In order to investigate the distribution of lesion size and to determine the background factors responsible for large infarcts, we examined CT findings in 88 consecutive patients with acute cardiogenic cerebral embolism of the internal carotid arterial system. Lesion size was determined by brain CT, and expressed as the “infarct index”. The typical CT finding was a sharply marginated lesion in the cortex corresponding to the occluded arterial territory, accompanied by mass effect. Over half of the cases showed an infarct index of 20% or less. Most cases had small lesions, with substantially fewer cases having large infarcts. The lack of large infarcts was attributable to early recanalization of the occuluded artery. Several background factors were implicated in the large infarcts, including elevated hematocrit, fibrinogen, arterial blood pressure, cardiothoracic ratio (as seen in chest X-rays), and a shortening of activated partial thromboplastin time (APTT). Factors implicated in the formation of a large embolus included increased blood viscosity and coagulability (caused by dehydration), and a hypertension-induced shift of the lower limit of autoregulation to a higher level. Further study is needed to determine whether such changes arise as the cause or the effect of a cerebral embolism.

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Spontaneously hypertensive rats (SHR) were used to study the effects of ion channel blockers on ischemic neuronal death. Transient cerebral ischemia was produced by occlusion of bilateral common carotid arteries for 10 minutes in combination with hypotension (50 mmHg). One, 2, 3, 4 or 7 days after ischemia, the animals were perfusion-fixed and their brains were processed for histological study. The number of intact neurons per millimeter (neuronal density) of the CAl region of hippocampus was investigated to assess the neuronal damage. Seven days after ischemia a significant decrease of the neuronal density was observed. The effect of ion channel blockers on delayed neuronal death in 7 days was then assessed. The calcium channel blocker, piperazinyl ethanol derivative (NC-1100) or the N-methyl-D-aspartate (NMDA) antagonist, dizocilpine (MK-801) was administered intravenously just before the induction of ischemia. A vehicle group was made by the same manner using saline. The neuronal densities of NC-1100 treated and MK-801 treated groups were 118.6±12.6/mm and 120.7±12.8/mm, respectively, while that of vehicle group was 73.3±16.5/mm. The NC-1100 treated and MK-801 treated groups showed significant protective effects compared to the vehicle group.
This study demonstrated that a calcium channel blocker and a NMDA antagonist protect against delayed neuronal death. It suggested that calcium influx through calcium channel and/or NMDA-linked ion channel plays an important role in delayed neuronal death in hippocampal CAl region.

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Many neuropathological investigations have suggested that periventricular hyper-intensity (PVH) lesions on MR-T₂ weighted image reflect ischemic change in these lesions. Intimate relation between PVH and dementia was also reported in some etiological studies. Nevertheless, only a few trial was performed in aspect of cerebral blood flow and metabolism. This study was planned to investigate the relation between PVH. ischemia and dementia using positron emission tomography (PET).
Thirty-three patients with subcortical cerebral infarction were classified under prevalence of PVH on MR-T₂ weighted image. PVH (+) group (n=-17) with severe PVH and PVH (-) group (n=16) without PVH were investigated. Neuropsychological examinations and DSM-III-R were classified them into two stages (none dementia and dementia). In addition, nine normal subjects were examined as control. Regional cerebral blood flow (CBF), oxygen extraction fraction (OEF), cerebral metabolic rate of oxygen (CMR02), cerebral blood volume (CBV) were measured by PET using C¹⁵O₂, ¹⁵O₂, ¹¹CO inhalation technique.
None dementia cases in PVH (+) group, significant decrease in CBF and significant increase in OEF were recognized in the region of frontal cingulate gyrus and PVH lesion compared to normal group. Such changes were also significant in compared to PVH (-) group without dementia. Meanwhile, in PVH (+) group with dementia, decrease in CBF coupled with increase in OEF and decrease in CMRO₂ were recognized in PVH lesion and all cortical regions as compared with normal group. In some cortical regions in PVH (+) group with dementia, especially in frontal cortical regions also showed showed such significant changes compared in PVH (-) group with dementia. CBV in the region of frontal cingulate gyrus and CBF/CBV ratio in PVH lesion in PVH (+) group showed significant decrease compared with normal group.
These results indicate the existence of “compensated hypoperfusion” in PVH lesion and cortical regions especially in the region of frontal cingulate gyrus in multiple infarction patients without dementia. Moreover, “ischemic hypoperfusion” was observed in both PVH lesion and cortical regions in multi-infarct dementia. These changes, which seemed to be caused by cerebroateriosclerosis, preceded the appearance of mental deterioration and persisted after dementia appeared. Our findings also showed PVH reflects severe ischemic change of brain in multiple cerebral infarction patient, not only dementia cases but also none dementia patients.

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To investigate whether does subjective symptoms, such as forgetfulness relate to silent brain infarction-like lesion (SBI), we studied relationship between subjective symptoms and MRI findings in 124 normal adults. SBI was diagnosed by T₁ and T₂ weighted image (horizontal, coronal and saggital plane) using 0.15 T MRI. Cognitive functions were evaluated by Okabe's Mini-mental state test (Shortened and modified version of Wechsler Memory Scale for Japanese aged) and Kohs' Block Design Test. Subjective symptoms (forgetfulness, decrease of motivation and concentration as mental symptoms (A group), headache, dizziness, tinnitus, numbness as physical symptoms (B group)) were examined by interview form. All subjects were divided into each 3 groups by these symptoms. Group A-I (57 subjects) had no mental symptom, A-II (46) had forgetfulness alone and A-III (21) showed forgetfulness with decrease of motivation and concentration. Group B-I (54) had no physical symptoms, B-II (43) had one of these and B-III (27) showed more than two of these symptoms. Group A-III showed significantly higher incidence of SBI (47.6%) than those in A-I (10.5%) and A-II group (10.9%). Group A-III showed significantly lower cerebral blood flow (CBF) and Okabe's score and higher self-rating depression scale (SDS) score than those in another two groups. Obsessional symptom score of Leyton's obsessional inventory was higher in group A-II and A-III than those in A-I. B group symptoms did not relate to aging, SBI, CBF, cognitive functions and SDS.
Conclusion : Feeling of forgetfulness with depressive state may relate to SBI. Feeling of forgetfulness alone is not caused by SBI, the difference between A-I and A-II group may be caused by aging and mild obsessional character.

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Background and purpose : There has been little reported on the safety and efficacy of intravenous recombinant tissue plasminogen activator (alteplase) in elderly patients with acute cerebral embolism. Recently, von Kummer at al reported on the efficacy and safety of a combination of alteplase and heparin therapy.
Methods : Eight patients (male 3, female 5, mean age 81.4 +/-3) with abrupt onset severe hemispheric stroke syndrome caused by middle cerebral artery (MCA) embolism were treated with 40 milligrams (20 million international unit) of alteplase by intravenous infusion over 60 minutes within a mean +/-SD of 134.1 +/-60.8 (range 90-268) min. after symptom onset. Heparinization was continued by an infusion of 5000-10000 IU per 24 hours after alteplase infusion. We evaluated cerebral blood flow change before and after treatment using ^99mTchexamethy propyleneamine oxime and single photon computed tomography (SPECT). We also examined neurological improvement and prognosis compared to age-matched patients (N=17, male 7, female 10, mean age 78.2 ± 8.4) with similar neurological symptoms, but their arrival at our hospital was over two hours after symptom onset, and they were treated with conventional therapy.
Results : Two patients showed marked improvement within several hours, but one patient experienced a second attack within three hours of initial onset. The SPECT study showed marked cerebral blood flow improvement of the affected hemisphere in two patients, partial in six, and unchanged in two. These findings correlated with their clinical improvement. The treated group showed a better clinical improvement and prognosis compared with the control group at the early phase, even six months after onset. One patient of treated group without reperfusion died because of severe edema, six patients of control group died from severe edema, hemorrhagic infarction, and congestive heart failure. There was no fatal hemorrhagic complication in the treated group.
Conclusion : Combined fibrinolytic therapy, alteplase and heparin was safe and effective even in elderly patients. Elderly patients with severe MCA embolism showed poor prognosis and high mortality, when they were treated with conventional therapy. Therefore further fibrinolytic therapy with the elderly are needed.

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Vascular renin-angiotensin system has been suggested to play an important role in cerebral vasoactivities. The aim of the present study was to examine the effect of inhibition of angiotensin converting enzyme by cilazapril on intra- and extracranial circulation, cerebral metabolism and its vasomotor responses.
The study was performed on 14 monkeys (macaca fuscata). Internal carotid blood flow (ICBF), vertebral blood flow (VBF), external carotid blood flow (ECBF) and femoral blood flow (FBF) were continuously measured by electromagnetic flowmeters with simultaneous measurements of blood pressure, pulse rate and PeCO₂. Cilazapril (3 mg/kg) was intravenously injected in order to inhibit angiotensin converting enzyme (ACE). Cerebral vasomotor responses were quantitatively tested by means of controlled changes in blood pressure, autoregulation index (Al : ΔCBF/ΔMABP, ml/min/mmHg) and controlled changes in PaCO₂, chemical vasomotor index (CVI : ΔCBF/ΔPaCO₂, ml/min/mmHg).
1) Blood pressure and pulse rate : Blood pressure showed a significant fall after ACE inhibition, but no significant change was observed in pulse rate.
2) Intra- and extracranial circulation : ICBF and VBF decreased significantly in parallel with ACE inhibition by cilazapril. However, ECBF and FBF increased temporally and then ECBF was significantly decreased but FBF showed no significant change following ACE inhibition.
3) Cerebral metabolism : No significant changes were obtained in CMRO₂ between before and after ACE inhibition.
4) CBF autoregulation : AI to induced hypotension became significantly lower following ACE inhibition (p<0.05), but AI to induced hypertension showed no significant differences between before and after ACE inhibition.
5) CBF chemical regulation : CVI to induced hypocapnia was significantly lower in the carotid arterial system after ACE inhibition (p<0.05), but there was no significant alteration of CVI to induced hypercapnia.
The data suggest that ACE inhibition by cilazapril reduces systemic blood pressure and has benefical effect on CBF autoregulation to induced hypotension.

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A 50-year-old man with left thalamo-mesencephalic hemorrhage showed ipsilateral monocular paresis of downgaze and contralateral monocular paresis of upgaze with mild depression of the contralateral eye in the primary position, right Horner's syndrome and convergence disturbance. Bell's phenomenon and conjugate horizontal eye movements were preserved. He didn't have disturbance of consciousness, motor and sensory impairments. The lesion may have affected either a unilateral rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) itself or the descending fibers from the caudomedial and the dorsolateral parts of the riMLF, with incomplete impairment of posterior commissure or the crossed fiber from the contralateral riMLF.
We present an unique disturbance of vertical eye movements caused by a hemorrhage localized in the thalamomesencephalic area. To our knowledge, there has been no previous report concerning these peculiar ocular signs. These findings of such a case support the current concept concerning the function of the riMLF.

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Three cases of multiple cerebral aneurysms associated with the persistent primitive trigeminal artery (PTA) are presented. They were all women, and had subarachnoid hemorrhage due to rupture of the aneurysm at the junction of the internal carotid (IC) and the posterior communicating arteries, which were treated with neck clipping. Each patient had another unruptured aneurysm in the cavernous portion of IC which was not treated, at the junction of the IC and the anterior choroidal arteries which was treated with wrapping, and at the junction of the IC and PTA, respectively. All the aneurysms developed on the same side as the PTA. The unruptured aneurysm of IC-PTA was successfully treated by balloon occlusion. Usefulness of balloon occlusion in the treatment of aneurysm of the IC-PTA is discussed. Literature is reviewed.

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A case of locek-in syndrome due to bilateral cerebral pedunclar infarction was reported.
A 67-year-old man, who suddenly suffered from vertigo and slurred speech, was admitted to our hospital. Neurological findings on admission disclosed horizontal nystagmus, slurred speech, dysphagia, tetraparesis with positive right Babinski reflex and dysmetria in both upper limbs. Ten days later, he became bedridden with complete tetraplegia and showed right lateral gaze palsy.
Three months later, pupils were equal in size and reacted to light. Right lateral gaze palsy was observed. He did not respond to pinpricks, but unpleasant stimuli of each limb produced eye closure without any limb movements. He could not speak, but he showed good comprehension by blinking in response to verbal comands.
Brain MRI (T₁ weighted image; TR/TE=500/13 msec) disclosed low signal intensity lesions in the bilateral cerebral peduncles and the paramedian portion of the pontine tegmentum and basilar portion of the pons. Compared with the former, the lesion of the basilar portion of the pons was very small. EEG was normal. Short latency somatosensory evoked potential (S-SEP) with stimuli of left median nerve showed diminishment of amplitudes for the P13-P14 and N18 potentials.
Locked-in syndrome was previously considered almost equivalent to ventral pontine syndrome. We reported a rare case of locked-in syndrome due to lesions in bilateral cerebral peduncles.

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A 62-year-old right handed man suddenly developed difficulty in reading and writing. Brain CT and MRI showed cerebral infarction in the left posterior inferior temporal lobe. Neurological examination revealed alexia with agraphia and, to a lesser extent, anomia and disturbance of verbal comprehension. Both reading and writing difficulties were prominent in Kanji compared with Kana. Copying letters was correctly performed. The patient recovered well from reading difficulty, but writing difficulty, especially in using Kanji, remained almost unchanged. Three-dimensional surface display with 123I-IMP showed cortical hypoperfusion areas in the lower half of the middle temporal gyrus and the inferior temporal gyrus. Cerebral blood flow in the angular gyrus and superior temporal gyrus was preserved.
Alexa with agraphia due to the left posterior inferior temporal lesion has been reported in Japan. However, the anatomical distribution of lesions responsible for alexia with agraphia remains to be elucidated. The present case suggests that cortical areas in the left lower middle temporal and inferior temporal gyri play an important role in Kanji reading and writing, especially in Kanji writing, and concurrence of amnestic aphasia.

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A 65-year-old man had four ischemic strokes during a 6-month-period, two episodes occurred prior to admission and other two occurred while he was hospitalized. He was a heavy smoker and tested positive for anticardiolipin IgG antibody. Furthermore, he had renovascular hypertension, diabetes mellitus and low serum HDL-cholesterol. Multiple ischemic lesions were demonstrated in both cerebral hemispheres on MRI. Neurological symptoms were bilaterally observed in the sensory and motor system. His blood pressure and blood glucose level were controlled by antihypertensive drugs and diet, respectively, and he quited smoking. Although ticlopidin (100 mg/day) was orally administered, two atacks still developed after the admission. A combination therapy of warfarin potassium (2 mg/day) and aspirin (81 mg/day) was replaced for ticlopidine. Since then, he has been free from further attacks for 6 months. Anticardiolipin antibody and other multiple risk factors might have made the patient susceptible to the recurrent brain infarction. A prophylactic therapy of warfarin potassium and aspirin seems to be of use in these patients.

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We reported a 57-year-old man with unilateral asterixis due to a right thalamic hemorrhage. In addition to the asterixis in left upper limb, he had left hemiparesis, mild consciousness loss, dysarthria, mild disturbance of the left position sense, and left cerebellar sign.
We confirmed a right thalamic hemorrhage with a mild hemorrhage into the right lateral ventricule on the computed tomography and delay of the central conduction time of short latency somatosensory evoked potential. We suggested that asterixis may be caused by the dysfunction of pyramidal tract, cerebellum, and reticular formation.

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