Potassium channels appear to be present in most cells and play an important role in regulation of the membrane potential. In cerebral blood vassels, four different potassium channels have been described: ATP-sensitive potassium channels, large conductance calcium-activated potassium channels, voltage-dependent patassium chonnels, and inward rectifier potassium channels. Activation of the ATP-sensitive and large conductance calcium-activated postassium channels appears to play an important role in the dilatory responses of cerebral blood vessels to diverse endogenous stimuli. The influence of these potassium channels is altered in disease states such as hypertension, diabetes, and atherosclerosis. It has been reported that an activator of ATP-sensitive potassiun channels effectively dilated spastic cerebral arteries following experimental subarachnoid hemorrhage. We have recently demonstrated that intracar-otid infusion of ATP-sensitive potassium channel openers can reduce ischemic neuronal damage in a focal ischemia model of the rats. It is possible therefore that modulation of the activity of potassium channels could provide a new therapeutic strategy for brain infarction and subarachnoid hemorrhage.

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Background: Post-stroke depression and apathy are not rare, and represent serious problems affecting the quality of life of stroke patients. However, few reports have evaluated the influence of apathy and depression on the cognitive functions of stroke patients. To investigate these problems, we examined certain relationships among cognitive functions.
Methods: The subjects comprised 57 stroke patients (51 cerebral infarction cases, 6 cerebral hemorrhage cases; mean agem 69.1 years). Apathy was assessed by using a revised apathy scale (Starkstein, 1993), and the depressive state was assessed by Zung's self-rating depression scale (SDS). The regional cerebral blood flow (rCBF) was measured by the Xe133 inhalation method. Cognitive functions were evaluated by revised version of Hasegawa's dementia rating scale, Okabe's mental scale, Kohs' block design test, verbal fluency, and a Kana pick-up test.
Results * Apathy was observed in 32 patients (56%), and 16 patients (28%) showed a depressive state. Thirteen patients had both. The apathy scale was significantly correlated with cognitive deficits (Kohs' block design test, verbal fluency and the Kana pick-up test) and with the duration after stroke. On the other hand, no significant correlations were noted between SDS and cognitive functions except for Okabe' s mental scale. There were no significant differences in apathy scores and SDS among the groups classified according to the severities of periventricular hyperintensity.
Conclusion: Apathy has a more significant influence on cognitive functions than does the depressive state, especially in terms of the performance IQ and frontal lobe functions.

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We studied disorders involving nocturnal blood pressure decrease in 33 patients with Binswanger's encephalopathy, evaluating the significance of non-dippers in this disease. When blood pressure was monitored over a 24-hour period (at 30-min intervals). non-dippers (mean night-time blood pressure greater than or equal to mean daytime blood pressure) were found to amount to 16 cases (48.5%). This rate was higher than that in patients with lacunar infarction (18.4%). Cases of non-dippers demonstrated more severe deficits in the vegetable-naming test, Kana pick-out test, and walking ability. MR imaging of non-dippers was characterized by marked periventricular hyperintensity and multiple small highintensity areas in the subcortical and brainstem regions. These findings were not related to intracranial large vessel stenosis on MR angiography and carotid plaque on B-mode ultrasonography. The presence of non-dippers among patients with Binswanger's encephalopathy would imply progress of the disease, associating with small vessel disease in the white matter and other parts of the brain.

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The expression profiles of cyclooxygenase-2 (COX-2) mRNA following transient and permanent middle cerebral artery (MCA) occlusion were studied using in situ hybridization. COX-2 immunoreactivity was also evaluated in permanent MCA occlusion. COX-2 mRNA was induced prominently in the ischemic cortex at 4 h of reperfusion following 30 min of transient occlusion and persistently until 24 h of the reperfusion period. With 90 min of transient occlusion and permanent occlusion, it was induced over a widespread region of the cerebral cortex except the ischemic region, medial striatum and bilateral hippocampi. Immunohistochemical investigations revealed COX-2 immunoreactivity in the large neuronal cells of the cerebral cortex, granule cells and pyramidal cells in the hippocampi at 24 h of permanent occlusion. In this study, COX-2 was shown to be induced in the surrounding and remote ares of the ischemic region as well as in the ischemic region itself. These data suggest that persistent acceleration of arachidonic acid metabolism might be elicited even in areas remote from the ischemic region.

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Recent evidence that apoptosis, programmed cell death, is at least partially involved in delayed neuronal death, prompted us to hypothesize that selective and vulnerable death in the hippocampal CAl sector may work in the direction of attenuating brain damage caused by further ischemic insults occurring in the future. Employing gerbils, we examined whether or not preconditioning with 5-min forebrain ischemia can ameliorate mortality and cell damage caused by 15-min forebrain ischemia given 10 days later. In a previous study, we found that gerbils preconditioned with 5-min forebrain ishcemia had a significantly attenuated mortality and body weight loss after 15-min forebrain ischemia, although the pathological findings for the brain tissues from 14-day survivors did not reveal any significant differences between the nonpreconditioned group and preconditioned group. In the present study, therefore, we examined the brain edema and pathological changes in gerbils at the time point when it was not yet known whether the asimals would die or survive. The brain edema at 2 hours, 2 days and 7 days after 15-min forebrain ischemia was significantly reduced in the preconditioned group (p<0.01). The pathological findings obtained by the Gallyas staining method also demonstrated less severe cell damage in the cerebral cortex and hypothalamus in the preconditioned group. The present data indicated that the ameliorating effect of preconditioning with 5-min forebrain ischemia on the mortality and body weight loss was well correlated with an attenuation of edema formation and cell damage in the brain.

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In a search for the simplest technical variations of photothrombosis we employed a krypton laser to induce photothrombotic cortical infarction in rats. The cortical region was irradiated by krypton laser transmission through the skull. The photosensitizing dye, rose bengal, at a body dose of 20 mg/kg was administered intravenously at a time interval of 90 sec. We confirmed reproducible infarction at laser powers of 5, 10 and 20mW, but not at 2mW. The rise in brain cortical temperature during irradiation with the laser beam applied directly to the cortex at 7 mW, which corresponds to 10mW used through skull, was less than 2°C; this was thus likely to avoid epiphenomena due to excess heat absorption. The advantages of our method may be summarized as follows. Highly reproducible infarcts can be produced, even though the model does not entail extensive surgery or opening of the skull. The 568-nm krypton laser does not require a high maintenance dye laser. Producing bilateral cortical intraction is also feasible. This thrombotic model affords useful standards for assessing the effects of antiplatelet treatment.

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We report a 39-year-old man with Wallenberg's syndrome due to dissecting aneurysm of the left vertebral artery following snowboarding injury. He was admitted to our hospital complaining of headache, nausea, vomiting, dysarthria and disturbance of swallowing at about one month following the injury. Clinically, he developed Wallenberg's syndrome. Head MRI demonstrated infarctions in the left dorsolateral part of the medulla oblongata and left cerebellar hemisphere and a flow void signal surrounded by a high signal area on TI- and T2-weighted images, suggesting a thrombus in the pseudo-lumen of the left vertebral artery. Vertebral angiography revealed an obstruction of the left vertebral artery, compatible with dissecting aneurysm. This might have been caused by overextension and rotation of the patient's neck. Although Wallenberg's syndrome due to dissecting aneurysm has been reported after minimal neck injuries incurred during skiing, etc., this is the first report to indicate that snowboarding injury can cause traumatic cerebrovascular disease.

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A 72-year-old right-handed woman was admitted to our hospital because of consciousness distrubance and left side weakness. She was found to have consciousness distrubance, anosognosis for left hemiplegia, left unilateral spatial neglect, dysarthria. left hemiplegia, left sensory disturbance, and left Babinski's sign. A brain CT scan on admission showed no infarction. Atral fibrillation was observed by electrocar-diography, and transthoracic echocardiography demonstrated an enlarged left atrium and mitral stenosis. anticoagulant therapy was initiated under a diagnosis of cardioembolic stroke in the territory of the right middle cerebral artery. However, a brain CT scan on the 3rd day revealed an infarction in the right thalamus, and no infarction in the right middle cerebral artery territory. Cerebral angiography on the 7 th day demonstrated occlusion of the right posterior cerebral artery. Brain MRI on the 13th day disclosed enhanced lesions in the right thalamus (almost the whole), right cerebral peduncle, right cerebellum and bilateral hippocampus. SPECT on the 5th day showed hypoperfusion in the basal ganglia and right temporal, parietal and frontal lobe. The left unilateral spatial neglect persisted for several days, and the anosognosia disappeared on the 15th day. The mechanism of anosognosia in this case is presumed to have involved (1) disturbance of the attention-arousal system due to right masive thalamic infarction, (2) left sensory disturbance, and (3) the presence of other lesions (bilateral hippocampus).

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A 62-year-old right-handed man with diabetes mellitus, suddenly experienced difficulty in writing.A physical examination at 40 days after the onset of this symptom was unremarkable. He exhibited non-fluent speech with a small voice. His performances on the Standard Language Test of Aphasia (SLTA) demonstrated moderate impairments in writing and animal naming, and slight impairment in object naming. Brain MRI demonstrated localized infarcts in the left centrum semiovale and left lateral occipilotemporal gyrus. ^99mTc-HMPAO SPECT revealed widespread hypoperfusion in the left middle cerebral artery (MCA) territory. Caroid ultrasonography suggested bilateral internal carotid artery occlusion, which was proved by cerebral angiography. The patient underwent left superficial temporal-middle cerebral arterial anastomosis, and soon after the surgery his spontancous speech and writing improved. At 2 months after the surgery, SPECT demonstrated improvement of the hypoperfusion in the left MCA territory, and the SLTA failed to dctect impairments any more. We speculate that not the infarcts but the widespread hypoperfusion area had caused his language disorder. Extracranial-intracranial bypass surgery may improve aphasia due to cerebral infarction in some cases. Screeing tests on the vascular system, employing SPECT and carotid ultrasonography, are vey important.

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We report 3 individuals from one family with intracranial aneurysms subarachnoid hemorrhage due to ruptured aneurysm at the junction between the left internal carotid artery and posterior communclating artery. Case 2 (a 55-year-old male) was found to have an unruptured cerebral aneurysm at the junction between the left internal carotid artery and posterior communicating artery. Case 3 (a 57-year-old male) was investigated by us, and demonstrated evidence of aneurysmal dilation at the junction between the left internal caroid artery and posterior communicating artery. All or these patients were operated on successfully. Familial intracranial aneurysms have been emphasized to show the following characteristics:(1) ease of rupture at younger ages as compared to not familial ones, (2) to be localized at the same site or a mirror site, (3) a greater likelihood to be multicentric, (4) flemale aneurysms somewhat outnumber male ones, and (5) a likelihood to runture at the same age. On the other hand, many problems remain, as follows: (1) securing a firm diagnosis as familial intracranial aneurysm, (2) which siblings should be anamined and when?, (3) is MRA maliable or not for accurate detection in order to avoid raise-nepative cases?, (4) deciding how to rical with infundibular dilatation, and (5) sctailed procedures and methods of follow-up. Strenous need to be made to resulve such problems. We discuss our 3 operated cases form among 8 siblings of one family and review some of the pertinent literature on familial intracranial aneurysms.

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We report a patient with cerebral terminal zone infarction who was waiting for an operation on rectal cancer. A 57-year-old woman with diabetes mellitus developed somnolence, total aphasia and right hemiparesis immediately after collection of blood (about 400 cc) for the purpose of preoperative aurologous blood donation. An MRI examination revealed left cerebral terminal zone infarction. Cerebral angiography demonstrated occlusion of the left internal carotid artery at the intracranial portion. This case suggested that inadvertent collection of blood from a patient with asymptomatic internal carotid artery stenosis or occlusion could be a potential source of hemodynamic infarction. Recently, preoper-ative autologous blood donations have frequently been practiced. We emphasize that patients who have risk factors of atherosclerosis should be evaluated for intra- or extra-cranial vascular disease by employing non-invasive techniques such as MR angiography or carotid ultrasonography.

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