Caplan reported the frontal artery sign as a bedside indicator of internal carotid artery occlusion. A 76-year-old man, who was normal except the previous history of transient ischemic attacks, drug-induced parkinsonism and multiple lacunar infarctions on CT scan, showed this sign in addition to the external carotid artery sign (ECS) of Olivarius.
His right superficial temporal artery was remarkably engorged (ECS), and its frontal branch had an anastomosis with the frontal artery of internal carotid origin. On palpation, the blood flow of the frontal artery was inverted (FAS).
On angiography, a complete obstruction of his right cervical ICA was confirmed and retrograde filling of intracranial ICA via ophthalmic artery was also observed.
The frontal artery sign is a good indicator of collateral flow in ICA occlusion, and is very diagnostic even if in an asymptomatic carotid occlusive disease.

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The authors describe a case of aneurysm arising from the fenestrated proximal anterior cerebral artery (A1 segment).
A 52-year-old female suddenly developed severe headache and vomiting, followed by disturbance of consciousness. At the other hospital, the patient was diagnosed subarachnoid hemorrhage by CT scan and lumbar puncture. On the 2nd day, she was translated to our hospital for the operation.
Angiographies demonstrated an aneurysm arising from the A1 segment with spastic irregular vascular wall. Therefore, the operation was performed immediately. When the neck of aneurysm was clipped, the small fenestration was found out at the A1 segment of the distal of it.
On the retrospective examination, the small fenestraton was just found out in the irregular wall of the A1 segment by the subtraction film of the left oblique C.A.G.
The patient had temporary mental disturbance due to suspected vascular accident at the 7th day after the operation. Although, she recovered soon without neurological deficit, but CT scan demonstrated low density area on the left anterior lobe.
In the literatures, the aneurysm at the fenestrated A1 segment has been reported only 8 cases. As these cases compared with out case, the relation of position between the neck of aneurysm and fenestration is not similar.
As an another characteristic in these reported cases, the rate of poor prognosis due to vasospasm is high (50%). This results suggest that the vasospasm is related to the fenestrated vascular wall.

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A 52-year-old woman with clinical manifestations of Winiwarter-Buerger's disease (thromboangiitis obliterans : TAO) developed an intracerebral hemorrhage. She had been suffering from gangrene of her fingers and toes for 13 years and had been receiving ticlopidine for the last three years. She was admitted to our hospital after a sudden onset of convulsive seizure and consciousness disturbance. CT scanning showed a walnut-sized high density area in the left frontal opercula. The left carotid angiography demonstrated tapering of posterior internal frontal artery as well as wide-spread narrowing of operculofrontal artery. Based on these angiographical findings and the patient's history of Winiwarter-Buerger's disease, a diagnosis of cerebral thromboangiitis obliterans (CTAO) was made. Our speculation is that the long term use of ticlopidine might have induced the intracerebral hemorrhage in this CTAO patient with possibly fragile cerebral vessels. The occurrance of intracerebral hemorrhage in this patient appears to claim precautious monitoring in high-dose antiplatelet therapy for patients with Winiwarter-Buerger's disease, especially for those with concomittant CTAO.

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Effects of oxygenation at high pressure (OHP) therapy on clinical outcomes and lactate concentration in cerebrospinal fluid (CSF) were studied in 32 cases with acute cerebral infarction. Another 12 cases who did not receive OHP were used as control.
CSF lactate level exceeded the normal range to 2.01 ± 0.58 (± SD) mmol/L at 3 or 4 days after the onset of the stroke. Following OHP treatment, the levels were lowered to 1.70 ± 0.26 mmol/L at 19 days and to 1.69 ± 0.24 mmol/L at 33 days, whereas the abnormally high levels remained (1.8-1.9 mmol/L) even at 30 days after the onset in the control group of patients.
The patients were devided into three groups according to the severity of the neurological deficit and the impaired consciousness; mild, moderate and severe groups. Neither the clinical course nor the levels of CFS lactate was different between OHP treated and control groups of mild as well as severe cases. In contrast, the neurological recovery in the moderately impaired patients was significantly better in OHP treatment group than in control one. CSF lactate levels in the former group were 1.95 ± 0.23 mmol/L before the treatment, followed by a marked decrease 1.58 ± 0.27 at 10 OHP and to 1.58 ± 0.21 at 20 OHP. In control group, the levels were 2.03 ± 0 mmol/L at first examination, and remained relatively high as 1.96 ± 0.34 mmol/L at 18 and 1.96 ± 0.07 at 32 hospital days.
These results suggest that OHP treatment seems to be effective in the case with moderate nenrological deficit in acute cerebral infarction.

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Consecutive 36 patients with cerebral embolism, admitted within 48 hours after onset, underwent serial echocardiographic and blood coagulation studies prospectively. The new formation of left atrial thrombi and/or the recurrence of embolic episode were documented in three of 36 patients within two weeks after initial embolic episodes.
The left atrial size in the recurrent group was larger than that in the non-recurrent group, and tendency to reduction of the left atrial size before recurrence was demonstrated by echocardiography. This phenomenon was associated with the increment of hematocrit value, which might reflect hemoconcentration. Blood coagulation study revealed lower plasma level of fibrinogen and relatively shorter partial thromboplastin time in the recurrent group. These results suggest the presence of hypercoagulable state and the plamsa fibrinogen consumption derived from thrombus formation in the recurrent group.

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In 21 patients (15 males and 6 females, mean age 62 years old) who developed the depressive state without dementia after stroke in the cerebral hemisphere, we studied the time course of the depression and its relation to the recovery of regional cerebral function evaluated by the change of regional cerebral blood flow (rCBF). Zung's self-rating depression scale (SDS) was administered for the quantitative evaluation of the depression. Regional CBF was measured with 133-Xe inhalation method.
Ten patients showed improvement in depressive state, but 7 patients had no change in SDS scores and 4 patients became more depressive during the mean follow-up periods of 7 months. The degree of improvement in depressive state was not significantly related to sex, age, duration from the attack, and mean blood pressure in the initial interview. The recovery of activities of daily living had also no relation to its improvement. On the other hand, the patients with higher cortical dysfunction or Parkinsonism showed poor improvement of the depression. The changes of mean rCBF was inversely correlated with that of SDS scores significantly (r=-0.77, p<0.001). Moreover, the improvement in depressive state were strongly related to the increase of rCBF in the anterior portion of the bilateral temporal lobe, in the posterior lower portion of the left frontal lobe, and in the right parietal lobe.
The depressive disorder after cerebrovascular accident may be closely related to the pathophysiology of the temporal lobe function.

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We report immunohistochemical findings of a case with recurrent carotid stenosis after endarterectomy. A 59-year-old female had restenosis of the carotid artery 2 years and 6 months after the first endarterectomy. Stenotic region was removed and bypassed with a saphenous vein graft. The arterial lumen showed whitish and glistering luminal surface with no ulceration. Microscopic findings is consistent with hyperplasia of spindle-shaped cells from media to intima. Immunohistochemical staining revealed that these cells contained smooth muslce actin. Therefore, hyperplasia of smooth muscle cells and migration of those from media to intima is a main cause of restenosis after endarterectomy.

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Clinical significance and pathogenesis of neurogenic hypernatremia were investigated in 38 patients with angiographically proven internal carotid artery (ICA) occulsion. Patients were classified into two groups : group A (died within 2 weeks) and group B (survived more than 2 weeks), and the changes of their sodium metabolism were studied. The number of cases indicating hypernatremia (serum Naγ150 mEq/l) in group A : 16/18 (89%) exceed group B : 1/20 (5%) (p<0.01). There was no significant difference between group A and B in the mean amount of the sodium administered, infusion volume, BUN, Ht and creatinine. In 16 cases of hypernatremia in group A, an increase in the K/Na ratio in urine and a decrease in sodium out-put/intake ratio to below 1 were observed from two days before the onset of hypernatremia. The hypothesis here is that an excessive reabsorption of sodium has led these results. However, no significant changes were observed in already-known hormons including aldosterone. And the CT findings show that low density area at the anterior portion of the IIIrd ventricle exists in all cases of group A (100%) while it exists in 4 to 20 cases of group B (20%).
The above results allow us to consider that neurogenic hypernatremia accompanied with acute phase of ICA occlusion brings about poor prognosis. As for the pathogenesis, the over-reabsorption of sodium related with the damage at the anterior portion of the IIIrd ventricle and with some unknown substance such as aldosterone were suggested.

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The purpose of the present study is to clarify the effect of nifedipine on local cerebral blood flow in patients with cerebral infarction. Local cerebral blood flow was measured in 10 patients aged 59.1 ± 9.1, who had the attack of cerebral infarction 1-3 weeks prior to the measurement. The cold xenon enhanced CT method using 35% Xe gas with in-vivo autoradiographic strategy was applied to measure the local cerebral blood flow (1-CBF). After the first measurement of 1-CBF, complete desaturation was performed and nifedipine (10 mg) was administered subligually. Then, the second set of scans for 1-CBF measurement after nifedipine and scan for local lambda value were made. Following the administration of nifedipine, the mean arterial blood pressure significantly decreased from 98.5 ±15.4 to 91.8 ± 12.6 mmHg (p<0.05). The mean CBF through the level of basal ganglia did not change following nifedipine administration (before nifedipine administration, 58.1 ± 12.5 ml/100 g brain/min; after nifedipine, 56.9 ± 10.2). The changes in CBF had no relationship with the degree of reduction in arterial blood pressure. The distribution of CBF improved after nifedipine administration in 4 cases, and re-distribution was observed in 3 cases. These findings suggest that cerebral blood flow did not uniformly decrease following nifedipine administration unless the decrease of blood pressure induced by nifedipine is prominent, and that nifedipine has direct vasodilatory effect on cerebral vessels.

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Experimental vasospasm of the cerbral arteries was produced in dogs by the double injection method. Somatosensory evoked potentials were recorded epidurally on the cerebral cortex and the second cervical vertebrae. Cerebral blood flow was measured by H₂ clearance technique. Angiography, taken periodically, revealed diffuse vasospasm of about 50% of the control vascular diameter at 48 hours after the second blood injection. However there was no significant delay of the central conduction time after the appearance of vasospasm. Regional cerebral blood flow was reduced to 33.1 ± 12.9 ml/100 g/min, nearly 70% of control blood flow, just after the first injection of autologous blood into the subarachnoid space. Then 20% flow reduction was observed at 48 hours after the second injection of autologous blood.
Our results confirmed that cisternal blood injection alone did not reduce the cerebral blood flow significantly despite the presence of angiographic vasospasm. Furthermore, it did not affect the central conduction time. This suggests that the vasospasm produced by cisternal blood injection does not induce a critical level of cerebral ischemia, which is frequently induced following ruptured cerebral aneurysm in clinical cases.
There is no argument that vasoactive substances derived from the extravasated blood induce vasospasm; however, vasospasm alone does not produce such severe cerebral ischemia. We would like to stress that initial brain damage induced by subarachnoid hemorrhage together with vascular tearing might be importatant for the occurrence of symptomatic vasospasm.

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We report a 63 year-old woman suffering from subclavian steal syndrome (SSS) due to severe stenosis of the left proximal subclavian artery. Her cheif complaint was dizziness when exercising her left arm. A difference in blood pressure between the two arms was the only abnormal physical finding. The reversed blood flow of the left vertebral artery was detected by Duplex ultrasonography examination (Duplex). She was treated by percutaneous transluminal angioplasty (PTA) for the stenosis of her left subclavian artery and the stenosis was improved.
But after 6 months she complained of the same symptom and we found by Duplex that her left vertebral artery blood flow was poor. We followed up her left vertebral artery blood flow using Duplex. Her left vertebral blood flow was reduced and the flow reversed. So we performed PTA again without any complication and the SSS was treated. She has had no re-stenosis since the second PTA.
Duplex is found to be a rapid, safe and accurate method for confirming clinically suspected SSS.
PTA can be repeated and is found to be an effective treatment for SSS due to subclavian stenosis.

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Recently the significance of MRI in the diagnosis of cerebrovascular disease has been recognized, and the findings of “Moyamoya Disease” have been reported utilizing strong magnetic field MRI scanner. In this paper we discuss the usefulness of MRI especially in the assessment of vascular abnormality in this disease.
At first, MRI and cerebral angiography in six cases of “Moyamoya Disease” were studied. The vascular diameter of cavernous portion in angiogram were compared with the degree of stenosis of that portion in MRI. There was good correlation between the degree of stenosis in angiography and that in MRI. Also MRI clearly revealed the stenosis or occlusion in the circle of Willis, and the development of “Moyamoya” vessel in basal ganglia.
Next, we examined the usefulness of fast scan, which is a new method obtaining the vascular enhanced image. In normal fast scan, images of each arteries of the circle of Willis such as terminal portion of ICA or proximal portion of ACA, MCA are constantly delineated in high intensity in contrast with brain parenchyma, skull bone, soft tissue, venous system, and CSF space which are visualized in low intensity in general. In the cases of “Moyamoya Disease”, each portion of the circle of Willis as well as cavernous portion of ICA showed stenotic change which are more clearly demonstrated in fast scan. And the development of “Moyamoya” vessels in basal cistern was also visualized in detail with good contrast. On the other hand, “Moyamoya” vessels in basal ganglia are not always visualized clearly.
As a result, vascular abnormality of “Moyamoya Disease” is evaluated finely and noninvasively in detail in MRI, and MRI is useful in screening and follow-up in this disease.

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“So-called” posterior communicating artery aneurysm usually mean the one arising from the internal carotid-posterior communicating junction. The aneurysms arising from the posterior communicating artery itself have been very rarely reported, and we report such a case.
A 40-year-old woman was referred to our clinic with the diagnosis of subarachnoid hemorrhage. Cerebral angiography revealed an aneurysm of the posterior communicating artery. She underwent an operation at day 1 and grade 2 (Hunt & Hess). A saccular aneurysm was found to be arising from the posterior communicating artery 3 mm distal to its origin from the internal carotid artery and projecting laterally and inferiorly. There was no branching observed around the neck. The aneurysm was clipped without difficulty. The patient was discharged without any neurological deficits.
The literature of this “true” posterior communicating artery aneurysm was reviewed, and technical points to be noted at surgery were discussed.

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We have investigated Metrizamide CT-cisternography in multi-infarct dementia (MID) : 29 cases, senile dementia of the Alzheimer type (SDAT) : 7 cases, normal pressure hydrocephalus (NPH) : 8 cases and spinocerebellar degeneration (SCD) : 3 cases.
By quantitative manner the differences of cerebrospinal fluid (CSF) flowdynamics in each group have been evaluated. In comparison with SCD which show normal CSF flow, MID show tendency to ventricular reflux and convexity stasis. No difference was seen between MID and SDAT. Though NPH shows stronger ventricular reflux than that or MID, the stasis in MID is more severe than that of NPH. In MID group subject of older than 70 years show more severe SCF flow disturbances. When divided into two groups by ADL (Activities of daily living) scale (full of 15 points) the group of less than 6 points show slight disturbances in comparison with that of more than 6 points. And the same is true in Hasegawas dementia rating scales, namely the group of less than 21 points (full of 32.5) shows slight disturbances in comparison with that of more than 21 points.
The flow dynamics pattern of slight ventricular reflux in 24 hours and stasis in convexity from 24 to 48 hours seems to be typical in either MID or SDAT. But such a pattern has never been reported in SCF flow dynamics studies. These findings may suggest that CSF flow disturbances have a close relation with aging and dementia.

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Regional cerebral blood flow (CBF) and brain atrophy were studied in 41 stroke patients with or without dementia aged over 65 years. CBF was measured using ¹³³Xe inhalation method at chronic stage (more than one month after the onset), and flow through gray matter (F1) and initial slope index (ISI) was calculated in each cerebral hemisphere. A ratio of maximum width of frontal horn of lateral ventricles and outer table of the skull (FHI), and a ratio of minimum width of cella media and outer table of the skull (CMI) were measured on CT scan. The presence and the degree of dementia was evaluated using Hasegawa's dementia rating scale.
F1 and ISI in the affected hemisphere were 37.1, 31.6 ml/100 g/min in dementia (pre-dementia and dementia), respectively, being significantly lower than 47.7, 37.7 ml/100 g/min in non-dementia (p<0.01, respectively). Such CBF reduction was found in the non-affected hemisphere as well as in the affected one. CMI was 0.248 in dementia, which was significantly greater than 0.217 in non-dementia, although there was no difference of FHI between dementia and non-dementia. F1 in severe dementia was 31.2 ml/100 g/min, being significantly lower than 40.1 ml/100 g/min in moderate dementia (p<0.05), although there were no differences of both FHI and CMI between the two groups. No specific localization of the hypoperfused area was noted in dementia.
Present results suggest that diffuse reduction of CBF is closely related with the development of dementia in stroke patients.

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