The authors studied the venous drainage system and its impairment in relation to risk of hemorrhage in 108 cases of supratentorial arteriovenous malformation (AVM). The proportion of AVM's undergoing hemorrhage (hemorrhagic rate) was calculated in relation to: 1) the number of draining veins (one, two, or three or more); 2) the presence or absence of impairment in venous drainage (severe stenosis or occlusion in draining veins); and 3) the location of draining veins (deep venous drainage alone, superficial venous drainage alone, or a combination of the two). Statistical analysis demonstrated that AVM's with the following characteristics had a high risk of hemorrhage: 1) one draining vein (hemorrhagic rate 89% in 54 patients); 2) severely impaired venous drainage (hemorrhagic rate 94% in 18 patients); and 3) deep venous drainage alone (hemorrhagic rate 94% in 32 patients). The present study suggests that the venous drainage system of AVM's is significantly associated with the risk of hemorrhage of these lesions. Therefore, careful preoperative angiographic evaluation of the venous drainage system is mandatory for decision making in the management of patients with AVM's.

No abstract

Currently, superficial temporal artery-middle cerebral artery (MCA) anastomosis, encephalomyosynangiosis (EMS), and encephalo-duro-arterio-synangiosis are used to treat moyamoya disease and are reported to effectively improve ischemic symptoms. All are methods of reversing the flow of blood from the external carotid artery system into the cortical branches of the MCA. As moyamoya disease advances, these operations alone will predictably not correct the deterioration in blood flow in the territory of the anterior cerebral artery. It was noted in a case of moyamoya disease with intraventricular hemorrhage that a burr hole, made in the frontal region for drainage purposes, induced marked neovascularization. Since then, similar frontal burr holes have been made in five juvenile cases of moyamoya disease; this procedure involved making a burr hole in both frontal bones and incising both the dura and the arachnoid membrane. In two cases a frontal burr hole in both frontal bones and incising both the dura and the arachnoid membrane. In two cases a frontal burr hole was placed simultaneously with EMS, and in the others the frontal burr hole was made following EMS. The clinical symptoms improved after the frontal burr hole was made, and dynamic computerized tomography revealed improved circulation in the frontal regions. Together with conventional surgical therapy for juvenile cases of moyamoya disease, this operation is considered beneficial both to the circulation in the frontal region and for the protection of frontal brain function.

The authors describe three cases of cervical radiculomyelopathy caused by calcium pyrophosphate dihydrate crystal deposition disease (CPPDcdd). Radiological investigations revealed nodular calcifications, 5 to 7 mm in diameter, in the cervical ligamentum flavum compressing the spinal cord. Light microscopic, scanning electron microscopic, and x-ray diffraction studies were performed on all three surgical specimens obtained by laminectomy. In two of the cases x-ray microanalysis and transmission electron microscope studies were also performed. This study defined the presence of two patterns of crystal deposition in the ligamentum flavum. One is a nodular deposit, in which hydroxyapatite crystals are seen in the central part of the nodules, with calcium pyrophosphate dihydrate (CPPD) being distributed thinly around them. The other pattern is a linear deposit seen in multiple ligaments and composed of pure CPPD, which causes minimal thickening of the ligaments. A transitional pattern between the two types was also observed. This study revealed details of the nodular deposition of crystals in the ligamentum flavum and demonstrates that CPPDcdd and so-called "calcification of the ligamentum flavum" are the same disease: namely, CPPDcdd. Hydroxyapatite is assumed to have been transformed from CPPD.

The assay of serum NSE and MBP levels provides a reliable laboratory indicator of the degree of brain damage and allows early prediction of the prognosis in patients with acute head injury.

We investigated the relationship between radiological findings and the nature of the cyst fluid and histological findings of six Rathke's cleft cysts. The results show that the majority (five of six cases) of symptomatic Rathke's cleft cysts exhibit no enlargement of the sella turcica on plain x-rays, which may be helpful in differentiating cystic pituitary adenoma in the radiological diagnostic process. Three cases with large cysts showing high-intensity T1-weighted magnetic resonance images harbored abundances of cholesterol crystal and hemosiderin pigment in the cyst walls. The high signal intensity in magnetic resonance images of Rathke's cleft cysts may be explained by hemorrhage and a deposition of cholesterol crystal and may be considered in certain cases of Rathke's cleft cyst, especially when they are large.

The present study suggested that intracarotid administration of bFGF (100 ng) can reduce infarct size after MCA occlusion. It was speculated that the increased CBF in the penumbral areas of MCA may contribute to contraction of infarct size.

✓ The pressure gradient of the venous pathway between the cortical vein and superior sagittal sinus was measured in adult mongrel dogs by recording the pressures of the bridging vein, lateral lacuna (proximal portion), and superior sagittal sinus, together with the systemic blood pressure while gradually increasing the intracranial pressure up to the level of mean systemic blood pressure. The pressure gradient between the lateral lacuna and the superior sagittal sinus was also measured under increased intracranial pressure. Pressures of the bridging vein and lateral lacuna were constantly 50 to 250 mm H2O higher than the intracranial pressure, regardless of the level of intracranial pressure. An abrupt drop in the intraluminal pressure was observed at a point 1 to 2 mm proximal to the junction of the lateral lacuna and the superior sagittal sinus, regardless of the level of intracranial pressure. It is concluded that gradual stenosis of the parasagittal venous pathways took place 1 to 2 mm proximal to the junction between the lacuna and the superior sagittal sinus, and thus cortical venous pressure was maintained 50 to 250 mm H2O higher than intracranial pressure. The authors believe that an “intracranial venous pressure regulation mechanism” exists at the junction of the lateral lacuna and the superior sagittal sinus.