Rapid Ossification of Epidural Hematoma in a Child: A Case Report / 대한신경손상학회지

The author present a rare case of rapid ossification of epidural hematoma (EDH) in a 5-year-old boy. At admission, the computed tomography (CT) revealed an EDH on left temporoparietal region. On the follow-up CT scan doing 14 days after traffic accident, the expansion of the former hematoma was not visible, but the hematoma accompanied by the thin hyperdense layer on the dura. On follow-up CT scans, the hematoma was decreased but the ossified layer progressing. After 6 months of conservative therapy, the hematoma was fully absorbed and the ossified lesion merged to inner table of the skull. Hence, rapid ossification of an EDH should be considered in children and serial follow-up CT scans must be conducted.

Metronidazole Induced Encephalopathy with Peripheral Polyneuropathy in Patient with Spinal Cord Injury

Metronidazole may produce a number of neurologic side effects including peripheral neuropathy, seizure, encephalopathy. We experienced neurological side effects of metronidazole. The 32-year-old female patient with spinal cord injury was diagnosed as encephalophathy and peripheral polyneuropathy resulting from complication of metronidazole. It was difficult to diagnose at first glance using clinical findings because of paraplegia due to spinal cord injury. But through magnetic resonance imaging with diffusion weighted imaging and electrophysiologic study, the patient showed to have characteristic abnormalities that of a person suffering from metronidazole-induced encephalopathy and peripheral polyneuropathy. Whether the symptoms were caused by a peripheral nerve lesion or MIE, the patient's paraplegia prevented to appear other symptoms, such as ataxic gait and seizure, from manifesting. In such case as this, an active differentiated diagnosis is crucial.

Metronidazole Induced Encephalopathy with Peripheral Polyneuropathy in Patient with Spinal Cord Injury

Metronidazole may produce a number of neurologic side effects including peripheral neuropathy, seizure, encephalopathy. We experienced neurological side effects of metronidazole. The 32-year-old female patient with spinal cord injury was diagnosed as encephalophathy and peripheral polyneuropathy resulting from complication of metronidazole. It was difficult to diagnose at first glance using clinical findings because of paraplegia due to spinal cord injury. But through magnetic resonance imaging with diffusion weighted imaging and electrophysiologic study, the patient showed to have characteristic abnormalities that of a person suffering from metronidazole-induced encephalopathy and peripheral polyneuropathy. Whether the symptoms were caused by a peripheral nerve lesion or MIE, the patient's paraplegia prevented to appear other symptoms, such as ataxic gait and seizure, from manifesting. In such case as this, an active differentiated diagnosis is crucial.

Role of Nitric Oxide in Leukocyte-Endothelial Interaction in Cerebral Venules during Reperfusion after Global Ischemia

OBJECTIVE: Reactive oxygen metabolites and polymorphonuclear leukocytes have been implicated in the pathophysiology of reperfusion injury. The mechanisms involved in superoxide-mediated leukocyte adherence remain unclear, however, nitric oxide(NO) may contribute to this response. The present study is undertaken to elucidate mechamisms controlling NO based mechanisms that regulated leukocyte-endothelial interactions in the cerebral vasculature after global cerebral ischemia and reperfusion. METHODS: Pial venular leukocyte adherence of anesthetized newborn piglets was quantified by in situ fluorescence videomicroscopy through closed cranial windows during basal conditions and during 2hours of reperfusion after global ischemia induced by 9minutes of asphyxia. Nitric oxide synthase(NOS) was inhibited by local window superfusion of L-nitroarginine(NA); superfusion of sodium nitroprusside(SNP) was used to donate NO. RESULTS: The mean number of adherent leukocytes to cerebral venules in the 9minutes asphyxia and 2hours reperfusion group were 161+/-19 compared with 13+/-4 in the nonasphyxial group. Superfusion of L-NA through the cranial window for 2hours resulted in leukocyte adherence similar to that observed during the initial 2hours of reperfusion after asphyxia. Leukocyte adherence was not additionally increased in asphyxic animal treated with L-NA. SNP inhibited asphyxia induced leukocyte adherence back to control levels. CONCLUSIONS: Nitric oxide inhibits leukocyte adherence to cerebral venules during the initial hours of reperfusion after asphyxia, and that NO supplementation inhibit asphyxia induced leukocyte adherence back to control levels. These results indicate that NO is an important factor in ischemia-reperfusion induced leukocyte adherence.