disease, including breast cancer, AIDS, Parkinson’s disease and multiple sclerosis, and affects all age groups and both genders. In the US and Europe, the magnitude of this epidemic has drawn national attention owing to the publicity received by injured athletes and military personnel. This increased public awareness has uncovered a number of unanswered questions concerning TBI, and we are increasingly aware of the lack of treatment options for a crisis that affects millions. Although each case of TBI is unique and affected individuals display different degrees of injury, different regional patterns of injury and different recovery profiles, this review and accompanying poster aim to illustrate some of the common underlying neurochemical and metabolic responses to TBI. Recognition of these recurrent features could allow elucidation of potential therapeutic targets for early intervention.

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          Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury.

          Ann C McKee, Robert Cantu, Christopher J Nowinski … (2009)
          Since the 1920s, it has been known that the repetitive brain trauma associated with boxing may produce a progressive neurological deterioration, originally termed dementia pugilistica, and more recently, chronic traumatic encephalopathy (CTE). We review 48 cases of neuropathologically verified CTE recorded in the literature and document the detailed findings of CTE in 3 profession althletes, 1 football player and 2 boxers. Clinically, CTE is associated with memory disturbances, behavioral and personality changes, parkinsonism, and speech and gait abnormalities. Neuropathologically, CTE is characterized by atrophy of the cerebral hemispheres, medial temporal lobe, thalamus, mammillary bodies, and brainstem, with ventricular dilatation and a fenestrated cavum septum pellucidum. Microscopically, there are extensive tau-immunoreactive neurofibrillary tangles, astrocytic tangles, and spindle-shaped and threadlike neurites throughout the brain. The neurofibrillary degeneration of CTE is distinguished from other tauopathies by preferential involvement of the superficial cortical layers, irregular patchy distribution in the frontal and temporal cortices, propensity for sulcal depths, prominent perivascular, periventricular, and subpial distribution, and marked accumulation of tau-immunoreactive astrocytes. Deposition of beta-amyloid, most commonly as diffuse plaques, occurs in fewer than half the cases. Chronic traumatic encephalopathy is a neuropathologically distinct slowly progressive tauopathy with a clear environmental etiology.
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            A new model of diffuse brain injury in rats. Part I: Pathophysiology and biomechanics.

            A Marmarou, M. A. Foda, W Van den Brink … (1994)
            This report describes the development of an experimental head injury model capable of producing diffuse brain injury in the rodent. A total of 161 anesthetized adult rats were injured utilizing a simple weight-drop device consisting of a segmented brass weight free-falling through a Plexiglas guide tube. Skull fracture was prevented by cementing a small stainless-steel disc on the calvaria. Two groups of rats were tested: Group 1, consisting of 54 rats, to establish fracture threshold; and Group 2, consisting of 107 animals, to determine the primary cause of death at severe injury levels. Data from Group 1 animals showed that a 450-gm weight falling from a 2-m height (0.9 kg-m) resulted in a mortality rate of 44% with a low incidence (12.5%) of skull fracture. Impact was followed by apnea, convulsions, and moderate hypertension. The surviving rats developed decortication flexion deformity of the forelimbs, with behavioral depression and loss of muscle tone. Data from Group 2 animals suggested that the cause of death was due to central respiratory depression; the mortality rate decreased markedly in animals mechanically ventilated during the impact. Analysis of mathematical models showed that this mass-height combination resulted in a brain acceleration of 900 G and a brain compression gradient of 0.28 mm. It is concluded that this simple model is capable of producing a graded brain injury in the rodent without a massive hypertensive surge or excessive brain-stem damage.
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              Oxidative stress caused by mitochondrial calcium overload.

              Tsung-I Peng, Mei-Jie Jou (2010)
              Mitochondrial oxidative stress has been reported as the result of respiratory complex anomalies, genetic defects, or insufficient oxygen or glucose supply. Although Ca(2+) has no direct effect on respiratory chain function or oxidation/reduction process, mitochondrial Ca(2+) overload can lead to reactive oxygen species (ROS) increase. Even though Ca(2+) is well known for its role as crucial second messenger in modulating many cellular physiological functions, Ca(2+) overload is detrimental to mitochondrial function and may present as an important cause of mitochondrial ROS generation. Possible mechanisms include Ca(2+) stimulated increase of metabolic rate, Ca(2+) stimulated nitric oxide production, Ca(2+) induced cytochrome c dissociation, Ca(2+) induced cardiolipin peroxidation, Ca(2+) induced mitochondrial permeability transition pore opening with release of cytochrome c and GSH-antioxidative enzymes, and Ca(2+)-calmodulin dependent protein kinases activation. Different mechanisms may exist under different mitochondrial preparations (isolated mitochondria vs. mitochondria in intact cells), tissue sources, animal species, or inhibitors used. Furthermore, mitochondrial ROS rise can modulate Ca(2+) dynamics and augment Ca(2+) surge. The reciprocal interactions between Ca(2+) induced ROS increase and ROS modulated Ca(2+) upsurge may cause a feedforward, self-amplified loop createing cellular damage far beyond direct Ca(2+) induced damage.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Dis Model Mech
                Journal ID (iso-abbrev): Dis Model Mech
                Journal ID (hwp): dmm
                Journal ID (publisher-id): DMM
                Title: Disease Models & Mechanisms
                Publisher: The Company of Biologists Limited
                ISSN (Print): 1754-8403
                ISSN (Electronic): 1754-8411
                Publication date (Print): November 2013
                Publication date (Electronic): 12 September 2013
                Volume: 6
                Issue: 6
                Pages: 1307-1315
                Affiliations
                [1 ]Department of Neurosurgery, UCLA, Los Angeles, CA 90095, USA
                [2 ]The Interdepartmental Program for Neuroscience, UCLA, CA 92697-3915, USA
                [3 ]The UCLA Brain Injury Research Center, Los Angeles, CA 90095-6901, USA
                [4 ]Department of Neurology, UCLA, Los Angeles, CA 90095, USA
                Author notes
                [* ]Author for correspondence ( mprins@ 123456mednet.ucla.edu )
                Article
                Publisher ID: 0061307
                DOI: 10.1242/dmm.011585
                PMC ID: 3820255
                PubMed ID: 24046353
                SO-VID: 848a3a3a-570f-4044-8578-149c1028a82f
                Copyright © © 2013. Published by The Company of Biologists Ltd
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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                Subject: At a Glance

                ScienceOpen disciplines: Molecular medicine
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                ScienceOpen disciplines: Molecular medicine

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