NeuroSci

Traumatic cervical spine injury in children and adolescents is uncommon but may cause major disability and prolonged critical care. This retrospective descriptive cohort characterizes patients aged 18 years or younger admitted to the Neurosurgical Intensive Care Unit (ICU) of a tertiary trauma center in New Delhi, India, during 2008–2015. Discharge status was classified as favorable (American Spinal Injury Association [ASIA] Impairment Scale D–E) or unfavorable (ASIA A–C or in-hospital death). We used chi-square tests with Yates’ continuity correction, with unadjusted odds ratios (ORs) and 95% confidence intervals (CIs). Among 112 patients, 83.0% were male, 85.7% were aged 9–18 years, and 77.7% had spinal canal compromise. Forty-seven patients (42.0%) had favorable and 65 (58.0%) had unfavorable discharge status, including nine in-hospital deaths (8.0%). Favorable status was associated with absence of spinal canal compromise (OR 6.67, 95% CI 2.40–18.54) and absence of the composite ICU complication indicator (OR 6.44, 95% CI 2.61–15.93), and with fracture rather than subluxation, absence of tracheostomy, and favorable admission ASIA category. No multivariable adjustment was performed; these exploratory, unadjusted associations do not establish independent or causal effects. The cohort provides descriptive data from an under-reported tertiary trauma setting and identifies variables for prospective multicenter study.

Nearly half of dementia cases are attributed to fourteen modifiable risk factors listed by the 2024 Lancet Commission; meal timing is not among them. Disrupted daily (circadian) rhythms are linked to faster neurodegeneration, yet it is unknown whether meal timing affects cognitive ageing. We review the evidence for the hypothesis that early time-restricted eating (eTRE) helps preserve cognition in older adults. We define eTRE as eating within a window of no more than 10 h, with at least 80% of daily energy eaten before 16:00. We evaluate three candidate pathways: daily rhythms in the removal of amyloid-beta and tau from the brain (glymphatic clearance), daily rhythms that keep brain inflammation low, and clock genes that support memory-related plasticity in the hippocampus. Nutrient-sensing and gut microbiota pathways are considered as alternatives. An AI co-scientist analysis, checked by the authors, suggested a “Dual-Gating” model: finishing meals early may lower nervous-system arousal and insulin levels at night, and both changes may favour brain clearance during sleep. We outline a three-arm trial (eTRE, late time-restricted eating, habitual eating) that tests whether any cognitive benefit is explained by changes in markers of clearance and inflammation. Meal timing remains a candidate exposure that needs prospective testing.

Persistent neurocognitive symptoms, such as “brain fog”, insomnia, or fatigue, are prevalent in PASC (post-acute sequelae of COVID-19, “Long COVID”), even after mild acute illness. However, evidence for the neural underpinnings of cognitive dysregulation and altered spontaneous neural activity is inadequate. EEG data were acquired during an inhibitory Go/NoGo task and wakeful rest from young, otherwise healthy adults with PASC approximately six months after recovery from mild COVID-19. Neurobehavioral indices were computed for correct and erroneous trials, resting state, and the questionnaire battery, and compared with a matched control (CONT) group of individuals not exposed to COVID-19. The PASC group reported higher cognitive difficulties, anxiety, depression, and sleep problems, consistent with the known symptomatic pattern. Despite intact task performance, neural indices indicated altered engagement of cognitive control in the PASC group on both correct and error trials, which was associated with less efficient responding. Moreover, co-oscillatory synchrony trended toward dysregulation during error commission in the PASC group. Altered neural indices of inhibitory control marginally correlated with spontaneous oscillatory slowing, potentially suggesting shared basic mechanisms. The overall pattern of PASC symptoms, altered neural activity during inhibitory control, and oscillatory slowing, is indicative of the core neural dysfunction characterizing PASC.