A new colorimetric method for the determination of serum lipid peroxide, free of the interference from sialic acids, was established. Then serum lipid peroxide values of 129 healthy controls and 117 patients with cerebrovascular diseases were determined by the new method.
In the procedure elaborated, serum lipid peroxide was precipitated with protein adding 5 volumes of 20°trichloroacetic acid to 0.5 ml of serum. After centrifugation at 3, 500 rpm for 10 min, the supernatant was decanted and the precipitate was washed once with 0.1N sulfuric acid. Then 2.5 ml of 0.1N sulfuric acid and 3.0 ml of 0.2% thiobarbituric acid (TBA) dissolved in 2M sodium sulfate were added to this precipitate, and reaction of lipid peroxide with TBA was performed by heating in boiling water bath for 30 min. After cooling in cold water, resulting chromogen was extracted with 4.0 ml of n-butyl alcohol by vigorous shaking. This was followed by centrifugation at 3, 000 rpm for 10 min and optical density of the organic phase was determined at the wavelength of 530 nm. In the new method, TBA reaction was performed in a weak acid medium, this was thought to inhibit the formation of TBA-reactive aldehyde derivatives of sialic acids. Besides presence of sodium sulfate might contribute to the elimination of the interference from sialic acids by depressing the rate of reaction with TBA through its enhancing effect on the ionic strength of the reaction mixture. This method was specific and useful for precise measurements of serum lipid peroxide.
Average serum lipid peroxide value in healthy controls was 3.6±0.87 nmol/ml. In controls, the value of those under 49 years of age was significantly lower as compared with those aged 50-59 and over 60. The average values of patients with cerebral infarction and cerebral hemorrhage were 4.5 ± 1.53 nmol/ml and 4.4±1.08 nmol/ ml, respectively, these values were significantly higher than that of controls. When classified by age, the difference between patients and controls was obvious in age groups of under 59. In controls, significant inverse relationship was observed between serum lipid peroxide and tocopherol.
These results may indicate the important role of lipid peroxide in cerebrovascular diseases and aging process. Although precise causal mechanism about the incrimination of lipid peroxide in cerebrovascular diseases was unclear, the possibility of its relation with platelet hypersensitivity and thrombotic vascular damage was envisaged.

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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 vaso-dilator 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, partly because of excessively weighed assessment on luxury perfusion phenomenon and partly because of undifferentiated assessment of the results both from the infarcted and the ischemic tissues.
In the previous consecutive studies, the author clarified that hypercapnia between 45 and 55 mmHg was beneficial in the development of collateral flow in areas of ischemia and simultaneous use of Mannitol solution did not offer any additional benefit for enhancement of decreased perfusion flow. However, our studies in the past were performed with an open cranium, even though experiment done after craniectomy undoubtedly provided very valuable information, mainly on better understanding of the dynamics of epicerebral circulation by fluorescein angiography and cortical blood flow studies by the ⁸⁵Kr clearance method. Since it is well known that elevation of PaCO₂ tends to induce an additional increase of intracranial pressure, the results achieved with an open cranium must be confirmed using a model with an enclosed compartment simulating clinical conditions in order to offer a safer application of CO₂, to humans.
Accordingly, a purpose of this part 3 was to measure cortical blood flow by ⁸⁵Kr and global miniregional cerebral blood flow by ¹³³Xe clearance under an environment of enclosed cranium, and also to monitor intracranial pressure (ICP) in the same model.
In results, between 43 and 50 mmHg of arterial carbon dioxide (PaCO₂), rCBF measured with both ⁸⁵Kr and ¹³³Xe clearances increased significantly. However, as PaCO₂ was elevated above this level, there was a definite dissociation in rCBF values from both isotopes. Cortical blood flow measured by ⁸⁵Kr decreases and conversely, global miniregional cerebral blood flow measured with ¹³³Xe continued to increase. Degree of elevation of ICP was 2.1 ±0.4 (SE) mmH₂O in response to 1 mmHg elevation of PaCO₂. Our conclusion, derived from the previous consecutive studies done with an open cranium, was confirmed in the investigation under enclosed compartment.

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High-density Lipoprotein (HDL) cholesterol and low-density lipoprotein (LDL) cholesterol were measured by a modified heparin-calcium method in 16 male patients with cerebral infarction confirmed by computerized tomography (CT) and in 15 male healthy subjects served as controls.
1) The patients with cerebral infarcts had significantly lower level of the HDL cholesterol than the controls.
2) The 7 cases with cerebral infarcts in the cortical arterial system determined by CT, showed more significantly lower ratio of HDL cholesterol to LDL cholesterol value than in 9 cases with infarctions in the perforating arterial regions.
It is therefore suggested that the significance of HDL cholesterol as a negative risk factor of cerebral infarction may differ according to the sites of vascular lesions.

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Acute vascular lesions of the cerebrobasal arteries were produced in rabbits by bilateral constriction of the common carotid artery. The vascular lesions were identified by visible deposits of carbon particles which were injected intravenously during the postoperative 3 days. Microscopical examination shows carbon deposits on the arterial walls with destruction of the internal elastic layer and degeneration of the medial muscle cells. These vascular lesions were frequently found in animals with severe constriction but not found in animals with slight one.

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Developments of hematomas and sites of bleeding were investigated and the volumes of the hematomas were measured with a modular optical planimeter in fifteen postmortem cases with primary pontine hemorrhage.
This disease was seen to be prevalent in cases aged between 40 and 70. Duration between onset and death varied from three hours to nine and half months, most of the cases dying within a week from the onset.
Clinical symptomatology was as follows : Disturbance of consciousness (most of cases showed coma), quadriplegia or hemiplegia, respiratory disturbance. myosis, decerebrate rigidity, etc.
Postmortem examination disclosed primary pontine hemorrhage could be divided into two types; tegmentobasilar (TB type) and tegmental (T type). The former type was seen in twelve cases, the latter in three cases. In TB type, primary sites of the hemorrhage were from the border zone of tegmental and basilar parts of the midpons. On the other hand, in T type, bleeding seemed to start from one side of the pontine tegmentum.
Measured volumes of hematomas varied from 0.5 ml to 96.99 ml (under 10 ml in T type, less than 20 ml in TB type within the pens, less than 40 ml in TB type with development of hematoma in the midbrain, and more than 40 ml in TB type with development of hematoma in the diencephalon). Developments of the hematoma were shown to spread in three directions in TB type. (1) Development into opposite side; (2) Development in ventrodorsal direction (hematomas can break into the fourth ventricle); (3) Upward development which causes midbrain or diencephalic hemorrhage. T type seemed not to develop out of the tegmentum on one side. No development to the medulla oblongata occurs in any type.
We conclude from findings of the fifteen postmortem cases that the primary pontine hemorrhage can be divided into two types, which show different sites of hemorrhage, different volumes, and different developments of hematomas.

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There have been only a few reports concerning the alteration of plasma renin activity in acute cerebrovascular disease. The purpose of this study was to investigate the alteration of plasma renin activity and its interrelationship with age, the type of stroke, clinical severity of stroke, urinary catecholamine excretion and blood pressure in acute cerebrovascular disease.
For assay of renin activity, blood samples were collected from every patients within 48 hours of an acute insult, and then periodical sampling of blood was carried out every seven days during three weeks of observation. Urinary catecholamine concentration was measured fluorometrically.
Of 21 patients with acute cerebrovascular disease who were examined in this study, 16 patients had cerebral infarction and the remaining 5 patients had intracerebral hemorrhage.
The following results were obtained in this study.
1) Significant inverse correlation (P<0.001) was found between age and plasma renin activity in acute cerebrovascular disease.
2) The mean value for renin activity was higher in intracerebral hemorrhage than in cerebral infarction but the difference was not statistically significant.
3) The patients with cerebral infarction whose clinical state was mild, had higher values for plasma renin activity than moderate or severe cases.
4) The blood pressure recorded at the time of blood sampling had no correlation with plasma renin activity, nor did the urinary catecholamine excretion.
5) No remarkable change was observed in plasma renin activity through the course of cerebrovascular disease from the onset to three weeks after.
In conclusion, there was a close relationship between plasma renin activity and age in the patient with acute cerebrovascular disease.
It was suggested that in any investigation of plasma renin activity, aging factor should not be ignored even in acute phase of cerebrovascular disease.

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Cerebral infarction is of two types, that is anemic and hemorrhagic. To investigate the clinical features of the hemorrhagic infaction (HI), we have studied 41 cases of HI in comparison with 163 cases of the anemic infaction (AI). The diagnosis was based on cerebrospinal fluid examinations, cerebral angiography and/or CT scan.
1) The majority of the cases with HI showed a completed type of stroke with sudden onset which was strongly suggestive of the cerebral embolism, while 70% of the cases with AI presented a progressive type of stroke.
2) The various types of cortical signs and homonymous hemianopsia were observed in high percentage in the HI group. These findings suggested that the occlusion of the main trunks of cerebral artery frequently occurred in HI group. The neck stiffness was observed in 59% of the cases in HI group. Therefore it is a useful symptom for making diagnosis of HI.
3) The disturbance of consciousness was observed in most of the cases in HI group. The consciousness was deteriorated during 2 to 3 days after the onset of stroke.
4) Less than 30% of the cases in HI group had the history of hypertension. The mean arterial pressure (MABP) in HI group was significantly higher (p<0.005) than that in AI group during 2 to 3 days after the onset of stroke, although, there was no significant difference between the two groups at the onset. This result suggested that the hypertension was not an apparent risk factor of HI, and elevated MABP might be consequence of acute cerebral edema caused by HI.
5) The prognosis for functional ability in cases with HI was poorer than that of AI. The mortality rate in HI group was much higher (24%) than that in AI group (6%).
6) The characteristic angiographical findings in HI group were occlusion of the main trunks of cerebral artery and its branches (recanalization was confirmed in 4 of 6 cases), residual stenosis, capillary blush with early venous filling and mass sign.
7) In HI group, scattered high and isodensity within the low density area were demonstrated on CT in 26% and 20%, respectively.
8) Sixty one percent of the cases in HI group was associated with the various types of cardiac diseases which could probably be source of embolism. This result indicated that HI occurred more frequently in cardiogenic cerebral embolism.

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A 46-year-old right-handed man who had suffered from cerebrovascular attack six years before, suddenly became completely deaf and made no response to spoken words, bell sounds or any other noises. Cortical symptom such as aphasia, alexia or agraphia was not observed. In addition, pure word deafness and auditory agnosia were not recognized in the course of recovery.
Computed tomography demonstrated a sharp defined high density area in the left insula and putamen indicating cerebral hemorrhage and scattered low density area in the right basal ganglia due to old stroke. Anterior horn of the lateral ventricle was compressed and shifted to the left. Pure tone audiometry performed on 13th day after the onset showed that the hearing loss was at the threshold of 40 dB in the right ear and 85 dB (1, 000Hz) in the left ear. On 23th day after the onset, the hearing loss was improved to the level of 20 dB in the right and 10 dB (1, 000 Hz) in the left with the recovery of clinical symptoms.
Results of clinical features and CT findings suggested that severe hearing loss observed in the present case was presumably due to bilateral subcortical lesions, presumably transecting the auditory radiations en route to the cortex. Possible roles of the auditory radiation for so-called cortical deafness have been discussed. Up to date, so-called cortical deafness possibly due to bilateral subcortical lesions has been reported on only 3 cases.

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