Journal of neurosurgery
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Journal of neurosurgery · Aug 2002
Absence of movement disorders after surgical resection of glioma invading the right striatum.
Despite the high frequency of striatal lesions, the rate of movement disorders reported in the literature is lower than expected (< 10%). To maximize the extent of resection in low-grade gliomas invading the right striatum, the authors performed a striatal resection in a series of 14 patients, observed the lack of movement disorders following these procedures, and discuss herein the mechanisms likely to explain these findings. ⋯ These findings show that the nondominant striatum can be removed in cases of glioma invasion without inducing even transitory movement disorders. This phenomenon could be explained by the combined resection of the two classes of striatal neurons, an associated pallidal and thalamocortical resection, or a compensatory recruitment of parallel networks. Thus, these results may allow the surgeon to maximize the extent of removal of low-grade gliomas involving basal ganglia. Striatal resection may induce transient hemiparesis and "athymhormic syndrome," however, necessitating that the patient be clearly informed before surgery.
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Journal of neurosurgery · Aug 2002
Ultra-early surgery for aneurysmal subarachnoid hemorrhage: outcomes for a consecutive series of 391 patients not selected by grade or age.
This study was undertaken to determine the outcomes in an unselected group of patients treated with semiurgent surgical clipping of aneurysms following subarachnoid hemorrhage (SAH). ⋯ The major risk of rebleeding after SAH is present within the first 6 to 12 hours. This risk of ultra-early rebleeding is highest for patients with poor grades. Securing ruptured aneurysms by surgery or coil placement on an emergency basis for all patients with SAH has a strong rational argument.
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Journal of neurosurgery · Aug 2002
Role of magnesium in the reduction of ischemic depolarization and lesion volume after experimental subarachnoid hemorrhage.
Ischemia-induced tissue depolarizations probably play an important role in the pathophysiology of cerebral ischemia caused by parent vessel occlusion. Their role in ischemia caused by subarachnoid hemorrhage (SAH) remains to be investigated. The authors determined whether ischemic depolarizations (IDs) or cortical spreading depressions (CSDs) occur after SAH, and how these relate to the extent of tissue injury measured on magnetic resonance (MR) images. In addition, they assessed whether administration of MgSO4 reduces depolarization time and lesion volume. ⋯ On the basis of their data, the authors suggest that CSDs play a minor role, if any, in the acute pathophysiology of SAH. Administration of Mg++ reduces the cerebral lesion volume that is present during the acute period after SAH. The neuroprotective value of Mg++ after SAH may, in part, be explained by a reduction in the duration of the ID of brain cells.