Spontaneous thoracic ventral spinal subdural hematoma mimicking a tumoral lesion: a case report.

INTRODUCTION: Spinal subdural hematoma is rare and can cause serious neurological symptoms. Sometimes, idiopathic spinal subdural hematoma can spontaneously occur without any identifiable underlying etiologies. In this report, we present such an uncommon case of paraplegia caused by idiopathic spinal subdural hematoma that was successfully managed by laminectomy. CASE PRESENTATION: A 45-year-old Chinese woman presented with sudden onset of progressive asthenia and numbness in both lower extremities, accompanied by difficulty in micturition. An initial non-contrast spinal magnetic resonance imaging at a local hospital suggested a spinal subdural tumoral hematoma at the T9 level. She was referred to our hospital and an emergency laminectomy from T8 to T10 was performed 22 hours after onset of her initial symptoms. However, nothing but a hematoma was identified during the operation, and a final diagnosis of spontaneous acute spinal subdural hematoma was concluded. She had partial return of sensations and voluntary movement after the operation. CONCLUSIONS: On imaging findings, spinal subdural hematoma could manifest as focal and independent from the dura matter, and, therefore, it should be included in the differential diagnosis of medullary compressive lesions.

[Expression and function of autophagy after ischemia/reperfusion in rats hippocampus neuron].

OBJECTIVE: To explore the expression of autophagy after ischemia/reperfusion and its possible function in rats hippocampus neurons. METHODS: After 2 hours oxygen-glucose deprivation and different periods time of reperfusion (OGD/R) treatment in primary hippocampal neurons, neuron viability was evaluated by MTT assay, specific structure of autophagosome and specific protein of autophagy microtubule-associated protein 1 light chain 3 B (LC3B) were detected by transmission electron microscope and immunofluorescence respectively. The inhibitor of autophagy 3-Methyladenine (3-MA) was also used to exam the viability of neurons. RESULTS: Treatment by OGD/R markedly reduced neuronal viability. Compared to the control group, autophagy existed in different time periods after OGD/R shown both in transmission electron microscope and immunofluorescence. Application of 3-MA significantly reduced neuronal viability. CONCLUSION: Oxygen-glucose deprivation can activate autophagy in rat hippocampus neurons, which may resist the injury during ischemia/reperfusion.