Distinct forms of depression and somatization following head injury: A neuropsychological framework and exploratory treatment paradigm for somatic symptoms and executive dysfunction following mild head injury

Abstract

Psychiatric symptoms following traumatic brain injury (TBI) pose a significant barrier to neurorehabilitation and impact survivor’s life satisfaction following injury. Depressive and somatization symptoms are common clinical presentations postinjury; however, due to the paucity of etiological models to explain these symptoms, treatment approaches are predominately “borrowed” from non-neurally compromised populations with similar clinical presentations. The orbitofrontal cortex (OFC) is particularly vulnerable in TBI, and serves to modulate autonomic arousal states. Varying severities of TBI have been linked to autonomic underarousal as measured by electrodermal activation (EDA). In a series of studies examining persons with mild head injury (MHI), the phenomenological presentation of depressive and somatization symptoms was examined in persons with and without MHI, and the relationship between these symptoms and autonomic underarousal was explored. In study one, MHI were found to be autonomically underaroused, reporting more somatic depressive symptoms relative to their no-MHI cohort, and the relationship between their injury severity and the intensity of their somatic depressive complaints was completely mediated by underarousal. Investigating somatization revealed MHI status as a moderator of the relationship between somatization and post-concussive symptoms, with MHI having a stronger positive association. Autonomic underarousal was found to be a complete mediator between the relationship between injury severity and their somatization symptoms. In study two, we experimentally manipulated autonomic arousal through brief cardiovascular exercise and evaluated whether this concomitantly improved somatic-based psychiatric complaints and neurocognitive functioning in persons with MHI. Study two replicated the somatic depressive mediation model of study one, and revealed that the experimental manipulation was effective in increasing autonomic arousal, and improving somatic-psychiatric complaints and neurocognitive status. Collectively, these findings suggest that depressive and somatization symptoms postinjury are phenomenologically and etiologically different in persons with a history of head injury relative to their non-neurally compromised counterpart, and autonomic underarousal and OFC dysfunction is a strong candidate for continued investigation as an etiological model for psychiatric symptoms postinjury. Reversal of underarousal may serve as an important therapeutic goal. Lastly, we propose the term “somatic underarousal” to describe this symptomatology as a means to avoid confusion with the historical roots of the term somatization.