## 10 Discussion
Other areas that showed reduced GM in TBI patients were the thalamus and the amygdala. In this context, thalamic atrophy was correlated with persistent post-traumatic headaches and with motor dysfunction in mTBI patients, while frontal and temporal lobe changes have been associated with cognitive impairment, memory and concentration issues, and behavioral changes that mTBI patients could develop. Changes in the amygdala volumes could be correlated with deficits in inhibitory control in patients who develop PTSD following mTBI [34]. \begin{table}
\begin{tabular}{c c c c} \hline \hline
**Study** & **Analysis** & \begin{tabular}{c} **Type of Injury and** \\ **Baseline Group** \\ \end{tabular} & \begin{tabular}{c} **Affected Areas** \\ \end{tabular} \\ \hline \hline \multirow{7}{*}{[PERSON] et al. [30]} & \multirow{7}{*}{MRI and VBM} & \multirow{7}{*}{48 Mtb patients vs. 37 HC} & \(\downarrow\) GM volumes in right hemisphere, lateral and medial portions of the sensorimotor cortex extending into the roclatic & \begin{tabular}{c} operculum, middle frontal gyrus, insula, \\ and temporal pole \\ \end{tabular} \\  & & & \(\downarrow\) WM volumes in the right hemisphere (superior fasciculus longitudinalis, arcuate fasciculus, and cortical-portine tracts) \\  & & & \(\uparrow\) WM volumes in the left arcuate fasciculus and left external capsule \\ \hline \hline \multirow{2}{*}{[PERSON] et al. [31]} & \multirow{2}{*}{\
\begin{tabular}{c} Regional volume and \\ asymmetry features \\ \end{tabular} } & \multirow{2}{*}{67 TBI patients} &
\begin{tabular}{c} Small structural volumes in the acute stage \\ (e.g., of the hippocampus, accumbens, \\ amygdala) predicting negative outcomes. \\ \end{tabular} \\ \hline \hline \multirow{2}{*}{[PERSON] et al. [32]} & \multirow{2}{*}{Volumetric changes} & \multirow{2}{*}{56 mTBI patients vs. 34 HC} & \(\downarrow\) thalamus and hippocampus volumes \\ \hline \hline \multirow{2}{*}{[PERSON] et al. [33]} & \multirow{2}{*}{Volumetric changes} & 25 mTBI patients vs. 18 HC & \(\downarrow\) GM volume \\  & & 20 mTBI/PTSD patients vs. 14 HC & \(\downarrow\) bilateral anterior amygdala volumes \\ \hline \hline \multirow{2}{*}{[PERSON] et al. [35]} & \multirow{2}{*}{GM density} & \multirow{2}{*}{24 mTBI patients vs. 16 HC} & \(\downarrow\) GM density in the dorsolateral prefrontal cortex, striatum, medial frontal, and temporal regions \\ \hline \hline \multirow{7}{*}{[PERSON] et al. [36]} & \multirow{7}{*}{Structural covariance} & \multirow{7}{*}{52 mTBI patients vs. 21 HC} & \(\downarrow\) GM volumes in the left supplementary motor area, the left frontal inferior orbital cortex, the left and right insular cortex, and the right supplementary temporal cortex \\  & & & \(\downarrow\) structural covariance in the right middle occipital cortex, the left fusiform cortex, the right middle temporal and cingulum and the left middle cingulum, the left supplementary temporal cortex \\ \hline \hline \end{tabular}
\end{table} 
Table 1: _Cont._However, based on the brain injury span and location, some of the symptoms could persist over time, never to remit, or even progress to more serious long-termed negative outcome, such as the chronic traumatic encephalopathy [3]. This could be the reason why the cerebellum, the basal ganglia, the hippocampus, the amygdala, and the thalamus also showed reduced GM volume following mTBIs. Stimuli perception and response, memory and learning, and emotion processing are also described as impaired in recurrent mTBI patients who later developed chronic traumatic encephalopathy [42]. A percentage of 40-80% of mTBI patients were shown to develop PCS with symptoms including headache, fatigue, irritability, dizziness, balance issues, affected sleep, poor memory and concentration, and increased sensitivity to light and noise. The symptoms were usually occurring shortly following brain injury and could persist for weeks or months [43]. Approximately 15% of patients developed persistent symptoms for more than 6 months or 1 year.