The purpose of the current study was to explore potential differences in pre- and post-concussion performance on a computerized neurocognitive concussion test between African American and White high-school and collegiate student-athletes. A prospective case-control design was used to compare baseline and 2- and 7-day post-concussion computerized neurocognitive performance and symptoms between 48 White and 48 African American athletes matched for age, gender, and concussion history. The Immediate Post-Concussion Assessment Cognitive Test (ImPACT) version 2.0 (NeuroHealth System, LLC, Pittsburgh, PA, USA) computer software program was used to assess neurocognitive function (i.e., verbal and visual memory, motor processing speed, and reaction time) and concussion symptoms. Regardless of race/ethnicity, there were significant decrements in computerized neurocognitive performance and increased symptoms following a concussion for the entire sample. African Americans and Whites did not differ significantly on baseline or post-concussion verbal memory, visual memory, reaction time, and total reported symptoms. However, African American participants were 2.4× more likely to have at least one clinically significant cognitive decline on ImPACT at 7 days post-concussion and scored lower at 7 days post-concussion compared with baseline on processing speed than White participants. The authors concluded that the baseline ImPACT test was culturally equivalent and construct valid for use with these two racial/ethnic groups. However, in contrast, the findings support deleterious performance for the African American athletes compared with the White athletes on the ImPACT post-concussion evaluation that is of critical clinical relevance and warrants further research.

In this paper, we investigate the potential for the development of a composite score investigating population-level phenotype changes in a mouse model of traumatic brain injury. Traumatic brain injuries (TBI) are a growing concern in the United States because the number of individuals impacted by TBI and associated symptoms is increasing, leading to a growing demand for research both in the clinical and preclinical setting. However, preclinical TBI modeling is complicated by the lack of inter and intra lab consistency in the assessment of behavioral and pathologic outcomes. Indeed, it remains unclear which behavior assessments are most useful in evaluating the effects of preclinical TBI. To investigate the relative contribution of various behavior tests in the assessment of preclinical TBI, three statistical models (simple linear regression, pairwise correlation, and factor analysis) were conducted on behavioral data from the Mannix-Meehan lab at Boston Children’s Hospital in Boston, Massachusetts, U.S.A. from 2012-2018. In this paper, a composite metric was created from the computation analysis of the three statistical methods. The score revealed MWM and EPM as the most potent behavioral tests. The Open Field and Rotarod test had a small impact on the outcome, but only in one of the three statistical models assessed. Thus, to effectively analyze treatment efficiencies, injury severity and long-term impairments, MWM and EPM are the best behavioral test for a mouse model. Furthermore, this method of analysis of entire populations of mice allows for more subtle phenotypic changes resultant from injury models to be revealed, and the generalizability of this model lends to widespread use.

Indiana University-Purdue University Indianapolis (IUPUI) / Traumatic brain injury (TBI) is a critical public health issue in the United States, affecting about 2.8 million people annually. Extensive cell death and neural degeneration directly and diffusively caused by the initial mechanical insult results in a wide range of neurological complications post-trauma. Learning and memory dysfunction is one of the most common complains. Hippocampal neuronal loss, together with other mechanisms, largely contributes to learning and memory impairment as well as other cognitive dysfunctions post-trauma. To date, no FDA-approved drug is available to target cell death or improve learning and memory following TBI. It is of great interest to develop alternative approaches targeting neural repair instead. Neural stem/progenitor cells (NSCs) in the adult hippocampus undergo life-long neurogenesis supporting learning and memory functions, thus hold great promise for post-traumatic neuronal replacement. The previous studies demonstrated that TBI transiently increase NSC proliferation. However, it is debated on whether TBI affects neurogenesis. The mechanism of TBI-enhanced NSC proliferation remains elusive. In the current studies, I have investigated post-traumatic neurogenesis after different injury severities, evaluated integration of post-injury born neurons, illustrated a molecular mechanism mediating TBI-enhanced NSC proliferation, proposed a de novo state of NSCs, and tested effects of a pharmacological approach on spatial learning and memory function recovery. My results demonstrated that post-traumatic neurogenesis is affected by injury severities, partially explained the pre-existing inconsistency among works from different groups. Post-injury born neurons integrate in neural network and receive local and distal inputs. TBI promotes functional recruitment of post-injury born neurons into neural circuits. Mechanistically, mechanistic target of rapamycin (mTOR) pathway is required primarily for TBI-enhanced NSC proliferation; NSCs feature a de novo alert state, in which NSCs are reversibly released from quiescence and primed for proliferation. Furthermore, my data demonstrated a beneficial role of ketamine in improving post-traumatic spatial learning possibly by activating mTOR signal in NSCs and/or promoting neuronal activity of post-injury born neurons. Together, my data support the feasibility of neurogenesis mediated neuronal replacement, provide a target for enhancing post-traumatic NSC proliferation and subsequent neurogenesis, and prove a potential pharmacological approach benefiting post-traumatic functional recovery in learning and memory. / 2021-11-04

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Mild Traumatic Brain Injury (mTBI) can be broken into two categories; complicated and uncomplicated. These categories are based on structural imaging scans during the assessment of the injury. If abnormalities appear in the scan, we refer to it as complicated. The present research aims at determining whether there are differences in the neuropsychological deficits in the presences of positive neuroimaging as opposed to negative neuroimaging. This was accomplished with meta-analytic techniques. It was found that neuroimaging does not predict neuropsychological functioning in the chronic state of mTBI.

Atrophy of the corpus callosum (CC) is a documented consequence of moderate-to-severe traumatic brain injury (TBI), which has been expressed as volume loss using quantitative magnetic resonance imaging (MRI). Other advanced imaging modalities such as diffusion tensor imaging (DTI) have also detected white matter microstructural alteration following TBI in the CC. The manner and degree to which macrostructural changes such as volume and microstructural changes develop over time following pediatric TBI and their relation to a measure of processing speed is the focus of this longitudinal investigation. As such, DTI and volumetric changes of the CC in participants with TBI and a comparison group at approximately three and 18 months post injury and their relation to processing speed were determined.

Researchers studying the long-term cognitive sequelae of mild traumatic brain injury (mTBI) have produced disparate results. Some studies have shown little to no long-term cognitive effects while others have shown that persistent cognitive sequelae continue to affect a subgroup of patients. Meta-analysis has been used to try to integrate these contrasting results to foster a coherent understanding of the cognitive outcomes following mTBI. However, previous meta-analyses of long-term cognitive sequelae have used studies from a period of mTBI research where methodological rigor has been called into question (Carroll, Cassidy, Holm, Kraus, & Coronado, 2004). Using studies from this period, meta-analysts found little to no effect for long-term cognitive sequelae after mTBI: g = 0.07, d = 0.12 (Binder, Rohling, & Larrabee, 1997), g = 0.11(Frencham, Fox, & Mayberry, 2005), and d = -0.07 (Rohling et al., 2011). The present meta-analysis was conducted to address problems with methodological rigor in the studies used in these previous meta-analyses and address differences in meta-analytic methodology (Pertab, James, & Bigler, 2009). Studies published between January 2003 and August 2010 were rated using the 4-tiered American Academy Neurology (AAN) guidelines for methodological rigor to ensure homogeneity and the methodological rigor of included studies. Seven studies were identified that met criteria for a rating of I or II and five met criteria for the lower ratings of III or IV. When studies of all ratings were combined, a significant effect of g = 0.45 was observed. When only studies rated I and II were combined, a significant effect of g = 0.52 was observed while a significant effect of g = 0.38 was observed when only studies rated III and IV were combined. These effect sizes for long-term cognitive sequelae are much larger than those found in previous meta-analyses. Based on these results, it is likely that methodological rigor and/or heterogeneity amongst included studies can impact meta-analytic effect sizes associated with long-term cognitive sequelae following mTBI. However, analyses did not show that more rigorous studies (i.e., those rated I or II) had significantly higher effect sizes than less rigorous studies (i.e., those rated III or IV), t(10) = .636, p = .845. This non-significant finding may be a result of the analysis being underpowered given the small k. Significant effects for neuropsychological domain were also observed and are reported. Additionally, a conceptual critique of mTBI is made with recommendations for future development of the rating system that Cappa, Conger, and Conger (2011) have put forth for objectively rating the methodological rigor of neuropsychological studies. Concerns are addressed related to the mTBI literature in the areas of mTBI definition, definition of cognitive impairment, problems with the constructs of post-concussion syndrome (PCS) and persistent post-concussion symptoms (PPCS), heterogeneity of outcome measurement, and unaccounted for variables.