Recurrent episodes of aggravation in left hemiparesis were observed in a case in which a mild hemoconcentration and a leftward shift of blood oxygen dissociation curve were confirmed. Improvement of left hemiparesis was noted after the combined therapy with exsanguination and isovolemic infusion of saline.
A pathophysiological discussion was also made with relation to cerebral circulation and various hemorheological factors.
A 63-year-old right-handed man was admitted on September, 22, 1978, complaining of recurrent attacks of weakness in the left extremities. He had had a ten year history of hypertension, for which hydrochlorothiazide had been administered. Two days prior to the admission he caught a cold and had a slight fever.
Physical examination at admission revealed an obese man with a blood pressure of 196/110 mmHg. No bruit was audible at the neck. He was alert and well oriented. The cranial nerves were intact except for slight flattening of the left nasolabial fold. He had a mild left hemiparesis with left sided hyperreflexia, however, he could walk without any support.
Laboratory examinations showed that hematocrit was 52%, hemoglobin 17.0 g/dl, red-cell count 5760000, white-cell count 9700, platelet count 199000. The erythrocyte sedimentation rate was 8 mm per hour. Platelet adhesiveness was 50%, and platelet aggulutination test was 39% (ADP) and 78% (collagen). The other routine laboratory data were in the normal range. An X-ray film of the chest revealed mild cardiac enlargement. An electrocardiogram demonstrated a normal rhythm with high voltage of R- wave and changes in ST- segment and T- wave consistent with left ventricular hypertrophy. Computed tomography of the brain, performed with and without contrast material, showed no abnormality. Cerebral angiography revealed only mild elongation of main branches of the carotid and vertebral arteries. Blood oxygen dissociation curve was measured by Hemox-Analizer (normal value of P50 was 25.6 mmHg.) and P50 was 24.7 mmHg.
After admission he slept for one hour, and when he awoke he noticed that he could not raise the left arm and leg. The blood pressure was 160/100 mmHg. Several minutes later he could raise his left arm and leg and at that tire time his blood pressure was raised to 200/110 mmHg. For following three hours several attacks of aggravation of left hemiparesis were occurred. During attack of aggravation of left hemiparesis, a trial of inhalation of 7% CO₂, with air induced immediate disappearance of left hemiparesis accompanied with an increase of cerebral blood flow (CBF) which was confirmed by a decrease of cerebral (A-V) O₂. After hyperventilation, an aggravation of left hemiparesis was reappeared accompanied with a decrease of CBF. After 400 ml exsanguination and isovolemic infusion of isotonic saline, the attacks of aggravation of left hemiparesis were subsided and CBF was increased. On the fourth day after the onset, blood oxygen dissociation curve showed a compensatory rightward shift and the aggravation of left hemiparesis was not induced any more after hyperventilation.
From these evidences it was surmised that the main pathogenic factors of cerebral circulation in the case were disturbance of microcirculation in the brain due to hemoconcentration and decreased oxygen transport.

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Fcr the purpose of deciding the minimum dose of antifibrinolytic agent for the conservative treatment of subarachnoid hemorrhage (SAH) in acute phase, we developed a method which was able to measure reduction in fibrinolytic activity of cerebrospinal fluid (CSF) within a short period of time. It was reproducible, and its value was expressed as t-AMCA score. CSF was collected every 30 minutes or six hours in nine cases of SAH who had been treated with an antifibrinolytic agent (t-AMCA) in a daily dose of 4-6 gram and the t-AMCA score obtained was compared with the dosage, t-AMCA concentration in the CSF, FDP in the CSF and daily excretion volume of CSF through the drainage.
It resulted in that the concentration of antifibrinolytic agent in the CSF was negativery correlated to the daily excretion volume of CSF, and revealed accumulation effect. The t-AMCA score usualy changed in a constant pattern for a term of administration, showed rebound fibrinolysis in the two hours after the administration and at the three days after the withdrawal, and revealed very increased fibrinolytic activity around the one week after the onset. FDP in the CSF was traced when the t-AMCA score had been continued over 5 more than 12 hours, and contrary it appeared when the t-AMCA score had been continued under 4 over 6 hours.

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As the prognosis of the vascular lesions in the brainstem has been believed very severe, few reports concerning to the clinical manifestations in the relation with the radiological findings have appeared. However, after the C.T. was available, the chances to make a definite diagnosis of the brainstem cerebrovascular diseases increased a lot. In this report, the authors verified the correlation among the clinical manifestations, radiological findings particularly C.T., and prognosis, using 16 cases of the hemorrhage and 17 cases of infarction as a material.
5 out of 16 cases of the brainstem hemorrhage were dead (mortality 31%). The authors classified these hemorrhagic cases into two groups. One is the group in which the hematoma localizes within the pons, and another is the group in which the hematoma spreads upward to the midbrain. This latter group showed a very poor prognosis or severe clinical features.
17 cases of the brainstem infarction showed the different clinical manifestations. No cases died so far. This infarction was also classified into two groups. One is the group of which the infarction is limited within the pons, and another is the group of which the infarction localized in the midbrain. Although the both of the groups survived, the functional prognosis obtained better in latter group.
In addition to these correlation, the techniques and methods to take fine pictures of the posterior fossa in C.T. was also discussed.

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There is abundant evidence that the cerebral vessels are anatomically innervated with both noradrenergic and cholinergic nervous system. The physiological role of these nerves is, however, still a matter of debate. Some investigators suggest that such nerves are physiologically vestgial and others insist on their important role in the autoregulation of cerebral blood flow.
The present study attempted to demonstrate action potentials from these nerves in the cerebral arterial walls and to examine their response to changes in blood pressure.
Fifty-four mongrel cats were anesthetized with 1.0% α-chloralose and 10% urethane followed by artificial respiration. The rectal temperature was kept at between 37° and 38 °C. Isolation of the pial arteries was performed by means of a microsurgical technique. Paraffin oil was used for maintenance of the local temperature and for insulation of the pial arteries. The action potentials were derived from the surface of the pial arterial walls by employing bipolar platinum electrodes, high sensitive preamplifiers (Bio-DC Amplifier, Model 1117, SAN-EI Instrument Co.), band-pass filters and a data analyzing computer (Signal Processor, Model 7T07, SAN-EI Instrument Co.). The discharges of action potentials were analyzed by using a program of pulse density variation and were recorded on an X-Y recorder. Blood pressure and respiration were measured continuously. Changes in blood pressure were induced by exsanguination and reinfusion of the blood.
Demonstration of action potentials from the pial arteries were successful in all the cats. The discharges increased significantly during induced hypotension and decreased during induced hypertension. Simultaneous recordings of EEG revealed no changes in frequencies during the same procedure. The discharges of both the action potentials and EEG disappeared following inhalation of pure nitrogen gas, asphyxia or injection of saturated KCl solution. The response to changes in blood pressure was inhibited in animals with brain swelling. The discharges from some pial veins revealed a similar response to those of the pial arteries during changes in blood pressure. On the other hand, the action potentials from the cerebral cortex or dura mater did not show a response.
Intravenous infusion of hexamethonium (C₆) diminished the discharges from the pial arteries in parallel with a fall in blood pressure. Both the discharges and blood pressure then gradually recovered with lapse of time. Even after such recovery, however, the response of the discharges to changes in blood pressure was completely abolished.
The discharges from the pial arteries also decreased markedly after inhibition of dopamine-β-hydroxylase by the administration of fusaric acid through a catheter placed in the lingual artery.
The above data suggest that the action potentials from the pial arterial walls are autonomic nervous discharges and have a close relation to the noradrenergic system.

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Incidence of headache in acute stage of cerebral infarction was studied in 86 patients. The diagnosis was confirmed by computerized tomography in all subjects. Headache occurred in 25 cases of 86 patients (29.1%). Of all patients, 72 cases had carotid system disease, and other 15 cases had vertebro-basilar system disease. Of 72 patients with carotid system disease, 15 cases had headache (20.8%). On the other hand, of 15 patients with vertebro-basilar system disease, 10 cases had headache (66.7%). The incidence of headache in patients with vertebrobasilar system disease was significantly higher than those in patients with carotid system disease (P<0.05). Of 72 patients with carotid system disease 47 cases had infarction in the area of penetrating branch, and 18 cases had infarction in the area of cortical branch. There was no significant difference on the incidence of headache between these two groups. As to the size of infarction there was significantly less frequencies of headache in patients with small infarction (P <0.05). There was no correlation between location of headache and infarcted area. There was no correlation between the incidence of headache and findings of cerebral angiography, initial pressure in lumbar puncture and content of CSF protein.

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Twenty-two cases of computed tomographies on reversible ischemic neurological deficit were analized retrospectively.
CT findings were classified in following three groups;
i) normal : 7 cases (31.8%)
ii) atrophic change and/or cerebral infarction : 7 cases (31.8%)
iii) intracerebral small hemorrhage : 8 cases (36.4%)
The results suggested that intracerebral hemorrhage is one of the causes of so-called RIND. The sites of hemorrhage are caudate nucleus, putamen, thalamus, paraventricle and subcortex. The size of hemorrhage is less than 1.3 cm. in diameter.
We would like to call the group with hemorrhage as “reversible hemorrhagic neurological deficit (RHND) against the ischemic group so-called RIND, and support the name calling the two groups genetically as “stroke with full recovery or “apoplexy with full recovery proposed by Loeb and Ohtomo et al.

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A series of 23 patients with brain stem vascular lesions, diagnosed by computerized tomography (CT), were experienced in our service and affiliated clinics for last 3 years. There were 15 patients with primary brain stem hemorrhage and 8 with brain stem infarction. These cases were classified into three categories with fulminant, severe and mild cases according to their clinical course. All of fulminant cases were died within few days from the onset of the disease. And severe cases were died within few weeks or severely disabled as vegetative state, even if they survived. Mild cases recovered to do themselves in ADL or returned to their social work. Of 15 patients with brain stem hemorrhage, 3 were classified into fulminant, and 7 were severe and 5 were mild cases. Of 8 patients with brain stem infarction, 3 were severe and 5 were mild cases. Generally, there was a tendency that infarction had rather milder course than hemorrhage. It was interesting to find that 33.3%of hemorrhagic patients were mild cases in our series.
Concerning the clinical signs and symptoms of 23 patients, “locked-in” syndrome was noted in 4, Foville's syndrome in 3, and Millard-Gubler's syndrome in 2 cases. It is known that abnormal eye movement are often seen in cases with brain stem lesions. In our series, however, only 9 patients showed MLF (medial longitudinal fasciculus) syndrome, conjugated deviation, ocular bobbing, skew deviation or one-and-a-half syndrome, but all of these clinical findings were transient.
In most patients, vascular lesions, identified by CT did fairly correspond to their neurological signs. However, there were some cases of which CT lesion did not correspond to their signs. The reasons for such discrepancy may be explained by limitation of the CT scanner resolution, influence of the angle of slice, presence of the artefact due to occipital bone and partial volume phenomenon in their visualization processes.
In the fulminant and severe cases, massive hematoma on CT was sited in the pontine region bilaterally and often extended up to the mid-brain or perforated into the fourth ventricle. In the mild cases, hematoma was small and localized in the pons unilaterally. On the other hand, severe infarcted cases often showed the large lesions bilaterally in the pans and mild cases showed the small lesions unilaterally. However, the CT lesions in infarction did not so well correspond to their clinical signs and symptoms as did in hemorrhage.

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A method for measurement of regional cerebral blood flow (rCBF) is described, based on 10 minute desaturation method after 1 minute inhalation of ¹³³Xe. Thirty-two collimated probes are placed over both hemispheres and brain stem-cerebellar regions. The rCBF data were obtained on 20 normal right-handed volunteers with an age range of 19 to 92 years (mean age 44). The subjects were requested to relax, keeping the eyes closed but not asleep. End-tidal ¹³³Xe curves are used for correction of recirculation. The blood flow of the fast compartment (gray matter) of the brain was calculated as well as the Initial Slope Index (ISI) as a flow index of predominantly gray matter, and the relative weight and the fractional flow of the fast compartment.
The mean gray matter flow value for the right hemisphere was 74.2+15.5 ml/100 g brain/min and that for the left was 74.3+15.3. The mean value of Initial Slope Index (ISI) for the right was 52.9+9.3 and that for the left was 52.6+8.8. There was actually no difference of the blood flow between both hemispheres.
The rCBF values were the highest frontally and the lowest parieto-occipitally on both dominant and non-dominant hemispheres. Those results were in good agreement with the values obtained by ¹³³Xenon intracarotid injection method.
It is concluded that ¹³³Xenon inhalation method is able to be used for rCBF measurement in man, and the rCBF values in Japanese healthy volunteers are almost same as the values reported by other investigators in US or Europe.

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A case of multiple intracerebral hemorrhage, supra-tentorial and infra-tentorial occurred almost simultaneously, is reported.
This 69-year-old man was transferred to Yokohama City University Hospital, because of motor aphasia and right hemiparesis of sudden onset. The computed tomography showed a small hematoma about 2 cm in diameter located in the left putaminal region, then he was decided to be treated conservatively, however, systolic hypertension had continued and his consciousness level had been going down and right abducens palsy developed in the next morning. Repeated computed tomography showed an another hematoma about 3 cm in diameter located in the right cerebellar hemisphere. Then, suboccipital craniectomy was carried out, the hematoma was removed urgently.
No case of multiple hematomas in which hemorrhage occurred supra- and infratentorial regions almost simultaneously has been reported as far as we know. In this case, the uncontrollable hypertension which followed hemorrhage is thought to be an etiological factor of the cerebellar hemorrhage.
The cases of multiple hematomas as like as just the authors reported may inci ease in number, since these hematomas will be diagnosed by the computed tomography nowadays.

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A case with a primitive trigeminal artery presented with homolateral intracranial carotid occlusion is reported. This 73-year-old female with hypertension has been well until on August 15, 1979, when acute onset of speech disturbance followed by unconsciousness lasting for several hours was developed. She was hospitalized with the diagnosis of transient ischemic attack in the left cerebral hemisphere. On August 25, a similar attack of the left hemisphere was recurred and the patient was referred to Omuta City Hospital. On admission, she was alert and right spastic hemiparesis and motor aphasia were noted. A general physical examination was normal except for hypertension as high as 190-90 mmH₂O. There were no history of previous neurological diseases nor cardiac diseases. CT scan demonstrated a localized small low density area on the left parietal lobe and mild brain atrophy. Left carotid angiogram showed an elongation of the internal carotid artery along the whole length with a primitive trigeminal artery which supplied the rostral basilar artery, left posterior cerebral artery and bilateral superior cerebellar artery. This indicated that the left internal carotid artery supplied the rostral part of the brain stem and cerebellum as well as the left cerebral hemisphere. The primitive artery was almost the same size as the cavernous portion of the carotid artery which showed a significant arteriosclerotic changes. Left retrograde brachial angiogram indicated that the caudal basilar artery was faintly filled via the left vertebral artery. The medical treatments including an antiagglutinating agents and vasodilators were started, however, right hemiparesis and mild motor aphasia were prolonged and fixed. On september 24, she was deteriorated again with resulting the prolonged unconsciousness when the occlusion of the left internal carotid artery at the cavernous portion distal to the bifurcation of the primitive artery was demonstrated on the left carotid angiogram. Based on the presence of the left primitive trigethinal artery, the definite arteriosclerotic changes in the carotid syphon and intractable hypertension in this case, reduced blood flow to the left anterior circulation might play a major role in the occurence of transient ischemic attacks leading to completed stroke due to the occlusion of the cavernous portion of the carotid artery when blood pressure was reduced. Although the clinical significance of the presence of a primitive trigeminal artery in the cases with occlusive cerebrovascular disease is not well understood, it would be concluded that the presence of the primitive artery may at least not be of major protective value for the patients with occlusive cerebrovascular disease as seen in the present case.

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The variation of the basal arteries of the brain were studied using 1, 017 autopsied cases of the aged. The results were as follows;
1) Anterior cerebral artery (ACA) : The calibers of the left and right ACAs were significantly differenat, one was two or more times greater than another, in 57 cases (5.6%). In 38 cases (3.8%) the left was greater, while in 19 cases (1.9%) the right was greater.
The hypoplasias of the pre-communical segments of the ACAs were found in 57 cases (5.7%), 12 in the left and 45 in the right.
2) Anterior communicating artery : It had been reported that the variations of the anterior communicating arteries, such as Y-form and net formation, were more frequent in Japanese than in Western population. However, the present results reviealed that no significant difference did present between the two.
3) Posterior cerebral artery (PCA) and posterior communicating artery (PComA) : In 307 PCAs (15.1%), the caliber of the PComA was far more greater than that of the pre-communical segment of the PCA (foetal type).
The calibers of the pre-communical segment of the PCA and the PComA were almost equal in 214 PCAs (10.5%) (transitional type).
The incidence of the cases with foetal types of the PCAs bilaterally (primitive type) was greater (77 cases, 7.6%) than the results reported from western countries (3.6%).
4) Vertebral artery (VA) : The significant difference in the calibers between left and right VAs, one was two or more times greater than another, was found in 282 cases (27.7%). In 187 cases (18.4%) the left was greater, in 64 cases (6.3%) the right was greater.
The hypoplasias of the VAs were found in 7 cases (0.7%), 3 in the left and 4 in the right.
The VAs, terminated in the posterior cerebeller artery without jointing basilar artery, were found in 14 cases (1.4%), 6 in the left and 8 in the right.

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A case, 53-year-old male, of recurrent intracerebral hematomas was reported. Any cause for the recurrent bleeding was not evident. During the previous 10 months he had had three episodes of subcortical hemorrhages in the different parts of the cerebral hemisphere. The hematomas were detected by computed tomography (CT); The hematoma examined on July 13 in 1979 was situated in the left frontotemporal region (Fig. 1), that on December 4 in 1979 was in the right temporal (Fig. 2), and that on January 14 in 1980 was in the left frontotemporal (Fig. 3). He had occasionally had a slight hypertension and albuminuria for several years. Carotid angiography and CT scan showed no evidence of tumor, angiomatous malformation and aneurysm. Any hemorrhagic tendency and inflammatory change were not present.

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