Psychological Effects of Traumatic Brain Injury from A Neurobiological Perspective

Pritam Dutta, M.Optom, FAAO

Clinical Optometry Practitioner, Chandraprabha Eye Hospital, Assam, India

Background

The Concussion in Sport Group (CISG) recognised in the most recent reiteration of the Consensus Statement on Concussion in Sport that psychological issues are commonly reported as a result of concussion and should be considered when managing individuals who have sustained sports-related concussions.⁽¹⁾ While adjustment problems and psychological symptoms are not uncommon after any type of traumatic brain injury, they are especially common in sports-related concussions, owing to situational factors (e.g. cognitive difficulties, pain, removal and/or possible retirement from play, and limited team/coach support). However, evidence suggests that neurobiological/pathophysiological alterations associated with a brain injury, regardless of severity, may be linked to the onset of psychological symptoms. ^(2-4)

The cortical-limbic hypothesis of depression proposed by Mayberg

Mayberg’s limbiccortical model of depression proposes that increased blood flow in the ventral limbic and paralimbic areas, which include the anterior insula and subgenual cingulate, and decreased blood flow in the neocortical and limbic regions, mediates depressive symptoms and melancholy (e.g., prefrontal, inferior parietal, dorsal anterior cingulate, posterior cingulate).⁽⁵⁾ Functional investigations of depression have shown hyperactivity in the ventromedial prefrontal cortex and hypoactivity in the dorsolateral prefrontal cortex, which is consistent with this finding.⁽⁶⁾

• Depression and Traumatic brain injury

Within the first three months after a mTBI, it is anticipated that 12–44 percent of people will experience some form of depression.⁽⁷⁾ Given that intracranial anomalies following traumatic brain injury are likely to include the frontal and temporal lobes, as well as the fronto-limbicsubcortical regions implicated in depression, depression is a common biological consequence of all severities of traumatic brain injury.⁽⁸⁾ The cortical-limbic hypothesis of depression has been supported by subsequent studies of depression following traumatic brain damage. Chen et al., found lower task-related activity in the dorsolateral prefrontal cortex, dorsal anterior cingulate cortex, insular cortex, thalamus, and striatum in athletes with post-concussive and depressive symptoms when compared to concussed athletes without depressive symptoms and healthy controls in an athlete sample.⁽²⁾ Chen et al., discovered that, while concussed athletes without depression had grey matter loss in the insular cortices as a result of the trauma, the concussed and the depressed group had even more grey matter volume loss in the medial frontal and temporal areas. Furthermore, the intensity of depressive symptoms was linked with less grey matter volume in the rostral anterior cingulate cortex, implying that higher levels of depressive symptoms were associated with less grey matter volume in this region of interest.

• Anxiety-related negative emotion in a limbic-medial prefrontal model

The limbic-medial prefrontal model, as described by Etkin, outlines how fear-related emotions are processed. Emotional processing has been linked to amygdala and insula hyperactivation when it comes to fear. These limbic systems, as well as other subcortical structures (such as the hypothalamus and periaqueductal grey), encode and record emotional impulses and trigger behavioural coordination. Because the amygdala is assumed to mediate fear-based reactions, exaggerated or excessive activation of this tissue has been linked to anxiety-related diseases.⁽⁹⁾

• Anxiety-related symptoms and traumatic brain injury

Damage to the prefrontal cortex, ventral frontal lobe, and anterior temporal lobe is common in traumatic brain injuries, and these areas are highly involved in the identification of emotionally important inputs and the regulation of responses to those stimuli.⁽⁹⁾  Rodents with a mild fluid percussion injury spent more time in the open arm of the behavioural apparatus, according to Shultz et al., ⁽¹⁰⁾ Reger et al., using generated lateral fluid percussion injuries and Pavlovian fear conditioning in a mouse paradigm, discovered that injured mice showed greater fear conditioning and over-generalization of learnt fear to conditioned and new circumstances.⁽⁴⁾

References

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