The contractile activity of arterial muscle cells is controlled by intracellular free Ca concentration. The membrane system, both of cell surface and internal organs, seemed to be responsible for controlling the myoplasmic Ca level. Calcium antagonists block cellular Ca in arterial strips in vitro.
In this study, the vasodilating effect of several Ca antagonists on late spasms in vivo was examined using dogs. Cinnarizine (Eisai), nifedipine (Bayer), verapamil (Eisai) and sodium nitroprusside were used as Ca antagonists.
Experimental vasospasms were induced in adult dogs by injecting about 5 ml, of fresh arterial blood into the cisterna magna.
Doses in this experiment were determined according to the drug's effectiveness in relaxing the contracted bovine basilar artery in Krebs solution. 5-HT-induced contraction was inhibited to about 20% of the maximum tension by 10^-6 M cinnarizine. The presence of 10^-6 M cinnarizine abolished K⁺-induced contraction almost completely. Similar results were obtained with verapamil and sodium nitroprusside. The suitable dose of nifedipine was 10^-8 M. The required dose of each drug was injected by one shot into the vertebral artery of a dog with cerebral vasospasms. Dilatation of the cerebral arteries was monitored by angiography 5, 15 and 30 minutes after administration of the drugs. Blood pressure, intracranial pressure and pulse rate were measured during intravenous application of these drugs in normal dogs.
Administration of Ca antagonists-cinnarizine, verapamil, sodium nitroprusside and nifedipine-released the late spasm in vivo for 15 to 30 minutes. Cinnarizine had no effect on blood pressure, intracranial pressure and pulse rate, while the other drugs decreased the blood pressure. Verapamil also decreased the pulse rate slightly. Therefore, cinnarizine gave the most satisfactory results. Sodium nitroprusside seemed to be dangerous because it markedly decreased blood pressure and increased intracranial pressure.
The author concludes, in general, that administration of any Ca antagonist is quite useful for the treatment of experimental late vasospasms.

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In vitro experiments were carried out to determine the inhibitory effects of several agents, especially a Ca⁺⁺ -blocker, nifedipine, on hemoglobin-induced contractions of dog basilar arteries.
Agents tested included methysergide, phentolamine, mepyramine, and aspirin. None of these agents significantly inhibited hemoglobin-induced contractions. This indicates that serotonin, norepinephrine, histamine, and prostaglandins are not involved in the contractile activity of hemoglobin. The inhibitory effect of cyclic AMP on hemoglobin-induced contractions was slight even at high concentrations.
In Ca⁺⁺-free solution, basilar arteries showed no response to hemoglobin. Nifedipine was found to be a highly potent inhibitor of hemoglobin-induced contractions. The inhibitory effect of nifedipine on hemoglobin-induced contractions was greater than that of papaverine.
These data suggest that nifedipine might be useful in the treatment of vasospasms following rupture of an aneurysm.

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Pathophysiological conditions following rupture of an aneurysm have not been sufficiently clarified. The present study was intended to analyze cerebral blood flow (CBF) and metabolism in patients with ruptured aneurysm sequentially. CBF measurements were performed 95 times on 53 patients by ¹³³Xe intracarotid injection method. O₂ content was measured by a spectrophotometer and gas analyzer. Glucose, lactate, and pyruvate were measured by enzymatic methods.
The reduction of CBF, CMRO₂, and CMRglucose and the increase of CVR correlated well with the severity of the clinical grade of Hunt & Hess in patients within 30 days after subarachnoid hemorrhage (SAH). It was found that the cerebral metabolism of the patients with diffuse type spasms inclined to anaerobic glycolysis. The reduction of CBF and CMRO₂ observed within 3 days after SAH, when spasm was rarely observed in carotid angiography, was probably caused by disturbances in micro-circulation.
Discrepancies of the cerebral metabolism and CBF, for example, reduction of CMRO₂ with almost normal CBF in Grade I and II, was observed in the period of recovery. High CSF pressure and high CSF lactate correlated relatively well with the severity of the clinical grades. CSF pressure and lactate content in CSF decreased gradually 14 days after SAH, and returned to the normal ranges 31 days after SAH. When CSF pressure was below 200 mmH₂O₂ its increase was correlated slightly with an increase of CBF, while CBF was inclined to decrease with the increase of CSF pressure when it was over 200 mmH₂O. In Grade IV patients, CBF and metabolism were disturbed in every period after SAH, and the prognosis was poor.

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During the period from October, 1977 through September, 1979, 1 1 cases of the spinal cord tumors were studied by either an EMI whole Body Scanner, CT 5005 (slice thickness: 13 mm) or EMI Head Scanner, CT 1010 (slice thickness: 10 mm). In eight cases except for lipomas, enhancement with intravenous injection of contrast medium (150 ml of 65% angiografin) was performed. Five cases received an intrathecal injection of metrizamide (170-250mgI/ml, 7-10 ml). The diagnoses were neurinomas in four cases, lipomas in three cases, meningiomas in two cases and astrocytomas in two cases.
Plain spinal CT is of diagnostic value in detecting bone changes and lipoma. Meningioma and neurinoma showed positive contrast enhancement and the extraspinal extension of the tumor is accurately outlined by spinal CT. CT metrizamide myelography visualizes the subarachnoid space and makes it possible to localize the tumor in the spinal canal in relation to the spinal cord. Localization of the tumor in axial plane is difficult and it is impossible to demonstrate the vascularity of the tumor and its relationship to the vessels.

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A treatment method for dural arterio-venous malformation of the posterior fossa was reported. The reported case was a 53 year-old male. The drainage veins were transverse and sigmoid venous sinuses. Under local anesthesia, 5 ml of aron alpha was injected through the occipital artery which was one of the main feeding arteries. Postoperative angiography revealed no opacification of the nidus even from the untreated tentorial artery. From this result it was considered that AVM was embolized almost completely. No side effects or complications of any nature occurred and the patients was discharged in ambulatory state. CT and cerebral angiography were performed six months after the operation with no evidence suggestive of recurrences. At present, one and half years after the operation, he lives well with no symptoms of recurrence.

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The dynamics of contrast medium were studied in RGC₅-transplanted and RSV-induced primary brain tumors of rats by soluble substance macro and micro-autoradiography. The distribution of ¹²⁵I-labeled meglumine diatrizoate in the brain, brain tumors and the liver was followed up to two hours after intravenous administration.
Immediately after administration, the contrast medium flowed in the blood vessels of the brain, but not in those of the tumors. It took about five minutes until the contrast medium flowed in almost all the blood vessels of the viable tumor tissues. This clearly proved a distinct delay in the vascular circulation within the tumor tissues in spite of the increased vascularity. Once it flowed in the blood vessels of the tumors, the contrast medium was rapidly extravasated into the viable tumor parenchyma five minutes after the administration. Spreading from the viable tumor tissues, the contrast medium accumulated in the area of central necrosis including the cyst, and the concentration of contrast medium in the necrotic zone and cyst became almost equal to that in the viable tumor tissues after about thirty minutes. The velocity of the washing out of contrast medium from the tumor tissues was very slow compared with that from the blood vessels or brain tissues. Two hours after administration, the contrast medium still remained dense in the areas of central necrosis, especially in the cyst, in contrast to the areas of the viable tumor tissues. In the peritumoral brain tissues, the contrast medium was not extravasated diffusely from the vessels. However, the contrast medium slowly spread from tumor tissues showing a high concentration of contrast medium to the peritumoral regions one or two hours after administration.
There was moderate and diffuse distribution of contrast medium in the brain tissues distant from the tumors only immediately after administration, possibly because of the transient breakdown of the blood-brain barrier due to high osmolality of the contrast medium. However, there was no distinct uptake of contrast medium in such areas thereafter.
The dynamics of the contrast medium were studied by calculating the tissue-blood ratio (TBR) of the concentration of the contrast medium in macroautoradiography. The TBR calculation enabled us to analyse the dynamics of the contrast medium quantitatively. This method shows the characteristics of the dynamics of the contrast medium in the brain and brain tumors and might be useful in the differential diagnosis of various lesions.

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A case of cerebral venous angioma is presented. A 13-year-old boy suffering from uncontrollable adversive seizures to the left was admitted to the Kagoshima University Hospital.
Neurologically slight hemiparesis on the left side was detected. In the electroencephalogram, spike-and-wave complexes were seen dominantly in the right frontal region. ^99mTc-pertechnetate brain scan demonstrated no abnormal activities.
Right common carotid angiography demonstrated no abnormalities in the arterial and capillary phases. However in the venous phase, a caput medusae-like or cone-shaped lesion was found in the white matter of the right frontal lobe and it consisted of numerous small veins. These veins drained centrally into a single large channel which coursed transcerebrally to reach the cortical surface and then drained into the vertex portion of the superior sagittal sinus.
Computerized tomography (CT) before contrast enhancement demonstrated a slightly atrophic area localized in the right frontal lobe. After contrast enhancement, linear high density was seen in the subcortex of the right frontal lobe.
Right frontal craniotomy was performed. The right frontal cortex was slightly atrophic and the angioma was extirpated surgically.
Postoperatively, the patient was uneventful and discharged without any neurological defects. Adversive seizures disappeared.
Histological examinations of the specimen revealed that these malformations consisted of numerous small veins separated by neural tissue and a cerebral venous angioma was diagnosed.
Cerebral venous angioma is relatively common at autopsy, whereas clinically, it is the rarest type of cerebral vascular malformations. In the literature, only 18 cases of cerebral venous angiomas demonstrated by angiography were reported, and there has been only one report of CT findings in cerebral venous angioma.

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A sequential study with computerized tomography (CT-scan) of two cases of chronic subdural hematoma was reported.
Case 1 was a 67-year-old man who had a mild head injury. The initial CT-scan taken after 24 days of his injury showed bilateral frontotemporal extracerebral low density areas. This was diagnosed as subdural effusion because of its location, shape and the Hounsfield unit (11.0). He was admitted to our hospital with complaints of headache, nausea, vomiting and left hemiparesis. The CT-scan on the 41st day after his injury showed bilateral extracerebral high density areas instead of the previous low density. An operation was performed, and membranes of a subdural hematoma were observed.
Case 2 was a 47-year-old man, who was admitted because of a mild head injury. The initial CT-scan (25 days) revealed bilateral extracerebral low density areas. This low density showed 11.7 in Hounsfield units suggesting subdural effusion. Follow-up CT-scans (after 76 days, 111 days, 113 days) demonstrated that chronic subdural hematoma had developed consequent on the post-traumatic subdural effusion. An operation disclosed a wellencapsulated hematoma.
The conclusions obtained in this study were as follows; (1) Development of the hematoma membrane does not start immediately after head injury. (2) Subdural effusion is formed a few days after head injury. (3) Then, neomembrane begins to form during a certain period of subdural effusion. (4) Existence of the isolated cerebrospinal fluid between the dura and arachnoid membrane is the most important factor forming subdural hematoma. (5) Repeated hemorrhaging into the cavity from this neo-membrane may cause chronic subdural hematoma.

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