Abstract
Purpose: The purpose of this study was to determine the level of excitability and inhibition, as well as the concentrations of excitatory and inhibitory neurotransmitters, in the motor cortex of individuals with acute and chronic symptoms from mTBI.Methods: Fifty-three individuals were assigned to one of four groups: (i) without history of mTBI (Control), (ii) within 72-h of diagnosis of mTBI (Acute), (iii) with history of mTBI and no remaining symptoms (Chronic Asymptomatic), and (iv) with chronic symptoms from mTBI, lasting at least 3 months post-injury (Chronic Symptomatic). Measures of corticospinal excitability and inhibition were obtained using transcranial magnetic stimulation (TMS). On the same day, measures of glutamate and GABA concentrations were obtained from the primary motor cortex (M1) using proton magnetic resonance spectroscopy.Results: MEP amplitude and area were both significantly lower in the Chronic Symptomatic group compared to the Control and Chronic Asymptomatic groups (p ≤ 0.05). Intracortical inhibition was not significantly different among groups (p = 0.14). The concentration of glutamate in M1 was similar between groups (p = 0.93) while there was a trend for a lower concentration of GABA in the Chronic Symptomatic group compared to the Acute group (p = 0.06).Conclusions: Individuals with chronic mTBI symptoms appear to have lower corticospinal excitability compared with acutely-injured individuals and asymptomatic controls, but the absence of differences in intracortical inhibition, and concentrations of excitatory and inhibitory neurotransmitters in M1 suggests that neurotransmitter changes in the human brain post-mTBI do not follow the pattern typically seen in the animal literature.
Highlights
Mild traumatic brain injury has been described as a diffuse injury that can impact both cognitive and motor function [1,2,3,4]
The results demonstrated that individuals with chronic symptoms from Mild traumatic brain injury (mTBI) had lower Motor Evoked Potential (MEP) amplitudes than individuals in the two control groups, indicating lower corticospinal excitability
While the time course of this cascade is unknown in humans, it is possible that the initial release of excitatory neurotransmitters in the brain following mTBI may resolve in the human brain by 72-h postinjury
Summary
Mild traumatic brain injury (mTBI) has been described as a diffuse injury that can impact both cognitive and motor function [1,2,3,4]. While acutely-injured individuals have consistently demonstrated a different neurophysiological profile compared with healthy controls [3, 8, 9], similar assessments in individuals with chronic symptoms have not been made. Little is known about the physiological characteristics of chronic mTBI and how they compare with characteristics of acute injury. Work in rodent models of mTBI suggests that immediately after a mechanical injury to the head, the brain enters a state of excitation as excitatory neurotransmitters, such as glutamate, are released [10]. Studies show that neurons injured following mTBI demonstrate a reduction in dendrite length and inhibited neuronal signaling, suggesting that mTBI may lead to a change in the excitatory/inhibitory balance post-injury [11]
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