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Objective/background Mild traumatic brain injuries (mTBI) are frequently associated with long-term, self-reported sleep disruption. Objective corroboration of these self-reports is sparse and limited by small sample sizes. The purpose of this study was to report on actigraphically-measured sleep outcomes in individuals with and without a history of recent mTBI in two U.S. cities (Boston, MA and Tucson, AZ). Patients/methods Fifty-eight individuals with a recent (within 18 months) mTBI and 35 individuals with no prior mTBI history were recruited for one of four studies across two sites. Participants completed a minimum of one week of actigraphy. Additionally, mTBI participants self-reported daytime sleepiness, sleep disruption, and functional sleep-related outcomes. Results In Boston, mTBI participants obtained less average sleep with shorter sleep onset latencies (SOL) than healthy individuals. In Tucson, mTBI participants had greater SOL and less night-to-night SOL variability compared to healthy individuals. Across mTBI participants, SOL was shorter and night-to-night SOL variability was greater in Boston than Tucson. Sleep efficiency (SE) variability was greater in Tucson than Boston across both groups. Only SOL variability was significantly associated with daytime sleepiness (r = 0.274) in the mTBI group after controlling for location. Conclusion Sleep quality, SOL and SE variability, are likely affected by mTBIs. Between-group differences in each site existed but went in opposite directions. These findings suggest the possibility of multiple, rather than a singular, profiles of sleep disruption following mTBI. Precision medicine models are warranted to determine whether multiple sleep disruption profiles do indeed exist following mTBI and the predisposing conditions that contribute to an individual's experience of sleep disruption.

Blue wavelength light has been used successfully as a treatment method for certain mood disorders, but, the underlying mechanisms behind the mood enhancing effects of light remain poorly understood. We investigated the effects of a single dose of 30 min of blue wavelength light (n = 17) vs. amber wavelength light (n = 12) exposure in a sample of healthy adults on subsequent resting-state functional and directed connectivity, and associations with changes in state affect. Individuals who received blue vs. amber wavelength light showed greater positive connectivity between the right amygdala and a region within the left dorsolateral prefrontal cortex (DLPFC). In addition, using granger causality, the findings showed that individuals who received blue wavelength light displayed greater bidirectional information flow between these two regions relative to amber light. Furthermore, the strength of amygdala-DLPFC functional connectivity was associated with greater decreases in negative mood for the blue, but not the amber light condition. Blue light exposure may positively influence mood by modulating greater information flow between the amygdala and the DLPFC, which may result in greater engagement of cognitive control strategies that are needed to perceive and regulate arousal and mood.

Mild traumatic brain injury (mTBI) can alter the structure of the brain and result in a range of symptoms, including elevated aggression. Neurological damage associated with mTBI is traditionally viewed as transient, yet a growing number of studies suggest long-lasting psychological and neurological changes following mTBI. However, research examining the neural basis of emotion processing in the chronic stage of mTBI recovery remains sparse. In the current study, we utilized resting state functional MRI to explore the association between default mode network connectivity and aggression in 17 healthy controls and 17 adults at least 6 months post-mTBI. The association between within-network connectivity and aggression was examined using general linear models, controlling for the effects of depression. Increased connectivity between the right hippocampus and midcingulate cortex was associated with elevated aggression in adults with mTBI, but not in healthy controls. The results provide evidence for a link between intrinsic functional network disruptions and the manifestation of postconcussive symptoms within chronic stages of recovery following mTBI. These findings expand upon the current research, providing evidence for the use of resting state functional connectivity as a potential biomarker of postconcussive aggression in chronic mTBI.

Introduction Sleep disruptions, including the increase of daytime sleepiness, are reported in roughly 70% of all individuals who have suffered a mild traumatic brain injury (mTBI). Prior research using magnetic resonance imaging (MRI) has identified associations between functional brain changes and daytime sleepiness following mTBI. In the present study, we aimed to identify whether structural differences in cortical thickness are associated with increased daytime sleepiness in adults with mTBI. Methods A total of 58 adults between 18 and 45 years of age (M=23.58±5.31) participated in the study, including 19 healthy controls and 39 individuals with a documented mTBI. Individuals with mTBI were further divided based on time-since-injury into a sub-acute (n=22) or chronic (n=17) group. Daytime sleepiness was assessed using the Epworth Sleepiness Scale (ESS) and cortical thickness was measured using high-resolution T1-weighted structural MRI. Whole-brain vertex-wise estimations of cortical thickness were calculated using FreeSurfer (v.6.0) and entered into a GLM to identify between-group differences in cortical thickness and the association with ESS. Results Significant differences in cortical thickness were found between the two mTBI groups (cluster-forming threshold p Conclusion More daytime sleepiness was associated with reduced inferior parietal cortical thickness in those 2 to 12-weeks post-injury, an association not observed in those 6 to 12-months post-injury or healthy controls. The inferior parietal lobule is part of the frontoparietal attention network and has been associated with vulnerability to sleep loss. Our findings suggest structural damage to the attention network following mTBI may be one factor affecting daytime sleepiness in mTBI. These findings may reflect a potential biomarker of sleep disturbances in mTBI. Support USAMRMC grant (W81XWH-12–0386).

Introduction Long-term sleep disruption, fatigue, and depression are common after mild traumatic brain injuries (mTBIs). Efficacious treatments for these disturbances in the context of mTBIs are lacking. Morning blue light therapy (BLT) effectively treats sleep disruption and improves mood. This study evaluated the treatment effects of morning BLT on post-mTBI daytime sleepiness, depression, and post-concussion symptoms. Methods 62 individuals (Boston: n=31; age: 23.11±7.20y; 17 females; days post-injury: 236.00±121.40; Tucson: n=31; age: 26.35±8.08y; 20 females; days post-injury: 272.94±167.69) received either BLT (n=30) or placebo amber light therapy (ALT; n=32). All participants completed the Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), Beck Depression Inventory (BDI), and Rivermead Post-concussion Symptom Questionnaire (RPQ3 and RPQ13 subscales) pre- and post-treatment. Treatment consisted of direct exposure to either blue or amber light (30 minutes each morning), delivered via tabletop light-box, over six weeks. Baseline and post-treatment values were compared to a non-mTBI, non-treated control sample (Tucson: n=32, age: 23.94±5.41y; 19 females). Results Baseline scores were higher in both mTBI light groups (BLT, ALT, respectively) than controls for the ESS (Cohen’s d=0.83, 0.83), PSQI (d=1.45, 1.71), BDI (d=1.46, 1.62), RPQ3 (d=1.72, 1.62) and RPQ13 (d=1.86, d=1.76). BLT resulted in lower within-group ESS (d=-0.58), BDI (d=-0.50), PSQI (d=-0.57), and RPQ13 (d=-0.45, p=0.005) scores. No improvements were seen following ALT. Minimal ESS score differences between the BLT and controls were observed after treatment (d=0.25). Conclusion Daily morning BLT resulted in moderate improvements in post-mTBI daytime sleepiness, sleep quality, depression, and post-concussion symptoms. These improvements may contribute to enhanced academic and job performance, post-mTBI quality of life, and general recovery. Future work is needed to clarify optimal dosage and precision medicine factors indentifying those most likely to benefit from morning BLT. Support This research was supported by multiple grants from the US Army Medical Research and Materiel Command (USAMRMC) to Dr. William D. S. Killgore, including W81XWH-11-1-0056 and W81XWH-14-1-0571.

Objective/Background Poor quality and inadequate sleep are associated with impaired cognitive, motor, and behavioral components of sport performance and increased injury risk. While prior work identifies sports-related concussions as predisposing factors for poor sleep, the role of sleep as a sports-related concussion risk factor is unknown. The purpose of this study was to quantify the effect of poor sleep quality and insomnia symptoms on future sports-related concussion risk. Patients/Methods In this study, 190 NCAA Division-1 athletes completed a survey battery, including the Insomnia Severity Index (ISI) and National Health and Nutrition Examination Survey (NHANES) Sleep module. Univariate risk ratios for future sports-related concussions were computed with ISI and NHANES sleepiness scores as independent predictors. An additional multiple logistic regression model including sport, sports-related concussion history, and significant univariate predictors jointly assessed the odds of sustaining a concussion. Results Clinically moderate-to-severe insomnia severity (RR = 3.13, 95% CI: 1.320–7.424, p = 0.015) and excessive daytime sleepiness two or more times per month (RR = 2.856, 95% CI: 0.681–11.977, p = 0.037) increased concussion risk. These variables remained significant and comparable in magnitude in a multivariate model adjusted for sport participation. Conclusion Insomnia and daytime sleepiness are independently associated with increased sports-related concussion risk. More completely identifying bidirectional relationships between concussions and sleep requires further research. Clinicians and athletes should be cognizant of this relationship and take proactive measures – including assessing and treating sleep-disordered breathing, limiting insomnia risk factors, improving sleep hygiene, and developing daytime sleepiness management strategies – to reduce sports-related concussion risk and support overall athletic performance.

Background: Sleep loss contributes to obesity through a variety of mechanisms, including neuroendocrine functioning, increased hunger, and increased food intake. Additionally, sleep loss alters functional activation within brain regions associated with reward and behavioral control. However, it remains unknown whether individual differences in baseline neural functioning can predict eating behaviors during total sleep deprivation (TSD). We used functional magnetic resonance imaging (fMRI) to test the hypothesis that individuals with increased baseline responsiveness within reward regions are more vulnerable to TSD-induced overeating. Methods: N=45 subjects completed several fMRI scans during a single pre-TSD session that included performance on the Multi-Source Interference Task (MSIT) and the n-back task. Subjects returned to the laboratory for an overnight TSD session, during which they were given ad libitum access to 10,900 kcal of food. Leftover food and packaging were collected every 6 hours (00:00, 06:00, 12:00) to measure total food consumption. Subjects reported sleepiness every hour and performed a food rating task every 3 hours. Results: Functional activation within the ventral striatum during the MSIT and n-back was positively correlated with total caloric and carbohydrate intake during the final 6 hours (06:00–12:00) of TSD. Activation within the middle and superior temporal gyri during the MSIT also correlated with total carbohydrates consumed. Food consumption was not correlated with subjective sleepiness, hunger, or food desire. Conclusions: Individual differences in neural activity of reward processing areas (i.e., nucleus accumbens) prior to sleep deprivation is associated with an individual’s propensity to overeat during subsequent sleep deprivation. This suggests that individual differences within reward processing pathways are potential key factors in sleep loss related overeating. Sleep loss and obesity are tightly linked. Both phenomena have been associated with increased neural activation in regions associated with reward, inhibitory control, and disrupted dopamine signaling. Elevated baseline reward sensitivity in the ventral striatum appears to be further compounded by sleep deprivation induced dysfunction in the reward neurocircuitry, increasing the likelihood of overeating. Our findings suggest that large individual differences in baseline responsiveness of hedonic reward pathways may modulate the association between sleep loss and obesity.

Context: The long-term effects of concussion on brain function during cognitive tasks are not fully understood and neuroimaging findings are equivocal. Some images show hyperactivation of prefrontal brain regions in previously concussed individuals relative to controls, suggesting increased cognitive resource allocation. Others show prefrontal hypoactivation and hyperactivation in other regions as a presumed compensatory mechanism. Given the relationship between sympathetic arousal and neural activation, physiologic measures of arousal, such as electrodermal activity, may provide additional insight into the brain's functional changes in those with a history of concussion. Objective: To quantify differences in electrodermal activity during a commonly used standardized neurocognitive assessment between individuals with or without a history of concussion. Design: Descriptive laboratory study. Setting: Research laboratory. Patients or Other Participants: Seven asymptomatic individuals with a self-reported history of physician-diagnosed, sport-related concussion (number of previous concussions = 1.43 ± 0.53; time since most recent concussion = 0.75 to 6 years, median = 3 years) and 10 individuals without a history of concussion participated in this study. Main Outcome Measure(s): All participants wore bilateral wrist electrodermal activity sensors during the Standardized Assessment of Concussion. We measured normalized phasic (reactive) electrodermal activity during each test element (orientation, immediate recall, concentration, delayed recall). Results: A significant group-by-test element interaction was present (P = .003). Individuals with a history of concussion had greater phasic activity during delayed recall (P < .001). Delayed-recall phasic activity was greater in both groups relative to the other elements. Conclusions: Delayed recall resulted in greater physiologic arousal in previously concussed individuals relative to healthy control participants, supporting previous neuroimaging findings of increased prefrontal cortex activity during memory tasks after concussion. Given similar task performance and arousal patterns across the test, our results suggest that previously concussed individuals incur additional cognitive demands in a short-delay recall task.

Light affects almost all aspects of human physiological functioning, including circadian rhythms, sleep–wake regulation, alertness, cognition and mood. We review the existing relevant literature on the effects of various wavelengths of light on these major domains, particularly as they pertain to recovery from mild traumatic brain injuries. Evidence suggests that light, particularly in the blue wavelengths, has powerful alerting, cognitive and circadian phase shifting properties that could be useful for treatment. Other wavelengths, such as red and green may also have important effects that, if targeted appropriately, might also be useful for facilitating recovery. Despite the known effects of light, more research is needed. We recommend a personalized medicine approach to the use of light therapy as an adjunctive treatment for patients recovering from mild traumatic brain injury.

Mild traumatic brain injury (mTBI) remains the most commonly reported head injury in the United States, and is associated with a wide range of post-concussive symptoms including physical, cognitive and affective impairments. Elevated aggression has been documented in mTBI; however, the neural mechanisms associated with aggression at the chronic stage of recovery remain poorly understood. In the present study, we investigated the association between white matter integrity and aggression in mTBI using diffusion tensor imaging (DTI). Twenty-six age-matched adults participated in the study, including 16 healthy controls (HCs) and 10 individuals in the chronic stage of recovery (either 6-months or 12 months post-mTBI). Psychological measures of aggression included the Buss-Perry Aggression Questionnaire and the Personality Assessment Inventory (PAI). Axonal pathways implicated in affective processing were studied, including the corpus callosum, anterior thalamic radiation, cingulum and uncinate fasciculus, and measures of white matter integrity included fractional anisotropy (FA), mean diffusivity (MD), radial diffusivity (RD) and axial diffusivity (AD). We found that adults with mTBI in the chronic stage of recovery had higher levels aggression. Individuals with mTBI also had greater RD in the corpus callosum compared to HCs, indicating reduced fiber integrity. Furthermore, we observed a significant association between reduced white matter integrity in the corpus callosum and greater aggression. Our findings provide additional evidence for underlying neuroanatomical mechanisms of aggression, although future research will be necessary to characterize the specific relationship between aggression and the white matter pathways we identified.

Background: Mild traumatic brain injuries (mTBIs) are a significant social, sport, and military health issue. In spite of advances in the clinical management of these injuries, the underlying pathophysiology is not well-understood. There is a critical need to advance objective biomarkers, allowing the identification and tracking of the long-term evolution of changes resulting from mTBI. Diffusion-weighted imaging (DWI) allows for the assessment of white-matter properties in the brain and shows promise as a suitable biomarker of mTBI pathophysiology. Methods: 34 individuals within a year of an mTBI (age: 24.4 ± 7.4) and 18 individuals with no history of mTBI (age: 23.2 ± 3.4) participated in this study. Participants completed self-report measures related to functional outcomes, psychological health, post-injury symptoms, and sleep, and underwent a neuroimaging session that included DWI. Whole-brain white matter was skeletonized using tract-based spatial statistics (TBSS) and compared between groups as well as correlated within-group with the self-report measures. Results: There were no statistically significant anatomical differences between the two groups. After controlling for time since injury, fractional anisotropy (FA) demonstrated a negative correlation with sleep quality scores (higher FA was associated with better sleep quality) and increasing depressive symptoms in the mTBI participants. Conversely, mean (MD) and radial diffusivity (RD) demonstrated positive correlations with sleep quality scores (higher RD was associated with worse sleep quality) and increasing depressive symptoms. These correlations were observed bilaterally in the internal capsule (anterior and posterior limbs), corona radiata (anterior and superior), fornix, and superior fronto-occipital fasciculi. Conclusion: The results of this study indicate that the clinical presentation of mTBI, particularly with respect to depression and sleep, is associated with reduced white-matter integrity in multiple areas of the brain, even after controlling for time since injury. These areas are generally associated not only with sleep and emotion regulation but also cognition. Consequently, the onset of depression and sleep dysfunction as well as cognitive impairments following mTBI may be closely related to each other and to white-matter integrity throughout the brain.

Purpose: To quantify differences in nonlinear aspects of performance on a seated visual-motor tracking task between clinically asymptomatic males and females with and without a self-reported mild traumatic brain injury history. Methods: Seventy-three individuals with a self-reported concussion history (age: 21.40 ± 2.25 years, mean ± SD) and 75 without completed the visual-motor tracking task (age: 21.50 ± 2.00 years). Participants pressed an index finger against a force sensor, tracing a line across a computer screen (visual-motor tracking). The produced signal's root-mean-square error (RMSE), sample entropy (SampEn, a measure of regularity), and average power (AvP) between 0 and 12 Hz were calculated. Results: Males with a history of 0 or 1 concussion had greater RMSE (worse performance) than females with 0 (p

STUDY OBJECTIVES: A number of subjective and objective studies provide compelling evidence of chronic postconcussion changes in sleep, yet very little is known about the acute effects of concussion on sleep quality and quantity. Therefore, the purpose of this prospective pilot study was to use actigraphy to examine the changes in sleep quality and quantity acutely following concussion at home rather than in a hospital or sleep laboratory. METHODS: Seventeen young adults (7 with acute concussion, 10 controls) were recruited for this study. All participants completed two 5-day testing sessions separated by 30 days from intake (controls) or day of injury (concussion). Participants wore actigraphs and kept a sleep journal. Sleep parameter outcomes included nighttime total sleep time (nTST), 24-h total sleep time (TST), wake after sleep onset (WASO), and sleep efficiency (SE). The coefficient of variation (CV) for each sleep parameter was computed for each session. RESULTS: nTST and TST CV was significantly greater in the concussion group. There is the additional indication that individuals with a concussion may require and obtain more sleep shortly after injury and subsequently have a shorter duration of sleep at 1 mo postinjury. This pattern was not seen in the measures of sleep quality (WASO, SE). CONCLUSION: Individuals with a concussion demonstrated increased nighttime sleep duration variability. This increase persisted at 1 mo postinjury and may be associated with previously documented self-reports of poor sleep quality lasting months and years after a concussion. Additionally, this increase may predispose individuals to numerous negative health outcomes if left untreated. Language: en