Journal of neurosurgery
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Journal of neurosurgery · Feb 2002
Case ReportsCerebellar hemorrhage arising postoperatively as a complication of supratentorial surgery: a retrospective study.
Postoperative cerebellar hemorrhage as a complication of supratentorial surgery is an increasingly recognized clinical entity. So far, it has remained unclear whether this complication constitutes an intraoperative or postoperative event. The observation of such cases prompted the authors to analyze retrospectively their series of supratentorial craniotomies. The aim of this study was to determine the incidence of cerebellar hemorrhage and its temporal relationship to supratentorial surgery. ⋯ The authors have demonstrated that cerebellar hemorrhage as a complication of supratentorial surgery arises not as an intraoperative event, but as a postoperative event. Resective nontumorous temporal lobe procedures place patients at particular risk for this complication. Evidence suggests that the complication might be precipitated by postoperative suction drainage.
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Journal of neurosurgery · Feb 2002
Case ReportsFar-lateral approach to intradural lesions of the foramen magnum without resection of the occipital condyle.
The goal of this study was to determine whether drilling out the occipital condyle facilitates surgery via the far-lateral approach by comparing data from 10 clinical cases with that from studies of eight cadaver heads. ⋯ On the basis of their findings the authors conclude that removal of the occipital condyle is not necessary for the safe and complete resection of anterior intradural foramen magnum tumors.
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Journal of neurosurgery · Feb 2002
Brain edema after experimental intracerebral hemorrhage: role of hemoglobin degradation products.
The mechanisms involved in brain edema formation following intracerebral hemorrhage (ICH) have not been fully elucidated. The authors have found that red blood cell lysis plays an important role in edema development after ICH. In the present study, they sought to determine whether degradation products of hemoglobin cause brain edema. ⋯ Hemoglobin causes brain edema, at least in part, through its degradation products. Limiting hemoglobin degradation coupled with the use of iron chelators may be a novel therapeutic approach to limit brain edema after ICH.
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Journal of neurosurgery · Feb 2002
Evaluation of the healing process after dural reconstruction achieved using a free fascial graft.
This study was undertaken to investigate the healing process and to delineate factors important for the survival of free fascial grafts used for dural repair. ⋯ Fascial grafts tolerated extraordinary intracranial pressures at 1 week postoperatively. Free fascial grafts can heal with durable fibrous tissue without the presence of a blood supply from an overlying vascularized flap.
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Journal of neurosurgery · Jan 2002
Cerebral tissue PO2 and SjvO2 changes during moderate hyperventilation in patients with severe traumatic brain injury.
The aim of this study was to investigate the effects of moderate hyperventilation on intracranial pressure (ICP), jugular venous oxygen saturation ([SjvO2], an index of global cerebral perfusion), and brain tissue PO2 (an index of local cerebral perfusion). ⋯ Ninety-four tests consisting of 20-minute periods of moderate hyperventilation (27-32 mm Hg) were performed on different days in 36 patients with severe traumatic brain injury (Glasgow Coma Scale score < or = 8). Moderate hyperventilation resulted in a significant reduction in average ICP, but in seven tests performed in five patients it was ineffective. The response of SjvO2 and brain tissue PO2 to CO2 changes was widely variable and unpredictable. After 20 minutes of moderate hyperventilation in most tests (79.8%), both SjvO2 and brain tissue PO2 values remained above the lower limits of normality (50% and 10 mm Hg, respectively). In contrast, in 15 tests performed in six patients (16.6% of the studied population) brain tissue PO2 decreased below 10 mm Hg although the corresponding SjvO2 values were greater than 50%. The reduction of brain tissue PO2 below 10 mm Hg was favored by the low prehyperventilation values (10 tests), higher CO2 reactivity, and, possibly, by lower prehyperventilation values of cerebral perfusion pressure. In five of those 15 tests, the prehyperventilation values of SjvO2 were greater than 70%, a condition of relative hyperemia. The SjvO2 decreased below 50% in four tests; the corresponding brain tissue PO2 values were less than 10 mm Hg in three of those tests, whereas in the fourth, the jugular venous O2 desaturation was not detected by brain tissue PO2. The analysis of the simultaneous relative changes (prehyperventilation - posthyperventilation) of SjvO2 and brain tissue PO2 showed that in most tests (75.5%) there was a reduction of both SjvO2 and brain tissue PO2. In two tests moderate hyperventilation resulted in an increase of both SjvO2 and brain tissue PO2. In the remaining 17 tests a redistribution of the cerebral blood flow was observed, leading to changes in SjvO2 and brain tissue PO2 in opposite directions. CCONCLUSIONS. Hyperventilation, even if moderate, can frequently result in harmful local reductions of cerebral perfusion that cannot be detected by assessing SjvO2. Therefore, hyperventilation should be used with caution and should not be considered safe. This study confirms that SjvO2 and brain tissue PO2 are two parameters that provide complementary information on brain oxygenation that is useful to reduce the risk of secondary damage. Changes in SjvO2 and brain tissue PO2 in opposite directions indicate that data obtained from brain tissue PO2 monitoring cannot be extrapolated to evaluate the global cerebral perfusion.