The Pathophysiology of Concussion

Abstract

Concussion is defined as a biomechanically induced brain injury characterized by the absence of gross anatomic lesions. Early and late clinical symptoms, including impairments of memory and attention, headache, and alteration of mental status, are the result of neuronal dysfunction mostly caused by functional rather than structural abnormalities. The mechanical insult initiates a complex cascade of metabolic events leading to perturbation of delicate neuronal homeostatic balances. Starting from neurotoxicity, energetic metabolism disturbance caused by the initial mitochondrial dysfunction seems to be the main biochemical explanation for most postconcussive signs and symptoms. Furthermore, concussed cells enter a peculiar state of vulnerability, and if a second concussion is sustained while they are in this state, they may be irreversibly damaged by the occurrence of swelling. This condition of concussion-induced brain vulnerability is the basic pathophysiology of the second impact syndrome. N-acetylaspartate, a brain-specific compound representative of neuronal metabolic wellness, is proving a valid surrogate marker of the post-traumatic biochemical damage, and its utility in monitoring the recovery of the aforementioned "functional" disturbance as a concussion marker is emerging, because it is easily detectable through proton magnetic resonance spectroscopy.

Imaging “Brain Strain” in Youth Athletes with Mild Traumatic Brain Injury during Dual-Task Performance

“…We have now shown that despite intact neuropsychological test performance, the lack of significant post-injury symptoms, and the absence of structural brain damage detected by conventional neuroimaging, differences exist in neural recruitment following mTBI in youth during working memory performance. Overall, these data support the hypothesis of a predominantly functional consequence following mTBI 18,95,96 and provides evidence for neural changes persisting well beyond the acute phase of injury.…”

The role of the cervical spine in post-concussion syndrome

“…In an effort to restore proper ion balance within the cell, the ATP pump is activated to a greater capacity requiring large amounts of ATP. The imbalance between increased ATP requirements, decreased ATP production and reduced cerebral blood flow quickly leads to an energy crisis within the brain known as spreading depression (Figure 1) [10,14].…”

“…The pathophysiology of mTBI during the acute phase of injury is becoming increasingly well-known suggesting ion imbalance, metabolic disruptions, blood flow abnormalities and autonomic nervous system (ANS) dysfunction as the main culprits [6,[10][11][12][13][14]. When attempting to search for potential mechanisms surrounding PCS; however, findings have been inconsistent and there remains no clear physiologic explanation for this disorder [9,15].…”

Update on Mild Traumatic Brain Injury: Neuropathology and Structural Imaging

“…Mild TBI is also an evolving, dynamic injury. [1][2][3][19][20][21] In brief, traumatic forces (e.g., linear, angular, pressure) induce localized physical stress in the brain that instigates a complex series of neurochemical and metabolic changes that may include substantial ionic fluxes, release of excitotoxic levels of neurotransmitters, hypermetabolism leading to energy depletion and hypometabolism, altered cerebral bloodflow and vascular reactivity, edema, and neuroinflammation. Multiple lines of evidence indicate that full return to baseline physiological state can be a prolonged process, requiring weeks or even months, rather than the few days once thought sufficient.…”

“…[1][2][3][19][20][21][22][23] The direction, speed, and extent of the induced local deformation(s) are critical factors. Primary (immediate) axon transaction (axotomy) is unlikely to occur.…”