Patients with ischemic cerebral infarction (except those with cerebral embolism) were retrospectively studied to determine the relationship between the prevention of recurrence and inhibition of platelet aggregation by ticlopidine. The subjects comprised 68 patients, including 50 males and 18 females, aged 70.2 ± 9.2 years on average. We measured the platelet aggregation induced by adenosine diphosphate (ADP) during a mean period of 30.2 months. Cerebral infarction and TIA recurred in 15 patients during this period. The oral administration of ticlopidine (200 mg/day or 300 mg/day) resulted in a significant inhibition of ADP-induced platelet aggregation. In contrast, no difference in platelet aggregation was observed between the recurrent group and non-recurrent group either before or after the treatment. However, there was a significant cumulative difference favoring the lower group over the higher group, when were divided on the basis of the below 15% (<15) and above 15% (≥15) for their platelet aggregation values. Serial measurements of the platelet aggregation during treatment were performed in at most patients, and the reproducibility was good. These results suggest that it is useful to determine the platelet aggregation with ADP and that it may be necessary to change the dose of ticlopidine when considering individual differences in antiplatelet effects with the drug.

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The auditory event-related potential (ERP), somatosensory evoked potentials (SEP), visual evoked potential (VEP) and brainstem auditory evoked potential (BAEP) were studied in 15 patients with Alzheimer's disease (AD), 16 patients with multi-infarct dementia (MID) due to subcortical infarctions and 15 normal control subjects. Both groups with dementia showed significant prolongation of the N200 and P300 latencies of the ERP as compared with those of the normal controls. In addition, patients with AD revealed significant prolongation of the P200 latency. Patients with MID showed significant prolongation of N13-N20 and N20-P40 of the SEP as compared with the normal controls, while patients with AD revealed only significant prolongation of N20-P40. There were no significant differences in P100 latency of the VEP among the three groups. The interpeak latencies between the I and V waves of the BAEP in patients with AD and MID were significantly longer than that of the normal controls. Thus, electrophysiological differences between MID and AD were noted in the ERP and SEP. The present results indicate that these two diseases with dementia exhibit abnormalities of evoked potentials, and also have some electrophysiological differences, which may be related to the underlying pathogenetic mechanisms. Measurement of multimodal evoked potentials, particularly of the SEP and ERP, may be helpful for the differential diagnosis of AD and MID.

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The present study focuses on the localization of ET-like immunoreactivity in the human stroke brain and on the expression of ET-1 in both the endothelium and astrocytes in relation to the healing process of occlusive cerebrovascular disease (CVD). Five patients with occlusive CVD were examined. Immunohistochemical studies on the human stroke brain were performed using rabbit polyclonal anti-human ET-1 antibody (Peptide Institude Inc., Japan). In each stroke brain, the immunohistochemical method demonstrated heterogeneous staining for ET-1, with different intensities of immunoreactivity among the central MCA, boundary MCA and non-MCA tetritories. Within the boundary MCA tetritory, the endothelial cells of the brain capillaries exhibited strong staining for ET-1 like immunoreactivity. Foot processes from astrocytes demonstrated ET-1 immunoreactivity, were attached and contributed to the formation of the preendothelial cell basement membrane. It was found that the foot processes of astrocytes encircled the endothelial cells with strong staining for ET-1 and also expressed ET-1 immunoreactivity. ET-1 can thus be produced by astrocytes and endothelium, with interection between them. Our data provide strong evidence ot suggest that the expressions of ET-1 in astrocytes and endothelium are closely related to the healing process of occlusive CVD.

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The relationship between the recurrence of ischemic stroke and the progression of carotid atherosclerosis was evaluated by B-mode carotid ultrasonography. The subjects comprised 90 consecutive patients with more than one carotid plaque (average age 64.6 ± 9.4 y.o.) who could be examined repeatedly after average intervals of 14.2 ± 6.0 months. Twelve patients (Group A) developed thrombotic stroke episodes during the study period, while the remaining 78 patients (Group N) did not. There was no significant difference in the severity of carotid atherosclerosis (plaque score : PS) between the two goups at the first observation. The control levels of risk factors for cerebral infarction during the period, and the percentage of patients on anti-platelet therapy were also not significantly different. The progression rate of PS was greater in Group A than in Group N (1.83 ± 1.30 vs. 0.95 ±1.03) (p <0.05). When comparisons were made among each site of the carotid arteries, the difference was remarkable just above (p<0.05) and below (p < 0.01) the flow divider. Furthermore, when Group A was divided into three subgroups with lacunar infarction (LI), TIA and atherothrombotic infarction (AI), the PS progression was significantly greater in TIA (p < 0.01) and AI (p<0.05) than in Group N. From the standpoint of the risk factors considered, good control of hypertension significantly suppressed the PS progression (p <0.001). Additionally, anti-platelet agent administration was considered to have a potential to suppress the progression of carotid lesions. The present findings clarified that the recurrence of thrombotic stroke (TIA and AI) was closely related to the progression rate of carotid atherosclerosis, and the progression rate appeared to be suppressed by good treatment of hypertension.

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We studied 44 emergent patients with cerebrovascular diseases 18 cases of subarachnoid hemorrhage, 15 of occlusive lesions, 7 of intracerebral hematoma and 4 of suspected subarachnoid hemorrhage using helical CT scan. The helical CT scan was performed with contrast medium at a rate of 3 ml/sec with a delay of 20 sec, and was carried out before conventional angiography. The reconstruction time of 3D-CTA was within 10 min. We were able to obtain findings for the lesion on 3D-CTA before those on conventional angiography. The 3D-CTA yielded excellent images of the vascular structures and anatomical relationships of the aneurysm, its neck and parent artery, and surrounding arteries. However, it proved difficult to visualize vessels of less than 1 mm in diameter, especially the perforating arteries. In occlusive diseases, the degree of stenosis depended on the changes in CT number thershold : at present, evaluations of the lesions should be made by conventional angiography. 3D-CTA using helical CT scan can thus be applied for emergent patients with cerebrovascular diseases. Surgical simulation images of 3D-CTA were especially useful at the time of operation.

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Recently, low-dose aspirin therapy for preventing cerebral thrombosis has become a popular procedure, based on the fact that high-dose aspirin would induce aspirin dilemma because aspirin inhibits the cyclooxygenase activity of not only platelets but also endothelial cells. However, even low-dose aspirin therapy is not sufficient to improve aspirin dilemma satisfactorily. We attempted to correlate the changes in platelet aggregability and serum prostanoids (6-ketoPGF_1α and thromboxane B₂) in the same patients while they were taking aspirin alone and while they were taking aspirin with beraprost (60 μg per day). The platelet aggregation was measured with an aggregometer using platelet-rich plasma with ADP (2.0 μM) and collagen (2.0 μg/ml). The serum 6-ketoPGF_1α and thromboxane B₂ were determined by radioimmunoassay. No difference was noted in the ADP-induced platelet aggregation, but the collagen-induced platelet aggregation was markedly inhibited by aspirin with beraprost. Concerning the prostanoids, no significant difference was noted in the levels of 6-ketoPGF_1α, but there was significant decrease in the levels of thromboxane B₂. The ratio of 6-ketoPGF_1α/thromboxane B₂, which is a useful parameter for judging the effects of antiplatelet agents, tended to become elevated but not significantly, while patients were taking aspirin and beraprost. In conclusion, low-dose aspirin together with beraprost may be more useful for avoiding dilemma than just aspirin alone.

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We examined the common carotid (CCAs) and internal carotid arteries (ICAs) by duplex sonography and the middle cerebal arteries (MCAs) by transcranial color-coded sonography (TCCS) in 50 volunteers (24 men, 26 women; mean age, 35 ± 9 years). We were able to measure the angle-corrected flow velocities of all arteries. The mean ± SD values for the flow velocities in the CCA, ICA, and MCA were 45.2 ± 7.6 cm/sec, 37.9 ± 9.8 cm/sec, and 83.1 ± 21.0 cm/sec, respectively. We analyzed the side-to-side ratio and correlation between the CCA and ICA, CCA and MCA, and ICA and MCA. The side-to-side ratio was calculated by dividing the faster velocity by the slower one. The side-to-side ratios for the CCA, ICA, and MCA were 1.2 ± 0.2, 1.2 ± 0.3, and 1.1 ± 0.1, respectively. There no significant correlation between the CCA and MCA (r=0.26) and ICA and MCA (r=0.30). However, a significant correlation existed between the CCA and ICA (r=0.50). We consider that duplex sonography and TCCS represent a potentialy practical technique for estimating cerebral blood flow. Our data should facilitate the process of defining normal and abnormal flow patterns for the extracerebral and intracerebral arteries.

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We report two cases with clustering of TIAs, i.e. crescendo TIA, who developed into cerebral infarction within a few days after the initial TIA attack. Case 1 was a man of 56 years of age with hypertension, and case 2 was a woman of 42 years of age with hypertension and diabetes mellitus. The former patient suffered from transient pure motor hemiparesis (face, upper and lower limb) 6 times during a period of 3 days, and the latter patient from transient sensorimotor stroke (face, upper and lower limb) 8 times during 3 days. Both developed into lacunar infarction in the territory of the cerebral basal ganglia despite intensive therapies including heparin administration. Neither case had cardiac arrythmia, cardiac diseases, blood coagulopathy, of cerebrovascular lesions. The mechanism of TIA in our cases was strongly considered to be in-situ small perforating vessel disease, such as lipohyalinosis. It is suggested that crescendo TIA, where the neurologic manifestation is lacunar syndrome and the mechanism can be explained by perforator lesions, is resistant to various kinds of preventive procedures and shows a poor prognosis, resulting in cerebral infarction within a short period. We discuss the particular characteristics of this type of TIA in relation to the literature.

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A case of optic aphasia, alexia without agraphia and color anomia associated with left posterior cerebral arteyr occlusion is reported. The 83-year-old right-handed man suddenly developed visual disturbance. Neuropsychological examinations did not reveal aphasia or gross mental deficits. The patient presented with alexia, agraphia, color anomia, and optic aphasia. His reading disturbance was severe. There was no difference among letters, words and sentences, or between Kana and Kanji. Writing disturbance was moderate. Copying of written material was impaired. He displayed severe naming disturbances when objects and pictures were presented to him visually. However, he could always describe the use of an item, and pantomime how the object was used. He named all common objects placed in either hand. His naming erros were rare when objects were presented as dictionary-like spoken verbal definitions or when the sounds specific to the objects were presented. He could easily categorize objects and photographs presented to him visually. He was always accurate when asked to select an item from a group of objects. Naming of colors was impaired. CT scan and MRI revealed infarcts of the left temporooccipital region and splenium. Cerebral angiogrpahy demonstrated occlusion of the ambient segment of the left posterior cerebral artery. The fundamental deficit in this patient could explained in terms of visuo-verbal disconnection due to lesions of he left tempporo-occlpital region and splenium.

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We experienced a case of a variant type of persistent primitive trigeminal artery (PTAV). An anomalous branch of the precavernous internal carotid artery is very rarely demonstrated angiographically. Its branch, originating at the level where the persistent primitive trigeminal artery is usually found but having no communication with the basilar artery, supplies vessels of the posterior fossa directly. Its location and course approcimated those of the supperior cerebellar artery. We report one case and review 75 reported cases. Based on a detailed assessment of these 76 cases, we emphasize the clinical significance of PTAV as follows : 1) it is readily be accompanied by cerebrovascular disease; and 2) it may be complicated with deficits of the cranial nerves including trigeminal neuralgia. The embryological mechanism and incidence of the artery are also discussed.

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