Microcirculatory disturbance can be responsible for the pathophysiology of cerebrovascular disorders. In this study, erythrocyte deformability was investigated in 48 cerebrovascular patients and 116 healthy controls as the index of blood filtrability in microcirculation.
Several hematological and blood chemical parameters were also determined to observe influences on the filtrability. Erythrocyte deformability was measured by the Reid's method and expressed as the deformability index (DI).
DI and ATP level decreased with advancing age both in controls and patients. DI and ATP level in patients were lower than those in controls. DI was directly proportional to ATP level both in controls and patients. Close relationship between DI and ATP level was ascertained by multivariate analysis of the data, although this relationship was revealed only in controls.DI was inversely proportional to hematocrit, hemoglobin, fibrinogen, and lactate levels in controls and directly to albumin in patients.
There were no significant differences in DI and ATP level between cerebral infarction and cerebral hemorrhage. Neither DI nor ATP level indicated arteriovenous gap.
In the cerebrovascular patients, decreased blood filtrability might predispose to the microcirculatory deterioration accompanied with sclerotic narrowing of arteries.

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Mitral valve prolapse has now become a well-known disease for cardiologists and many authors have reported several secondary complications. They are arrhythmias, mitral regurgitation, bacterial endocarditis and sudden death. In addition, neurological disturbances such as transient ischemic cerebral attacks, partial non-progressive stroke were reported a few years ago. We recently experienced one case with mitral valve prolapse and completed stroke. The lack of clinical report in Japan as for cerebral infarction with this pathological condition merits this case report. The authors reviewed an association among transient ischemic cerebral attacks, stroke and mitral valve prolapse in the literature. And we emphasized that echocardiography was very useful for the screening of the ischemic cerebrovascular diseases secondary to the emboli originated from the heart.
A 65-year-old right-handed female was admitted to our hospital because of left-hemiplegia in February, 1980. The physical examination and chest X-ray revealed arrhythmia and cardiomegaly. Electrocardiogram showed atrial fibrillation and left ventricular hypertrophy. But she had no abnormal heart sounds and murmurs on auscultation. The neurological findings were left hemiplegia with extensor planter reflex, ocular conjugate deviation to the right side, and disturbed consciousness. Computed tomography (CT) showed no abnormal density on admission. The right carotid angiography performed on the 1st day after onset demonstrated an occlustion of the middle cerebral arterial branch and collaterals from the anterior cerebral artery. Repeated CT on the following day showed a large low density area in the territory of the anterior and the middle cerebral artery. The angiographic findings were suspected to reflect the prior recanalization of an embolic occlusion of the internal carotid artery, or that of multiple arteries retrospectively. Echocardiography was performed to study any embolic source in the heart six after onset. Two-dimensional echocardiography demonstrated mitral valve prolapse without other anatomical changes. M-mode scan also revealed pansystolic bowing or hammocking of the anterior mitral leaflet. But phonocardiography revealed no mid-systolic click or systolic murmur.
Afte admission, she slowly showed clinical improvement enough to walk with a brace. But she often complained of precordial pain and palpitation after exercise or even at rest. Therefore we performed angiocardiography to scrutinize the causes of chest pain and atrial fibrillation. Left ventriculography showed mitral valve prolapse involving both posterior and anterior mitral leaflets with regurgitation of mild degree on the 27th day after onset. The selective coronary angiography showed slight luminal irregularity without any significant occluded lesion. Her cardiac complaints were, we considered, possible secondary to idiopathic mitral valve prolapse. After the administration of aspirin and nitroglycerin, she scarcely complained of chest pain.

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The serum lipoproteins were separated into ultra-watersoluble (UWS) and non-watersoluble (Non-WS) lipoproteins by 72 hours flowing water dialysis.
This paper was studied on the method of fractionation of UWS-Lp and Non-WS-Lp, and the significances of those lipo-proteins in stroke.
The subjects are 19 cases with cerebral thrombosis (CT), 6 cases with cerebral haemorrhage (CH) and 10 healthy persons (controls).
There were no obvious differences in serum total cholesterol and total triglyceride levels between controls and stroke patients.
But UWS-Lp-cholesterol levels in CH are higher than those in CT, and Non-WS-Lp-cholesterol levels in CT were higher than those in CH and controls.
Although there were no differences among three groups in UWS-Lp-triglyceride levels, Non-WS-Lp-triglyceride levels in stroke were higher than those in controls.
The serum total binding hexose levels in stroke are higher than those in controls. Those high levels were caused by high levels with Non-WS-binding hexose without UWS-binding hexose.
It is useful for studying lipid metabolism in stroke to separate serum lipoprotein into two kinds of UWS-lipoprotein and Non-WS-lipoprotein.

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The role of the heart in an embolic stroke has been given much attention through previous patholoical and epidemiological studies. We have examined patients having embolic stroke by two dimensional echocardiography in order ot investigate the pathological changes of the heart and the presence of intracardiac thrombi. One hundred thirty eight infarcted patients were examined by echocardiography. They were admitted within 48 hours after onset and were diagnosed as having cerebral infarction by both physical and neuroradiological findings. The short axial view and long axial view were taken in addition to M-mode scanning. The left ventriculography and/or coronary angiography were performed, if necessary, for diagnosis.
The abnormalities found other than rheumatic heart diseases were hypertrophic type cardiomyopathy in 10, congestive type cardiomyopathy in 2, mitral valve prolapse in 3 and mitral annulus calcification in 4 cases. Rheumatic heart diseases have been well recognized as embolic sources in stroke patients. But mitral annulus calcification (MAC) has not been given much attention as an embolic source, although several descriptions on the pathologic anatomy of MAC have appeared over that past seven decades.
The echocardiography in the 4 cases of MAC showed a dense, linear echo behind the mitral valve that moved anteriorly with systole, similar to the motion of the posterior left ventricular wall. On scanning from the left ventricle to the left atrium this dense band of echoes stopped abruptly at the junction between the left ventricle and left atrium. It was difficult to differentiate this band of echoes from the posterior mitral valve leaflet and from the posterior wall of the left ventricle. Two-dimensional echocardiography provided a more exact display of anatomic relationships than the M-mode thechnique.
The ages of patients with MAC were 69, 73, 80 and 81 years respectively. Two of them were females. Calcifications of mitral annulus were demonstrated by the plain chest X-P or fluoroscopy in 2 cases. All cases showed left ventricular dilatation on chest X-P. Three cases showed atrial fibrillations and the other one had ventricular premature contractions on ECG. Intracardiac thrombi were not found in any cases by echocardiography. Two autopsied cases had no intracardiac thrombi. The internal carotid artery occlusion was confirmed in two cases, and the latter 2 cases had stenotic lesions on internal carotid arteries. On CT scan, 2 cases had low density areas on the territory of middle cerebral artery and 1 on the territory of both anterior and middle cerebral arteries. One case had no abnormal CT findings.
Our data suggest that two-dimensional echocardiography is necessary for investigating cardiac abnormalities including MAC in infarcted patients. The concomitant lesions of internal carotid artery and MAC have to be paid more attension in order to estimate MAC as an embolic source in cerebral infarction.

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It is known that mortality and morbidity during the acute phase of a stroke are related to transtentorial herniation resulting from severe brain edema. The importance of transtentorial herniation with ischemic brain edema has been cverlookea in cerebral infarction, and no appropriate management for its prevention has been devised.
Two cases demonstrating severe brain edema due to acute cerebral infarction resulting from occlusion of the unilateral internal carotid artery were presented, and both patients underwent decompressive surgery and one survived. We reviewed the literature and discussed indications for surgical decompression.
Among reported 32 patients 17 died following the operation (mortality rate 53%). 16 patients were underwent surgical decompression within 2 weeks, whose preoperative neurological findings were stupor or coma in 16, 11 presented pupillary abnomality, 5 showed decerebrated or decorticate posturing, and 4 presented respiratory disturbance,
Computerized tomography scans were useful in diagnosing cerebral infarction with transtentorial herniation.
The clinical course, neurological signs and CT findings facilitated determination of indications for decompressive surgery. The signs and symptoms showing impending herniation were useful indicator of the timing of its surgery. If there has been irreversible damage to the brain stem, surgery will not result in any benefit. These findings are deep coma, dilated and fixed pupils, midline fixed eye position, and negative oculovestibular and corneal reflexies.
Further medical and surgical management are required in such situation, and therefore neurological and neurosurgical intensive care is recommeded.

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Direct injection of ¹³³Xe has been used for measurements of cerebral blood flow (CBF) in internal carotid arterial territory, but little is known as to whether this technique can be utilized for measurements of CBF within the vertebrobasilar artery system. This study investigated a validity of ¹³³Xe injection into the vertebral artery for CBF measurement of infratentorium.
A catheter was inserted into either left or right vertebral artery through the femoral artery under florescopic control to directly inject 1-2 mCi of ¹³³Xe. Similar catheter procedures were used for CBF measurement for the internal carotid artery. Four probes as well as seven probes fitted with collimaters of 40 mm lenght and 17 mm diameter were placed respectively over posterior fossa and cerebral hemisphere. Cerebral blood flow values for vertebrobasilar arterial system (V-CBF) and for internal carotid arterial system (I-CBF) were calculated from the initial part of clearance curves.
Measurements were made in 7 patients with infra-tentorial stroke. The patients' clinical severities were of different degrees. The results obtained could be summarized as follows : (1) The more severe the grade of disturbed consciousness, the more apparent the decrease of V-CBF. (2) In patients with mild disturbance of consciousness, the decrease of V-CBF was more prominent compared to I-CBF. (3) In comatose or semicomatose patients. I-CBF and V-CBF were markedly reduced showing indentical values. These results indicate the possibility and clinical usefulness of V-CBF measurement in stroke patients.

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Wallenberg's syndrome is characterized by acute bulbar paralysis and dissociated sensory disturbance due to ischemic damage of the lateral portion of the medulla oblongata. This syndrome occurs more often due to occlusion of the vertabral artery than the posterior inferior cerebellar artery (PICA).
This was a report of a case of hypoplastic right vertebral artery and PICA which were considered to be a cause of Wallenberg's syndrome.
This 46 year old female with essential hypertension of five years' duration suddenly developed nausea, vomiting, headache, vertigo, dysarthria and dysphagia. Wallenberg's syndrome was diagnosed on the basis of the neurological examination. Bilateral vertebral angiography was performed one month after the onset. Left vertebral angiography was unremarkable, but right vertebral angiography revealed a hypoplastic right vertebral artery. The PICA was also hypoplastic, particularly in its proximal segment. From the distal portion of the vertebral artery to the proximal segment of the PICA, the arterial wall was irregular, suggesting recanalization of thrombotic occlusion.

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A perifocal low density area in C.T. plays an important role to determine the prognosis of the lesion, although its genesis is still controversial.
In this report, the perifocal low density area of the hypertensive basal ganglionic hematoma was evaluated, concerning to its time course in pre- and post-operation, and to the correlation with its histological findings.
The conclusions were obtained as follows :
1) The perifocal low density area can appear within three hours after the attack, particularly in a fulminant case. The low density area is usually occupied by the fluid with blood and CSF which has been certified in the operation at a super-acute stage after the attack.
2) The low density area consisted of brain edema, brain swelling and brain destruction which were certified by the histological study, apperars around six hours after the attack.
3) The low density area with a mass effect is usually observed for two weeks after the removal operation. This duration seems to be longer than our pervious (pre C.T. era) understanding about the duration of the existence of the brain edema, particularly in cases of the incomplete removal of the hematoma, the low density area with the mass effect is observed for more than two weeks after the operation. This fact suggests to give the anti-hyper ICP drugs in longer days than the duration of our previous understanding.

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Electrocardiographic changes were studied in 46 patiants with subarachnoid hemorrhage (SAH), in 34 patients with intracerebral hemorrhage (ICH) and 13 patiants with brain tumors (BT) as a control group. Those EKG alterations were analyzed in respect to gravity and prognosis of those patients. The patients with past history of ischemic heart diseases had been excluded in this study.
In 8 cases with SAH and ICH, the EKGs before and after attacks were compared. Electrocardiographic changes were noted in 36 cases of SAH (78.3%), in 27 cases of ICH (79.4%) and in 4 cases of BT (30.8%). In SAH, wide deep negative T was one of characteristic EKG changes.
In SAH, prolonged QT_c (U) was found more in the cases higher grading of Hunt and Kosnik. Vasospasm in SAH and intraventricular hemorrhage in ICH were the factors bringing about more EKG alterations. In ICH, left ventricular hypertrophy and ST alterations were commoner findings compared to others. Those EKG changes had no co-relation with serum electrolyte and enzyme changes, but some co-relation with higher serum glucose level.
In the fatal cases, and in the cases with GI bleeding and hyperthermia in their clinical course, more marked EKG changes were noted. For the etiology of those EKG alterations, neuronal factors rather than humoral ones were suggested. For the trarget areas, the hypothalamus and its vicinity were considered. More precise clinical investigations and animal experiments are to be followed after this prospective study in future.

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Changes in the electrical activity of the brain were studied for 7 days following 30 min, 1 hr or 2 hr occlusion of blood flow, using the thalamic infarction model in the dog which was produced by means of simultaneous occlusion of middle cerebral artery, internal carotid artery, anterior cerebral artery and distal portion of posterior communicating artery.
Discussion is made of the relationship between thalamus EEG changes and the histological findings obtained at autopsy on the 7th day with regard to the development of cerebral infarction.
1) All 2 animals which had undergone 30 min vascular occlusion showed, subsequent to release of occlusion, rapid return of fast wave components which had disappeared during occlusion. On the third day, the presence of mildly slow waves was seen, but these disappeared by the 5th day and electrical activity similar to the preoperative state was seen on the 7th day. Histologically, either no signs of infarction or extremely mild signs were seen.
2) Among the animals undergoing 1 hr occlusion, 2 patterns were observed : one in which recovery to a preoperative state occured, and one in which ultimately complete flattening of electrical activity occures. In both groups, slow waves in the 3 Hz region were predominant until the 3rd day, but on th 5th day 2 animals exhibited fast wave components and nearly complete recovery by the 7th day. Histologically, small infarctic foci were found. The second group showed no fast wave components on th 5th day, and in the 1 dog which then showed slow wave components, complete flattening occurred by the 7th day. Infarciec foci were found to cover 1/2 of the thalamus.
3) In the animals undergoing 2 hr occlusion, there was slight slow waves apparent until the 3rd day, but thereafter until the 7th day, complete flattening occurred. Large infarctic foci were seen throughout the thalamus in all of these dogs.
From the above findings, it was concluded that sequential changes in thalamic electrical activity closely correlate with histological findings.

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In order to examine the role of noradrenergic nerve system in autoregulation of cerebral blood flow, the effect of fusaric acid (FA), inhibitor of dopamine-β-hydroxylase, on autoregulatory response of pial arteries was investigated by the vidicon camera system in 8 cats.
Before the inhibition, the pial arteries were dilated by exsanguination and constricted by reinfusion. Intravenous administration of FA (50 mg/kg) produced a significant dilation of the pial arteries and a decrease of mean arterial blood pressure (MABP). About 30 minutes after the administration, autoregulatory response of the pial arteries was re-examined. Contrary to the experiments before inhibition, pial arteries were constricted by exsanguination and dilated by reinfusion.
Cerebral vasomotor index (-Δdiameter (μ) /MABP (mmHg)) (VMI) was calculated for evaluation of the autoregulatory response of the pial arteries. Before FA administration, VMI was +0.397±0.302 in exsanguination and was +0.343±0.237 in reinfusion. But after FA administration, they changed to -0.294±0.236, -0.299±0.301 respectively (p<0.001).
These results indicated that the function of the nerve terminal of noradrenergic system has an important role in the neurogenic process of autoregulation of cerebral blood flow.

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Non-invasive methods, such as radioisotope angiography, oculoplethsmography, and ultrasonic Doppler flowmetry, are used for the detection of caroid artery lesion. However, these methods are qualitative, and diagnostic accuracies are inferior to arteriography. On the other hand arteriography needs catheterization. So we tried to use CT scan and intravenous contrast enhancement for the diagnosis of carotid artery disease.
A CT/T scanner (X-2) was used, which enabled to produce computer reconstruction image of the carotid artery by use of the arrange program. 12 sequential axial images of the neck (between heights ofC2 and C5) were obtained before and during infusion of contrast material. Analysis of sequential axial images and reformatted images were obtaned in patients with cerebrovascular disease. Carotid arteriography were made in 53 arteries, lesions with stenosis and/or occlusion were demonstrated in 26/53 arteries. Intravenous CT carotid-angiography revealed lesions with stenosis and/or occlusion in 25/53 arteries. Results of statistical analysis were as follows; overall diagnostic accuracy 52/53 (98%), diagnostic sensitivity 25/26 (96%) and diagnostic specificity 27/27 (100%), respectively.
Moreover, intravenous CT carotid-angiography provided following benefits beyond arteriography.
1) Minimal calcification of the carotid wall and precise localisation of atheromatous plaque could be detected.
2) Patent arterial lumen above the occluded lesion could be found out.
3) CT carotid-angiography would be suitable for the follow-up study after carotid endoarterectomy because of the unnecessity of catheterization.
4) Thrombus formation in the internal jugular vein could be grasped.

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Dopamine, which is known to raise systemic blood pressure by stimulating alpha and beta-adrenergic receptors, also causes vasodilatation of the kidney and other organs by stimulating the specific dopamine receptors. It has been demonstrate in animals that either dopamine or dopamine agonist leads to cerebral vasodilatation, witch is blocked by its antagonists. These findings suggest that the specific dopamine receptors may exist in the cerebral arteries of certain animals. However, effects of dopamine on cerebral blood flow (CBF) is still obscure in human. The present study was performed in this respect.
The subjects comprised of 11 patiants with ischemic cerebrovascular diseases and 3 patients with degenertive diseases. The CBF was measured by the Argon inhalation method before and during intravenous administration of dopamine. Argon gas tension of arterial and internal jugular venous blood was continuously moniterd using the mass-spectrometer, and CBF was calculated by desaturation curve using the Fick princilpe. Dose-responses to dopamine were investigated in 6 subjects and autoregulation of CBF was examined by head-up tilting in 8 cases before and during dopamine.
The CBF was significantly increased from 41.3±7.9 (ml/100 g brain/min) to 46.1±8.9 (12% increase) after intravenous infusion of dopamine at a rate of 2μg/kg·min. Mean values for cerebral oxygen consumption before and after dopamine administration were 2.77±0.77, and 2.85±0.66 (ml/100 g brain/min), respectively, indicating that the drug had no significant effect on cerebral metabloism. During dopamine administration mean arterial blood pressure was slightly lowered and cerebrovascualr resistance was significantly reduced from 2.46±0.54 (mmHg/ml/100 g brain/min) to 2.15±0.51, although arterial blood gases and pH remained unchanged. Dopamine-induced 10% increase in CBF was not altered by changing infusion rate from 1 to 4 μg/kg · min but slightly reduced by high dose administration (8 μg/kg · min). On the other hand, autoregulation of CBF was not affected by dopamine.
The results suggest that small doses of dopamine may exert a direct vasodilating action on the cerebral arteries by stimulation of the specific dopamine receptors.

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The purpose of the present study was to investigate the possibility to estimate CBF autoregulation and cerebrovascular CO₂ reactivity by the retinal vascular responsiveness to changes in perfusion pressure and in arterial carbon dioxide tension (Paco₂).
The retinal arterial diameter and its response to changes in blood pressure and in Paco₂ were measured by means of a fundus camera in 6 control subjects without intracranial lesion, 15 patients with cerebrovascular disease (CVD), 2 with Shy-Drager syndrome and 3 with spinocerebellar degeneration.
Reduction of effective mean arterial blood pressure (effective MABP) was induced by the postural change from a recumbent to an erect position. The increase of Paco2 was induced by 5% CO₂ inhalation for 3 to 5 minutes in sitting position.
Changes in diameter of the retinal vessels were quantitatively analysed by the use of Retinal Vascular Index (RVI) (-a change in diameter (%) / a change in effective MABP (mmHg)) and Retinal Vascular CO₂ Reactivity Index (CO₂-I) (a change in diameter (%) / a change in Paco₂ (mmHg))
The results obtained were summarized as follows :
1) Both RVI and CO₂-I in patients with CVD were significantly lower when compared with those in control subjects (p<0.001 and p<0.05, respectively).
RVI in cases with acute CVD (<a month from stroke) and chronic CVD (>a month from stroke) was both significantly lower than that in control subjects (p<0.001 and p<0.05, respectively). RVI in acute CVd was lower than that in chronic CVD, but the difference was not significant. CO₂-I in cases with acute CVD was significantly lower than that in control subjects (p<0.001), but there was no significant difierence in CO₂-I between chronic CVD and control subjects.
In cases with unilateral CVD, RVI in both affected and non-affected side of the lesion was significantly lower when compared with that in control subjects (p<0.001 and p<0.02, respectively), but there was no significant difference in RVI between affected and non-affected side. CO₂-I was slightly lower in non-affected side and moderately lower in affected side whem compared with that in control subjects, but these difference was not significant among three groups.
2) In patients with Shy-Drager syndrome with severe impairment of the autonomic nervous system, RVI was significantly lower than that in control subjects (p<0.01). CO₂-I, however, did not show any significant difference between Shy-Drager syndrome and control subjects.
In patients with spino-cerebellar degeneration without impairment of the autonomic nervous system, RVI and CO₂-I were not significantly different from those in control subjects.
The above data indicate that the autonomic nervous system plays a role in the mechanism of autoregulation of retinal blood flow and that the mechanism is independent of chemical control of retinal vessels mediated by carbon dioxide.
Present results of the retinal vessels are compatible with the previous data of autoregulation and CO₂ reactivity obtained from the cerebral vessels. It is concluded that the observation of the retinal blood flow autoregulation and retinal vascular CO₂ reactivity are a useful method to estimate the CBF autoregulation and cerebrovascular CO₂ reactivity.

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Elevation of serum amylase activity has been reported in a variety of conditions without clinical manifestation of pancreatic disease, such as postoperativi state, hypoxemia or head trauma.
We measured serum amylase activity and plasma noradrenaline in 60 patients with acute cerebrovascular disease. The highest value of the serum amylase activity was 6380 S.U./dl (normal range 70 to 220 S.U./dl) in cerebral hemorrhage. The mean serum amylase activity for cerebral hemorrhage, subarachnoid hemorrhage and cerebral infarction was 668±51 (SEM) S.U./dl (N=26), 489±83 (SEM) S.U./dl (N=7), and 146±2 (SEM) S.U./dl (N=27), respectively. The mean value for serum amylase activity was significantly higher in cerebral hemorrhage or subarachnoid hemorrhage than in cerebral infarction (p<0.05). The serum levels of amylase activity well reflected the level of consciousness and prognosis. Serum amylase activity reached the highest level within a few days following onset, and then gradually decreased towards a normal level over the next 7 to 9 days. In addition, hyperamylasemia was associated with increased plasma levels of noradrenaline. These findings suggest that in the acute stage of cerebrovascular disease, amylase is released into the circulating blood presumably from the pancreas or the salivary glands associated with the excitement of sympathetic nervous activity.

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An autopsy case of secondary diabetes insipidus associated with subarachnoideal hemorrage, which had been considered a rare cause of diabetes insipidus, was reported.
The patient was a 54-year-old male who was admitted to our hospital on April 17, 1978 with the chief complaints of severe headache and vomitting. He had hypertension for 10 years. Two weeks prior to admission he experienced transient headache. In the morning of April 12, 1978 he developed severe headache associated with vomitting after defecation. His headache was containued until the time of admission.
On physical examination the patient was awake and alert. General physical examinations were unremarkable except for high blood pressure (156/90 mmHg) and mild nuchal rigidity. Fundoscopic examination revealed the hypertensive changes (KW IIa).
The lumbar puncture revealed that the opening pressure was 220 mmH₂O, and the CSF was bloody. One and a half hours after admission, patient became deeply comatous suddenly, and the pupils became dilated and fixed to light. And occasionaly apnea was noted; therefore, dexamethazone was administered and oxygen inhalation was started. However, the apnea continued and the patient was placed on the respirator. Thereafter, polyuria developed; the urine volume was 600 to 1340 ml/hr with the specific gravity of 1.0041.006. Following the administration of vasopressin, the urine volume decreased and the specific gravity of the urine increased. However, the patient did not recover and expired 43 hours after the admission.
Postmortem examinations revealed subarachnoideal hemorrage due to the rupture of the aneurysm of the left anterior communicating artery, which penetrated to the ventricular system. Histological findings revealed that the hypothalamus was necrotic; especially, the supraoptic and paraventricular nucleus were disappeared, and the anterior and posterior lobe of the pituitary were also necrotic.

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