Plasma cyclic adenosine 3', 5'-monophosphate (cAMP) and cyclic guanosine 3', 5'-monophosphate (cGMP) levels were measured by the competitive radioimmunoassay method in 13 patients with cerebral infarction and 8 patients with intracerebral hemorrhage soon after onset. Control studies were performed on out-patients more than 3 months after cerebral stroke and 225 normal volunteers. The results are as follows : 1) The mean plasma cAMP and cGMP levels of normal volunteers were 20.7±3.8 and 4.7±1.6 pmol/ml respectively with the cAMP/cGMP ratio of 4.8±1.7. 2) All the 11 patients in acute phase of cerebral infarction, who ultimately survived, showed almost normal levels of plasma cAMP and increased levels of plasma cGMP with significant difference from controls (p<0.001) on the first day of stroke, showing cAMP/cGMP ratio definitely lower than controls. Two patients, died in the course of acute cerebral infarction showed moderately increased plasma levels of cAMP and slightly increased plasma levels of cGMP with normal cAMP/cGMP ratio. 3) Five patients, died of intracerebral hemorrhage showed markedly increased plasma levels of cAMP, with scarcely increased plasma levels of cGMP, on the first day of stroke, with higher cAMP/cGMP ratio than that in patients in acute stage of cerebral infarction and controls. 4) The daily plasma levels of cAMP and cGMP were determined at least during the first week after onset in acute cerebral infarction. In survival cases, plasma cGMP kept in higher levels than controls, while plasma cAMP remained almost within normal range. Normalization of plasma cGMP level was found earlier in cases with more marked and rapid improvement than in cases with delayed improvement. 5) The inverse correlation was demonstrated between plasma cGMP levels and the Frithz's prognostic scores in 22 cases with acute cerebral infarction within 72 hours after onset with coefficient (r=0.53, p<0.02). From these findings, it was suggested that determination of plasma cGMP level in acute stage of cerebral infarction may be useful for the evaluation of its prognosis.

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The prognosis of spontaneous (hypertensive) intracerebral hematoma associated with the intraventricular hemorrhage were discussed with the base of computerized tomography (CT) findings in their acute stage.
104 (47%) out of 219 patients with hypertensive intracerebral hemorrhage revealed intraventricular hemorrhage in our service from January 1978 to December 1980. In these cases infratentorial, cerebellar and pontine hemorrhage were not included. Namely, 22 out of 93 cases of putaminal hemorrhage, 47 out of 61 cases in thalamic type, 30 out of 39 cases in combined type and 5 out of 26 cases in subcortical type were demonstrated the ventricular hemorrhage by CT examination, respectively.
In early period of CT utilization, the ventricular hemorrhage had generally been accepted as one of serious signs from the knowledges, which had been obtained from postmortem examination in such cases. Recent experiences, however, suggested that cases of intracerebral hematoma with the ventricle rupture were not always resulted to the poor prognosis. In this paper, following factors, which may influence the prognosis of such cases, were selected and investigated in our series of the cases.
These factors were :
1) hematoma size
2) intraventricular blood extention to 3rd and 4th ventricle
3) acute enlargement of the ventricle
4) disappearance of the ambient cistern
5) extension of hematoma to the hypothalamus
6) level of consciousness at admission time
Cases, which had extension of the hematoma to the 3rd and 4th ventricle, were clearly divided into two contradictory group, namely, poor and good prognostic group. They showed nearly equal occurance. However, it was noted that cases with the cast formation below the third ventricle resulted poor prognosis.
Statistical analysis of our cases led the following conclusions i.e. the influencing factors of the poor outcome are :
1) hematoma size is larger than 3×3 cm
2) combination of acute ventricular enlargement, disappearance of the ambient cistern and hypothalamic extension of hematoma
3) cast formation of blood in the 3rd and 4th ventricle
And, it is our impression that, if there are cases without abovementioned three findings, the immediate ventricular drainage will not be indicated but existence of increased intracranial pressure or critical condition.

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After C.T. was available, the pathological changes of the surrounding areas from the main lesion can be observed by C.T.
In this paper, the effect of the massive ventricular clot to the surrounding areas in the hypertensive ganglionic hemorrhage was histologically verified, paticularlly focusing to the changes of the nerve cells.
The results obtained were as follows :
1. The nerve cells had been transformed by effects of ventricular hematoma daily after the attack.
2. This transformation of the nerve cells was ischemic degeneration.
3. It is known that the stage which suggests the nerve cells to recover functionally is the stage of the nuclear eccentory or central chromatolysis of the nerve cells. We knew that this stage was the 3rd day from the attack.
4. If the effect of ventricular hematoma was prevented by 3 days, the nerve cells would be recoverd.
These results suggested that the early removal of the massive ventricular clot might be recommended.

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The number of stroke patients in the Shizuoka prefecture during the period between 1978 and 1979 was estimated based on the results obtained from a questinaire sent to 17 major hospitals, most of which are possessed of CT scan and division of neurosurgery. The data collected were analyzed with respect to stroke incidence by age and sex, type-specific frequency of stroke, the number of operated stroke and the number of deaths by stroke within the hospital.
The mortality statistics of stroke in the whole prefecture obtained from the local public health center was also compared with that of admitted cases.
The results were as follows :
1) Total number of deaths by stroke in the whole prefecture in 1977 was 4994 (total population of 3.43 million in Shizuoka prefecture), 68.9% of which belonged to the age group of above 70 years old.
2) On the contrary, of whole stroke patients who were admitted in the major hospitals mentioned above, 65% belonged to the age group of between 40-69 years old.
3) On the type-specific frequency of stroke in the admitted patients, cerebral infarction was 41.0%, cerebral hemorrhage was 30.9% and intracranial aneurysm was 18.6%.
4) The mortality rate during admission was 36% in cerebral hemorrhage, 27% in intracranial aneurysm and 11% in the cerebral infarction.
5) From the above data it was estimated that the total number of stroke incidence in some district would be as 4 or 5 times more than the total number of death by stroke.

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The present study was performed to investigate whether or not there are any differences in clinical features and outcome of cerebral embolism depending on the underlying (cardiac) disorders.
Forty eight patients with cerebral embolism were selected from 274 consecutive cases of acute cerebral infarction. Diagnostic criteria for cerebral embolism were reported elsewhere.
Underlying embologenic disorders were divided into three major categories, namely valvular heart disease (20 cases), arrhythmia of various types (17 cases, majority of them was fixed atrial fibrillation), and miscellaneous disorders such as bacterial endocarditis, acute myocardial infarction, etc.... Sources of emboli were unknown in two cases.
Mean ages of the patients with valvular heart disease (VHD) and those with arrhythmia (AR) were 53.6 and 69.4 years old. The former was significantly younger than the latter. Female was predominant in VHD group.
Disturbed consciousness of various degree, ranging from stupor to coma, was seen in approximately 60% of the patients in both VHD and AR groups. Functional outcome was, however, more unfavorable in AR group than in VHD group. Forty eight percent of the patients with arrhythmia and 20% of those with valvular heart disease became disabled at the time of discharge. This difference in outcome is probably due to an older mean age in AR group than in VHD group. Five patients died in VHD group, two of them due to recurrent embolizations to the abdominal organs, while only one died in AR group due to massive cerebral damage.
Occlusion of cerebral arteries was found in all cases of both VHD and AR groups, when the cerebral angiography was performed within three days of illness. There was no difference in the site of arterial occlusion and in the incidence of reopening of the occluded vessels between the two groups. However, arterial occlusion with visible emboli were more frequently seen in VHD group than in AR group.
The size of ischemic lesion on computed tomography (CT), which was expressed as a ratio of areas of low attenuation value to the hemispheric square measure, was 26.9±27.1% (mean±SD) in VHD group and 32.1±23.0% in AR group. There was no significant difference between the two groups in the size of cerebral lesions and in the incidence of hemorrhagic infarction as judged by CT.
After admission 16 systemic embolic episodes occurred in 11 out of 20 patients with valvular heart disease, but only two episodes in two cases of AR group. In VHD group, 13 episodes were in the vascular systems outside the brain (including the extremities). When the embolic episodes preceeding the present admission were included, 46 systemic embolic episodes occurred in 20 cases of VHD group (2.3 episodes per patient), and 21 episodes in 17 patients of the AR group (1.2 episodes per patient).
Thus, the patients with valvular heart disease suffered from recurrent arterial embolization more frequently than those with arrhythmia alone, although the latter tended to show more unfavorable functional outcome than the former, probably due to advanced age.

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In the occlusion of internal carotid artery (ICA), collateral blood flow is supplied either via the circle of Willis (large vessel collaterals) or through small vessel anastmoses such as cortical anastmotic channels or the anastmoses between external carotid arterial system and ophthalmic artery (small vessel collaterals). Efficiency difference between these two types of collaterals was studied in 40 patients with ICA occlusion using ¹³³Xe inhalation rCBF measurements.
Materials and Methods : Forty patients with chronic cerebral infarction due to ICA occlusion were subjected to this study. There were 35 males and 5 females with ages ranging from 39 to 76 years. On the basis of four-vessel angiography, these patients were divided into two groups, one receiving collateral flow mainly from the circle of Willis (n=27) and the other with collaterlas mainly through small vessel anastmoses (n=13). Each group was further divided into two subgroups according to the CT findings, one with large cerebral infarcts and the other with small infarcts. The regional cerebral blood flow (rCBF) was measured by ¹³³Xe inhalation methods, and cerebrovascular resistence in occluded hemisphere was estimated from rCBF values and mean blood pressure. In 11 cases, rCBF measurement was repeated 2 weeks to 5 months afterward, when blood pressure decreased spontaneously or due to administration of hypotensive agents.
Results : At the time of first rCBF measurement, mean blood pressure in cases of small vessel collaterals was generally higher than in those of large vessel collaterals. The mean hemispheric rCBF in occluded hemisphere was significantly reduced in patients with large infarcts compared to those with small infarcts, whether they had large vessel collaterals or small vessel collaterals. The rCBF in cases of large vessel collaterals and in those of small vessel collaterals was the same, if the size of infarcts was the same. Patients with small vessel collaterals had, however, significantly higher cerebrovascular resistence compared to those with large vessel collaterals, even if compared in groups with same size of infarcts. When blood pressure decreased spontaneously or after administration of hypotensive agents, rCBF showed little changes in patients with large vessel collaterals. On the other hand, marked rCBF reduction occurred in 3 of 6 patients with small vessel collaterals.
Comments : In the present study, cerebrovascular resistence in cases of small vessel collaterals was shown to be higher than that in cases of large vessel collaterals. This might be partly attributed to differences of blood pressure level, which virtually existed between two groups at the time of rCBF measurement. However, blood pressure difference does not seem to be the main reason for these results, since rCBF in cases of small vessel collaterals tended to decrease following blood pressure reduction, suggesting that autoregulatory response was impaired in this group. In small vessel collaterals, blood flow must pass through resistent vessels twice, while in large vessel collaterals only once. It is considered that high cerebrovascular resistence in cases of small vessel collaterals is mainly attributed to such an inefficiency in this type of collateral circulation. In order to supply sufficient blood flow to occluded hemisphere through small vessel collaterals, considerably high blood pressure may be required.

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Not many studies have been done in patients with hypertensive intracerebral hemorrhage (HIH) to evaluate their regional cerebral blood flow (rCBF). Any previous studies about rCBF in patients with HIH did not say the relationship between the change of rCBF and motor function.
Our study was performed in patients with HIH during resting state and investigated the correlation between mean cerebral blood flow (MCBF) and hematoma volume, duration from the attack, motor function, findings of CT scan. rCBF was measured in 50 patients with putaminal hemorrhage by the¹³³Xe intracarotid injection method.
The results were as follows :
1) The averages of MCBF in each duration within one year showed similar values, averaged about 30ml/100 g/min..
There was, however, a significant difference between the averages of MCBF within one year and that of over one year.
2) There was the close correlation between hematoma volume and MCBF within 3 months from the attack. Most of the cases having had the hematoma over 100 ml showed a relatively low value around 30 ml/100 g/min..
3) Most of cases continued low flow value for a long term, but which was independent on hematoma volume. A few cases with small hematoma revealed a good recovery of MCBF in short time. This findings was not always associated with the recovery of motor function.
4) There was a good relationship between the degree of motor disturbance and reduction of MCBF. The group with severe motor disturbance (Ueda's stages I, II and III) showed less value than 30ml/100 g/min..
5) The cases with a compression against internal capsule on CT scan showed various courses of recovery of MCBF and good recovery of motor function. While, the cases with destruction of internal capsule on CT scan showed less value at second investigation than at the first. However, there is no correlation between the recovery of motor function and that of MCBF in two groups.

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Autonomic nervous function is assumed to be deranged in the acute stage of cerebrovascular diseases (CVD), but no systematic evaluation of the function has ever been attempted in the disease. The purpose of the present study was to investigate the time course of the noradrenergic nervous function in patients with CVD from the view point of circulatory catecholamines.
Nineteen patients had occlusive CVD which consisted of 13 hemispheric and 6 brainstem infarctions. Hemorrhagic CVD consisted of 9 intracerebral and 10 brainstem hemorrhages. Blood samples were obtained serially from the onset up to 60 days after the stroke. Plasma catecholamines were measured with the method of high speed liquid chromatography. In hemorrhagic CVD without ventricular rupture, both plasma norepinephrine and epinephrine remained within normal range until 30 hours after the attack, then started to increase reaching an initial peak on the third day which was followed by second peak on the twelfth day. The mean curves of the time course for plasma catecholamines in occlusive CVD had two peaks, the first one on the third day and the second one on the eleventh day, similar to the peaks observed in hemorrhagic CVD. In the patients with ventricular rupture both catecholamine values were markedly elevated and reached to their highest values immediately after the onset of the disease. All patients with plasma norepinephrine over 800 pg/ml expired in the acute stage. The increase of plasma norepinephrine or epinephrine induced by head-up tilting reached its maximal level on the eleventh day, corresponding to the second peak of the basic catecholamine levels.
The above results confirmed the clinical assumption that the autonomic nervous function is deranged in the acute stage of stroke.

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This report contains a 13 year old boy of Duchenne's progressive muscular dystrophy (DMP) who suffered from cerebral embolism of possible cardiac origin.
The patient had muscular symptoms of DMP since the age of 2-3, together with mental retardation. He had been in National Nishitaga Hospital and educated there since the age of 6. During a month prior to onset of stroke, he was on 100 mg/day of diethylstilbestrol diphosphate in order to supress frequent and openly-performed masturbation.
On March 7th 1980, abruptly appeared loss of consciousness with right hemiplegia, conjugated deviation and vomiting. Motor aphasia was also noted next day when his consciousness became almost clear. 5 days later, on admission, right hemiplegia, motor aphasia and gynecomastia were noted in addition to apparent physical signs of DMP.
His brain CT taken 4 days after the onset showed a low density area in the left hemisphere, involving the internal capsule, lenticular nuclei and neighboring structures.
Angiograms taken 7 days after onset revealed an occlusion of the left carotid artery at its bifurcation to the anterior and middle cerebral arteries. Right retrograde carotid-vertebral angiograms showed completely normal arterial visualization including the left anterior cerebral artery. There were no findings suggestive of arteriosclerosis or inflammatory changes of the arterial wall. Angiograms taken 25 days after onset demonstrated recanalization of the occluded part.
His chest roentgenogram and ECG showed a marked cardiomegalia (CTR 63%) and myocardial damages frequently seen in DMP. Moreover, the mitral valve prolapse was strongly suggested by echocardiograms.
Laboratory examinations were within normal ranges except moderate leucocytosis, elevated CPK, slightly shortened bleeding time and elevated serum estrone for his age.
The possible roles of the mitral valve prolapse and estrogen intaken in production of cerebrovascular accident in the present case were discussed.

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A 32-year-old woman developed a sudden onset of vertigo, nausea and vomiting six days after she noted facial palsy on the left side. She had a history of pain in her left elbow accompanied by low grade fever three months prior to this episode. On admission, the blood pressure was 126/68 mmHg and heart sounds were normal. She was alert and well orientated. Neurological examinations revealed horizontal nystagmus, left facial nerve palsy of a peripheral type, hearing disturbance of the left ear, incoordinations of the left upper and lower extremities, and unsteadiness of gait. Raynaud's phenomenon and splinter hemorrhage of the nail were also noted while she was hospitalized. In addition to these symptoms, laboratory examinations disclosed marked proteinuria, increased blood sedimentation rate, positive LE cell tests and existence of the antibodies to DNA, suggesting that she was in an active stage of systemic lupus erythematosus (SLE). The CT scan performed 4 days after the onset showed a relatively large area of low density in the left cerebellar hemisphere, which was enhanced by the contrast medium after two weeks. Reexamination of CT seven months later demonstrated the clearly recognizable area of low density with well-defined margins, which was indicative of infarcted tissue. Vertebral angiography revealed stenosis of the left superior cerebellar artery at its origin. From the results of these examinations she was diagnosed as having cerebellar infarction probably due to cerebral vasculitis caused by SLE. To the best of our knowlege, this is the first report of the case with cerebellar infarction associated with SLE in Japan.

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