Stress is well known to increase the severity of somatization and insomnia. A recent major stressor that could have influenced the severity of these presentations was world-wide COVID-19 Pandemic. Somatization is the physical expression of stress and emotional distress that can manifest itself throughout various corporal domains and can be a comorbidity to insomnia. Headaches represent some of the most common complaints associated with brain injuries and neurological disorders but are common in somaticized disorders as well. In large survey study we examined whether exercise was associated with severity of somatization and headaches. We hypothesized that both healthy individuals and those with insomnia who exercised during the pandemic would report less severe somatic symptoms and headaches than those who did not.

A large survey was sent out to 4,073 individuals to measure their experience in numerous domains during the COVID-19 pandemic. This survey included a short symptom questionnaire used to measure somatization and the Insomnia Scale Index to measure insomnia. These questionnaires were administered along with a “yes or no” question on whether the participants exercised regularly in that period. A univariate ANOVA was performed to analyze the data to determine if exercise during the pandemic was beneficial in the reduction of somatic symptoms and headache severity. Furthermore, these tests were run to determine if the effect was greater on those with insomnia.

The effect of insomnia and exercise on total somatic symptoms were significant at F(1, 3445)=650.5, p<0.001 and F(1, 3445)=26.1, p<0.001, respectively. For reported headache severity, there was a significant effect of exercise F(1, 4073)=14.5, p<0.001 and insomnia F(1, 4073)=160.5, p<0.001; therefore, those who exercised reported less severe headaches and those who suffered from insomnia reported more severe somatic symptoms. This meant that those who exercised reported less severe somatization and headaches than those who didn’t and those with insomnia reported more severe somatization and headaches than healthy individuals. However, the interaction between exercise and insomnia on overall somatization severity was not significant at F(1, 3445)=3.4, p=0.066 nor for reported headache severity F(1, 4073)=0.81, p=0.370. Despite there not being a significant interaction, the benefit of exercise was slightly greater on healthy individuals than those with insomnia.

Those with insomnia reported more severe headaches and overall somatic symptoms than non-insomniacs regardless of whether they exercised or not. Exercise did make a difference on the reported severity of headaches and somatization in both groups; however, the benefit of exercise on headaches and somatization was greater in individuals who do not suffer from insomnia. Thus, exercise was noted to be beneficial to those in the general population and those suffering from insomnia as it can potentially reduce the severity of somatization and headaches. Of course, this research was cross sectional and correlational, so the directionality of the effects cannot be inferred. For future research, it would be instrumental to use experimental methods to help determine the duration and type of exercise that may optimize its potential benefits on headaches and somatic symptoms.

mTBI is trauma to the brain due to a blow or other mechanical force affecting the head. Prior research has established that common symptoms of mTBI include decreased sleep quality and onset/worsening of emotional dysregulation. However, there is little published research investigating how sleep disruption and depressive symptoms are experienced at varying stages of mTBI. We hypothesized that sleep disruption would change with differing time since injury, and that depressive symptoms should accordingly. Additionally, since females tend to have higher rates of depression, we predicted that there would be a significant difference between the sexes at different stages post-mTBI.

This study included 145 healthy adults, split into six groups, comparing healthy controls consisting of 15 males (Mage=23.67, SD=5.066) and 17 females (Mage=25.35, SD=7.035) to individuals who had mTBI, 41 males (Mage=26.88, SD=8.509) and 72 females (Mage=23.79, SD=6.898) at five points post-mTBI: 2 weeks and 1, 3, 6, and 12 months. The Pittsburgh Sleep Quality Index (PSQI) global score was used to assess individual sleep quality and disturbances; higher scores indicated poorer sleep quality. The Beck Depression Index (BDI-II) was used to assess characteristics and symptoms of depression. We adjusted the score to exclude item 16, which measures changes in sleep. Higher scores indicate more severe depressive symptoms. We conducted a multivariate analysis of variance and Pearson correlation to examine whether there were significant differences in sleep and depression at different stages of mTBI for each sex.

We discovered that sleep quality was worse at chronic stages of mTBI (i.e, 12M, p=<.001), than at acute stages (2W, p=.049), and compared to healthy controls. There were also significant differences in depression scores compared to healthy controls at 2W, p=.008, 3M, p=<.001, and 6M, p=.012, but not 12M, p=.313, suggesting that depressive symptoms resolved by 12M in those with mTBI. To explain this, we investigated sex differences, as males tend to experience fewer depressive disorders than females. However, females reported fewer depressive symptoms than males at chronic stages of mTBI. This finding was not statistically significant as females had a Mbdi_total=6.84, SD=7.98 and males had a Mbdi_total=5.38, SD=6.078; still, this could be due to the low statistical power of the study, and with a larger sample size, could produce statistically significant differences between the sexes. Despite this, there is a statistically significant difference in the depression score for females between 2W and 12M post-mTBI (p=.046; effect size of d=.99). Comparatively, males showed no significant divergence between depression and sleep scores.

Sleep disruption and depressive symptoms were correlated in individuals with mTBI in both acute and chronic stages; however, at 12M, there was a decrease in this correlation due to females exhibiting fewer depressive symptoms in combination with greater sleep disruption in the chronic phase of mTBI. Further research investigating the relationship between depression and sleep quality by looking at females with a much larger sample size would be helpful in clarifying these associations.

Resiliency has been shown to attenuate and even protect against cognitive impairment from mental and physical stressors. Recently, it has been demonstrated that individuals who score high in psychological resilience tend to have less impairment following a mTBI.The COVID-19 pandemic proved to be an uncertain time for many. Periods of isolation, unemployment, and of course, sickness, meant more time at home. The partial or complete breakdown of an individual’s day-to-day routine paired with the stress of the pandemic has reinforced the need for psychological resilience. This analysis investigates the relationship between self-reported routine adherence and an individual’s corresponding psychological resilience. We hypothesize that individuals who maintained a structured daily routine during the pandemic will have higher levels of psychological resilience, enabling them to better handle periods of extreme stress.

8963 English-speaking adults (18-92 years old; 59.5% female) from across the U.S. completed an online, monthly cross-sectional (∼1000 participants per month), battery of questions that included the Connor-Davidson Resilience Scale (CD-RISC), and a self-reported sleep and routine rating(s) between June 2020 and April 2021. We measured the level of an individual’s routine by adding the self-reported survey scores of waking at the same time and maintaining a routine throughout the day. Both questions were scored 0-4 (Likert-style) for a score range of 0 to 8; higher scores indicated a higher adherence to a daily structure. Weeknight sleep (Sun-Thurs) was a self-reported average of the hours of sleep obtained over the past 4 weeks. A two-way ANCOVA was used to analyze the effects that routine had on subsequent psychological resilience scores while controlling for average sleep duration.

A significant main effect routine on psychological resilience was found F(8,8953) =227, p=<.00001 after controlling for average reported weeknight sleep. An independent t-test was performed to determine the differences between those who fall above and below the average score (M= 5.1) for routine adherence. Individuals who were above average in adherence (M=71.1, SD=15.5) had significantly higher CD-RISC scores than individuals who did not (M=59.2, SD=16.7); t(9166)=35.1, p <0.001.

Individuals who maintained a more structured day throughout the pandemic were more likely to score higher on psychological resilience assessments than those who did not. Chronic stress is known to contribute to the development and exacerbation of many common psychiatric conditions like anxiety and depression. These results suggest that having a regular routine may have positive effects on an individual’s ability to bounce back from stressful cognitive and psychological events. This relationship should be further investigated in clinical populations as a potential intervention or adjunctive treatment for common neuropsychiatric conditions.

It is well known that there are differences between men and women in anxiety and aggression. Moreover, prior research has shown an association between anxiety and aggression but the strength of these associations in males and females has not been well characterized, and it remains unclear whether such associations are driven by comorbid disorders such as posttraumatic stress disorder (PTSD) or substance abuse. Therefore, we examined these associations in a large sample of males and females, and statistically controlled for the aforementioned potential confounding variables.

A total of 13,313 adults completed the survey on Amazon Mechanical Turk between April 2020 and April 2021, including 5,598 females (Mage=36.4, SD=11.9) and 7,654 males (Mage=37.81, SD=12.7). Aggression was measured using the Buss Perry Aggression Questionnaire (BPAQ), while the Generalized Anxiety Disorders (GAD-7) scale was used to gauge anxiety levels. PTSD was assessed with the PC-PTSD scale, and alcohol misuse was assessed with the Alcohol Use Disorders Inventory (AUDIT). Data were analyzed with zero-order correlations and linear regression to control for the effects of PTSD and alcohol misuse. Lastly, we used a Fisher r-to-z transformation to compare the correlations between males and females for both physical and verbal aggression with anxiety.

Higher aggression (i.e., BPAQ) was correlated with greater anxiety (i.e., GAD; r(13213)=0.482, p<0.0001)). This association between anxiety and aggression held even when other potential confounders were controlled, such as PTSD (p<0.0001), and alcohol misuse, p<0.0001. Additionally, the correlation between anxiety and physical aggression was significantly stronger in males than females (z=5.02, p<0.0001), a pattern that was also true for the association between anxiety and verbal aggression (z=4.13, p<0.0001).

Our findings suggest that there is a linear relationship between the severity of anxiety and the severity of both verbal and physical aggression, that these associations tend to be stronger among males, and are not accounted for by associated conditions such as PTSD or alcohol misuse. This data augments existing research on the factors that contribute to aggression and further suggest that anxious feelings are more directly associated with aggression in males. These findings raise the possibility that interventions that target anxiety may prove helpful in reducing aggressive behavior among males. It may be fruitful for future work to identify neural systems that are associated with both anxiety and aggression and which are also modulated by sex. While measures of neurochemistry were not collected here, prior research has suggested that there are sex differences in brain systems that rely on serotonergic neurotransmission and arginine vasopressin, which could provide a target for future work.

Previous research indicates that women tend to struggle with insomnia at higher rates both prior to and during the global COVID-19 pandemic; however, not much research has investigated the extent to which insomnia correlates with comorbid problems, including aggression, depression, anxiety, PTSD severity, and alcohol use between the sexes. On a neurobiological level, insomnia could be associated with those mood disorders due to the effects of sleep disturbance on serotonergic and GABA neurotransmission, and males might experience such associations at a lower frequency due to their increased rates of serotonin synthesis. Consequently, we hypothesized that women would demonstrate higher prevalence of the aforementioned comorbidities during COVID than males due to higher rates of insomnia reported in women during COVID.

We surveyed a total of 13,313 adults, with 5,598 females (Mage=36.4, SD=11.9) and 7,654 males (Mage=37.81, SD=12.7) using Amazon Mechanical Turk between April 2020 and April 2021. Insomnia was measured using the Insomnia Severity Index (ISI), while levels of depression, anxiety, PTSD severity, and alcohol use, and aggression were assessed through Patient Stress Questionnaires (PSQs) and the Buss Perry Aggression Questionnaire (BPAQ).

As expected, there were significant positive correlations between ISI and BPAQ (r(13306)=0.364, p<0.0001), PSQ Depression (r(13300)=0.694, p<0.0001), PSQ Anxiety (r(13211)=0.627, p<0.0001), PSQ PTSD (r(13305)=0.444, p<0.0001), and PSQ Alcohol (r(12915)=0.218, p<0.001). The strength of these associations was significantly higher in males than females in almost all categories: aggression (z=4.27, p<0.0001), depression (z=2.41, p=0.016), anxiety (z=3.16, p=0.0016), and alcohol use (z=5.89, p<0.0001) - not significant for PTSD severity (z=1.48, p=0.14).

We found that insomnia was more strongly correlated with comorbid emotional and behavioral problems among males than females. This stands in contrast to our initial hypothesis, as the findings suggest that men who suffer from greater insomnia are more likely to experience those four comorbidities than females. This suggests that sex may play a role in the association between sleep disturbances and other clinical presentations relevant to neuropsychology. Further work will be necessary to identify the neurobiological mechanisms that drive the sex differences in these associations. While the present findings cannot determine the causal direction of the association, it will be crucial to determine the directionality of these associations and the mechanisms that lead to differences in expression between the sexes.

Mild traumatic brain injury (mTBI) remains one of the most silent recurrent head injuries reported in the United States. mTBI accounts for nearly 75 percent of all traumatic brain injuries in the American population. Brain injury is often associated with impulsivity, but the association between resting state functional connectivity (rsFC) and impulsivity at multiple stages since time-since-injury (TSI) is unclear. We hypothesized that rsFC within the default mode network (DMN) would predict impulsivity across multiples stages of recovery in mild TBI.

Participants healthy controls (HC: n=35 total [15 male, 20 female], age M=24.40, SD=5.95; mTBI: n=121 total [43 male; 78 female], age M=24.76, SD=7.48). Participants completed a cross-sectional study design at various post-injury time points ranging from (2W, 1M,3M,6M,12M). Participants a neuroimaging session and behavioral tasks including a psychomotor vigilance task. Impulsivity was assessed as a combination of false starts and impulsive responses on behavioral tasks. The neuroimaging session included a rsFC scan. To predict impulsivity from brain connectivity, we conducted a series of stepwise linear regression analyses with the 11 functional brain connections (extracted as Fisher’s z-transformed correlations between regions) as predictors and each of the 13 neurocognitive factor scores separately. We focus here on the outcomes for the impulsivity factor.

Results showed greater positive connectivity between the and Right Frontal Pole and the anterior cingulate cortex (ACC; seed) (ß = .158, t = 1.98, p = .049) which was associated with greater impulsivity. Individuals in the 2W group demonstrated one significant predictor (R = .632, R2 = .399, F = 5.32, p = .050). Largely, there was greater positive connectivity between the Right Frontal Pole and the ACC (seed) and (ß = .632, t = 2.31, p = .050) which was associated with higher impulsivity at the 2W time-since-injury. No predictors emerged for the 1M, 3M, or 6M conditions. However, individuals in the 12M group demonstrated two significant predictor connections (R = .497, R2 = .247, F = 5.73, p = .007). Overall, a linear combination of greater negative (anticorrelated) connectivity between the Right Frontal Pole and the mPFC (seed) (/? = -.576, t = -3.53, p = .002) and greater positive connectivity between the Paracingulate Cortex (seed) and the Left Lateral Prefrontal Cortex (ß = .368, t = 2.14, p = .039) was also associated with greater impulsivity in individuals with mTBI at 12M.

These findings suggest functional connectivity between the anterior node of the DMN and prefrontal cortex regions involved in behavioral control was predictive of higher impulsivity in individuals with mTBI at 2W and 12M post injury, but not at other time frames. Interestingly, these connections differed at the two time points. Acutely, greater impulsivity was associated with greater connectivity among regions involved in error detection, exploration, and emotion. At one year, the connections involve regions associated with error monitoring and inhibitory processes. This may reflect compensatory strategy development during recovery.

Mild traumatic brain injury (mTBI) remains one of the most prevalent brain injuries, affecting approximately one-in-sixty Americans. Previous studies have shown an association between white matter integrity and aggression at chronic stages (either 6-months or 12 months post-mTBI) however, the association between white matter axonal damage, neuropsychological outcomes, and elevated aggression in multiple stages since time-since-injury (TSI) is unclear. We hypothesized that functional connectivity between the default mode network (DMN), a key brain network involved in cognitive, self-reflective, and emotional processes, and other cortical regions would predict elevated aggression and emotional disturbances across multiples stages of recovery in mild TBI.

Participants healthy controls (HC: n=35 total [15 male, 20 female], age M=24.40, SD=5.95; mTBI: n=121 total [43 male; 78 female], age M = 24.76, SD=7.48). Participants completed a cross-sectional study design at specific post-injury time points ranging from (2W, 1M,3M,6M,12M). Participants completed a comprehensive neuropsychological battery and a neuroimaging session, including resting state functional connectivity (FC). Here, we focus on the FC outcomes for the DMN. During the neuropsychological assessment, participants completed tests that measured learning and memory, speed of information processing, executive function, and attention. To predict neuropsychological performance from brain connectivity, we conducted a series of stepwise linear regression analyses with the 11 functional brain connections (extracted as Fisher’s z-transformed correlations between regions) as predictors and each of the 13 neurocognitive factor scores separately.

Consistent with our hypothesis, one predictor materialized as significant (R = .187, R2 = .035, F = 5.55, p = .020) for the Total Sample. Largely, positive connectivity between Right Inferior Frontal Gyrus and the PCC (seed) was associated with increased aggression in the Total Sample of all participants (ß = .187, t = 2.36, p = .020). One predictor materialized as significant in Individuals the 2W group, (R = .719, R2 = .518, F = 8.58, p = .019). In general, greater negative (anticorrelated) connectivity between the Left Lateral Occipital Cortex (ß = -.719, t = -2.93, p = .019) and the PCC (seed) and was associated with greater aggression at 2W, but no predictors emerged at 1M or 3M. Individuals in the 6M group showed one significant predictor (R = .675, R2 = .455, F = 16.71, p = .001). Specifically, greater positive connectivity between the Right Lateral Occipital Cortex (/? = .675, t = 4.09, p = .001) and PCC (seed) was associated with greater aggression at 6M. No associations were evident at 12M.

Overall, these findings suggest functional connectivity between the posterior hub of the DMN and cortical regions within the occipital cortex was predictive of higher aggression in individuals with mTBI. However, the direction of this connectivity differed at 2W versus 6M, suggesting a complex process of recovery that may contribute differentially to aggression in patients with mTBI. As these regions are involved in self-consciousness and visual perception, this may point toward future avenues for aiding in functional recovery of emotional dysregulation in patients with persistent post-concussion syndrome.