Peritumoral edema is one of the most serious complications of intracranial neoplasms; however, the exact pathogenesis of this condition is still unknown. To explore the effect of macrophages in brain tumors on the pathogenesis of peritumoral edema, 42 specimens of primary or metastatic brain tumors were studied. Frozen sections were examined by an immunoperoxidase staining technique with anti-Leu-M3 monoclonal antibody. Eight of 14 gliomas demonstrated Leu-M3-positive cell (macrophage) infiltration. The two glioblastomas showed a moderate or marked degree of macrophage infiltration. Twelve of 16 meningiomas demonstrated varying degrees of macrophage infiltration. All six metastatic brain tumors exhibited prominent macrophages in intra- and peritumoral tissues. Four acoustic neurinomas and two hemangioblastomas showed a slight to moderate degree of macrophage infiltration. Excellent correlation was found between the degree of macrophage infiltration seen on immunoperoxidase staining and the peritumoral edema detected on computerized tomography brain scans of patients with supratentorial tumors, especially meningiomas. Macrophages are known to secrete various substances (including arachidonate metabolites) that may interfere with vascular permeability. These data suggest that macrophages infiltrating brain tumors may play an important role in the pathogenesis of peritumoral edema.

Cervical spinal cord stimulation (SCS) was used to increase cerebral blood flow (CBF) in 10 patients with secured cerebral aneurysms in Hunt and Hess grade 3 or 4 and with Fisher group 3 subarachnoid hemorrhage (SAH). The patients underwent preemptive electrical stimulation through a percutaneous lead following aneurysm surgery. All patients also received hypervolemic therapy and nicardipine. Efficacy of the treatment was evaluated using xenon computed tomography and cerebral angiography. The CBF in the distribution of the middle cerebral artery significantly increased following SCS (p < 0.05). Four of 10 patients showed angiographic vasospasm, but none developed severe sequelae of cerebral vasospasm. The overall outcome was good or excellent in seven of the 10 patients. No serious adverse effects due to SCS were observed. Fluid management and calcium antagonist have a beneficial effect on cerebral vasospasm following SAH, but is not tolerated or is ineffective in some patients. SCS as an adjunctive therapy for cerebral vasospasm following SAH may have a favorable effect on outcome.

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Ruptured vertebrobasilar dissecting aneurysm is usually treated surgically because rebleeding negatively affects outcome. However, the risk of rebleeding decreases markedly once several hours have passed from the initial bleeding. Moreover, surgery-related complications are not rare. We describe seven patients with ruptured vertebrobasilar dissecting aneurysm. To prevent rebleeding during the acute stage, we treated all seven patients conservatively with fentanyl instead of emergency surgery. During the follow-up period (mean 20 months), no patient suffered rebleeding. Conservative treatment with fentanyl administration may be a good option for management of ruptured vertebrobasilar dissecting aneurysm during the acute stage.