Journal of neurotrauma
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Journal of neurotrauma · Apr 2015
Structured interview for Mild Traumatic Brain Injury after military blast: interrater agreement and development of diagnostic algorithm.
The existing gold standard for diagnosing a suspected previous mild traumatic brain injury (mTBI) is clinical interview. But it is prone to bias, especially for parsing the physical versus psychological effects of traumatic combat events, and its inter-rater reliability is unknown. Several standardized TBI interview instruments have been developed for research use but have similar limitations. ⋯ The accuracy of this algorithm, when applied against the actual physician consensus in sample 2, was almost perfect (correctly classified = 97%; Cohen's kappa = 0.91). In conclusion, we found that highly trained clinicians often disagree on historical blast-related mTBI determinations. A fully structured interview algorithm was developed from their consensus diagnosis that may serve to enhance diagnostic standardization for clinical research in this population.
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Journal of neurotrauma · Apr 2015
Randomized Controlled TrialProlonged mild therapeutic hypothermia versus fever control with tight hemodynamic monitoring and slow rewarming in patients with severe traumatic brain injury: a randomized controlled trial.
Although mild therapeutic hypothermia is an effective neuroprotective strategy for cardiac arrest/resuscitated patients, and asphyxic newborns, recent randomized controlled trials (RCTs) have equally shown good neurological outcome between targeted temperature management at 33 °C versus 36 °C, and have not shown consistent benefits in patients with traumatic brain injury (TBI). We aimed to determine the effect of therapeutic hypothermia, while avoiding some limitations of earlier studies, which included patient selection based on Glasgow coma scale (GCS), delayed initiation of cooling, short duration of cooling, inter-center variation in patient care, and relatively rapid rewarming. We conducted a multicenter RCT in patients with severe TBI (GCS 4-8). ⋯ The overall rates of poor neurological outcomes were 53% and 48% in the therapeutic hypothermia and fever control groups, respectively. There were no significant differences in the likelihood of poor neurological outcome (relative risk [RR] 1.24, 95% confidence interval [CI] 0.62-2.48, p = 0.597) or mortality (RR 1.82, 95% CI 0.82-4.03, p = 0.180) between the two groups. We concluded that tight hemodynamic management and slow rewarming, together with prolonged therapeutic hypothermia (32-34 °C) for severe TBI, did not improve the neurological outcomes or risk of mortality compared with strict temperature control (35.5-37 °C).
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Journal of neurotrauma · Apr 2015
Multicenter StudyCould a traumatic epidural hematoma on early CT tell us about its future development? A multi-center retrospective study in China.
Our aim for this study was to quantitatively develop an early epidural hematoma (EDH) natural evolutionary curve and assess association of the most common radiological signs of initially nonsurgical supratentorial EDHs on early computed tomography (CT), in addition to their CT time for EDH enlargement. We retrospectively reviewed pertinent data of supratentorial EDH cases with CT ≤ 6 h postinjury (1997-2013) in three medical institutions in Shanghai. Cases involved were divided into six groups according to their initial CT time postinjury (≤ 1, 1-2, 2-3, 3-4, 4-5, and 5-6 h for groups 1 through 6, respectively). ⋯ Multi-variate analysis succeeded in determining two risk factors for EDH enlargement ≥ 30 mL and EDH enlargement requiring an operation for EDH cases with an early CT/EDH volume >10 mL on CT performed ≤ 2 h and EDH located at the temporal or temporoparietal region on CT ≤ 1 h post brain injury. Using recursive partitioning analysis, "high-risk" identification criteria were derived to predict EDH enlargement ≥ 30 mL with sensitivity of 90.5% (95% confidence interval [CI], 77.9-96.2), specificity of 60.1% (95% CI, 54.3-65.7), and EDH enlargement requiring surgery with sensitivity of 100.0% (95% CI, 89.9-100.0), and specificity of 59.9% (95% CI, 54.1-65.4). A redo-CT 5 ∼ 6 h post impact for cases at high risk is recommended.
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Journal of neurotrauma · Apr 2015
Characterizing self-reported sleep disturbance following mild traumatic brain injury.
Sleep disturbance after mild traumatic brain injury (mTBI) is commonly reported as debilitating and persistent. However, the nature of this disturbance is poorly understood. This study sought to characterize sleep after mTBI compared with a control group. ⋯ These results indicate a difference in the magnitude and nature of perceived sleep disturbance after mTBI compared with controls, where persons with mTBI report poorer sleep quality and greater sleep-related impairment. Sleep quantity and timing did not differ between the groups. These preliminary findings should guide the provision of clearer advice to patients about the aspects of their sleep that may change after mTBI and could inform treatment selection.
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Journal of neurotrauma · Apr 2015
Inhibition of injury-induced cell proliferation in the dentate gyrus of the hippocampus impairs spontaneous cognitive recovery following traumatic brain injury.
Neurogenesis persists throughout life in the neurogenic regions of the mature mammalian brain, and this response is enhanced after traumatic brain injury (TBI). In the hippocampus, adult neurogenesis plays an important role in hippocampal-dependent learning and memory functions and is thought to contribute to the spontaneous cognitive recovery observed after TBI. Utilizing an antimitotic agent, arabinofuranosyl cytidine (Ara-C), the current study investigated the direct association of injury-induced hippocampal neurogenesis with cognitive recovery. ⋯ We found that a 7-day infusion of Ara-C significantly reduced the total number of BrdU(+) and DCX(+) cells in the dentate gyrus (DG) in both hemispheres. Moreover, inhibition of the injury-induced cell proliferative response in the DG completely abolished the innate cognitive recovery on MWM performance at 56-60 days postinjury. These results support the causal relationship of injury-induced hippocampal neurogenesis on cognitive functional recovery and suggest the importance of this endogenous repair mechanism on restoration of hippocampal function.