Journal of neurosurgery
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Journal of neurosurgery · Feb 1996
Effects of spinal cord stimulation on the flexor reflex and involvement of supraspinal mechanisms: an experimental study in mononeuropathic rats.
The physiological mechanisms responsible for pain relief caused by spinal cord stimulation (SCS) are essentially unknown and recent experimental data are sparse. In the present study the authors explored the possible involvement of supraspinal mechanisms in the effects of SCS applied in rats with experimental mononeuropathy produced by sciatic nerve ligation according to the method of Bennett and Xie or that of Seltzer, et al. Confirming results of a previous study undertaken by the authors, the thresholds of the early component of the flexor reflex (latency 8-12 msec), which is mediated by A fibers, were significantly lower in the nerve-ligated than in the intact leg. ⋯ There was no effect on the late component of the reflex in either leg. The results indicate that this effect of SCS in mononeuropathic rats does not necessarily involve supraspinal mechanisms; instead SCS is operative at a spinal, segmental level. In view of the similarities between the effects of therapeutic SCS on cutaneous hypersensibility in patients with peripheral neuropathic pain and the effects demonstrated in neuropathic rats, the clinical pain relief achieved with SCS may be produced, at least partially, by intraspinal mechanisms.
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Journal of neurosurgery · Feb 1996
Case ReportsMiddle cerebral artery dissecting aneurysm with persistent patent pseudolumen. Case report.
The extremely rare condition of an ischemic right middle cerebral artery dissecting aneurysm with persistent patent pseudolumen is described. In the majority of cases of dissecting aneurysms, the pseudolumen persists for a very short time, probably because reentry from the pseudolumen is minimal or nonexistent. In contrast, the present case was assumed to have sufficient reentry from the bypass flow in the pseudolumen. Endothelial formation both in the true lumen and the pseudolumen was suggested as the possible mechanism of the stabilized double lumen.
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Journal of neurosurgery · Feb 1996
Case ReportsPosttraumatic intradiploic meningoencephalocele. Case report.
A case of posttraumatic intradiploic meningoencephalocele is reported. The patient presented with a progressively enlarging lump in the left parietal area approximately 8 months after a blunt trauma. ⋯ These findings were confirmed at surgery. In addition, the cyst was found to have a lining of arachnoid membrane.
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To determine the incidence of, and risk factors for, the occurrence of rebleeding between admission and early operation (ultra-early rebleeding) in patients with spontaneous subarachnoid hemorrhage (SAH), the authors reviewed the cases of 179 patients admitted within 24 hours after their last attack of SAH. Thirty-one (17.3%) of these patients had ultra-early rebleeding despite scheduling of early operation (within 24 hours after admission). The incidence of rebleeding significantly decreased as the time interval between the last attack and admission increased. ⋯ Multivariate analysis revealed that the following three factors were independently associated with ultra-early rebleeding: the level of enhancement of platelet sensitivity; the time interval between the last attack and admission; and the level of thrombin-antithrombin complex. On the basis of these findings, the authors suggest that many of the risk factors for ultra-early rebleeding are interrelated. A particularly high risk of ultra-early rebleeding was observed in those patients 1) who had platelet hypoaggregability; 2) who were admitted shortly after their last SAH; and 3) whose thrombin-antithrombin complex levels were extremely high and were thus in severe clinical condition.
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The mechanism by which intracerebral hemorrhage leads to the formation of brain edema is unknown. This study assesses the components of blood to determine if any are toxic to surrounding brain. Various solutions were infused stereotactically into the right basal ganglia of rats. ⋯ On the other hand, activation of the coagulation cascade by adding prothrombinase to plasma did produce brain edema. The edema response to whole blood could be prevented by adding a specific thrombin inhibitor, hirudin, to the injected blood. This study indicates that thrombin plays an important role in edema formation from an intracerebral blood clot.