Introduction: Traumatic brain injury (TBI) frequently affects the frontal cortex, which can have widespread behavioural effects including disruption to the reward system. This disruption may manifest clinically as anhedonia, the reported loss of interest or pleasure thought to be linked to dysfunction in reward circuitry. It may also be measured experimentally through tasks probing various facets of reward including motivation, effort, anticipation, and reward responsivity. Notably, anhedonia is a core symptom of Major Depressive Disorder (MDD). Thus, the presence of anhedonia and reward dysfunction post-TBI may predict the future development of psychiatric disorders including MDD. The aim of this current review is to synthesize the published literature on reward processing and anhedonia in TBI, and to discuss the psychiatric implications of these findings.

Methods: A literature search was conducted to identify and summarize the published literature on reward processing and anhedonia in TBI populations using the search engine PubMed, with no restriction on publication year. The review was limited to primary research papers which enrolled adult participants and were available in English.

Results: The literature search identified 155 articles, of which 21 articles met criteria for inclusion. Across included studies, the most frequently used measure of reward (n=9) was the Iowa Gambling Task (IGT), which probes various facets of reward including anticipation, hedonic response, and feedback integration. These studies generally demonstrated impaired performance on the IGT in TBI as compared to non-injured controls, though some conflicting results were found, possibly due to small sample sizes. Reward valuation, assessed through temporal discounting and auction tasks, was also shown to be impaired in TBI across studies. At the neurophysiological level, electroencephalography (EEG) studies consistently demonstrated that rewarding stimuli were not processed by TBI patients in the same way as controls. Few studies measured anhedonia in TBI; one reported an association between anhedonia and damage to the ventrolateral prefrontal cortex. Two included studies also reported the effectiveness of various therapeutic options, including psychotherapy and pharmacological agents that target the reward system (e.g. dopamine agonists) in improving reward function post-TBI.

Implications: Findings of this review underscore the value of assessing anhedonia and reward deficits following TBI. Importantly, anhedonia may be a key factor in the development of psychiatric sequelae post-injury, as this symptom has shown promise in predicting MDD onset and treatment outcome. Therefore, the presence of anhedonia and reward processing dysfunction following TBI may be a potential marker of risk for depression.

Anhedonia and reward-related deficits in traumatic brain injury: Implications for development of depression post-injury