Traumatic Brain Injury: A Review and High-Field MRI Findings in 100 Unarmed Combatants Using a Literature-Based Checklist Approach

Nevada Imaging Centers, Las Vegas, Nevada, USA.
Journal of neurotrauma (Impact Factor: 3.71). 04/2009; 26(5):689-701. DOI: 10.1089/neu.2008.0636
Source: PubMed


This study reviewed the literature for the extent of neuroimaging findings in boxers, indicative of traumatic brain injury (TBI) as identified in magnetic resonance imaging (MRI). The study then utilized a systematic checklist approach to assess 100 unselected consecutive 1.5- and 3.0-Tesla MRI examinations of professional unarmed combatants to determine the extent of identifiable TBI findings. The percentage of positive findings and the localization of lesions were quantified using the checklist that included the MRI findings previously reported in the medical literature. Seventy-six percent of the unarmed combatants had at least one finding that may be associated with TBI: 59% hippocampal atrophy, 43% cavum septum pellucidum, 32% dilated perivascular spaces, 29% diffuse axonal injury, 24% cerebral atrophy, 19% increased lateral ventricular size, 14% pituitary gland atrophy, 5% arachnoid cysts, and 2% had contusions. Statistical relationships were found between number of bouts and lateral ventricular size (tau-b = 0.149, p = 0.0489), with years of fighting correlating with the presence of dilated perivascular spaces (tau-b = 0.167, p = 0.0388) and diffuse axonal injury (tau-b = 0.287, p = 0.0013) findings. The improved resolution and increased signal-to-noise ratio on 1.5- and 3.0-Tesla high-field MRI systems defines the range of pathological variations that may occur in professional unarmed combatants. Additionally, the use of a systematic checklist approach insures evaluation for all possible TBI-related abnormalities. This knowledge can be used to anticipate the regions of potential brain pathology for radiologists and emergency medicine physicians, and provides important information for evaluating unarmed combatants relative to their safety and long-term neurocognitive outcome.

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Available from: Thomas G Perkins, Mar 15, 2015
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    • "The hippocampus, a key brain structure for cognition, is particularly vulnerable to TBI. The earliest and most severe neuropathological changes occur in the hippocampus after TBI [5], [6]. However, molecular mechanisms underlying hippocampal alterations and cognitive impairments following TBI remain elusive. "
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    ABSTRACT: Traumatic brain injury (TBI) is a common cause for cognitive and communication problems, but the molecular and cellular mechanisms are not well understood. Epigenetic modifications, such as microRNA (miRNA) dysregulation, may underlie altered gene expression in the brain, especially hippocampus that plays a major role in spatial learning and memory and is vulnerable to TBI. To advance our understanding of miRNA in pathophysiological processes of TBI, we carried out a time-course microarray analysis of microRNA expression profile in rat ipsilateral hippocampus and examined histological changes, apoptosis and synapse ultrastructure of hippocampus post moderate TBI. We found that 10 out of 156 reliably detected miRNAs were significantly and consistently altered from one hour to seven days after injury. Bioinformatic and gene ontology analyses revealed 107 putative target genes, as well as several biological processes that might be initiated by those dysregulated miRNAs. Among those differentially expressed microRNAs, miR-144, miR-153 and miR-340-5p were confirmed to be elevated at all five time points after TBI by quantitative RT-PCR. Western blots showed three of the predicated target proteins, calcium/calmodulin-dependent serine protein kinase (CASK), nuclear factor erythroid 2-related factor 2 (NRF2) and alpha-synuclein (SNCA), were concurrently down- regulated, suggesting that miR-144, miR-153 and miR-340-5p may play important roles collaboratively in the pathogenesis of TBI-induced cognitive and memory impairments. These microRNAs might serve as potential targets for progress assessment and intervention against TBI to mitigate secondary damage to the brain.
    PLoS ONE 08/2014; 9(8):e103948. DOI:10.1371/journal.pone.0103948 · 3.23 Impact Factor
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    • "Based on a number of bTBI studies that implicate the hippocampus in the development of neurobehavioral symptoms, we expected to detect injury-induced structural and/or volumetric changes in this region due to its involvement in TBI3435. We previously found significantly increased numbers of apoptotic, TUNEL-positive cells in the hilus and granular cell layer of the hippocampus as early as 2 h post-injury in both single- and multiple-injured rats36. "
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    ABSTRACT: Mild blast-induced traumatic brain injury (mbTBI) poses special diagnostic challenges due to its overlapping symptomatology with other neuropsychiatric conditions and the lack of objective outcome measures. Diffusion tensor imaging (DTI) can potentially provide clinically relevant information toward a differential diagnosis. In this study, we aimed to determine if single and repeated (5 total; administered on consecutive days) mild blast overpressure exposure results in detectable structural changes in the brain, especially in the hippocampus. Fixed rat brains were analyzed by ex vivo DTI at 2 h and 42 days after blast (or sham) exposure(s). An anatomy-based region of interest analysis revealed significant interactions in axial and radial diffusivity in a number of subcortical structures at 2 h only. Differences between single- and multiple-injured rats were largely in the thalamus but not the hippocampus. Our findings demonstrate the value and the limitations of DTI in providing a better understanding of mbTBI pathobiology.
    Scientific Reports 05/2014; 4:4809. DOI:10.1038/srep04809 · 5.58 Impact Factor
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    • "In addition to the developmental presence of the CSP, the cavity may also be generated from injury, thought to result from acceleration– deceleration forces causing a tearing (or fenestration). The CSP has been linked with traumatic brain injuries (TBIs), particularly to professional boxers (Corsellis et al., 1973; Cabanis et al., 1986; Bogdanoff and Natter, 1989; Jordan, 2000; McCrory, 2002; Orrison et al., 2009; Handratta et al., 2010), but also fatal traffic accidents (Pittella and Gusmao, 2005). While the physical fenestration of a head injury resulting in a CSP clearly has different mechanisms from that of a developmental presence, patients with both head injuries and neurodevelopmental disorders share many symptoms that are attributed to functions of the limbic system and underperform on many neuropsychological measures. "
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    ABSTRACT: The cavum septum pellucidum (CSP) is a fluid-filled cavity in the thin midline structure of the septum pellucidum. The CSP has been linked to several neurodevelopmental disorders, but it also occurs as a result of head injury. The aims were to assess the presence and characterization of the CSP in youth with traumatic brain injury (TBI), to assess whether injury severity or IQ measures were related to CSP size, and to examine brain morphometry changes associated with the CSP size. Ninety-eight survivors of TBI and 34 control children underwent magnetic resonance imaging (MRI). Numerous methods were used to define the presence and characterization of the CSP including length, classification of abnormally large CSP, rating of the CSP, and volume. There was no difference in presence of CSP between TBI patients and controls; however, there was larger and more severely graded CSP in the patient group. Size of the CSP correlated positively with injury severity, and regions that correlated most significantly with CSP size were the right entorhinal cortex and bilateral hippocampus. Characterizing the CSP and related brain changes may provide important information concerning disturbances seen after a TBI.
    06/2013; 213(3). DOI:10.1016/j.pscychresns.2013.03.001
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