Changes in personality after mild traumatic brain injury from primary blast vs. blunt forces

Mendez, Mario F.; Owens, Emily M.; Jimenez, Elvira; Peppers, Dominique; Licht, Eliot A.

doi:10.3109/02699052.2012.722252

Cited by 30 publications

(14 citation statements)

References 71 publications

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“…6a ). Klhl2 in CA1 pyramidal cells may serve as a novel link between mTBI and the increased tendency for neuroticism observed in blast TBI 40 . Arhgap32 is primarily upregulated in CA subtype 2 cells in mTBI.…”

Section: Resultsmentioning

confidence: 99%

Single cell molecular alterations reveal target cells and pathways of concussive brain injury

et al. 2018

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The complex neuropathology of traumatic brain injury (TBI) is difficult to dissect, given the convoluted cytoarchitecture of affected brain regions such as the hippocampus. Hippocampal dysfunction during TBI results in cognitive decline that may escalate to other neurological disorders, the molecular basis of which is hidden in the genomic programs of individual cells. Using the unbiased single cell sequencing method Drop-seq, we report that concussive TBI affects previously undefined cell populations, in addition to classical hippocampal cell types. TBI also impacts cell type-specific genes and pathways and alters gene co-expression across cell types, suggesting hidden pathogenic mechanisms and therapeutic target pathways. Modulating the thyroid hormone pathway as informed by the T4 transporter transthyretin Ttr mitigates TBI-associated genomic and behavioral abnormalities. Thus, single cell genomics provides unique information about how TBI impacts diverse hippocampal cell types, adding new insights into the pathogenic pathways amenable to therapeutics in TBI and related disorders.

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Section: Resultsmentioning

confidence: 99%

Single cell molecular alterations reveal target cells and pathways of concussive brain injury

et al. 2018

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“…It has been reported that blast forces alone can cause deleterious behavioral changes when evaluated with selected measures of personality (35). Blast exposure has also been linked to self-perceived cognitive decline in soldiers with mbTBI (36).…”

Section: Discussionmentioning

confidence: 99%

The Temporal Pattern of Changes in Serum Biomarker Levels Reveals Complex and Dynamically Changing Pathologies after Exposure to a Single Low-Intensity Blast in Mice

et al. 2015

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Time-dependent changes in blood-based protein biomarkers can help identify the pathological processes in blast-induced traumatic brain injury (bTBI), assess injury severity, and monitor disease progression. We obtained blood from control and injured mice (exposed to a single, low-intensity blast) at 2-h, 1-day, 1–week, and 1-month post-injury. We then determined the serum levels of biomarkers related to metabolism (4-HNE, HIF-1α, ceruloplasmin), vascular function (AQP1, AQP4, VEGF, vWF, Flk-1), inflammation (OPN, CINC1, fibrinogen, MIP-1a, OX-44, p38, MMP-8, MCP-1 CCR5, CRP, galectin-1), cell adhesion and the extracellular matrix (integrin α6, TIMP1, TIMP4, Ncad, connexin-43), and axonal (NF-H, Tau), neuronal (NSE, CK-BB) and glial damage (GFAP, S100β, MBP) at various post-injury time points. Our findings indicate that the exposure to a single, low-intensity blast results in metabolic and vascular changes, altered cell adhesion, and axonal and neuronal injury in the mouse model of bTBI. Interestingly, serum levels of several inflammatory and astroglial markers were either unchanged or elevated only during the acute and subacute phases of injury. Conversely, serum levels of the majority of biomarkers related to metabolic and vascular functions, cell adhesion, as well as neuronal and axonal damage remained elevated at the termination of the experiment (1 month), indicating long-term systemic and cerebral alterations due to blast. Our findings show that the exposure to a single, low-intensity blast induces complex pathological processes with distinct temporal profiles. Hence, monitoring serum biomarker levels at various post-injury time points may provide enhanced diagnostics in blast-related neurological and multi-system deficits.

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“…Limitations include a modest sample size, all male subjects, no predeployment testing, 16 no direct comparison with identically assessed non-blast-related subjects with TBI, no formal assessment of combat exposure intensity, and absence of genetic data. We cannot rule out deficits in cognitive or behavioral domains not tested, 47,48 nor early cognitive impairments that resolved before follow-up evaluation. Likewise, Negative correlation with sustained vigilance, assessed using the hit rate block change measure from the Conners Continuous Performance Test, where similarly lower Z-scores indicate worse performance.…”

Section: Discussionmentioning

confidence: 99%

Functional Status after Blast-Plus-Impact Complex Concussive Traumatic Brain Injury in Evacuated United States Military Personnel

MacDonald

Johnson

Nelson

et al. 2014

Journal of Neurotrauma

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Fundamental questions remain unanswered about the longitudinal impact of blast-plus-impact complex traumatic brain injuries (TBI) from wars in Iraq and Afghanistan. This prospective, observational study investigated measures of clinical outcome in US military personnel evacuated to Landstuhl Regional Medical Center (LRMC) in Germany after such "blast-plus" concussive TBIs. Glasgow Outcome Scale-Extended assessments completed 6-12 months after injury indicated a moderate overall disability in 41/47 (87%) blast-plus TBI subjects and a substantial but smaller number (11/18, 61%, p=0.018) of demographically similar US military controls without TBI evacuated for other medical reasons. Cognitive function assessed with a neuropsychological test battery was not different between blast-plus TBI subjects and controls; performance of both groups was generally in the normal range. No subject was found to have focal neurological deficits. However, 29/47 (57%) of blast-plus subjects with TBI met all criteria for post-traumatic stress disorder (PTSD) versus 5/18 (28%) of controls (p=0.014). PTSD was highly associated with overall disability; 31/34 patients with PTSD versus 19/31 patients who did not meet full PTSD criteria had moderate to severe disability (p=0.0003). Symptoms of depression were also more severe in the TBI group (p=0.05), and highly correlated with PTSD severity (r=0.86, p<0.0001). Thus, in summary, high rates of PTSD and depression but not cognitive impairment or focal neurological deficits were observed 6-12 months after concussive blast-plus-impact complex TBI. Overall disability was substantially greater than typically reported in civilian non-blast concussive ("mild") patients with TBI, even with polytrauma. The relationship between these clinical outcomes and specific blast-related aspects of brain injuries versus other combat-related factors remains unknown.

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Changes in personality after mild traumatic brain injury from primary blast vs. blunt forces

Abstract: These results suggest that blast forces alone can cause negativistic behavioural changes when evaluated with selected measures of personality. Further research on isolated blast-force mTBI should focus on these personality changes and their relationship to blast over-pressure.

Cited by 30 publications

References 71 publications

Single cell molecular alterations reveal target cells and pathways of concussive brain injury

Single cell molecular alterations reveal target cells and pathways of concussive brain injury

The Temporal Pattern of Changes in Serum Biomarker Levels Reveals Complex and Dynamically Changing Pathologies after Exposure to a Single Low-Intensity Blast in Mice

Functional Status after Blast-Plus-Impact Complex Concussive Traumatic Brain Injury in Evacuated United States Military Personnel

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