We examined the course of PTSD symptoms in a cohort of U.S. Marines (N = 867) recruited for the Marine Resiliency Study (MRS) from a single infantry battalion that deployed as a unit for 7 months to Afghanistan during the peak of conflict there. Data were collected via structured interviews and self-report questionnaires 1 month prior to deployment and again at 1, 5, and 8 months postdeployment. Second-order growth mixture modeling was used to disaggregate symptom trajectories; multinomial logistic regression and relative weights analysis were used to assess the role of combat exposure, prior life span trauma, social support, peritraumatic dissociation, and avoidant coping as predictors of trajectory membership. Three trajectories best fit the data: a low-stable symptom course (79%), a new-onset PTSD symptoms course (13%), and a preexisting PTSD symptoms course (8%). Comparison in a separate MRS cohort with lower levels of combat exposure yielded similar results, except for the absence of a new-onset trajectory. In the main cohort, the modal trajectory was a low-stable symptoms course that included a small but clinically meaningful increase in symptoms from predeployment to 1 month postdeployment. We found no trajectory of recovery from more severe symptoms in either cohort, suggesting that the relative change in symptoms from predeployment to 1 month postdeployment might provide the best indicator of first-year course. The best predictors of trajectory membership were peritraumatic dissociation and avoidant coping, suggesting that changes in cognition, perception, and behavior following trauma might be particularly useful indicators of first-year outcomes.

We engineered a transdermal neuromodulation approach that targets peripheral (cranial and spinal) nerves and utilizes their afferent pathways as signaling conduits to influence brain function. We investigated the effects of this transdermal electrical neurosignaling (TEN) method on sympathetic physiology under different experimental conditions. The TEN method involved delivering high-frequency pulsed electrical currents to ophthalmic and maxillary divisions of the right trigeminal nerve and cervical spinal nerve afferents. Under resting conditions, TEN significantly suppressed basal sympathetic tone compared to sham as indicated by functional infrared thermography of facial temperatures. In a different experiment, subjects treated with TEN reported significantly lower levels of tension and anxiety on the Profile of Mood States scale compared to sham. In a third experiment when subjects were experimentally stressed TEN produced a significant suppression of heart rate variability, galvanic skin conductance, and salivary α-amylase levels compared to sham. Collectively these observations demonstrate TEN can dampen basal sympathetic tone and attenuate sympathetic activity in response to acute stress induction. Our physiological and biochemical observations are consistent with the hypothesis that TEN modulates noradrenergic signaling to suppress sympathetic activity. We conclude that dampening sympathetic activity in such a manner represents a promising approach to managing daily stress.

The current study provides a comprehensive analysis and integration of the literature on the social network correlates of individual innovation. Reviewing the extant literature, we cluster existing network measures into five general properties—size, strength, brokerage, closure, and diversity. Using meta-analysis, we estimate the population effect sizes between these network properties and innovation. Results showed that brokerage had the strongest positive relation to innovation, followed by size, diversity, and strength. Closure, by contrast, had a weak, negative association with innovation. In addition, we offer a path-analytic integration of the literature proposing and testing the direct and indirect effects of the five properties on innovation. We suggest that network size and strength impact innovation through a web of relations with the more proximal features of brokerage, closure, and diversity. Our path-analytic integration considers the two dominant perspectives on the effects of social networks—brokerage versus closure—simultaneously allowing us to establish their relative efficacy in predicting innovation. In addition, our model highlights that network strength can have both negative and positive effects (via different direct and indirect pathways) and thus inherently involves a tradeoff. We discuss the implications of these results for future research and practice.

Large cohort studies suggest that most military personnel experience minimal posttraumatic stress disorder (PTSD) symptoms following warzone deployment, an outcome often labeled resilience. Very low symptom levels, however, may be a marker for low exposure, not resilience, which requires relatively high-magnitude or high-frequency stress exposure as a precondition. We used growth mixture modeling (GMM) to examine the longitudinal course of lifetime PTSD symptoms following combat exposure by disaggregating deployed U.S. Marines into upper, middle, and lower tertiles of combat exposure. All factor models fit the data well; Tucker-Lewis Index (TLI) and comparative fit index (CFI) values ranged from .91 to .97. Three distinct trajectories best explained the data within each tertile. The upper tertile comprised True Resilience (73.2%), New-Onset Symptoms (18.3%), and Pre-existing Symptoms (8.5%) trajectories. The middle tertile also comprised True Resilience (74.5%), New-Onset Symptoms (16.1%), and Pre-existing Symptoms (9.4%) trajectories. The lower tertile comprised Artifactual Resilience (86.3%), Pre-existing Symptoms (7.6%), and New-Onset Symptoms (6.1%) trajectories. True Resilience involved a clinically significant symptom increase followed by a return to baseline, whereas Artifactual Resilience involved consistently low symptoms. Conflating artifactual and true resilience may inaccurately create the expectation of persistently low symptoms regardless of warzone exposure.

Achieving optimal human performance that involves cognitive or physical work requires quality sleep and a positive mental attitude. The ascending reticular activating system (RAS) represents a powerful set of endogenous neuromodulatory circuits that gate and tune global brain responses to internal and external cues, thereby regulating consciousness, alertness, and attention. The activity of two major RAS nuclei, the locus coeruleus (LC) and pedunculopontine nucleus (PPN), can be altered by trigeminal nerve modulation. Monosynaptic afferent inputs from the sensory components of trigeminal nerve branches project to the trigeminal sensory nuclear complex (TSNC), which has direct and polysynaptic connections to the LC and PPN. We previously found high-frequency (7 -11 kHz) transdermal electrical neuromodulation (TEN) of the trigeminal nerve rapidly induces physiological relaxation, dampens sympathetic nervous system responses to acute stress, and suppresses levels of noradrenergic biomarkers. Given the established roles of LC and PPN neuronal activity in sleep regulation, psychophysiological arousal, and stress, we conducted three studies designed to test hypotheses that modulation of the TSNC can improve sleep quality and mood in healthy individuals (n = 99). Across a total of 1,386 days monitored, we observed TEN modulation of trigeminal and cervical nerves prior to sleep onset produced significant improvements in sleep quality and affective states, quantified using clinically validated surveys, overnight actigraph and heart rate recordings, and biochemical analyses compared to baseline or sham controls. Moreover, we observed some frequency dependence in that TEN delivered at lower frequencies (TENLF; 0.50 -0.75 kHz) was significantly more effective at improving sleep quality and reducing anxiety than higher frequency TEN waveforms. Collectively our results indicate that transdermal electrical neuromodulation of trigeminal and cervical nerve branches can influence TSNC activity in a manner that significantly improves sleep quality and significantly reduces stress. We conclude that biasing RAS network activity to optimize sleep efficiency and enhance mood by electrically modulating TSNC activity through its afferent inputs holds tremendous potential for optimizing mental health and human performance.