Background and PurposeThe functional outcome of traumatic brain injury (TBI) varies widely. The aim of this study was to identify the factors predicting outcome following TBI.MethodsWe prospectively enrolled acute TBI patients, and assessed them clinically and radiologically using brain magnetic resonance imaging (MRI). Functional outcome was measured using the Glasgow Outcome Scale (GOS) at 3 months after TBI. A GOS score of ≤4 was regarded as an unfavorable outcome. We performed multivariate analysis to investigate the association between clinicoradiological variables and outcome.ResultsForty-two patients completed the clinical evaluation in the acute phase and outcome measurement at 3 months. Motorcycle accident was associated with unfavorable outcome [odds ratio (OR)=38.3, p=0.022]. If the patients were the victims of the accident, they were more likely to have an unfavorable outcome (OR=21.3, p=0.037). All seven patients with a low Glasgow Coma Scale (GCS) score (i.e., ≤8) at 24 or 48 h after TBI were also found to have an unfavorable outcome. The presence of diffuse axonal injury (DAI) was a significant predicting factor of an unfavorable outcome (OR=8.48, p=0.042).ConclusionsMotorcycle accident, being an accident victim, and a lower GCS score at 24 hours or more after the accident were found to be unfavorable prognostic variables. DAI was the only radiologic variable predicting an unfavorable outcome. Thus, it is important to identify DAI by applying MRI in the acute phase.
Spinal epidural abscess (SEA) is a rare infection with a high rate of mortality and morbidity, which requires urgent surgery. Although surgery is the mainstay of treatment, some investigators currently report good outcomes after medical treatment. Thus, the optimal treatment option is debatable without established guidelines for standard of care. Moreover, surgery in elderly SEA patients is challenging because of comorbidities and perioperative risks. Methods: We retrospectively reviewed the medical records of 16 elderly patients with SEA, including 6 males and 10 females, ranging in age from 69 to 88 years (mean 75 years). Fourteen patients underwent open surgery, and 2 underwent aspiration biopsy as well as antibiotic treatment. We statistically analyzed variables related to clinical outcomes. The mean follow-up duration was 21.6 months. Results: Twelve patients had comorbidities, and 5 had other systemic infections. Four and 3 patients had a history of spinal intervention and spinal fusion surgery, respectively. Finally, 7 patients completely improved and 2 were moderately disabled. Another 2 patients were severely disabled and 5 died during antibiotic treatment. Most mortalities were due to comorbidities. SEA in elderly patients with comorbidities was associated with high mortality rates. Furthermore, delayed surgery was significantly related to poor neurological outcomes, whereas other variables were not significantly related to the outcomes of SEA in elderly patients. Conclusion: We identified a statistically significant relationship between neurological outcome and comorbidity (p= 0.026), predisposing conditions (p=0.010), and time to surgery (p=0.014), suggesting that early surgery should be considered, even in elderly SEA patients.
Although preparation of early-stage bone-marrow-derived mesenchymal stem cells (BM-MSCs) is critical for successful cell transplantation therapy, no culture system offers a sufficient number of early-stage BM-MSCs for cell transplantation. Accordingly, we developed a culture system capable of producing a large number of early-stage BM-MSCs by using gelatin-coated matrix. The greatest retrieval and proliferation rates of the earliest-stage rat BM-MSCs were detected in bone-marrow-derived cells cultured on 1% (wt/v) gelatin-coated matrix, which showed significantly greater colony forming unit-fibroblast number, diameter, and total cell number. Moreover, continuous culture of the earliest-stage BM-MSCs on 1% (wt/v) gelatin-coated matrix resulted in a maximum of 21.2 ± 2.7 fold increase in the cumulative total number of early-stage BM-MSCs at passage 5. BM-MSCs generated in large quantities due to a reduced doubling time and an increased yield of cell population in S/G2/M phase showed typical fibroblast-like morphology and no significant differences in BM-MSC-related surface marker expression and differentiation potential, except for an increased ratio of differentiation into a neurogenic lineage. The use of gelatin-coated matrix in the retrieval and culture of BM-MSCs contributes greatly to the effective isolation and mass production of early-stage BM-MSCs.
Neuronal loss (death) occurs selectively in vulnerable brain regions after ischemic insults. Astrogliosis is accompanied by neuronal death. It can change the molecular expression and morphology of astrocytes following ischemic insults. However, little is known about cerebral ischemia and reperfusion injury that can variously lead to damage of astrocytes according to the degree of ischemic injury, which is related to neuronal damage/death. Thus, the purpose of this study was to examine the relationship between damage to cortical neurons and astrocytes using gerbil models of mild and severe transient forebrain ischemia induced by blocking the blood supply to the forebrain for five or 15 min. Significant ischemia tFI-induced neuronal death occurred in the deep layers (layers V and VI) of the motor cortex: neuronal death occurred earlier and more severely in gerbils with severe ischemia than in gerbils with mild ischemia. Distinct astrogliosis was detected in layers V and VI. It gradually increased with time after both ischemiae. The astrogliosis was significantly higher in severe ischemia than in mild ischemia. The ischemia-induced increase of glial fibrillary acidic protein (GFAP; a maker of astrocyte) expression in severe ischemia was significantly higher than that in mild ischemia. However, GFAP-immunoreactive astrocytes were apparently damaged two days after both ischemiae. At five days after ischemiae, astrocyte endfeet around capillary endothelial cells were severely ruptured. They were more severely ruptured by severe ischemia than by mild ischemia. However, the number of astrocytes stained with S100 was significantly higher in severe ischemia than in mild ischemia. These results indicate that the degree of astrogliosis, including the disruption (loss) of astrocyte endfeet following ischemia and reperfusion in the forebrain, might depend on the severity of ischemia and that the degree of ischemia-induced neuronal damage may be associated with the degree of astrogliosis.
Although cavernous hemangiomas occur frequently in the intracranial structures, they are rare in the spine. Most of spinal hemangiomas are vertebral origin and "pure" epidural hemangiomas not originating from the vertebral bone are very rare. Our spinal hemangioma case is extremely rare because of its "pure" epidural involvement and intralesional hemorrhage. A 64-year-old man presented with progressive paraparesis from two months ago. His motor weakness was rated as grade 4/5 in bilateral lower extremities. He also complained of decreased sensation below the T4 sensory dermatome, which continuously progressed to the higher dermatome level. Magnetic resonance imaging demonstrated thoracic spinal tumor at T3-T4 level. The tumor was located epidural space compressing thoracic spinal cord ventrally. The tumor was not involved with the thoracic vertebral bone. We performed T3-5 laminectomy and removed the tumor completely. The tumor was not infiltrating into intradural space or vertebral bone. The histopathologic study confirmed the epidural tumor as cavernous hemangioma. Postoperatively, his weakness improved gradually. Four months later, his paraparesis recovered completely. Here, we present a case of pure spinal epidural cavernous hemangioma, which has intralesional hemorrhage. We believe cavernous hemangioma should be included in the differential diagnosis of the spinal epidural tumors.
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