Traumatic brain injury (TBI) often results in traumatic axonal injury and white matter (WM) damage, particularly to the corpus callosum (CC). Damage to the CC can lead to impaired performance on neurocognitive tasks, but there is a high degree of heterogeneity in impairment following TBI. Here we examined the relation between CC microstructure and function in pediatric TBI. We used high angular resolution diffusion-weighted imaging (DWI) to evaluate the structural integrity of the CC in humans following brain injury in a sample of 32 children (23 males and 9 females) with moderate-to-severe TBI (msTBI) at 1–5 months postinjury, compared with well matched healthy control children. We assessed CC function through interhemispheric transfer time (IHTT) as measured using event-related potentials (ERPs), and related this to DWI measures of WM integrity. Finally, the relation between DWI and IHTT results was supported by additional results of neurocognitive performance assessed using a single composite performance scale. Half of the msTBI participants (16 participants) had significantly slower IHTTs than the control group. This slow IHTT group demonstrated lower CC integrity (lower fractional anisotropy and higher mean diffusivity) and poorer neurocognitive functioning than both the control group and the msTBI group with normal IHTTs. Lower fractional anisotropy—a common sign of impaired WM—and slower IHTTs also predicted poor neurocognitive function. This study reveals that there is a subset of pediatric msTBI patients during the post-acute phase of injury who have markedly impaired CC functioning and structural integrity that is associated with poor neurocognitive functioning. SIGNIFICANCE STATEMENT Traumatic brain injury (TBI) is the primary cause of death and disability in children and adolescents. There is considerable heterogeneity in postinjury outcome, which is only partially explained by injury severity. Imaging biomarkers may help explain some of this variance, as diffusion weighted imaging is sensitive to the white matter disruption that is common after injury. The corpus callosum (CC) is one of the most commonly reported areas of disruption. In this multimodal study, we discovered a divergence within our pediatric moderate-to-severe TBI sample 1–5 months postinjury. A subset of the TBI sample showed significant impairment in CC function, which is supported by additional results showing deficits in CC structural integrity. This subset also had poorer neurocognitive functioning. Our research sheds light on postinjury heterogeneity.

The effects of mild–moderate partial sleep deprivation on affective and cognitive functioning were evaluated in a naturalistic home environment, mimicking short sleep typically caused by demands from work or society. A total of 52 healthy individuals aged 18–35 was included in an 11-day study protocol. Participants slept at home, and sleep patterns were observed using actigraphs and sleep diaries. After maintaining habitual sleep for 7 days, the participants were asked to sleep 2 hours less than their average sleep duration for the last three nights of the study protocol. A not-X continuous performance test was administered at 9 am (± 90 minutes) on days 1, 4, 8 (habitual sleep), 9 and 11 (sleep deprivation). Performance-based measures included response accuracy and speed. Participant-reported measures included how well the participants felt they performed and how exhausted they were from taking the test, as well as positive and negative affect. There was a significant change in reaction time, number of commission errors, subjective performance, subjective exertion, and positive affect across the visits. Specifically, there was a linear decrease in reaction time, performance, and positive affect throughout the study, and a significant quadratic trend for commissions and exertion (first decreasing, then increasing after sleep deprivation). The univariate tests for omissions and negative affect were not significant. We conclude that sleeping 1.5–2 hours less than usual leads to faster response speed, but more commission errors and decreased positive affect. This indicates that individuals become more impulsive and experience less positive affect after a period of short sleep.

Blue-depleted lighting reduces the disruptive effects of evening artificial light on the circadian system in laboratory experiments, but this has not yet been shown in naturalistic settings. The aim of the current study was to test the effects of residing in an evening blue-depleted light environment on melatonin levels, sleep, neurocognitive arousal, sleepiness, and potential side effects. The study was undertaken in a new psychiatric hospital unit where dynamic light sources were installed. All light sources in all rooms were blue-depleted in one half of the unit between 06:30 pm and 07:00 am (melanopic lux range: 7–21, melanopic equivalent daylight illuminance [M-EDI] range: 6–19, photopic lux range: 55–124), whereas the other had standard lighting (melanopic lux range: 30–70, M-EDI range: 27–63, photopic lux range: 64–136), but was otherwise identical. A total of 12 healthy adults resided for 5 days in each light environment (LE) in a randomized cross-over trial. Melatonin levels were less suppressed in the blue-depleted LE (15%) compared with the normal LE (45%; p = 0.011). Dim light melatonin onset was phase-advanced more (1:20 h) after residing in the blue-depleted LE than after the normal LE (0:46 h; p = 0.008). Total sleep time was 8.1 min longer (p = 0.032), rapid eye movement sleep 13.9 min longer (p < 0.001), and neurocognitive arousal was lower (p = 0.042) in the blue-depleted LE. There were no significant differences in subjective sleepiness (p = 0.16) or side effects (p = 0.09). It is possible to create an evening LE that has an impact on the circadian system and sleep without serious side effects. This demonstrates the feasibility and potential benefits of designing buildings or hospital units according to chronobiological principles and provide a basis for studies in both nonclinical and clinical populations.

Survivors of moderate-severe Traumatic Brain Injury (TBI) are at risk for long-term cognitive, emotional, and behavioural problems. This prospective cohort study investigated self-reported executive, emotional, and behavioural problems in the late chronic phase of moderate and severe TBI, if demographic characteristics (i.e., age, years of education), injury characteristics (Glasgow Coma Scale score, MRI findings such as traumatic axonal injury (TAI), or duration of posttraumatic amnesia), symptoms of depression, or neuropsychological variables in the first year after injury predicted long-term self-reported function. Self-reported executive, emotional, and behavioural functioning were assessed among individuals with moderate and severe TBI (N=67, age range 15–65 years at time of injury) 2–5 years after TBI, compared to a healthy matched control group(N=72). Results revealed significantly more attentional, emotional regulation, and psychological difficulties in the TBI group than controls. Demographic and early clinical variables were associated with poorer cognitive and emotional outcome. Fewer years of education and depressive symptoms predicted greater executive dysfunction. Younger age at injury predicted more aggressive and rule-breaking behaviour. TAI and depressive symptoms predicted Internalizing problems and greater executive dysfunction. In conclusion, age, education, TAI, and depression appear to elevate risk for poor long-term outcome, emphasising the need for long-term follow-up of patients presenting with risk factors.

Motor skills have previously not been reported in young adults born with very low birth weight (VLBW), although they are commonly reported in children and adolescents. To compare fine and gross motor skills in VLBW young adults with matched term-born controls, and to study longitudinal changes in the VLBW group. A geographically based follow-up study of a VLBW group and a control group. Thirty-six VLBW (birth weight ≤ 1500 g) young adults, including four participants with cerebral palsy (CP), and 37 matched controls (birth weight ≥ 10th centile) were examined at 14 and 23 years of age. Fine and gross motor skills were assessed using Grooved Pegboard test (GP), Trail Making Test-5 (TMT-5), Movement Assessment Battery for Children-2 (Movement ABC-2) and High-level Mobility Assessment Tool (HiMAT). VLBW young adults were slower than controls on GP (p = 0.026) and TMT-5 (p < 0.001). Mean total Movement ABC-2 score was 69.7 ± 20.2 in the VLBW group compared with 74.1 ± 14.4 in the control group (p = 0.017). Differences were also seen in manual dexterity and balance. Additionally, HiMAT showed reduced balance and speed in gross motor skills in the VLBW group. The proportion of participants with motor problems did not change between age 14 and 23. After exclusion of participants with CP, scores were essentially the same. VLBW young adults had overall poorer fine and gross motor skills compared with controls. Reduced speed seemed to be an underlying problem. Longitudinal findings indicate that VLBW children have not outgrown their motor problems when entering adulthood.