In the diagnosis of primary traumatic brain injury it is important to know the mechanical background of the injury. Clinical observations show that the natures and locations of brain injuries well correspond to the particular fashion and site of the blow. Although experimental observations show that the mass movement of the brain occur at the moment of the blow, theoretically brain injury occur by the combinations of translational and/or rotational acceleration where the skull is rigid and distortion injury where the skull is elastic. Thus, coup and contrecoup injury, gliding contusion, intermediate injury can be well comprehended and foreseen by applying the above mechanisms. Modifying factors are the irregularity of the skull base and the presence of the tentorium etc.
The stochastic diagnosis of traumatic intracranial hematoma is a good example of a clinical application of mechanical analysis. There are many items in the table for stochastic diagnosis. But the most significant information are the state and course of consciousness after the impact, the direction of the blow, and the side of neurological signs. Consciousness disturbance concerns the presence of the hematoma. The direction of the blow and the side of the neurological signs concern the type and the side of the hematoma. Only those three items can make the diagnosis correct no less than 90%.
To take notice of the mechanical action of the blow is important and is the first step to deepen the comprehension of head trauma.

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In the acute stage of selected cerebrovascular occlusive disease, it is essential to prevent the 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, carbon dioxide, which is a potent cerebral vasodilator without reduction of systemic blood pressure in the intact brain tissue, has been considered. However, in spite of the numerous investigations done in the last decade, its effectiveness on the increase of cerebral blood flow into ischemic areas still remains controversial.
Therefore, the present study was undertaken to re-evaluate an effectiveness of carbon dioxide on microregional cerebral blood flow (rCBF) in areas of ischemia which was produced by occlusion of the canine middle cerebral artery, by means of beta-emitting ⁸⁵Kr and gamma-emitting ¹³³Xe clearance techniques, fluorescein angiography and measurement of diameters of arteries. Between 45 and 55 mmHg of arterial carbon dioxide pressure (PaCO₂), rCBF measured with ⁸⁵Kr and ¹³³Xe clearances increased significantly. This was confirmed also by fluorescein angiography. However, when PaCO₂ was elevated above 55 mmHg, there was a remarkable dissociation in the rCBF values from both isotopes. The cortical blood flow values measured by ⁸⁵Kr clearance method decreased and conversely, the global miniregional blood flow values measured by ¹³³Xe continued to increase. Arteries of less than 50μ in diameter, in the areas of ischemia, dilated significantly during hypercapnia.
At a PaCO₂ above 65 mmHg, progressive subpial hemorrhage and extravasation of dye were observed as side effects of hypercapnia. Finally, the authors conclude that PaCO₂ between 45 and 55 mmHg is beneficial in enhancement of perfusion flow in areas of ischemia.

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In terms of increase of perfusion flow into an area of ischemia, carbon dioxide must be one of the most promising candidates, even though complete agreement has still not been obtained.
A controversial, but attractive point in this field is that there is a discrepancy between experimental results obtained by beta-emitting ⁸⁵Kr and gamma-emitting ¹³³Xe clearance techniques.
To resolve this discrepancy in the results from the two isotopes, the experiment of this series were undertaken and our first report clarified that between 45 and 55 mmHg of arterial carbon dioxide pressure (PaCO₂), microregional cerebral blood flow (rCBF), measured with both the ⁸⁵Kr and ¹³³Xe clearance techniques, increased significantly.
However, in the same study, as PaCO₂ was elevated above this level, there was a remarkable dissociation in rCBF change as measured by each isotope.
The cortical blood flow measured with ⁸⁵Kr clearance method decreased and conversely, global miniregional cerebral blood flow measured by ¹³³Xe continued to increase steadily.
In our first report, occurrence of subpial hemorrhage, extravasation of dye and increase of brain volume were considered as possible factors contributing to decrease in cortical blood flow by ⁸⁵Kr clearance following a stage of its definite increase. In that report, the former two factors were analyzed in detail.
Since cerebrovascular occlusive disease in humans tends to produce intracranial hypertension of varying degrees, depending upon secondary brain edema, the elevation of intracranial pressure by inhalation of carbon dioxide must be carefully investigated.
If two methods of management, increase of perfusion flow by inhalation of carbon dioxide and reduction of increased brain volume by infusion of hypertonic solution are compatible on treatment and are capable of extending the range of PaCO₂ which permits an increase of cortical blood flow measured with ⁸⁵Kr clearance, an application of carbon dioxide to humans will be much safer and its therapeutic indication will be much wider.
Therefore, Part 2 of our experiments was done with administration of 20% mannitol solution, using the same materials and methods as in the previous experiment and a comparison of the results with and without mannitol was made.
In results, between 45 and 55 mmHg of PaCO₂, cortical blood flow measured with the ⁸⁵Kr clearance method, increased significantly with a gradual decline at PaCO₂ higher than this level, which was very similar to the previous work done without mannitol. With the combined use of these two agents, subpial hemorrhage of more marked degree was observed at a PaCO₂ above 65 mmHg with extravasation of dye appearing at lower PaCO₂ level than with hypercapnia alone.
The use of mannitol combined with hypercapnia appeared to be harmful.

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On administration of antibiotics by the intrathecal or intraventricular route for purposes of meningitis therapy, it is necessary to decide the dosage by considering the concentration in the regions where the dispersion of antibiotic is worst. For the purpose of investigating the antibiotic concentration in CSF at the region of administration and at remote regions gentamycin (GM) or sulbenicillin (SBPC) were administered in the CSF cavity to 16 cases who did not have CSF circulation disorders and the concentration was measured in CSF in several regions.
The lowest antibiotic level in cases of intraventricular administration was in the lumbar CSF the highest concentration.
Among them being 0.18±0.09% of dose concentration which was calculated theoretically as the concentration of antibiotic in 1 ml solution. The highest concentration in the CSF collected at the same time from the chiasmatic cistern was 0.22-0.83%.
With intrathecal administration, the concentration was lowest in the ventricle, the highest concentration among them being 0.05±0.02%. The highest concentrations in the upper cervical CSF were 1.14±0.39%.
Severe side effects observed when administering antibiotics in the CSF cavity are disturbances of consciousness, respiratory and circulatory disorders and other brain stem symptoms. During the 5 years from 1971 to 1976 at the Department of Neurosurgery, the number of cases who were treated by administration of antibiotics in the CSF cavity either during meningitis or clinical research was approx. 70, and in two cases among these transient brain stem symptoms were observed. Also observed were cases who developed light degree intraventricular bleeding, or vomiting, and diffuse flashing of skin, but there were no fatalities or cases of aftereffects. Based on the literature or on the experiences in this department, the safe dosage when administering antibiotics in the CSF cavity should be 50 mg or less for CET, CER and SBPC, and 12 mg or less for GM.

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The authors report the role of local inflammatory mechanisms in outer membranes to define the physiopathogenesis of the chronic subdural hematoma enlargement. The outer membranes in 20 adult patients of chronic subdural hematoma were investigated by means of light and electron microscopy.
Microscopically, perivascular small hemorrhage and hemosiderin as well as fibroblasts, hemosiderin-laden macrophages, eosinophiles and plasma cells were found around the sinusoidal channels. Perisinusoidal hemorrhage, especially red blood cells were, usually, separated from the hematoma cavity by the fibrous layer. Several sinusoids could be seen coalesced to form multiple small cavities in outer membranes, with a fibroblast like lining. Such small hemorrhagic cavities, although not often, may rupture to communicate with the hematoma cavity.
Ultrastructurally, the endothelial cells of sinusoids were rich in organelles, especially rough E.R., free ribosomes, mitochondrias, pinocytotic vesicles, and endothelial specific bodies. The site of vascular leakage was identified in several sinusoids as an endothelial gap, in the range of 1-8 μ in diameter, presumably formed by separation at intercellular junctions. Perivascular exudation of plasma lead to destruct the extracellular matrix of the sinusoidal layer. Extensive accumulations of endogenous amorphous material and irregularly arranged thin collagen fibers showed interstitial edema. Fibroblasts manufacture tropocollagen molecules within the activated rough E.R., which are then secreted onto the cell surface and gradually polymerized into visible microfibrils and collagen fibers. Interstitial edema, ultimately, disappears in the fibrous layer. The fibrous layer is generally characterized by numerous collagen fibers, fibroblasts, serum proteins and only a few capillaries, some of which show direct openings into the hematoma cavity. Some perivascular edematous fluid in the sinusoidal layer may pass through the fibrous layer into the hematoma cavity.
Under scanning electron microscopy, red blood cells and fibrin strands or sheets were seen especially around the outlets of the fibrous layer capillaries.
The results indicate that outer membranes, once developed, enlarge chronic subdural hematoma by ruptures of small hemorrhagic cavities formed in outer membranes, direct hemorrhage from the fibrous layer capillaries, and exudation of perisinusoidal edematous fluid into the hematoma cavity.

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The authors have surveyed the causative bacteria for postoperative meningitis past four years (1972-1975), and obtained the result that 78% of those was gram-negative bacteria.
Ten dogs were given single shot injection of either Cephalothin (CET), Chloramphenicol (CP) or Sulbenicillin (SB-PC), and the blood and the cerebrospinal fluid concentration of these drugs were measured. The results revealed that Chloramphenicol was higher than Cephalothin or Sulbenicillin in cerebrospinal fluid concentration.
The antibiotics were administered subcutaneously or intravenously to patients with aneurysm of cerebral artery, head injury, tumor near pituitary gland or hydrocephalus who had continuous ventricullar drainage and were comparatively stable in condition. The transit of antibiotics to the cerebrospinal fluid were measured for six hours.
As the result, Cefazolin (CEZ) moved in the most and Cephaloridine (CER) did in more than Cephalothin. The transit of Sulbenicillin and Gentamicin (GM) were not sufficient. The maximum values of each antibiotics found in the cerebrospinal fluid were as follows; 2.6 mcg/ml after subcutaneous injection of lg CEZ, 0.58 mcg/ml after intravenous single shot injection of 2g CER and 0-3.6 mcg/ml after intravenous drip injection of 2g CET. The transit of Gentamicin and Sulbenicillin to cerebrospinal fluid was not recognized. These values are not enough to maintain MIC (minimum inhibitory concentration for growth of bacteria) for gram-negative bacteria.
From those data, it is advisable to administer a large dosis of antibiotics systemically for certain length of time. Considering the side-effects caused by the large dosis administration of antibiotics systemically, it is necessary to treat the intracranial infection with both systemic administration and the intrathecal administration of antibiotics.

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Seventy-five studies of regional cerebral blood flow (rCBF) were performed in 42 patients with ruptured intracranial aneurysms. The measurement of rCBF was made by ¹³³Xe intra-arterial method using 32 detectors. A computer system was used for automatic calculations of rCBF by stochastic and initial flow analysis. The changes in rCBF were analyzed under various pathophysiological conditions following rupture of intracranial aneurysms and were discussed with special reference to occurrence of focal ischemia and abnormal vascular response. The results were as follows;
1) The degree of flow abnormalities and the occurrence of focal ischemia correlated well with the clinical grade of neurological deficits. Most of the grade IV patients (classification of Hunt and Hess) showed marked decrease of mean CBF, which was below 30 ml/100 g/min. Furthermore, these patients also had marked ischemic foci, where the rCBF was below 20 ml/ 100 g/min.
2) Most of the patients with angiospasm showed focal ischemia in the regions supplied by the involved arteries. All of the patients with diffuse angiospasm of severe grade showed focal areas of decreased flow below 30 ml/100 g/min, in addition to a diffuse reduction in rCBF. The relief of angiospasm was followed by the increase of mean CBF, and rCBF in the ischemic focus.
3) The patients with low density lesions in CT showed more depressed values of mean CBF than those without low density lesions, but there was little difference in rCBF in the ischemic foci between both groups.
4) Severe neurological deficits were found in cases with intracerebral hematoma and hydrocephalus. rCBF studies showed focal decreased flow below 30 m1/100 g/min corresponding to the area of hematoma as well as generalized reduction in rCBF. Twelve studies in patients with hydrocephalus showed marked reduction in mean CBF, which was below 30 ml/100 g/min.
5) Imparied CO₂-response and autoregulation were found in patients with severe neurological deficits, severe degree of angiospasm and marked depression of mean CBF.

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A case of cavernous angioma was reported. A 20-year-old woman was admitted because of 10 year's seizure episodes. Electroencephalography (EEG) in another hospital had shown high voltage slow waves in the right frontal area. This EEG abnormality progressed gradually. Brain scintigraphy, carotid angiography and computerized tomography revealed a tumor of the right frontal lobe. A craniotomy was performed and the tumor situated at the anterior part of the right cingular gyrus was removed totally without any neurological deficits.
The tumor 3 cm in diameter, was well encapsulated and spongy containing fresh blood. Histologically, the tumor had many vascular cavities with the walls lined with a single layer of endothelial cells, had no glial cells between the vascular cavities and was diagnosed as a cavernous angioma. This was the first case of cavernous angioma among our experiences of 1, 364 brain tumors. The characteristics of this rare tumor were also discussed with a review of 15 cases reported in Japan.

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