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Most children recover from mild traumatic brain injury (mTBI), but some experience persistent neurocognitive effects. Understanding is limited due to methodological differences and a lack of pre-injury data. The study aimed to assess changes in neurocognitive outcomes in children following mTBI compared to orthopedic injury (OI) and non-injured (NI) controls, while accounting for pre-injury functioning.
Method:
Data were drawn from the Adolescent Brain and Cognitive Development (ABCD) study, a prospective longitudinal cohort. The sample included children with mTBI between the 1-year and 2-year follow-ups (n = 83), identified by parent report of head injury with memory loss or loss of consciousness, compared to children who experienced OI within the same period (n = 231) and an NI control group (n = 218). Changes in neurocognitive outcomes from baseline to the 2-year follow-up between groups (mTBI vs. OI; mTBI vs. NI) were estimated using linear mixed-effects models, accounting for demographic, behavioral, genetic, and white matter microstructural covariates.
Results:
At baseline prior to injury, the mTBI group demonstrated better performance on picture vocabulary and crystallized composite scores than the OI group. At post-injury, after adjusting for pre-injury baseline differences, children who sustained an mTBI were no different in any measure of neurocognitive outcomes compared to OI and NI controls.
Conclusions:
The findings highlight the importance of accounting for pre-injury differences when evaluating neurocognitive outcomes following pediatric mTBI. Neurocognitive differences within a year post-injury may be more related to pre-existing individual factors rather than the injury itself, underscoring the need for a comprehensive approach in studying pediatric mTBI.
Patients with posttraumatic stress disorder (PTSD) exhibit smaller regional brain volumes in commonly reported regions including the amygdala and hippocampus, regions associated with fear and memory processing. In the current study, we have conducted a voxel-based morphometry (VBM) meta-analysis using whole-brain statistical maps with neuroimaging data from the ENIGMA-PGC PTSD working group.
Methods
T1-weighted structural neuroimaging scans from 36 cohorts (PTSD n = 1309; controls n = 2198) were processed using a standardized VBM pipeline (ENIGMA-VBM tool). We meta-analyzed the resulting statistical maps for voxel-wise differences in gray matter (GM) and white matter (WM) volumes between PTSD patients and controls, performed subgroup analyses considering the trauma exposure of the controls, and examined associations between regional brain volumes and clinical variables including PTSD (CAPS-4/5, PCL-5) and depression severity (BDI-II, PHQ-9).
Results
PTSD patients exhibited smaller GM volumes across the frontal and temporal lobes, and cerebellum, with the most significant effect in the left cerebellum (Hedges’ g = 0.22, pcorrected = .001), and smaller cerebellar WM volume (peak Hedges’ g = 0.14, pcorrected = .008). We observed similar regional differences when comparing patients to trauma-exposed controls, suggesting these structural abnormalities may be specific to PTSD. Regression analyses revealed PTSD severity was negatively associated with GM volumes within the cerebellum (pcorrected = .003), while depression severity was negatively associated with GM volumes within the cerebellum and superior frontal gyrus in patients (pcorrected = .001).
Conclusions
PTSD patients exhibited widespread, regional differences in brain volumes where greater regional deficits appeared to reflect more severe symptoms. Our findings add to the growing literature implicating the cerebellum in PTSD psychopathology.
Humanitarian mine action (HMA) stakeholders have an organized presence with well-resourced medical capability in many conflict and post-conflict settings. Humanitarian mine action has the potential to positively augment local trauma care capacity for civilian casualties of explosive ordnance (EO) and explosive weapons (EWs). Yet at present, few strategies exist for coordinated engagement between HMA and the health sector to support emergency care system strengthening to improve outcomes among EO/EW casualties.
Methods:
A scoping literature review was conducted to identify records that described trauma care interventions pertinent to civilian casualties of EO/EW in resource-constrained settings using structured searches of indexed databases and grey literature. A 2017 World Health Organization (WHO) review on trauma systems components in low- and middle-income countries (LMICs) was updated with additional eligible reports describing trauma care interventions in LMICs or among civilian casualties of EO/EWs after 2001.
Results:
A total of 14,195 non-duplicative records were retrieved, of which 48 reports met eligibility criteria. Seventy-four reports from the 2017 WHO review and 16 reports identified from reference lists yielded 138 reports describing interventions in 47 countries. Intervention efficacy was assessed using heterogenous measures ranging from trainee satisfaction to patient outcomes; only 39 reported mortality differences. Interventions that could feasibly be supported by HMA stakeholders were synthesized into a bundle of opportunities for HMA engagement designated links in a Civilian Casualty Care Chain (C-CCC).
Conclusions:
This review identified trauma care interventions with the potential to reduce mortality and disability among civilian EO/EW casualties that could be feasibly supported by HMA stakeholders. In partnership with local and multi-lateral health authorities, HMA can leverage their medical capabilities and expertise to strengthen emergency care capacity to improve trauma outcomes in settings affected by EO/EWs.
Apolipoprotein E (APOE) E4 is the main genetic risk factor for Alzheimer’s disease (AD). Due to the consistent association, there is interest as to whether E4 influences the risk of other neurodegenerative diseases. Further, there is a constant search for other genetic biomarkers contributing to these phenotypes, such as microtubule-associated protein tau (MAPT) haplotypes. Here, participants from the Ontario Neurodegenerative Disease Research Initiative were genotyped to investigate whether the APOE E4 allele or MAPT H1 haplotype are associated with five neurodegenerative diseases: (1) AD and mild cognitive impairment (MCI), (2) amyotrophic lateral sclerosis, (3) frontotemporal dementia (FTD), (4) Parkinson’s disease, and (5) vascular cognitive impairment.
Methods:
Genotypes were defined for their respective APOE allele and MAPT haplotype calls for each participant, and logistic regression analyses were performed to identify the associations with the presentations of neurodegenerative diseases.
Results:
Our work confirmed the association of the E4 allele with a dose-dependent increased presentation of AD, and an association between the E4 allele alone and MCI; however, the other four diseases were not associated with E4. Further, the APOE E2 allele was associated with decreased presentation of both AD and MCI. No associations were identified between MAPT haplotype and the neurodegenerative disease cohorts; but following subtyping of the FTD cohort, the H1 haplotype was significantly associated with progressive supranuclear palsy.
Conclusion:
This is the first study to concurrently analyze the association of APOE isoforms and MAPT haplotypes with five neurodegenerative diseases using consistent enrollment criteria and broad phenotypic analysis.