The effects of the Ca²⁺ entry blocker nilvadipine on the diameter of the brain surface microvessels of rats were studied in vivo using intravital fluorescence microscopy and a closed cranial window technique under an intracranial pressure of 5-7 mmHg. Intravenous Na⁺-fluorescein was used as a blood-brain barrier (BBB) and vessel marker. The BBB function, as determined by the barrier marker, remained intact during the entire observation period. Nilvadipine (10^-10-10^-6M) and/or vehicle were dissolved in artificial cerebrospinal fluid (CSF). Superfusion of the brain surface with artificial CSF with and without vehicle had no effect on vessel diameters. Nilvadipine dilated pial arterioles in a dose-dependent manner. The arterioles were dilated significantly at concentrations of ≥10^-9M when compared with resting diameters. The diameters of venules were not affected by nilvadipine. The results suggest a possible mechanism for the nilvadipine-induced increase in the cerebral blood flow under physiological conditions.

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The magnitude and time course of histological and neuroradiological changes due to interstitial hyperthermia in normal cerebral white matter were investigated in eight adult Japanese monkeys. A cooling system enveloping a 2450-MHz microwave antenna was inserted stereotactically into the brain under general anesthesia. A point located 5 mm away from the surface of the cooling system was used as the reference point (RP). Hyperthermia was given to maintain the RP at 43°C for 60 minutes. Two animals were sacrificed under general anesthesia following the intravenous administration of Evans blue, immediately and 1, 3, and 7 days after treatment. After removing the brain, histological changes were investigated. Magnetic resonance (MR) imaging was performed at 1, 3, and 7 days after treatment. Evans blue extravasation was most prominent in the region heated to 43°C or above immediately after treatment. MR imaging showed obvious enhancement in the region heated to 43°C or above I day after treatment, related to the disruption of the blood-brain barrier (BBB) by hyperthermia. Three days after treatment, ring-like enhancement with a central low-intensity area was seen in the region heated to about 43°C, caused by BBB disruption and slight neovascularization. One week after treatment, an enhanced ring was observed in the region heated to less then 43°C which surrounded a low-intensity area. The enhancement seen 1 week after treatment was caused by prominent neovascularization. T₂-weighted imaging showed a high-intensity area, caused by edema, most prominent 3 days after treatment. Thus chemotherapeutic agents should be given just before the end of hyperthermia.

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The metabolism of the brain was investigated in eight patients with peritumoral edema, six patients with ischemic stroke, and 28 normal controls using proton magnetic resonance (MR) spectroscopy. The MR studies were performed using a 1.5-T whole-body imaging and spectroscopy system with a 1500-msec repetition time (TR) and a 270-msec echo time (TE). The peak areas for N-acetyl-aspartate (NAA), choline-containing compounds (Cho), creatine and phosphocreatine (Cr), and lactate (Lac) were measured, and the NAA/Cr, Cho/Cr, and Lac/Cr ratios were calculated. To quantify and compare the serial spectra, relaxation effects were investigated by acquisitions at two different points (TRs or TEs) and by monoexponential fitting. The normal NAA/Cr and Cho/Cr ratios were 2.76 and 1.09, respectively. Lac could not be identified in normal brains. In ischemic stroke and peritumoral edema, significantly increased Lac/Cr and decreased NAA/Cr ratios were observed. Resolution of peritumoral edema was associated with normalized NAA/Cr ratio and disappearance of Lac. The T₁ relaxation times of the metabolites were similar in normal brain and peritumoral edema, but the T₂ values were significantly shortened. Serial measurements of T₂ values in two patients with peritumoral edema showed gradual normalization corresponding to improvement of the edema. To absolutely quantify metabolite concentrations in edema, changes in relaxation times should be considered.

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The usefulness of magnetic resonance (MR) angiography using the three-dimensional time-of-flight method for the characterization of symptomatic middle cerebral artery (MCA) occlusive lesions was evaluated in 10 patients with MCA occlusion and 10 with MCA stenosis. All lesions were symptomatic and documented by conventional angiography. There was no false-negative MR angiogram that failed to demonstrate the MCA occlusive lesion. MR angiography correctly evaluated the location of lesions and the difference between stenosis and occlusion. Stenosis appeared as a focal signal loss (< 1.0 cm) of the MCA at the site of stenosis, and occlusion as a complete signal loss of the MCA distal to the site of occlusion. However, MR angiography could not distinguish diffuse stenosis and one point stenosis demonstrated by conventional angiography. MR angiography is a useful noninvasive, diagnostic method for evaluating occlusive lesions of the MCA in symptomatic patients.

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A strategy for surgical management, including the approach and preoperative evaluation, of pituitary adenoma invading the skull base is described. Preoperative evaluation requires a balloon occlusion test of the internal carotid artery (ICA) to determine tolerance to occlusion. Failure to tolerate occlusion indicates administration of brain protective agents and/or a bypass procedure before tumor removal. The transsphenoidal, pterional, orbitofrontomalar, and infratemporal fossa approaches are all suitable for various tumor locations. A combined orbitofrontomalar and extended frontal approach allows removal of tumor with extensive invasion and is suitable for bypass procedures. Preoperative evaluation of ICA occlusion can prevent development of hemodynamic stroke.
We treated five patients with pituitary adenoma invading the skull base, including two primary and three recurrent cases. All symptoms improved, but temporary oculomotor nerve disturbance occurred in three patients and anosmia in one. Reoperations for recurrent pituitary adenomas were effective in reversing the symptoms. No hemodynamic stroke was seen postoperatively. These tumors, except for drug-responsive cases, are indicated for skull base surgery.

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One case of an aneurysm in the P₃ segment and two cases of aneurysms in the P₄ segment of the posterior cerebral artery are described. The P₃ aneurysm in a 60-year-old female and a P₄ aneurysm in a 63-year-old male were clipped or coated via the occipital interhemispheric approach. The other P₄ aneurysm in a 73-year-old female was clipped via a hematoma cavity. The occipital interhemispheric approach should be selected for small or large P₃ aneurysms and for P₄ aneurysms associated with slack brain, as brain retraction is minimal and the approach to the aneurysm is straightforward.

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Six infective endocarditis patients who developed cerebral bacterial aneurysm were reviewed to clarify the indications and timing for cerebral angiography to achieve early detection of unruptured aneurysms. All cerebral bacterial aneurysms were confirmed either angiographically or at autopsy. All patients were treated conservatively. Four patients died due to ruptured aneurysm. Four of the six patients showed the signs and symptoms of cerebral and/or systemic embolism, followed by rupture or detection of cerebral bacterial aneurysm. Prodromal signs and symptoms of embolism in patients with infective endocarditis should be considered as indicators for cerebral angiography to detect cerebral bacterial aneurysms before rupture.

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A 39-year-old male presented with rapidly growing recurrent primary intracranial malignant lymphoma, manifesting as intractable headache, recent memory disturbance, and left hemiparesis during the previous month. He had received irradiation and chemotherapy for primary intracranial malignant lymphoma 15 months before admission. Signs of uncal herniation developed soon after admission. High-dose intra-arterial corticosteroid infusion followed by intra-arterial chemotherapy (etoposide and cisplatin) successfully relieved the symptoms of uncal herniation. Magnetic resonance imaging demonstrated a dramatic remission in the size of the tumor and associated mass effect. Sequential administration of corticosteroid and chemotherapy agents is a possible treatment for recurrent malignant lymphoma.

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A 79-year-old male presented with recurrent maxillary ameloblastoma with intracranial invasion into the left orbit, previously histologically diagnosed as benign ameloblastoma. Skull x-ray films and computed tomography showed the multicystic mass had destroyed the skull base. The tumor was nearly completely removed. However, microscopic examination revealed residual tumor cells around the left optic nerve. Histological examination found no malignant transformation in the tumor specimen. Aggressive complete removal of maxillary ameloblastoma should be attempted even in cases of intracranial invasion.

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A 51-year-old female presented with an extremely unusual cerebellar porencephalic lesion manifesting as progressive cerebellar signs and cranial nerve pareses. T₁-weighted magnetic resonance imaging demonstrated a low-signal-intensity area in the left cerebellar hemisphere suggesting a cavity communicating with the fourth ventricle. Histological study showed the wall of the cavity contained nonspecific gliosis. A diagnosis of porencephaly was made.

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