Advances in neuroimaging of traumatic brain injury and posttraumatic stress disorder.
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ABSTRACT:
SUBMITTER: Van Boven RW
PROVIDER: S-EPMC3233771 | biostudies-other | 2009
REPOSITORIES: biostudies-other
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Project description:IntroductionNeurocognitive problems associated with posttraumatic stress disorder (PTSD) can interact with impairment resulting from traumatic brain injury (TBI).Research questionWe aimed to identify neurocognitive problems associated with probable PTSD following TBI in a civilian sample.Material and methodsThe study is part of the CENTER-TBI project (Collaborative European Neurotrauma Effectiveness Research) that aims to better characterize TBI. For this cross-sectional study, we included patients of all severities aged over 15, and a Glasgow Outcome Score Extended (GOSE) above 3. Participants were assessed at six months post-injury on the PTSD Checklist-5 (PCL-5), the Trail Making Test (TMT), the Rey Auditory Verbal Learning Test (RAVLT) and the Cambridge Neuropsychological Test Automated Battery (CANTAB). Primary analysis was a complete case analysis. Regression analyses were performed to investigate the association between the PCL-5 and cognition.ResultsOf the 1134 participants included in the complete case analysis, 13.5% screened positive for PTSD. Probable PTSD was significantly associated with higher TMT-(B-A) (OR = 1.35, 95% CI: 1.14-1.60, p < .001) and lower RAVLT-delayed recall scores (OR = 0.74, 95% CI: 0.61-0.91, p = .004) after controlling for age, sex, psychiatric history, baseline Glasgow Coma Scale and education.Discussion and conclusionPoorer performance on cognitive tests assessing task switching and, to a lesser extent, delayed verbal recall is associated with probable PTSD in civilians who have suffered TBI.
| S-EPMC9560676 | biostudies-literature
Project description:PurposeTraumatic brain injury (TBI) and posttraumatic stress disorder (PTSD) have emerged as independent risk factors for an earlier onset of Alzheimer's disease (AD), although the pathophysiology underlying this risk is unclear. Postmortem studies have revealed extensive cerebral accumulation of tau following multiple and single TBI incidents. We hypothesized that a history of TBI and/or PTSD may induce an AD-like pattern of tau accumulation in the brain of nondemented war veterans.MethodsVietnam War veterans (mean age 71.4 years) with a history of war-related TBI and/or PTSD underwent [18F]AV145 PET as part of the US Department of Defense Alzheimer's Disease Neuroimaging Initiative. Subjects were classified into the following four groups: healthy controls (n = 21), TBI (n = 10), PTSD (n = 32), and TBI+PTSD (n = 17). [18F]AV1451 reference tissue-normalized standardized uptake value (SUVr) maps, scaled to the cerebellar grey matter, were tested for differences in tau accumulation between groups using voxel-wise and region of interest approaches, and the SUVr results were correlated with neuropsychological test scores.ResultsCompared to healthy controls, all groups showed widespread tau accumulation in neocortical regions overlapping with typical and atypical patterns of AD-like tau distribution. The TBI group showed higher tau accumulation than the other clinical groups. The extent of tauopathy was positively correlated with the neuropsychological deficit scores in the TBI+PTSD and PTSD groups.ConclusionA history of TBI and/or PTSD may manifest in neurocognitive deficits in association with increased tau deposition in the brain of nondemented war veterans decades after their trauma. Further investigation is required to establish the burden of increased risk of dementia imparted by earlier TBI and/or PTSD.
| S-EPMC6451714 | biostudies-literature
Project description:ObjectiveGiven the high prevalence and comorbidity of combat-related PTSD and TBI in Veterans, it is often difficult to disentangle the contributions of each disorder. Examining these pathologies separately may help to understand the neurobiological basis of memory impairment in PTSD and TBI independently of each other. Thus, we investigated whether a) PTSD and TBI are characterized by subcortical structural abnormalities by examining diffusion tensor imaging (DTI) metrics and volume and b) if these abnormalities were specific to PTSD versus TBI.MethodWe investigated whether individuals with PTSD or TBI display subcortical structural abnormalities in memory regions by examining DTI metrics and volume of the hippocampus and caudate in three groups of Veterans: Veterans with PTSD, Veterans with TBI, and Veterans with neither PTSD nor TBI (Veteran controls).ResultsWhile our results demonstrated no macrostructural differences among the groups in these regions, there were significant alterations in microstructural DTI indices in the caudate for the PTSD group but not the TBI group compared to Veteran controls.ConclusionsThe result of increased mean, radial, and axial diffusivity, and decreased fractional anisotropy in the caudate in absence of significant volume atrophy in the PTSD group suggests the presence of subtle abnormalities evident only at a microstructural level. The caudate is thought to play a role in the physiopathology of PTSD, and the habit-like behavioral features of the disorder could be due to striatal-dependent habit learning mechanisms. Thus, DTI appears to be a vital tool to investigate subcortical pathology, greatly enhancing the ability to detect subtle brain changes in complex disorders.
| S-EPMC5256941 | biostudies-literature
Project description:Mild traumatic brain injury (mTBI) is often characterized by deficits in response inhibition, which can contribute to marked social and occupational dysfunction. mTBI often occurs in the context of psychologically traumatic events. This can cause posttraumatic stress disorder (PTSD), which also impedes response inhibition. The overlap or distinction in these inhibitory deficits in mTBI and PTSD is unclear. This study aimed to assess behavioral, neurophysiological, and neuroimaging indices of response inhibition in mTBI by also assessing these parameters in healthy controls (HC) and PTSD participants. Participants with mTBI (without PTSD) (n = 46), PTSD (without mTBI) (n = 41), and HC (n = 40) were assessed during a response inhibition task (the Go/NoGo task) during neuropsychological testing and separate functional magnetic imaging and event-related potentials sessions. PTSD symptom severity was assessed with the Clinician-Administered PTSD Scale. Both mTBI and PTSD participants performed more omission errors on the Go/NoGo task and were associated with greater N2 amplitude, greater left inferior parietal activation and reduced connectivity of the left inferior parietal cluster and left angular gyrus compared to HC. There were no differences between mTBI and PTSD on any of these measures. These findings highlight that both mTBI and PTSD contribute to neural dysfunction during response inhibition, and arguably these occur due to distinct mechanisms. In the context of the common comorbidity between these two conditions, strategies to address response inhibition deficits in mTBI may need to consider causative factors underpinning neurological insult of mTBI and psychological effects associated with PTSD.
| S-EPMC7905369 | biostudies-literature
Project description:BackgroundBrain volumes in regions such as the hippocampus and amygdala have been associated with risk for the development of posttraumatic stress disorder (PTSD). The objective of this study was to determine whether a set of regional brain volumes, measured by magnetic resonance imaging at 2 weeks following mild traumatic brain injury, were predictive of PTSD at 3 and 6 months after injury.MethodsUsing data from TRACK-TBI (Transforming Research and Clinical Knowledge in TBI), we included patients (N = 421) with Glasgow Coma Scale scores 13-15 assessed after evaluation in the emergency department and at 2 weeks, 3 months, and 6 months after injury. Probable PTSD diagnosis (PTSD Checklist for DSM-5 score, ≥33) was the outcome. FreeSurfer 6.0 was used to perform volumetric analysis of three-dimensional T1-weighted magnetic resonance images at 3T obtained 2 weeks post injury. Brain regions selected a priori for volumetric analyses were insula, hippocampus, amygdala, superior frontal cortex, rostral and caudal anterior cingulate, and lateral and medial orbitofrontal cortices.ResultsOverall, 77 (18.3%) and 70 (16.6%) patients had probable PTSD at 3 and 6 months. A composite volume derived as the first principal component incorporating 73.8% of the variance in insula, superior frontal cortex, and rostral and caudal cingulate contributed to the prediction of 3-month (but not 6-month) PTSD in multivariable models incorporating other established risk factors.ConclusionsResults, while needing replication, provide support for a brain reserve hypothesis of PTSD and proof of principle for how prediction of at-risk individuals might be accomplished to enhance prognostic accuracy and enrich clinical prevention trials for individuals at the highest risk of PTSD following mild traumatic brain injury.
| S-EPMC7946719 | biostudies-literature
Project description:ObjectiveTo examine whether experiencing a traumatic brain injury (TBI) on a recent combat deployment was associated with postdeployment binge drinking, independent of posttraumatic stress disorder (PTSD).MethodsUsing the 2008 Department of Defense Survey of Health Related Behaviors among Active Duty Military Personnel, an anonymous survey completed by 28 546 personnel, the study sample included 6824 personnel who had a combat deployment in the past year. Path analysis was used to examine whether PTSD accounted for the total association between TBI and binge drinking.Main measuresThe dependent variable, binge drinking days, was an ordinal measure capturing the number of times personnel drank 5+ drinks on one occasion (4+ for women) in the past month. Traumatic brain injury level captured the severity of TBI after a combat injury event exposure: TBI-AC (altered consciousness only), TBI-LOC of 20 or less (loss of consciousness up to 20 minutes), and TBI-LOC of more than 20 (loss of consciousness >20 minutes). A PTSD-positive screen relied on the standard diagnostic cutoff of 50+ on the PTSD Checklist-Civilian.ResultsThe final path model found that while the direct effect of TBI (0.097) on binge drinking was smaller than that of PTSD (0.156), both were significant. Almost 70% of the total effect of TBI on binge drinking was from the direct effect; only 30% represented the indirect effect through PTSD.ConclusionFurther research is needed to replicate these findings and to understand the underlying mechanisms that explain the relationship between TBI and increased postdeployment drinking.
| S-EPMC4395509 | biostudies-literature
Project description:Neuroimaging genetic studies that associate genetic and epigenetic variation with neural activity or structure provide an opportunity to link genes to psychiatric disorders, often before psychopathology is discernable in behavior. Here we review neuroimaging genetics studies with participants who have Posttraumatic Stress Disorder (PTSD). Results show that genes related to the physiological stress response (e.g., glucocorticoid receptor and activity, neuroendocrine release), learning and memory (e.g., plasticity), mood, and pain perception are tied to neural intermediate phenotypes associated with PTSD. These genes are associated with and sometimes predict neural structure and function in areas involved in attention, executive function, memory, decision-making, emotion regulation, salience of potential threats, and pain perception. Evidence suggests these risk polymorphisms and neural intermediate phenotypes are vulnerabilities toward developing PTSD in the aftermath of trauma, or vulnerabilities toward particular symptoms once PTSD has developed. Work distinguishing between the re-experiencing and dissociative sub-types of PTSD, and examining other PTSD symptom clusters in addition to the re-experiencing and hyperarousal symptoms, will further clarify neurobiological mechanisms and inconsistent findings. Furthermore, an exciting possibility is that genetic associations with PTSD may eventually be understood through differential intermediate phenotypes of neural circuit structure and function, possibly underlying the different symptom clusters seen within PTSD.
| S-EPMC5056798 | biostudies-literature
Project description:PURPOSE:Aggressive driving contributes to the high rates of postdeployment motor vehicle-related injury and death observed among veterans, and veterans cite problems with anger, aggressive driving, and road rage as being among their most pressing driving-related concerns. Both posttraumatic stress disorder (PTSD) and traumatic brain injury (TBI) have been associated with driving-related deficits in treatment-seeking samples of veterans, but the relative contribution of each of these conditions to problems with aggressive driving in the broader population of combat veterans is unclear. METHOD:?2 and logistic regression analyses were used to examine the relative association of PTSD, TBI, and co-occurring PTSD and TBI to self-reported problems with road rage in a sample of 1,102 veterans living in the mid-Atlantic region of the United States who had served in Afghanistan or Iraq. RESULTS:Results indicate that controlling for relevant demographic variables, PTSD without TBI (odds ratio = 3.44, p < .001), and PTSD with co-occurring TBI (odds ratio = 4.71, p < .001) were associated with an increased risk of road rage, but TBI without PTSD was not. CONCLUSIONS:Our findings suggest that PTSD, with or without comorbid TBI, may be associated with an increased risk of aggressive driving in veterans. Clinical implications for treating problems with road rage are discussed, including use of interventions targeting hostile interpretation bias and training in emotional and physiological arousal regulation skills. (PsycINFO Database Record
| S-EPMC5941924 | biostudies-literature
Project description:BackgroundLimitations in everyday functioning are frequently reported by veterans with a history of mild traumatic brain injury (mTBI) and/or posttraumatic stress disorder (PTSD). Multiple factors are associated with functional disability among veterans, including depression, poor social support, cognition, and substance use. However, the degree to which these factors, particularly cognitive capacities, contribute to functional limitations remains unclear.MethodsWe evaluated performance on tests of processing speed, executive functioning, attention, and memory as predictors of functioning on the World Health Organization Disability Assessment Scale (WHODAS) 2.0 in 288 veterans. Participants were placed in one of the following groups: PTSD-only, mTBI-only, mTBI + PTSD, and neither PTSD nor mTBI (deployed control group). Cognitive test performances were evaluated as predictors of WHODAS 2.0 functional ratings in regression models that included demographic variables and a range of mood, behavioral health, and postconcussive symptom ratings.ResultsMultiple cognitive test performances predicted WHODAS 2.0 scores in the deployed control group, but they generally did not predict functioning in the clinical groups when accounting for demographics, mood, behavioral health, and postconcussive symptoms.ConclusionsIn veterans with mTBI and/or PTSD, cognitive test performances are less associated with everyday functioning than mood and postconcussive symptoms.
| S-EPMC8916049 | biostudies-literature
Project description:ObjectivesMilitary service members risk acquiring posttraumatic stress disorder (PTSD) and mild-traumatic brain injury (mTBI), with high comorbidity. Owing to overlapping symptomatology in chronic mTBI or postconcussion syndrome (PCS) and PTSD, it is difficult to assess the etiology of a patient's condition without objective measures. Using resting-state functional MRI in a novel framework, we tested the hypothesis that their neural signatures are characterized by functionally hyperconnected brain regions which are less variable over time. Additionally, we predicted that such connectivities possessed the highest ability in predicting the diagnostic membership of a novel subject (top-predictors) in addition to being statistically significant.MethodsU.S. Army Soldiers (N = 87) with PTSD and comorbid PCS + PTSD were recruited along with combat controls. Static and dynamic functional connectivities were evaluated. Group differences were obtained in accordance with our hypothesis. Machine learning classification (MLC) was employed to determine top predictors.ResultsFrom whole-brain connectivity, we identified the hippocampus-striatum connectivity to be significantly altered in accordance with our hypothesis. Diffusion tractography revealed compromised white-matter integrity between aforementioned regions only in the PCS + PTSD group, suggesting a structural etiology for the PCS + PTSD group rather than being an extreme subset of PTSD. Employing MLC, connectivities provided worst-case accuracy of 84% (9% more than psychological measures). Additionally, the hippocampus-striatum connectivities were found to be top predictors and thus a potential biomarker of PTSD/mTBI.ConclusionsPTSD/mTBI are associated with hippocampal-striatal hyperconnectivity from which it is difficult to disengage, leading to a habit-like response toward episodic traumatic memories, which fits well with behavioral manifestations of combat-related PTSD/mTBI. Hum Brain Mapp 38:2843-2864, 2017. © 2017 The Authors Human Brain Mapping Published by Wiley Periodicals, Inc.
| S-EPMC6867178 | biostudies-literature