Lumbar Epidural Varix Mimicking Disc Herniation.

Lumbar radiculopathy is generally caused by such well-recognized entity as lumbar disc herniation in neurosurgical practice; however rare pathologies such as thrombosed epidural varix may mimic them by causing radicular symptoms. In this case report, we present a 26-year-old man with the complaint of back and right leg pain who was operated for right L4-5 disc herniation. The lesion interpreted as an extruded disc herniation preoperatively was found to be a thrombosed epidural varix compressing the nerve root preoperatively. The nerve root was decompressed by shrinking the lesion with bipolar thermocoagulation and excision. The patient's complaints disappeared in the postoperative period. Thrombosed lumbar epidural varices may mimic lumbar disc herniations both radiologically and clinically. Therefore, must be kept in mind in the differential diagnosis of lumbar disc herniations. Microsurgical techniques are mandatory for the treatment of these pathologies and decompression with thermocoagulation and excision is an efficient method.

The neuroprotective effect of acute moderate alcohol consumption on caspase-3 mediated neuroapoptosis in traumatic brain injury: the role of lysosomal cathepsin L and nitric oxide.

Our aim in this study was to investigate the effect of moderate acute alcohol administration on cysteine protease mediated neuronal apoptosis and nitric oxide production in the traumatic brain injury. A total of 29 adult Sprague-Dawley male rats weighing 250-300 g were used. The rats were allocated into four groups. The first group was the control (sham-operated) group in which only a craniotomy was performed, the others were alcohol, trauma and trauma+alcohol groups. Caspase-3 enzyme activity in the trauma group increased significantly in comparison with the control group. The alcohol given group showed a decreased caspase-3 enzyme activity compared to the trauma group. The level of caspase-3 enzyme activity in the alcohol+trauma group decreased in comparison to the trauma group. SF/FEL ratio of cathepsin-L enzyme activity in the trauma group was significantly higher than in the control group. Our results indicate that moderate alcohol consumption may have protective effects on apoptotic cell death after traumatic brain injury. Protective effects of moderate ethanol consumption might be related to inhibition of lysosomal protease release and nitric oxide production.