A multimodal imaging study in US veterans of Operations Iraqi and Enduring Freedom with and without major depression after blast-related concussion

Veterans Affairs San Diego Healthcare System, USA.
NeuroImage (Impact Factor: 6.36). 05/2010; 54 Suppl 1:S69-75. DOI: 10.1016/j.neuroimage.2010.04.269
Source: PubMed

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.

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    • "Recent advances and the emergence of newer functional imaging techniques such as Diffusion Tensor Imaging (DTI), fl uorodeoxyglucose positron emission tomography (FDG-PET), Single Photon Emission Computed Tomography (SPECT) and functional Magnetic Resonance Imaging (fMRI) have shown great potential in detecting brain tissue damage that are invisible in CT and MRI. These newer technologies therefore, may have a signifi cant potential in diagnosing mTBI in future (Brenner, 2011; Matthews et al., 2011). The availability of these imaging tools, however, is very limited and will require further experimental validation and correlation with the neurophysiological paradigms of TBI. "
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    • "th both PTSD and depression , common areas of volume reduction were located in the PFC ( Kroes , Rugg , Whalley , & Brewin , 2011 ) . An fMRI study demonstrated that veterans with both mTBI and MDD showed greater activity in the amygdala , and less activity in dorsolateral PFC , than veterans with mTBI only during an emotional face matching task ( Matthews et al . , 2011 ) . Robertson , Manly , Andrade , Baddeley , and Yiend ( 1997 ) have argued that in addition to motor response inhibition , the Go / NoGo task is a measure of sustained attention . Both motor response inhibition and / or lapses of attention can produce high NoGo error rates . In our experiment , the 90 / 10 blocks might have been more m"
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    ABSTRACT: Combat veterans with post-traumatic stress disorder (PTSD) can show impairments in executive control and increases in impulsivity. The current study examined the effects of PTSD on motor response inhibition, a key cognitive control function. A Go/NoGo task was administered to veterans with a diagnosis of PTSD based on semi-structured clinical interview using DSM-IV criteria (n = 40) and age-matched control veterans (n = 33). Participants also completed questionnaires to assess self-reported levels of PTSD and depressive symptoms. Performance measures from the patients (error rates and reaction times) were compared to those from controls. PTSD patients showed a significant deficit in response inhibition, committing more errors on NoGo trials than controls. Higher levels of PTSD and depressive symptoms were associated with higher error rates. Of the three symptom clusters, re-experiencing was the strongest predictor of performance. Because the co-morbidity of mild traumatic brain injury (mTBI) and PTSD was high in this population, secondary analyses compared veterans with PTSD+mTBI (n = 30) to veterans with PTSD only (n = 10). Although preliminary, results indicated the two patient groups did not differ on any measure (p > .88). Since cognitive impairments could hinder the effectiveness of standard PTSD therapies, incorporating treatments that strengthen executive functions might be considered in the future. (JINS, 2012, 18, 1-10).
    Journal of the International Neuropsychological Society 05/2012; 18(5):917-26. DOI:10.1017/S1355617712000458 · 3.01 Impact Factor
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    • "US veterans from OEF with major depression after blast-related concussion showed greater regional activation (compared with blast-related concussed veterans without depression) in a limbic region (amygdala) during fear trials. During these fear trials of depressed veteran's postconcussion symptoms, activation is reduced in the dorsolateral prefrontal cortex, a fear inhibitory brain region (Matthews et al., 2010). Thus, it seems that the prefrontal cortex, medial temporal regions, hippocampus, amygdala, and corpus callosum represent brain regions of interest in TBI. "
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    ABSTRACT: As US military service members return from the wars in Iraq and Afghanistan with elevated rates of traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD), attention has been increasingly focused on TBI/PTSD comorbidity, its neurobiological mechanisms, and novel and effective treatment approaches. TBI and PTSD, and their comorbid conditions, present with a spectrum of common clinical features such as sleep disturbance, depression, anxiety, irritability, difficulty in concentrating, fatigue, suicidality, chronic pain, and alterations in arousal. These TBI and PTSD disorders are also thought to be characterized by overlapping neural mechanisms. Both conditions are associated with changes in hippocampal, prefrontal cortical, and limbic region function because of alterations in synaptogenesis, dendritic remodeling, and neurogenesis. Neural changes in TBI and PTSD result from pathophysiological disturbances in metabolic, cytotoxic, inflammatory, and apoptic processes, amongst other mechanisms. Neurotrophins have well-established actions in regulating cell growth and survival, differentiation, apoptosis, and cytoskeleton restructuring. A body of research indicates that dysregulation of neural brain-derived neurotrophic factor (BDNF) is found in conditions of TBI and PTSD. Induction of BDNF and activation of its intracellular receptors can produce neural regeneration, reconnection, and dendritic sprouting, and can improve synaptic efficacy. In this review, we consider treatment approaches that enhance BDNF-related signaling and have the potential to restore neural connectivity. Such treatment approaches could facilitate neuroplastic changes that lead to adaptive neural repair and reverse cognitive and emotional deficits in both TBI and PTSD.
    Behavioural pharmacology 09/2010; 21(5-6):427-37. DOI:10.1097/FBP.0b013e32833d8bc9 · 2.19 Impact Factor
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