A multimodal imaging study in US veterans of Operations Iraqi and Enduring Freedom with and without major depression after blast-related concussion
ABSTRACT Although the exact number of affected individuals is unknown, it has been estimated that approximately 20% of U.S. veterans of Operations Enduring Freedom (OEF) and Iraqi Freedom (OIF) have experienced mild traumatic brain injury (mTBI) (i.e., concussion), which is defined as a brief loss or alteration of consciousness from a blow or jolt to the head. Blast exposure is among the most common causes of concussion in OEF-OIF warriors. Although the mechanism is unknown, major depressive disorder (MDD) after head injury is common. The purpose of this study was to use diffusion tensor imaging (DTI) and functional magnetic resonance imaging (fMRI) to examine the structural and functional neural correlates of MDD in OEF-OIF combat veterans with a self-reported history of blast-related concussion. We hypothesized that subjects in the MDD group (i.e., individuals with a history of blast-related concussion who were experiencing current MDD) relative to individuals in the non-MDD group (i.e., individuals with a history of blast-related concussion but no current or lifetime history of MDD) would show amygdala hyperactivity and disruption of white matter tracts connecting prefrontal and limbic brain regions. To test these hypotheses, 11 MDD and 11 non-MDD individuals underwent DTI and performed a validated emotional face matching task during fMRI. MDD relative to non-MDD individuals showed greater activity during fear matching trials in the amygdala and other emotion processing structures, lower activity during fear matching trials in emotional control structures such as the dorsolateral prefrontal cortex and lower fractional anisotropy (FA) in several white matter tracts including the superior longitudinal fasciculus (SLF). Greater depressive symptom severity correlated negatively with FA in the SLF. These results suggest a biological basis of MDD in OEF-OIF veterans who have experienced blast-related concussion, and may contribute to the development of treatments aimed at improving the clinical care of this unique population of wounded warriors.
SourceAvailable from: Kevin KW Wang
Dataset: Balakathiresan Biomarkers Ch 3+
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ABSTRACT: Despite substantial investments, traumatic brain injury (TBI) remains one of the major disorders that lack specific pharmacotherapy. To a substantial degree, this situation is due to lack of understanding of the pathophysiological process of the disease. Experimental TBI research offers controlled, rapid, and cost-effective means to identify the pathophysiology but translating experimental findings into clinical practice can be further improved by using the same or similar outcome measures and clinically relevant time points. The pathophysiology during the acute phase of severe TBI is especially poorly understood. In this Mini review, I discuss some of the incongruences between current clinical practices and needs versus information provided by experimental TBI research as well as the benefits of designing animal experiments with translation into clinical practice in mind.Frontiers in Neurology 03/2015; 6:47. DOI:10.3389/fneur.2015.00047
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ABSTRACT: Traumatic brain injury (TBI) causes a wide variety of neuropsychiatric disturbances associated with great functional impairments and low quality of life. These disturbances include disorders of mood, behavior, and cognition, and changes in personality. The diagnosis of specific neuropsychiatric disturbances can be difficult because there is significant symptom overlap. Systematic clinical evaluations are necessary to make the diagnosis and formulate a treatment plan that often requires a multipronged approach. Management of TBI-associated neuropsychiatric disorders should always include nonpharmacological interventions, including education, family involvement, supportive and behavioral psychotherapies, and cognitive rehabilitation. Pharmacological treatments include antidepressants, anticonvulsants, antipsychotics, dopaminergic agents, and cholinesterase inhibitors. However, evidence-based treatments are extremely limited, and management relies on clinical empiricism and resemblance of TBI neuropsychiatric symptom profiles with those of idiopathic psychiatric disorders. Although the understanding of TBI-associated neuropsychiatric disorders has improved in the last decade, further research is needed including prospective, longitudinal studies to explore biomarkers that will assist with management and prognosis as well as randomized-controlled studies to validate pharmacological and nonpharmacological treatments. The current review summarizes the available literature in support of a structured, systematic evaluation approach and treatment options as well as recommendations for further research directions. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.Seminars in Neurology 02/2015; 35(1):64-82. DOI:10.1055/s-0035-1544241 · 1.78 Impact Factor