October 3, 2023
Mild traumatic brain injury (MTBI) and concussions are topics of significant focus in neurology research. While they're often used interchangeably in medical literature, MTBI encompasses a broader spectrum of brain injuries, including intracranial hemorrhages. The aftermath of a concussion results in numerous physiological changes in the brain, lasting anywhere from hours to weeks. This period sees impaired neurotransmission, deregulation of ions, and compromised energy metabolism. The brain's vulnerability increases post-concussion, making it susceptible to changes in pressure and blood flow. Crucially, concussions result in diffuse injuries across the brain rather than localized ones, indicating the widespread implications of even a mild traumatic event on neural structures.

Mild traumatic brain injury (MTBI) is frequently categorized under the classification of concussion in numerous medical publications. Yet, this synonymy is often approached with caution, as other injuries such as intracranial haemorrhages (intra-axial hematoma, epidural hematoma, and subdural hematoma) might not always be excluded in MTBI or mild head injury contexts. In instances where MTBI is coupled with abnormal neuroimaging, it might be categorized as “complicated MTBI.” Although the term “concussion” tends to denote a temporary impairment of brain functionality, “MTBI” leans more towards representing a pathophysiological condition. It is worth noting that current clinical neurology practices gravitate towards using explicit descriptions of the injury’s specifications rather than general terms like “concussion.”

The aftermath of a concussion triggers a series of physiological alterations in the brain, that can last from a few hours to several weeks, initiating a myriad of pathological responses. While these responses predominantly hamper neuronal and brain operations, it is observed that a significant majority of affected brain cells can revert to their metabolic processes. A minimal subset might undergo apoptosis subsequent to the injury.

Central to the neural disturbance post-concussion is the hampered neurotransmission and the deregulation of ions. An excess release of excitatory neurotransmitters, such as glutamate, post-injury precipitates excessive neuronal firing. This hyperactivity generates an ionic imbalance, primarily of potassium and calcium, across neuronal cell membranes, analogous to excitotoxicity. Such ionic disequilibrium, particularly neuronal depolarization, demands that ion pumps operate beyond their usual capacity, subsequently increasing the energy demands of the cells. This hypermetabolic state, potentially lasting days to weeks, juxtaposed with an unexplained reduced cerebral blood flow, plunges the brain into an “energy crisis,” as cells grapple with reduced glucose supplies.

Simultaneously, there seems to be a decline in mitochondrial activity, compelling cells to shift towards anaerobic metabolism, elevating lactate levels. The brain, post-concussion, becomes critically susceptible to variations in intracranial pressure, blood flow, and anoxia for a duration spanning from minutes to days. Research on animal models suggests that during this interval, even marginal alterations in blood flow can be fatal to a vast number of neurons.

Concussions predominantly result in diffuse brain injuries rather than focal ones. This implies that the repercussions are disseminated across a vast expanse of the brain rather than being concentrated at a specific locus. Concussions are often perceived as a milder variant of diffuse axonal injury due to the potential for minor axonal damage from stretching. Empirical research involving primate models has revealed tissue damage, including minor petechial haemorrhages and axonal injuries. Such axonal damages have been detected post-mortem in individuals with a history of concussion, although these might be influenced by inadequate cerebral blood flow stemming from other injuries.

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