Search

This study investigated the use of resting-state electroencephalography (EEG) data to help differentiate posttraumatic stress disorder (PTSD) symptom factors. The sample, 147 combat-exposed OIF/OEF (Operation Iraqi Freedom/Operation Enduring Freedom) Veterans and service members, was a polytrauma population with variable PTSD and mild traumatic brain injury (mTBI) diagnoses. Participants completed the PTSD Checklist (PCL) and resting-state EEG was assessed for 10 minutes, with eyes closed. Regional averages of absolute power in alpha, beta, delta, and theta frequency bands were computed to estimate a single EEG common factor per band. An oblique 4 common-factor model was then fit to the 17 PCL items that included a residual EEG factor as an exogenous predictor with the group mean effect of mTBI on the EEG factor removed. Separate comparative model testing sequences for the alpha, beta, delta, and theta EEG factor frequency bands were conducted. An inverse relationship of delta and theta frequency bands on avoidance and numbing symptom factors (but not re-experiencing and hyperarousal) was found. Results provide evidence for possible neurobiological basis for the 4 PTSD symptom factors.

Objective: Insomnia and behavioural health symptoms 1 year after traumatic brain injury (TBI) were examined in a clinical sample representative of veterans who received inpatient treatment for TBI-related issues within the Veterans Health Administration., Methods: This was a cross-sectional sub-study (n = 112) of the Polytrauma Rehabilitation Centres' traumatic brain injury model system programme. Prevalence estimates of insomnia, depression, general anxiety, nightmares, headache and substance use, stratified by injury severity, were derived. Univariate logistic regression was used to examine unadjusted effects for each behavioural health problem and insomnia by injury severity., Results: Participants were primarily male, < 30 years old and high school educated. Twenty-nine per cent met study criteria for insomnia; those with mild TBI were significantly more likely to meet criteria (43%) than those with moderate/severe TBI (22%), χ(2)(1, n = 112) = 5.088, p ≤ 0.05. Univariable logistic regression analyses revealed depressive symptoms and general anxiety were significantly associated with insomnia symptoms after TBI of any severity. Headache and binge drinking were significantly inversely related to insomnia symptoms after moderate/severe TBI, but not MTBI., Conclusions: Veterans with history of TBI, of any severity, and current insomnia symptoms may be at increased risk for depression and anxiety 1 year after TBI.

Vestibular symptoms are persistent and problematic sequelae of blast exposure. Several lines of evidence suggest that these symptoms often stem from injury to the central nervous system. Current methods of assessing the vestibular system have described vestibular deficits that follow traumatic brain injury and differentiate blunt and blast trauma but have not examined the full range of vestibular functions that depend on the cerebral structures above the midbrain. Damage to the central vestibular circuits can lead to deficits in vital processes of spatial perception and navigation, in addition to dizziness and disequilibrium, and may also affect emotional functioning, particularly noradrenergically modulated states of anxiety. Perceptual functions can be assessed to determine the extent of central nervous system involvement in vestibular symptoms and to provide greater confidence when vestibular dysfunction is to be excluded. The ability to detect central vestibular dysfunction will significantly enhance our response to the dizziness and balance symptoms that are a common source of distress for Veterans.

Objective: Long-term changes to EEG spectra after mild traumatic brain injury (mTBI, i.e., concussion) have been reported; however, the role of injury characteristics in long-term EEG changes is unclear. It is also unclear how any chronic EEG changes may underlie either subjective or objective cognitive difficulties, which might help explain the variability in recovery after mTBI. Methods: This study included resting-state high-density electroencephalography (EEG) and mTBI injury data from 340 service members and veterans collected on average 11 years after injury as well as measures of objective and subjective cognitive functioning. The average absolute power within standard bands was computed across 11 spatial regions of the scalp. To determine how variation in brain function was accounted for by injury characteristics and aspects of cognition, we used regression analyses to investigate how EEG power was predicted by mTBI history characteristics [number, number with post-traumatic amnesia and witnessed loss of consciousness (PTA + LOC), context of injury (combat or non-combat), potentially concussive blast exposures], subjective complaints (TBIQOL General Cognitive and Executive Function Concerns), and cognitive performance (NIH Toolbox Fluid Intelligence and premorbid IQ). Results: Post-traumatic amnesia (PTA) and loss of consciousness (LOC), poorer cognitive performance, and combat experience were associated with reduced power in beta frequencies. Executive function complaints, lower premorbid IQ, poorer cognitive performance, and higher psychological distress symptoms were associated with greater power of delta frequencies. Multiple regression confirmed the relationship between PTA + LOC, poor cognitive performance, cognitive complaints, and reduced power in beta frequencies and revealed that repetitive mTBI was associated with a higher power in alpha and beta frequencies. By contrast, neither dichotomous classification of the presence and absence of mTBI history nor blast exposures showed a relationship with EEG power variables. Conclusion: Long-term alterations in resting EEG spectra measures of brain function do not appear to reflect any lasting effect of a history of mTBI or blast exposures. However, power in higher frequencies reflects both injury characteristics and subjective and objective cognitive difficulties, while power in lower frequencies is related to cognitive functions and psychological distress associated with poor long-term outcomes after mTBI. [ABSTRACT FROM AUTHOR]

Transcranial magnetic stimulation (TMS) is a non-invasive treatment protocol for treating several psychiatric conditions, including depression, migraine, smoking cessation, and obsessive-compulsive disorder. Past research suggests that TMS treatment outcomes vary based on neuroanatomy, functional connectivity, and tractography-based structural connectivity. In a previous study, 26 mild to moderate traumatic brain injury (mTBI) patients underwent repetitive transcranial magnetic stimulation (rTMS) and showed improvements in depression, post-concussive symptoms, and sleep dysfunction. The present study was a secondary analysis of that data. Anatomically accurate head models were derived from magnetic resonance imaging (MRI), and finite element analysis simulations were performed to mimic empirical data collection. This allowed for examination of the roles that age, brain scalp distance (BSD), gray matter volume (GMV), site-specific electrical field strength (EFS), and depolarized gray matter volume (DGMV) had on resting motor threshold (RMT) at the precentral gyrus (PreCG). We also investigated how EFS simulated at the dorsolateral prefrontal cortex (DLPFC) and RMT influenced rTMS treatment outcomes. Linear regression showed BSD was associated with EFS, RMT, and DGMV supporting efforts to derive accurate parameters from MRI-based modeling. Furthermore, linear mixed effects modeling showed RMT was associated with EFS and DGMV at the PreCG when age and individual neuroanatomy was accounted for suggesting MRI based anatomy and simulated EFS potentially determine TMS dosage. We did not observe any significant relationship between any of the measures from this study on empirically collected rTMS outcomes in mTBI suggesting further investigations into the mechanisms behind these outcomes are needed. [ABSTRACT FROM AUTHOR]

Spectral information from resting state EEG is altered in acute mild traumatic brain injury (mTBI) and in disorders of consciousness, but there is disagreement about whether mTBI can elicit long term changes in the spectral profile. Even when identified, any long-term changes attributed to TBI can be confounded by psychiatric comorbidities such as PTSD, particularly for combat-related mTBI where postdeployment distress is commonplace. To address this question, we measured spectral power during the resting state in a large sample of service members and Veterans varying in mTBI history and active PTSD diagnosis but matched for having had combat blast exposure. We found that PTSD was associated with decreases in low frequency power, especially in the right temporoparietal region, while conversely, blast-related mTBI was associated with increases in low frequency power, especially in prefrontal and right temporal areas. Results support the idea that long-term neurophysiological effects of mTBI share some features with states of reduced arousal and cognitive dysfunction, suggesting a role for EEG in tracking the trajectory of recovery and persisting vulnerabilities to injury. Additionally, results suggest that EEG power reflects distinct pathophysiologies for current PTSD and chronic mTBI. [ABSTRACT FROM AUTHOR]

In military populations, traumatic brain injury (TBI) also holds potential to increase impulsivity and impair mood regulation due to blast injury effects on ventral frontal cortex – to put military personnel at risk for suicide or substance abuse. We assessed a linkage between depression and impaired behavioral inhibition in 117 blast-exposed service members (SM) and veterans with post-concussion syndrome (PCS), where PCS was defined using a Rivermead Postconcussive Symptom Questionnaire (RPQ) modified to clarify whether each symptom worsened compared to pre-blast. Center for Epidemiological Studies-Depression Scale (CES-D) scores, PTSD Checklist 5 (PCL-5) scores, and RPQ raw subscale scores correlated positively with commission and perseverative errors on the continuous performance test II (CPT-II). In contrast, the number of RPQ symptoms ostensibly worsened post-blast did not correlate with impulsive errors on the CPT-II. These data replicate earlier findings that link increased affective symptomatology to impaired behavior inhibition in military TBI populations, but where additional effects on impulsivity from the blast itself remain equivocal. [ABSTRACT FROM AUTHOR]