Articles: traumatic-brain-injuries.
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This study evaluates the applicability of S100B levels, mean maximum velocity (Vmean) over time, pulsatility index (PI), intracranial pressure (ICP), and body temperature (T) for the prediction of the treatment of patients with traumatic brain injury (TBI). Sixty patients defined by the Glasgow Coma Scale score ≤ 8 were stratified using the Glasgow Coma Scale into 2 groups: favorable (FG: Glasgow Outcome Scale ≥ 4) and unfavorable (UG: Glasgow Outcome Scale < 4). The S100B concentration was at the time of hospital admission. ⋯ The unfavorable outcome is defined by significantly higher levels of all parameters, except T. A favorable outcome is defined by S100B < 3 mg/L, PI < 2.86, ICP > 25 mm Hg, and Vmean > 40 cm/s. The relationships provided may serve as indicators of the results of the TBI treatment.
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Hyperhidrosis is clinical symptom of various diseases and is an important clinical feature of paroxysmal sympathetic hyperactivity (PSH). Traumatic brain injury (TBI) is known to be most common condition associated with PSH, and PSH has been mainly reported in moderate and severe TBI. However, very little has been reported on PSH or hyperhidrosis in mild TBI patients. ⋯ By contrast, the apparent diffusion coefficient values for both sides of the hypothalamus were significantly higher in the patient group than in the control group (P < .05). In conclusion, we detected hypothalamic injuries in patients who showed hyperhidrosis after mild TBI. Based on the results, it appears that hyperhidrosis in patients with mild TBI is related to hypothalamic injury.
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Dexmedetomidine was found to be protective against traumatic brain injury (TBI) in animal studies and safe for use in previous clinical studies, but whether it improves TBI patient survival remains to be determined. We sought to answer this question by analyzing data from the MIMIC clinical database. ⋯ Dexmedetomidine may improve the survival of TBI patients. It should be used with careful avoidance of hypotension.
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Journal of neurosurgery · Sep 2022
Complications associated with early cranioplasty for patients with traumatic brain injury: a 25-year single-center analysis.
Cranioplasty is a technically simple procedure, although one with potentially high rates of complications. The ideal timing of cranioplasty should minimize the risk of complications, but research investigating cranioplasty timing and risk of complications has generated diverse findings. Previous studies have included mixed populations of patients undergoing cranioplasty following decompression for traumatic, vascular, and other cerebral insults, making results challenging to interpret. The objective of the current study was to examine rates of complications associated with cranioplasty, specifically for patients with traumatic brain injury (TBI) receiving this procedure at the authors' high-volume level 1 trauma center over a 25-year time period. ⋯ In this cohort of patients with TBI, early cranioplasty, including ultra-early procedures, was not associated with higher rates of complications. Early cranioplasty may confer benefits such as shorter or fewer hospitalizations, decreased financial burden, and overall improved recovery, and should be considered based on patient-specific factors.
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Journal of neurotrauma · Sep 2022
Fluvoxamine confers neuroprotection via inhibiting infiltration of peripheral leukocytes and M1 polarization of microglia/macrophages in a mouse model of traumatic brain injury.
Neuroinflammation is an important mediator of secondary injury pathogenesis that exerts dual beneficial and detrimental effects on pathophysiology of the central nervous system (CNS) after traumatic brain injury (TBI). Fluvoxamine is a serotonin selective reuptake inhibitor (SSRI) and has been reported to have the anti-inflammatory properties. However, the mechanisms and therapeutic effects of fluvoxamine in neuroinflammation after TBI have not be defined. ⋯ Fluvoxamine treatment promoted microglial/macrophage phenotypic transformation from pro-inflammatory M1-phenotype to anti-inflammatory M2-phenotype in in vivo and in vitro experiments. In addition, fluvoxamine treatment attenuated neuronal apoptosis, blood-brain barrier (BBB) disruption, cerebrovascular damage, and post-traumatic edema formation, thereby improving neurological function of mice subjected to TBI. These findings support the clinical evaluation of fluvoxamine as a neuroprotective therapy for TBI.