It has been established that the contractile system in cerebral vascular smooth muscle involves myosin and actin, which form thick and thin filaments, respectively and that their activities are regulated by the intracellular free Ca²⁺ concentration. The membrane system, both the cell surface and intracellular organelles, seems to be responsible for controlling the myoplasmic Ca²⁺ level.
An attempt was made to show the localization of intracellular Ca²⁺, which might play a key role on the regulation of contractile elements in bovine cerebral arteries. The pyroantimonate precipitate method was used. For quantitative chemical analysis of the pyroantimonate precipitates, the sections were analyzed with an energy dispersive X-ray microanalyzer (EDAX 711) attached to a transmission scanning electron microscope; the output of the analyzer was processed by a computer system. A distinct peak at 3, 620 eV, which was considered as a combined peak of Sb-Lα and Ca-Kα lines, was always observed in all the precipitates examined, indicating that the precipitates may serve as a valid measure of Ca²⁺ localization.
When the muscle cells were fixed after 50 minutes of soaking in high-K Krebs solution (127 mM-K substituted for Na) containing 10.8 mM Ca, the precipitates were mostly observed at the plasma membrane, the sarcoplasmic reticulum, the mitochondria and the nuclei. It was not, however, possible to decide whether the precipitates on the plasma membrane were located on its inner surface or its outer surface. In this condition, the muscle cells were completely relaxed during fixation.
If the preparations were fixed without pretreatment, they showed marked tension development in response to the pyroantimonate-osmium solution. The precipitates were mostly distributed randomly in the myoplasm of the muscle cells fixed during mechanical activity, while the precipitates were rarely seen at the plasma membrane, the sarcoplasmic reticulum and the mitochondria.
The results obtained in these experiments are in general agreement with previous reports on different kinds of smooth muscles, strongly suggesting that the Ca²⁺ accumulated at the plasma membrane, the sarcoplasmic reticulum and the mitochondria is released into the myoplasm to cause contraction in bovine cerebral arterial smooth muscle.

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In the acute stage of selected cerebrovascular occlusive disease, it is essential to prevent irreversible neuronal changes caused by ischemic insult by restoring decreased cerebral blood flow through appropriate methods. As an active and non-surgical method for enhancement of perfusion flow, inhalation of carbon dioxide has been considered.
Previous experiments of the authors clarified that mild hypercapnia between 43 to 55 mmHg was effective in enhancing perfusion flow in the area of ischemia. However, an additional verification of effectiveness of mild hypercapnia was needed with respect to restoration of neuronal activity in ischemic brains.
Accordingly, somatosensory evoked potential (SEP) as well as regional cerebral blood flow (rCBF) were monitored under mild hypercapnia in ischemic brains of dogs produced by occlusion of a middle cerebral artery.
Under normocapnia, the primary component (V₁) of the evoked potential was depressed by 53.8% with a 31.3% decrease of rCBF 30 minutes following occlusion of a middle cerebral artery.
During mild hypercapnia, recovery of SEP by 63.4% was noted with an increase of rCBF by 23.4%.
The authors concluded that mild hypercapnia was beneficial not only in increasing rCBF but also in restoring neuronal activity in acute ischemic brains of a mild degree.

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Flow rates and flow patterns of cerebrospinal fluid shunts were evaluated in 55 cases of normally functioning shunts (Rickham-Holter shunts: 20, Pudenz shunts: 35). After approximately 0.05 ml of 100μ Ci of ^99mTcpertechnetate was injected into a reservoir, the radioactivity clearance half-time (T1/2) was determined. Then, a flow rate (F ml/min) was calculated according to the formula established in the previous studies: log₁₀ (F) = -1.8 log₁₀ (T1/2) +0.019 in the standard Rickham reservoir and logo (F)= -1.3 log₁₀ (T1/2)+0.087 in the Pudenz 12 mm reservoir. From the 109 observations evaluating flow rates and their patterns it became apparent that CSF flow through the implanted shunts was not continuous but rather sporadic, depending upon the patient's posture and the intraventricular pressure. The difference in the shunt devices showed no influence at all. In sitting positions flow rates of more than 0.1 ml/min were usually observed, whereas in supine positions flow rates ranged from 1.0 ml/min to 0.01 ml/min or below. When flow rates were determined sequentially in both sitting and supine positions, those in the sitting position were higher than those in the supine positions in 96%, and furthermore, in 33% the lowest flow rates were in the supine position. Flow rates and their patterns were found basically consistent in cases reexamined at long intervals of 10 days and 2, 6 and 12 months.

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CT-scans made it possible to estimate the age of intracranial hematomas which had been almost impossible in conventional radiological studies. However, attenuation values of hematomas only reflect the concentration of hemoglobin in the hematoma and do not always indicate the age of the hematoma. This report proposes the usefulness of measurement of the methemoglobin to total hemoglobin (oxyhemoglobin and methemoglobin) ratio to determine the hematoma age more accurately.
Both the attenuation of hematomas in CT and the concentrations of total hemoglobin, oxyhemoglobin and methemoglobin in the hematomas of 75 cases of intracerebral hematoma, 34 cases of acute and subacute extracerebral hematoma and 29 cases of chronic subdural hematoma were analysed. Using a phantom, the correlation between the attenuation values and the concentration of hemoglobin was also studied.
The results supported the previous reports that the attenuation values of hematoma depended mainly on the concentration of total hemoglobin. It was shown that, in cases of intracerebral hematoma and acute extracerebral hematoma, chronological decrease of the attenuation values was well correlated with the decrease in concentration of total hemoglobin and with the increase in the ratio of methemoglobin.
On the other hand, in more than half (69%) of chronic subdural hematomas, the attenuation values or the concentration of hemoglobin and the amount of methemoglobin were not well correlated with the elapsed time from the trauma. Their attenuation values were much higher, and the methemoglobin was much lower than those of the standard curves obtained from the cases of intracerebral hematomas. These findings strongly indicated that recurrent or intermittent hemorrhages had occurred during the enlarging process of chronic subdural hematomas. It was also suggested that hematomas with low ratios of methemoglobin might be rather fresh even with hypodense CT findings.

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Following neurosurgical operations, diabetes insipidus or SIADH is often observed, the former characterized b) polyuria, hypernatremia and a low plasma level of arginine vasopressin (AVP) ; and the latter by hyponatremie and a high plasma level of AVP. In this study, plasma levels of AVP, human growth hormone (HGH), nicotine stimulated neurophysine (NSN), estrogen stimulated neurophysine (ESN), sodium and creatinine; plasma osmolarity and urine output were measured during neurosurgical operations. Plasma levels of AVP, NSN, ES? and HGH were assayed by radio-immunoassay. Plasma AVP and NSN rose to the highest level towards the end of each operation in parallel with the change of plasma HGH levels. Significant correlation was observed betweerr the plasma levels of AVP [y: (pg/ml)] and NSN [x: (ng/ml)]; y=2.lx+6.5 (r=0.64, P<0.01). It is thought that the elevation of plasma levels of AVP and NSN towards the end of the operation is mainly caused by surgical stress.
There were no significant correlations between the level of AVP in plasma and plasma osmolarity or between the former and change in blood pressure during the period of observation. It is suggested that these two factor: which are important in regulating the AVP level under physiological conditions may not be critical in the elevation of AVP by neurosurgical procedures.
From the course of AVP levels in plasma, it was considered that surgical stress after manipulation of the dura mater may be the main factor evoking the course of AVP release, resulting in retention of free water.

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Of 14 patients of craniopharyngioma including seven cases in children under the age of 15 and seven cases in adults operated on between 1973 and 1979, 13 patients showed diabetes insipidus (DI) in the postoperative period.
Records of these 13 patients with DI after surgery on craniopharyngiomas were reviewed to find out any difference in incidence and duration of DI between children and adults. In 10 of these 13 cases, antiduretic hormone (ADH) in plasma was measured by radioimmunoassay. Of the 13 patients in this series, seven were children and six were adults. There was little difference in the duration of DI between children and adults. However, there were two early deaths in adult cases.
Plasma ADH levels of patients who had DI postoperatively were below 1.1 μU/ml. Plasma ADH values increased after administration of pitressin in one case.
There was a case which showed low value of plasma ADH below 0.5 μU/ml 40 months after surgery, although clinical manifestation of DI had been disappeared. It was suggested that to prevent fluid and electrolyte disturbances, early administration of pitressin was recommended with strictly controlled fluid input. It was also indicated that a long term follow-up would be necessary for the treatment of postoperative DI.

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Infantile acute subdural hematoma is clinically characterized by generalized convulsions, preretinal hemorrhage and bulging fontanelles occurring shortly after mild head injury mostly in infancy and in early childhood. In its mild form, the patient stays awake, though more or less irritable for several days, and mostly passes undiagnosed unless subdural tapping is performed. In its severer form, the patient lapses into a stuporous or comatose state with hemiplegia and/or other grave signs and sometimes dies.
It is said that the majority of infantile chronic subdural hematomas originates from infantile acute subdural hematomas, although there are few documented cases reported as such. Four cases of infantile chronic subdural hematomas with a precedent history of infantile acute subdural hematomas were presented.
Case 1 was a 14 month-old boy with CT and surgical evidence of bilateral chronic subdural hematoma. At the age of 9 months he had had a history of mild head injury followed by an immediate convulsion and a bulging fontanelle. Case 2 was a 15 month-old boy with the left hemiplegia and CT evidence of the right chronic subdural hematoma and of the right calcarine infarction. At the age of twelve months, he had had a mild occipital head injury followed by an immediate convulsion and disturbed consciousness. Case 3 was a seven month-old boy with CT evidence of bilateral subdural hematoma which was evacuated surgically. Three weeks prior to this, he fell down followed by an immediate convulsion and preretinal hemorrhage. CT taken two hours posttrauma documented the presence of an acute bilateral subdural hematoma. Case 4 was a twelve month-old girl with CT evidence of a left chronic subdural hematoma biconvex in shape. At the age of eight months, she had had a mild head injury followed by vomiting and a generalized convulsion. CT examination at that time was reported to show a thin acute subdural hematoma. This, however, had been considered thin enough to be treated conservatively. CT taken one month and two months, respectively, after the trauma showed widened low density areas over both hemispheres as well as prominent sulci and enlarged ventricles. These were mis-interpreted to indicate “brain atrophy”.
The four cases of infantile chronic subdural hematomas reported here all had clinical evidence strongly suggestive of the presence of the preceeding acute subdural hematoma. One of them, moreover, had CT documentation of its presence. It may be concluded that infantile acute subdural hematoma, if untreated or neglected, is an important etiology of infantile chronic subdural hematoma.

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Eight cases with coexistence of a brain tumor and cerebral aneurysms were found through the review of the authors' series of 198 brain tumors over a period of eight years. They were treated successfully with no operative mortality. Histological diagnoses of these eight tumors were meningiomas in four, pituitary adenomas in two, a glioblastoma multiforme and an acoustic neurinoma. Clinical significance of the coexistence was discussed with special stress on etiology. It can be incidental in many cases. However, in three out of eight cases, hemodynamic change due to peripherally located tumors was suspected as a cause of aneurysm development in their proxymal arteries.

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A case of cerebral arterial vasospasm following removal of a large chromophobe putuitary adenoma by the subfrontal approach was presented. The patient, a 48-year-old male, suffered from progressively disturbed vision. He also complained of headache, easy fatigability, and decreased libido. The axillary and pubic hair was decreased. He suffered complete loss of vision in the right eye and a temporal field cut in the left eye. Both optic disks were pale due to optic nerve atrophy. Plain skull X-rays showed an enlarged sella turcica without any calcification.
Computed tomography showed homogenous contrast enhancement of a tumor in the sellar region which extended to the suprasellar region. Angiographic studies demonstrated lateral displacement of the internal carotid artery, elevation of the anterior cerebral artery, and a large homogenous vascular stain from the late arterial phase to the late venous phase without vasospasm.
A right frontotemporal craniotomy was performed. A gross total removal of the tumor was accomplished. No vascular spasm was evident at the time of closure. The pathological diagnosis was a chromophobe pituitary adenoma.
The postoperative course was uneventful except for diabetes insipidus until the seventh postoperative day, when the patient developed a left hemiplegia and became stuporous. Emergent angiography showed severe vasospasms around the right internal carotid artery bifurcation extending to the C₁, A₁, and M₁ portions. Precontrast computed tomography revealed a slightly high-dense area in the basal cistern.
The vasospasm disappeared almost completely in right carotid angiography on the twenty-third postoperative day. On the thirtieth postoperative day, he remained demented, in a state of urinary incontinence, and still had the left hemiplegia. On the forty-fifth postoperative day, computed tomography showed marked ventricular dilatation with periventricular lucency. A ventriculo-peritoneal shunting operation was performed to treat the communicating hydrocephalus. His clinical symptoms gradually improved. Seven months after surgery, he was able to walk by himself with a cane.
Seven other cases were included in the discussion. The mechanism underlying this unusual complication was thought to be postoperative bleeding in the basal subarachnoid space, although a hypothesis that chemical vasoactive agents are liberated from the tumor bed into the subarachnoid space can not be ignored.

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