Abstract
Mild traumatic brain injury (TBI) results in chronic affective disorders such as depression, anxiety, and fear that persist up to years following injury and significantly impair the quality of life for patients. Although a great deal of research has contributed to defining symptoms of mild TBI, there are no adequate drug therapies for brain-injured individuals. Preclinical studies have modeled these deficits in affective behaviors post-injury to understand the underlying mechanisms with a view to developing appropriate treatment strategies. These studies have also unveiled sex differences that contribute to the varying phenotypes associated with each behavior. Although clinical and preclinical studies have viewed these behavioral deficits as separate entities with unique neurobiological mechanisms, mechanistic similarities suggest that a novel approach is needed to advance research on drug therapy. This review will discuss the circuitry involved in the expression of deficits in affective behaviors following mild TBI in humans and animals and provide evidence that the manifestation of impairment in these behaviors stems from an amygdala-dependent emotional processing deficit. It will highlight mechanistic similarities between these different types of affective behaviors that can potentially advance mild TBI drug therapy by investigating treatments for the deficits in affective behaviors as one entity, requiring the same treatment.
Highlights
Traumatic brain injury (TBI) is a serious public health concern that affects over 1.5 million people each year and results in the death and disability of thousands, with mild traumatic brain injury (TBI) comprising the greatest proportion of these cases (Kay et al, 1993; Coronado et al, 2011; McMahon et al, 2014)
Neurobiological studies have suggested that the amygdala is a key brain region involved in emotional processing (Phelps and Ledoux, 2005; Pessoa, 2010; Kim et al, 2011; Korgaonkar et al, 2019), and its impairment is associated with the manifestation of the affective disorders seen after TBI (Han et al, 2015; Hoffman et al, 2019)
Because of the high comorbidity and mechanistic similarities across depression, anxiety, and fear, we suggest that they should be considered as a collective deficit in emotional processing stemming from impairment within the amygdala
Summary
Traumatic brain injury (TBI) is a serious public health concern that affects over 1.5 million people each year and results in the death and disability of thousands, with mild TBI comprising the greatest proportion of these cases (Kay et al, 1993; Coronado et al, 2011; McMahon et al, 2014). Depression, anxiety, and fear/post-traumatic stress disorder (PTSD) are affective behavioral impairments that are among the most frequently reported behavioral problems that manifest in the chronic period following mild TBI (Baldassarre et al, 2015; Ellis et al, 2015; Horn et al, 2016; Bunt et al, 2020). The severity of these deficits is known to vary by sex, in that women are more prone to exhibiting affective disorders postinjury (Broshek et al, 2005; Bunt et al, 2020). Because of the high comorbidity and mechanistic similarities across depression, anxiety, and fear, we suggest that they should be considered as a collective deficit in emotional processing stemming from impairment within the amygdala
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