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
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AbstractPsychiatric 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.
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Social competence following mild head injury and moderate traumatic brain injury: Investigating the neuropsychological relationships between arousal, social decision-making and depressionRobb, Sean; Department of PsychologyClient-directed long-term rehabilitative goals and life satisfaction following head injury emphasize the importance of social inclusion, rather than cognitive or physical, outcomes. However, very little research has explored the socio-emotional factors that pose as barriers to social reintegration following injury. This study investigates social barriers following head injury (i.e., decision-making - Iowa Gambling Task [IGT] and mood – depression) and possible amelioration of those challenges (through treatment) in both highly functioning university students with and without mild head injury (MHI) and in individuals with moderate traumatic brain injury (TBI). An arousal manipulation using emotionally evocative stimuli was introduced to manipulate the subject’s physiological arousal state. Seventy-five university students (37.6% reporting a MHI) and 11 patients with documented moderate TBI were recruited to participate in this quasi-experimental study. Those with head injury were found to be physiologically underaroused (on measures of electrodermal activation [EDA] and pulse) and were less sensitive to the negative effects of punishment (i.e., losses) in the gambling task than those without head injury, with greater impairment being observed for the moderate TBI group. The arousal manipulation, while effective, was not able to maintain a higher state of arousal in the injury groups across trials (i.e., their arousal state returned to pre-manipulation levels more quickly than their non-injured cohort), and, subsequently, a performance improvement was not observed on the IGT. Lastly, head injury was found to contribute to the relationship between IGT performance and depressive symptom acknowledgment and mood status in persons with head injury. This study indicates the possible important role of physiological arousal on socio- emotional behaviours (decision-making, mood) in persons with even mild, non-complicated head injuries and across the injury severity continuum.
Neural and Behavioural Consequences of Chronic Inflammation following Spinal Cord InjuryAllison, David; Applied Health Sciences ProgramThis thesis investigated the influence of chronic inflammation on several neural/behavioural disorders following spinal cord injury (SCI) including depression, cognitive impairment, neuropathic pain, and somatic nerve deficits. Ample evidence exists to suggest that the immune system communicates with, and influences the nervous system both centrally and peripherally. Pro-inflammatory cytokines have been shown to influence the nervous system directly by altering ion channel kinetics, as well as indirectly by altering enzyme function thereby resulting in changes in critical neuroactive compounds. Proinflammatory mediators have been shown to up-regulate the enzyme indoleamine 2,3 dioxygenase (IDO) resulting in the accelerated degredation of serotonin precursor tryptophan (TRP) and increased production of TRP metabolites such as kynurenine (KYN). They have also been shown to upregulate the enzyme cyclooxygenase (COX) resulting in the increased production of pain inducing eicosanoids such as prostaglandin E2 (PGE2). Immune dysfunction in the form of chronic inflammation may therefore contribute to the severity of behavioural disorders such as depression and cognitive impairment, as well as neural disorders such neuropathic pain and somatic nerve deficits. SCI is typically associated with not only a state of chronic inflammation but also a drastically higher prevalence of each of the aforementioned neural and behavioural disorders. This makes SCI an ideal population to study the interaction between the immune and nervous systems, and assess the potential efficacy of novel treatment strategies which target the immune system for the management of such disorders. A 3-month anti-inflammatory diet was utilized as a treatment intervention for the purpose of reducing chronically elevated levels of pro-inflammatory mediators. This intervention allowed for the assessment of each of the outcome variables of interest at baseline (under an elevated inflammatory status) as well as at 1-month and 3-months during the intervention (under a reduced inflammatory state). Changes in inflammation were assessed by the quantification of serum pro (IL-1β, IL-2, IL-6, IFN-У, TNF-α, CRP) and anti-inflammatory (IL-4, IL-10, IL-1RA) cytokines. Cytokine-induced alterations in enzyme function and corresponding changes in neuroactive compounds were assessed by tryptophan (TRP), the competing amino acids phenylalanine (PHE), tyrosine (TYR), leucine (Leu), isoleucine (Ile), and valine (Val), the tryptophan metabolite kynurenine (KYN), and the pain-inducing eicosanoids prostaglandin E2 (PGE2) and leukotriene B4 (LTB4). In addition to such molecular indices, actual changes in each of the outcome variables of interest were assessed. Levels of depression were assessed by questionnaire via the Center for Epidemiological Studies Depression Scale (CES-D). Cognitive function (in the form of verbal learning) and memory was assessed via the California Verbal Learning Test (CVLT). Neuropathic pain was assessed via the Neuropathic Pain Questionnaire (NPQ). Somatic nerve function was assessed by EMG, including the assessment of nerve conduction velocity and signal amplitude in both motor and sensory nerves. The intervention significantly reduced serum concentrations of pro-inflammatory mediators in the treatment group (n=12) by 28%, while no significant change was found in the control group (n=8). Among other changes in amino acids, the most notable was that the change in the KYN/TRP ratio (an indicator of IDO activity) and the TRP/LNAA ratio (an indicator of TRP availability for serotonin synthesis) was significantly different between groups. The treatment group showed a significant reduction in scores of depression, as well as a significant reduction in sensory neuropathic pain scores. No significant changes were observed in regards to somatic nerve conduction and most indices of cognitive function (with the exception of the ability to avoid incorrect responses on the CVLT). These results may suggest a substantial role for chronic inflammation in depression and neuropathic pain following SCI and provide a potential alternative treatment strategy for the management of such intractable disorders.