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CSME|CAPDA Medico-Legal Summit - Dr. Sherese Ali
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Neurobiology of Mild Traumatic Brain Injury
Dr. Sherese Ali, MD FRCPC

The neuropsychiatric symptomatology and accompanying disability which often accompany mild traumatic brain injury (TBI), without a history of direct head impact or loss of consciousness can be prolific and appear disproportionate to the mechanism of injury. It remains a controversial and debatable issue and there are varying opinions regarding an organic basis of these complaints. Indeed, the gravitational forces associated with daring roller coaster rides can, in many cases, exceed those associated with a low-impact motor vehicle accident. An understanding of the neurobiological components, can help in determination of psychiatric impairment ratings related to mild TBI. The conditions under which this controversial entity rests on a solid neurobiological foundation include both impact forces but inertial forces. The distribution of lesions from both impact and inertial forces is not random. Impact forces lead to frontal and temporal contusions in the base of the brain with hemorrhagic defects in the orbitofrontal surface, dorsolateral prefrontal cortex, cerebellum and the anterotemporal poles. Inertial forces act on 1) axons, 2) vasculature and 3) fulcrum of upper brainstem. Axons of the corpus callosum and subcortical white matter tracts are particularly vulnerable and can lead to deficits in multitasking, selective attention, recall of registered information. When vasculature is stretched, bridging veins are particularly susceptible, which can lead to subarachnoid and subdural hemorrhages with their associated clinical correlates. Inertial forces cause the brain to rotate in an anterior-posterior plane along the fulcrum of the upper brainstem which houses cells of the reticular activating system, therefore causing sequelae of impaired alertness and hypersomnolence. Furthermore, secondary injury occurs when damage from inertial injury evolves over time and includes, among many processes, massive release of neurotransmitters in vulnerable pathways which including dopaminergic (mesolimbic and mesocortical), serotonergic and cholinergic. Therefore, despite an ostensibly “mild” mechanism of injury the consequences of mild TBI may be substantial with non-random geographic distribution of injury to specific regions and neurotransmitter pathways which are critical to behavioral modulation and cognitive function. Mild TBI can therefore result in various dysexecutive syndromes, disorders of social comportment, disorders of motivation and psychiatric disorders. Single mild brain injury used to be thought of as a minor event with a uniformly good prognosis. The most current understanding is that a mild TBI is not a single event but moreover a process. It may be this single event that initiates a chronic illness such as chronic traumatic encephalopathy. The risk of dementia with a single injury causing a mild TBI is highly debatable, however, and repetitive injury is required. Neuropathological studies show abnormal protein aggregates and tauopathy in repetitive mild TBI and severe TBI, but short-term, uncertain pathology in single mild TBI.

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