OBJECTIVE : We analyzed the incidence and types of strokes in cancer patients, and evaluated the clini-cal utility of coagulation and fibrinolytic markers in cancer patients as compared to non-cancer patients.
METHODS : A retrospective review of all ischemic strokes between January 2000 and December 2005 was conducted. Seventy-four patients (males, 53; females, 21) were identified. Age, gender, cancer diagnosis and histology, and vascular risk factors were recorded. The following coagulation and fibrinolytic parameters were examined : thrombin-antithrombin III complex (TAT), FDP D-dimer, α₂-plasmin inhibitor/plasmin complex (PIC), antithrombin III (AT-III), fibrinogen (FIB), and platelet cell count.
RESULTS: The strokes were embolic in 45 patients (60.8%) and thrombotic in 29(39.2%). The most com-mon primary tumor was gastric cancer (23%). The most common histopathology was adenocarcinoma (60.8%). Both mean D-dimer levels were higher in the malignant patients as compared to the controls (D-dimer: 15.4 ± 21.6μg/ml vs. 3.9 ± 6.8μg/ml, p<0.05). An increased serum CA19-9 level was correlated with the serum D-dimer level (CA19-9 vs. D-dimer : R = 0.37, p<0.05) .
CONCLUSION : Activation of the coagulation system in cancer patients was more closely related to the cause of stroke than in patients without cancer ; that is to say, increased serum D-dimer levels might have the possibility to become predictors of stroke onset.

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Inflammation of the vascular endothelium is reported to cause atheromatous plaques and worsened athe-rosclerosis. It has been found that stroke patients with atherosclerotic lesions present increased inflammatory markers in the chronic stage. Focal inflammation following ischemia causes expansion of the stroke volume, and even oxidative stress plays an important role in the pathogenesis of vascular injury. It is critical therefore to minimize the effects of inflammation in order to improve the treatment and outcome of stroke patients. Ischemic stroke patients who were admitted to hospital within 24 hr of the onset were enrolled into the present study (n=104). The subjects were classified into the following groups based on their MRI and MRA findings : embolic stroke (n=30), atheromatous stroke (n=29), lacunar stroke (n=41), and arterial dissection (n=4). Inflammatory markers, such as high-sensitive CRP (hsCRP), TNFgbα, IL-6 and oxidized LDL, were sampled on admission. The NIHSS was used for assessment of the clinical severity, which was observed on the first and 28^th days from the onset. The oxidized LDL was significantly elevated in all groups on admission. The hsCRP was significantly elevated in the embolic and atheromatous stroke groups. A significant correlation with the NIHSS was noted for the IL-6 of the embolic stroke group and for the TNFα of the lacunar stroke group. A deteriorating outcome was related to an increased level of IL-6 in the embolic stroke group. In conclusion, increases of inflammatory markers, observed in the acute phase, may indicate the severity of stroke lesions.

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Background and Purpose: The neurological severity of acute ischemic-stroke is evaluated worldwide using the National Institutes of Health stroke scale (NIHSS). In Japan, the Japan Stroke Scale (JSS) which was developed originally in Japan is also used. Several reports have suggested the efficacy of stroke scales for the evaluation of acute ischemic stroke receiving thrombolytic therapy. We assess the clinical usefulness of the NIHSS and JSS in cases receiving local intra-arterial thrombolysis (LIT). Methods: Neurological severity was assessed before, immediately after, and at 24 hours and one month after LIT using the NIHSS and JSS. We evaluated outcome at discharge based on the modified Rankin Scale (mRS) and the Barthel index (BI) score. Results: Sixteen patients receiving LIT underwent assessment by the NIHSS and the JSS. The NIHSS score was significantly related to the JSS score at each time of measucement. The mRS score at discharge was significantly related to both the stroke scale scores at 24 hours and those at one month after LIT. When the NIHSS score improved immediately by 2 or more after LIT and the JSS score improved by 0.65 or more, the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) for a good outcome (mRS 5 2) at discharge were 0.75 vs. 0.75, 1.00 vs. 0.875, 1.00 vs. 0.875, and 0.80 vs. 0.778, respectively. Conclusion: Periodical evaluation of the NIHSS and JSS in patients with acute middle cerebral artery occlusion receiving LIT is useful for predicting patient outcome at discharge.

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Purpose : We evaluated the clinical features of patients with subarachnoid hemorrhage (SAH) at our hospital. Methods : 430 patients with SAH were analyzed retrospectively. Results : At admission, 259 patients (60%) revealed a poor Hunt & Kosnik (H&K) grade (IV or V). Among these 259 patients, 100 demonstrated cardiopulmonary arrest at admission. We detected the cause of SAH in 274 patients (64%) : 272 patients were bleeding from cerebral aneurysms, and 2 were bleeding from arteriovenous malformations. Aneurysmal clipping was performed in 129 patients and coil emobolization was performed in 56 patients. At the time of discharge, 129 patients (30%) showed good recovery, 36 patients (8%) showed moderate disability, 32 patients (7%) showed severe disability, 3 patients (1%) were in a persistent vegetative state, and 230 patients (54%) were dead. Conclusion : About 60% of the SAH patients who were admitted to our hospital had a poor H&K grade and poor outcome.

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An analysis of published clinical studies was made using the technique of meta-analysis to evaluate the effectiveness of edaravone, a brain-protective agent, against lacunar infarction. An electronic information search was conducted employing three key words (edaravone, stroke, and humans), and abstracts from major scientific meetings were explored by undertaking a manual search for the abstracts. The authors of the extracted reports were asked to cooperate with the study and to provide related data. From the 35 reports for which authors' approval was obtained, we selected those which met the following criteria for metaanalysis : (1) studies involving a control group and 10 or more patients treated with edaravone, (2) studies in which mRS was one of the variables analyzed, and (3) there was no significant difference in severity on admission between the edaravone-treated group and the control group. The selected 14 reports were subjected to pooled-analysis for the effectiveness of edaravone against lacunar infarction. When the functional outcome of the patients with lacunar infarction was evaluated using the percentage of cases rated as mRS 0-1, the outcome was slightly better in the edaravone-treated group, with an odds ratio of 1.41 (95%CI : 1.01-1.97), and this difference was statistically significant. These findings suggest that the functional outcome of patients with lacunar infarction can be improved by treatment with edaravone.

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Background and purpose : Migraine is a rare but important etiologic factor of brain infarction in young people. We investigated the relationship between migraine and brain infarction.
Methods : Seven patients (6 females and one male) who suffered brain infarction after migraine attacks were included. The mean age at cerebral infarction was 30.0 (range, 22 to 45) years old.
Results : Two patients suffered migraine with aura and 5 patients suffered migraine without aura before the brain infarction. Six patients had vertebral-basilar and posterior cerebral artery lesions and one patient had middle cerebral artery lesions. None of the patients had hypertension, hyperlipidemia, diabetes, or cardiogenic diseases. Beta-thromboglobulin and platelet factor IV were elevated in 85.7% of the patients. Antinuclear antibody was positive in 57.1 % of the patients. One patient was IgM anti-cardiolipin antibody positive, and 2 patients were lupus anticoagulant positive.
Conclusion : Our results suggested that brain infarction can be caused by exposure to a hypercoagulable state, and could be related to autoimmune abnormalities or anti-phospholipid antibodies.

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We examined the clinical features of our cases of subarachnoid hemorrhage of unknown etiology (SAHUE) which were not diagnosed for the origin of their bleeding at initial cerebral angiography. Thirtyfour cases which could not be diagnosed for the origin of their bleeding on initial cerebral angiography among 325 consecutive cases of non-traumatic subarachnoid hemorrhage that were admitted to our hospital between February 1997 and June 2005 were included. We defined the 15 cases of unknown etiology and with no rebleeding to date as Group A, and the 19 cases where the origin of the bleeding was found or which rebled as Group B, and compared the clinical features of the two groups. Group B was worse as regards the symptoms on admission, the volume of the hematoma on CT scans, the severity of symptomatic vasospasm, the existence of hydrocephalus and the prognosis as compared to Group A. Among our 34 cases of SAHUE, the origin of the bleeding was identified in 15 cases. Overall, internal carotid artery aneurysms (six cases) and vertebrobasilar artery aneurysms (six cases) were tended to show a higher frequency. Five cases out of the 6 internal carotid artery aneurysms were so-called internal carotid artery anterior wall aneurysms (ICA). In our series of SAHUE, approximately half of the cases were truly unknown for the origin of their bleeding, and normal SAH with ruptured aneurysm was included at a higher frequency than we thought. We should bear in mind that a SAHUE with a bad prognosis could be a case of ruptured ICA.

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The difference in functional prognosis by the time of transfer to convalescence sickbed was evaluated from the acute stage sickbed in 59 stroke patients using the motor FIM. The whole home return rate was 79.6%. The motor FIM at admission, in the patient group which was transferred within 1 month of development of symptoms, improved from 50.5 to 75.4 (FIM gain, 24.9) at discharge. The motor FIM in the group transferred at less than 2 months improved from 51.6 to 66.1 (FIM gain, 14.5), and that in the group transferred at less than 3 months improved from 38.3 to 50.3 (FIM gain, 12.0). Even if viewed according to each FIM, in all items, differences were evident between each FIM. Moreover, the home return rates were 91.6%, 73.0%, and 25.0%, respectively. It was considered that a motor FIM of around 70 represented a turning point in the discharge destination (home or institution). Accordingly, in order to aim at an ADL of this level, it is required that the patient be transferred from the acute term sickbed smoothly, and within 1 month of development of symptoms at the latest.

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We describe a 67-year-old man with atherothrombotic stroke who had a carotid mobile lesion and underwent carotid endarterectomy in the acute phase of stroke. He was admitted to our institute because of sudden development of aphasia and right hemiparesis. MRI diffusion-weighted images revealed multiple high intensity lesions in the left internal carotid artery (ICA) territory. Carotid ultrasonography demonstrated that the central part of the low-echoic plaque in the left ICA was moving concomitantly with the arterial pulsation in association with floating thrombus in the distal portion. Transcranial Doppler detected micro-embolic signals in the middle cerebral artery. Artery-to-artery emboli originating from a carotid mobile lesion were considered to be the cause of the acute ischemic stroke. Despite antithrombotic therapy, the mobility of the carotid plaque remained unchanged for more than 3 days. Carotid endarterectomy was then performed at 4 days after admission in order to prevent stroke recurrence. Following the endarterectomy, the patient showed good functional recovery without recurrence of stroke. On histopathological examination, the carotid mobile lesion was found to represent an intra-plaque hemorrhage accompanied by capsular rupture, a high-risk state of cerebral ischemia. A carotid mobile lesion detected by echosonography, as found in our case, may represent a high-risk state of cerebral ischemia. In such cases, carotid endarterectomy may be recommended to prevent ischemic stroke even in the acute phase of stroke.

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A 104-year-old woman suddenly developed right hemiplegia and aphasia due to cardioembolic stroke. At onset, she fell down and bruised her face. Although computed tomography (CT) did not demonstrate apparent intracranial hemorrhage, diffusion-weighted and FLAIR magnetic resonance imaging (MRI) revealed a small amount of subdural hematoma. Accordingly, we did not use intravenous recombinant tissue-type plasminogen activator for her stroke. MRI appears to be more capable of detecting intracranial hemorrhage than does CT. For patients with hyperacute ischemic stroke who have a recent history of head injury, MRI may be advantageous over CT as a decisive diagnostic tool for indicating thrombolytic therapy.

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Background : The clinical features of dural arteriovenous fistula (dural AVF) vary from mild complaints to life-threatening symptoms. Methods : Twenty-eights patients diagnosed as dural AVF were studied. All imaging findings, clinical features, and treatment procedures were retrospectively analyzed. Results : The dural AVFs were located in the cavernous sinus (n = 13), transverse sigmoid sinus (n = 7), anterior cranial fossa (n = 4), marginal sinus (n = 1), and craniocervical junction (n = 3). According to Borden's classification, 18 patients were of type I, 8 of type II, and 2 of type III, respectively. The patient presentations were asymptomatic in 5 cases (28%) and mild in 7 cases (39%) of type I, and aggressive in 5 cases (63%) of type II. Hemorrhagic episodes were seen in 2 cases of types II and III. Drainer clipping was performed in 4 patients, direct sinus packing in 2, endovascular embolization in 12, irradiation in 2, and observational management in 8. Eighteen patients (64%) achieved a resolution of their preexisting symptoms, 9 patients (32%) remained asymptomatic or stable with moderate disabilities, and one patient died with subarachnoid hemorrhage. Conclusion : Proper management procedures depending on each of the clinical findings or angiographical patterns should lead to a benign course for dural AVF.

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Although reversible diffuse white matter signal changes caused by dural arteriovenous fistula (DAVF) are well known, studies on changes in the cortical gray matter have not been described. This report deals with a case of multiple DAVF associated with widespread but reversible high-intensity areas in the cortical gray and white matter detected on MR imaging and featuring status epilepticus. A 62-year-old man with a history of previous cerebral infarction and convulsions presented in a confused state. One day after the onset of confusion, he developed status epilepticus, while mild right hemiparesis was observed. T₂ weighted MR imaging revealed a diffuse and widespread hyperintensity area in the left cortical gray matter. Fluid-attenuated in-version recovery (FLAIR) imaging demonstrated additional extensive high-intensity lesions in the gray and subcortical white matter of the left occipital, parietal and temporal lobes. The left thalamus and right cerebellar hemisphere also showed high-intensity abnormalities. Angiography revealed multiple dural arteriovenous fistulas associated with the superior sagittal sinus as well as left transverse sinus thrombosis. The abnormalities seen on MR imaging except for the ischemic region in the left white matter improved after control of the status epilepticus and embolization of the DAVF. Reversible gray matter signal changes induced by status epilepticus have been reported, but not in the case of DAVF. In our patient, cytotoxic and vasogenic edema due to venous hypertension may have caused the diffuse and marked but reversible abnormalities.

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We assessed the current status of urgent medical services for patients with acute in-hospital stroke before the era of rt-PA. Nineteen consecutive patients with acute in-hospital stroke were enrolled. The main causes of hospitalization were cardiac disease in 10 and digestive disease in 3 patients. The major subtypes of stroke were cardioembolic stroke (n=5) and atherothrombotic infarction (n=5). The median NIHSS score was 5.5, and 4 patients suffered stroke during sleep. The median delay in detection from onset was 5.7 hours. In the late detected group, tendencies for having a lower NIHSS score and/or for suffering during sleep were observed. Acute in-hospital stroke was common at the cardiology department. The delay in detection may be longer for patients with mild symptoms and/or onset during sleep.

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