Alia L. Yasen

Acute and longitudinal changes in motor cortex function following mild traumatic brain injury.

Abstract Primary objective: To evaluate excitability and inhibition of the motor cortex acutely and longitudinally following mild traumatic brain injury (mTBI). Research design: A longitudinal paired case-control design was used to examine cortical excitability and inhibition in 15 adults who had sustained an mTBI (mean age = 20.8 ± 1.2 years) and 15 matched control participants (mean age = 21.1 ± 1.3 years). Methods and procedures: Participants visited the lab within 72 hours of injury and again at 1, 2, 4 and 8 weeks post-injury. During each visit, transcranial magnetic stimulation was used to examine resting motor threshold (RMT), motor evoked potential peak-to-peak amplitude (MEPamp) and cortical silent period (CSP) duration of the first dorsal interosseous muscle. Main outcomes and results: There were no differences between groups in RMT (p = 0.10) or MEPamp (p = 0.22) at 72 hours post-injury or across the 2-month testing period (p ≥ 0.68), indicating similar cortical excitability. However, the CSP duration was higher in individuals with mTBI, indicating greater intra-cortical inhibition compared with the control group at 72 hours post-injury (p = 0.03) and throughout the 2 months of recovery (p = 0.009). Conclusions: mTBI appeared to have little effect on cortical excitability, but an acute and long-lasting effect on intra-cortical inhibition.

Motor cortex inhibition is increased during a secondary cognitive task

The purpose of this study was to assess the effect of a cognitive task on motor cortex excitability and inhibition. Transcranial magnetic stimulation of the motor cortex was performed on 20 healthy individuals (18-24 years; 9 females) to measure motor evoked potentials (MEPs) and cortical silent periods at baseline, during, and following a secondary cognitive task. The MEP amplitude increased from 0.50 ± 0.09-0.87 ± 0.50 mV during a secondary cognitive task (p = .04), and returned to baseline (0.48 ± 0.31 mV; p = .90) posttask. The CSP duration also increased from 93.48 ± 28.76-113.6 ± 33.68 ms (p = .001) during the cognitive task, and returned to baseline posttask (89.0 ± 6.9 ms; p = .88). In the presence of a cognitive task, motor cortex excitability and inhibition were both increased relative to baseline. The increase in inhibition may help to explain the motor deficits experienced while performing a secondary cognitive task.

Cortical and Physical Function after Mild Traumatic Brain Injury

Purpose The aim of this study was to prospectively examine the association between intracortical inhibition and functional recovery after mild traumatic brain injury (mTBI). Methods Twenty individuals with mTBI and 20 matched control participants were assessed using transcranial magnetic stimulation, the Attentional Network Test, and gait analysis. Hierarchical linear modeling was used to longitudinally examine potential differences between groups and relationships in the pattern of recovery in cortical silent period (CSP) duration, cognitive reaction time, and single- and dual-task walking speeds across five testing time points. Individuals with mTBI were assessed within 72 h of injury, and again at 1 wk, 2 wk, 1 month, and 2 months postinjury. After initial testing, control participants followed a similar timeline. Results At the 72-h time point, the group with mTBI had longer reaction time (b = −91.76, P = 0.01), similar single-task walking speed (b = 0.055, P = 0.10), and slower dual-task walking speed (b = 0.10, P = 0.012) compared with control participants. The CSP duration also tended to be longer in individuals with mTBI than controls at the 72-h time point (b = −16.34, P = 0.062). The change is CSP duration over time was not significantly associated with the change in reaction time (b = −0.19, P = 0.47), single-task walking speed (b = 0.0001, P = 0.53), or dual-task walking speed (b < 0.001, P = 0.68). Conclusion Although cognitive and motor functions were significantly impaired in the mTBI group acutely after injury, levels of intracortical inhibition were not associated with recovery in either functional domain.

Reliability of glutamate and GABA quantification using proton magnetic resonance spectroscopy

The consistency and reliability of proton magnetic resonance spectroscopy (1H-MRS) assessments of neurotransmitter concentration has not been widely examined over multiple days. The purpose of this study was to determine the reliability of glutamate and GABA measures using a single-voxel 1H-MRS protocol in healthy men and women. Glutamate and GABA quantitations were obtained from the primary motor cortex (M1) and the dorsolateral prefrontal cortex (DLPFC) in 13 healthy individuals across 3 data collection sessions, including a baseline (Visit 1), 2-week (Visit 2), and 2-month time point (Visit 3). Glutamate concentrations were similar across visits in M1 (p=0.72) and the DLPFC (p=0.52). Reliability across days was excellent in M1 (R=0.93), and in the DLPFC (R=0.99). GABA concentrations were similar across visits in M1 (p=0.44) and in the DLPFC (p=0.59). Reliability of GABA concentration across days was excellent in M1 (R=0.93), and in the DLPFC (R=0.97). 1H-MRS is a reliable method for quantifying glutamate and GABA concentration in M1 and the DLPFC in humans.

Glutamate and GABA concentrations following mild traumatic brain injury: a pilot study

Animal models of mild traumatic brain injury (mTBI) suggest that metabolic changes in the brain occur immediately after a mechanical injury to the head. Proton magnetic resonance spectroscopy (1H-MRS) can be used to determine relative concentrations of metabolites in vivo in the human brain. The purpose of this study was to determine concentrations of glutamate and GABA in the brain acutely after mTBI and throughout 2 mo of recovery. Concentrations of glutamate and GABA were obtained using 1H-MRS in nine individuals who had suffered an mTBI and nine control individuals in two brain regions of interest: the primary motor cortex (M1), and the dorsolateral prefrontal cortex (DLPFC), and at three different time points postinjury: 72 h, 2 wk, and 2 mo postinjury. There were no differences between groups in concentrations of glutamate or GABA, or the ratio of glutamate to GABA, in M1. In the DLPFC, glutamate concentration was lower in the mTBI group compared with controls at 72 h postinjury (d = 1.02), and GABA concentration was lower in the mTBI group at 72 h and 2 wk postinjury (d = 0.81 and d = 1.21, respectively). The ratio of glutamate to GABA in the DLPFC was higher in the mTBI group at 2 wk postinjury (d = 1.63). These results suggest that changes in glutamate and GABA concentrations in the brain may be region-specific and may depend on the amount of time that has elapsed postinjury. NEW & NOTEWORTHY To our knowledge, this is the first study to examine neurotransmitter concentrations in vivo at multiple time points throughout recovery from mild traumatic brain injury in humans.