Background and purpose: Striatocapsular infarction (SCI) has been well recognized as subcortical infarcts mainly corresponding to the region of lenticulostriate arteries. Stroke mechanisms are mostly associated with embolic mechanisms and less frequently with middle cerebral atherothrombotic disease (MCAD). Although intracranial atherosclerosis is prevalent in Japan, SCI caused by MCAD has not yet been systematically studied. We therefore conducted the present study to elucidate the stroke mechanism of SCI caused by MCAD.
Subjects and methods: We selected 56 patients who had middle cerebral artery occlusion or stenosis, and classified patients into 3 groups: 1. 10 patients with pure SCI, 2. 5 with SCI plus, 3. 41 with non-SCI.
Results: Progressive motor deficits were found in 5 patients with pure SCI (50%), 3 with SCI plus (60%) and 17 with non-SCI (41%). Severe disability expressed by modified Rankin Scale on discharge was found in 9 patients with pure SCI (90%), 3 with SCI plus (60%) and 23 with non-SCI (56%). Middle cerebral artery occlusion was found in 7 patients and stenosis was found in 3 patients in the SCI group.
Conclusions: Patients with pure SCI and SCI plus exhibited a higher prevalence of progressive motor deficits and severe disability as compared to non-SCI. Three patients with SCI appeared to be caused by middle cerebral artery stenosis, and we speculated that penetrating arteries were occluded by atherothrombolic plaque. As SCI often shows neurological deterioration in the acute stage, the precise mechanism of infarcts should be further explored and intensive treatment should be tailored.

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Objective: This study was to investigate the effects of the angiotensin II (Ang II) AT1 receptor antagonist valsartan on blood pressure (BP) and cognitive functions in cerebrovascular hypertensive patients.
Methods: Nineteen patients aged 58–75 years with moderate essential hypertension (DBP > 90 mmHg and/or SBP > 140 mmHg, for more than six months after stroke onset) were assigned to once daily (o.d.) treatment with valsartan 80 mg for 8 months. The patients were examined every 4 months during the study, with pre-dose BP (standard mercury sphygmomanometer, Korotkoff I and IV) recorded at each visit. Cognitive function was evaluated at the pre-dose point and after 4 and 8 months of active treatment by means of four tests (MMSE, Trail making test A & B, WMS-R and Rey’s complex figure test).
Results: Valsartan had a clear antihypertensive effect, and led to a significantly greater reduction in SBP/DBP at 8 months (from 155.8/81.2 mmHg to 139.9/74.3 mmHg; paired-t test, 0.01). Valsartan significantly increased the verbal memory score (+8.1%; P < 0.01 vs baseline, Wilcoxon signed rank test), but did not induce any significant changes in any of the other cognitive function test scores.
Conclusion: These findings indicate that, in cerebrovascular hypertensive patients, 8 months of treatment with valsartan 80 mg o.d. is significantly effective in reducing BP, and improves some of the components of cognitive function, particularly verbal memory function.

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Background and Purpose: The relationship between increased exercise and improvement in motor paralysis in stroke patients was examined in relation to changes in the medical insurance system concerning rehabilitation.
Methods: Subjects were 122 stroke patients (6-session group) who performed 5 or 6 exercise sessions while the maximum number of exercise sessions permitted by medical insurance was 6 sessions (2 hours) and 45 patients (9-session group) who performed 7, 8, or 9 exercise sessions while the upper limit was 9 session. They underwent subacute rehabilitation in the Kaifukuki rehabilitation ward. Five motor items of the Stroke Impairment Assessment Set (SIAS) were evaluated on admission and at discharge and were compared between the two groups. We also performed a stratified analysis by degree of paralysis on admission.
Results: SIAS motor scores were higher in the 9-session group than in the 6-unit group before stratification. When we restricted the analysis to patients with moderate lower extremity paralysis or mild upper extremity paralysis on admission, SIAS motor scores at discharge and the increase in these scores were higher in the 9-unit group than in the 6-unit group.
Conclusions: Increasing the number of exercise sessions from 6 to 9 sessions per day improved motor paralysis.

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The aim of this study was to examine the efficacy of stroke treatments in an intra-hospital referral model, by investigating the outcome of acute cerebral infarction. During a recent 3-year period, 456 consecutive acute cerebral infarctions, including 170 lacunar, 151 atherothrombotic, 116 cardioembolic and 19 other ischemic strokes were treated in acute stroke therapies. The outcome was evaluated using both the modified Rankin Scale (mRS) and home-recovery rate.
By an analysis of mRS 0-2 rates as a good outcome, mortality, home-recovery rate, and determining the stroke type on admission is useful to assess the outcome of acute cerebral infarction. NIH stroke scale (NIHSS) on admission as a clinical assessment of gravidity is useful for the prospective evaluation of outcome on discharge. Cases with Functional Independence Measure (FIM) score over 90 at the end of acute therapy and those with an FIM score under 89 with a significant gain of FIM points during convalescent rehabilitation could recover to home. FIM score and FIM gain points are useful for judging the necessity of convalescent rehabilitation and estimating the possibility of home recovery. By an analysis of mRS 3 and 4 cases, convalescent rehabilitation has been more beneficial, resulting in a 77% home-recovery rate.
It is useful to evaluate stroke treatment for acute cerebral infarctions in an intra-hospital referral model, because of the seamless coordination from acute stroke therapy to convalescent rehabilitation, by clarifying a prospective evaluation on admission and necessity of successive rehabilitation.

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We retrospectively evaluated the clinical features and outcomes of acute spinal cord infarction (SCI). We examined the records of 14 patients with SCI (7 males and 7 females; age range, 22 to 74 years; median age, 63 years) who had been admitted to our departments between April 1997 and September 2008. Six of the 14 patients had no cardiovascular risk factors. Two patients had cervical disc herniation close to the ischemic lesion. Regarding clinical features, 11 patients had anterior spinal artery syndrome, one had Brown-Séquard syndrome, and two had transverse syndromes. The initial symptom was pain in eight patients, weakness in four patients, and sensory disturbance in two patients. All patients had an acute or sudden onset and a monophasic clinical course. Eight patients were treated with antithrombotic therapy, one with corticosteroids, and five with both antithrombotic therapy and corticosteroids. At the time of discharge, six patients could walk without assistance (favorable outcome). Patients who were female, had long cord lesions, had transverse syndromes, or presented with weakness tended to have a poor outcome.

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We examined the communication between recovery rehabilitation hospitals and acute hospitals in terms of access to functional prognosis information of patients at discharge. We enrolled 240 stroke patients (153 men and 87 women) who used the local critical pathway in this study. Collection and completeness of used local critical pathways, physical and cognitive function at transfer, improvement in recovery rehabilitation hospitals, and final outcome were investigated. As results, 46 (22.5%) and 33 (16.2%) pathways were found to be incomplete in acute and recovery rehabilitation hospitals, respectively. Time to transfer to a recovery rehabilitation hospital was 29.5±14.2 days. Mean length of stay in a recovery rehabilitation hospital was 101.1±57.0 days. After discharge, 143 patients (74.5%) returned home, 13 (6.8%) entered a convalescent ward or hospital, 29 (15.1%) went to a nursing care facility, and 7 (3.6%) had other outcomes. There was obvious difference in mean length of stay and ADL improvement per day (FIM efficiency) among the referred recovery rehabilitation hospitals. In conclusion, all healthcare facilities using the local critical pathway need to have a common recognition of stroke rehabilitation. By using the local critical pathway network system, rehabilitation staff in acute hospitals should proactively contribute to the qualitative improvement of rehabilitation in stroke patients during the recovery period.

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Objectives: The use of thrombolytic therapy with intravenous alteplase (rt-PA therapy) was investigated by prefectures and secondary medical service areas to clarify the current status and regional gaps of medical practice for acute ischemic stroke.
Subjects and methods: We collected all records of rt-PA use during the first 4 years after its approval from the government. Changes in the incidence of rt-PA therapy (the annual number of rt-PA therapy per 100,000 population over 65 years old) were calculated for each secondary medical service area, and the time trends in the use of rt-PA therapy were investigated for each area.
Results: It was estimated that 22,491 patients underwent rt-PA therapy during the 4 years after its approval. Per 100,000 people aged 65 years or older, the number of patients who received rt-PA therapy has increased with time. Of 348 secondary medical service areas, the number of service areas where rt-PA therapy had never been conducted decreased from 61 service areas (18%) in the 2nd year to 44 service areas (13%) in the 4th year. There were regional gaps of the percent use of rt-PA therapy among prefectures and secondary medical service areas.
Conclusions: Government needs to play a central role in taking positive educational activities for stroke and in improving systems for emergency transportation and other relevant measures across barriers among the authorities concerned.

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A 76-year-old woman suffered from intractable paroximal arterial fibrillation after aortic valve replacement for aortic stenosis. The patient developed complete right hemiplegia and motor aphasia on the fifteenth day after surgery. At the onset of stroke, the patient’s NIHSS score was 16. Initial head CT revealed neither hemorrhage nor early ischemic changes. Complete occlusion of the distal M1 portion of the middle cerebral artery was identified via 3D-CT angiography. Intravenous recombinant tissue plasminogen activator (rt-PA) therapy was initiated 140 minutes after the onset of symptoms. The patient showed remarkable improvement (the NIHSS score reduced to 4) without the occurrence of surgical site bleeding. The risk of ischemic stroke is increased during the perioperative period, especially after cardiac surgery. Intraarterial thrombolysis for postoperative stroke has been reported. However reports of intravenous rt-PA administration for postoperative stroke are scarce because postoperative stroke mostly occurs within 2 weeks of surgery and are excluded based on the guidelines. This report contributes to the investigation of the efficacy and safety of intravenous rt-PA administration.

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A 95-year-old woman who exhibited drowsiness, anosognosia, left facial palsy and left hemiparesis with sensory loss was transferred to our institution 30 minutes after onset. Her NIHSS score was 14 and cranial computed tomography (CT) showed neither high density area nor early CT findings. Except for relative precautions (high age, prior ischemic stroke and use of aspirin), the clinical information indicated that intravenous rt-PA therapy (IVtPA) would be appropriate. When the therapy was started 70 minutes after the stroke onset, neurological deficits rapidly improved, and magnetic resonance diffusion weighted images showed a small localized infarction in the right parietal lobe. Clinical conditions were stable until she developed headache and vomiting 15 hours after IVtPA. Emergent CT revealed bilateral hematomas in the cerebellar hemispheres and subsequently a ventricular drainage was performed. Her clinical conditions gradually improved, but she died of congestive heart failure on day 52. As one of the complications after IVtPA, extraischemic cerebral hematomas occur in the brain region without visible ischemic damage that is remote from an ischemic infarct. Although this kind of hemorrhage is an infrequent complication, the outcome is quite unfavorable. Therefore, care of such complications should be taken when considering thrombolytic therapy for very elderly patients.

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Case report: We report a right-handed, 52-year-old woman who presented with gradually progressive apathy and abulia. She had been diagnosed as having obesity, hyperlipidemia, and hypertension. She previously had a lively character but became apathetic and abulic. These neuropsychiatric symptoms gradually worsened over a week. Neuropsychiatric examination showed a mild depressive state, dysfunction of the left frontal lobe and mild cognitive dysfunction. Brain MRI showed infarction extending from the capsular genu to the corona radiata in the left hemisphere, corresponding to the territory of the medial lenticulostriate arteries (LSA). MRA showed no severe stenosis in the bilateral MCA and flow sensitive black blood MRA showed reduced number of LSA, leading to the diagnosis of branch atheromatous disease (BAD) in the left capsular genu. After admission, she received anti-thrombotic therapy, and then her symptoms gradually resolved.
Discussion: Capsular genu infarction seemed to have damaged the anterior or inferior thalamic peduncles, leading to the thalamo-cortical disconnection and neuropsychiatric symptoms. Although BAD is known to cause progressive sensorimotor symptoms, the present patient showed no apparent neurological deficits except progressive neuropsychiatric symptoms. To our knowledge, 39 cases of capsular genu infarctions have been reported to present with neuropsychiatric symptoms. However, almost all of the cases show other neurological deficits as well. Therefore, progressive psychiatric symptoms are rare but should be considered as the sole symptoms in BAD for its proper and prompt treatment.

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We reported a case of a previously healthy 25-year-old woman who presented with sudden headache, speech disturbance, and left-sided weakness. Her brain diffusion weighted MR image (DWI) showed a small region of high signal intensity in the right claustrum and MR angiography (MRA) demonstrated segmental narrowing of the right terminal portion of the internal carotid artery (C1). Considering her clinical features and characteristic MR findings, we diagnosed her with ischemic stroke due to arterial dissection of the C1 and started conservative treatment.
After her admission, however, several ischemic attacks due to the dissecting C1 recurred. Follow-up DWI and MRA performed 4 days after the onset revealed new ischemic lesions in the right hemisphere and aneurysmal formation just proximal to the stenosis of the C1. Cerebral angiography performed on the same day showed a segmental narrowing of the C1 and an aneurysmal outpouching just proximal to the stenosis. By adjusting antithrombotics to the optimal dose on the basis of evaluation for the intracranial condition by repetitive DWI and MRA, with concerns about both the recurrence of ischemic attacks and occurrence of subarachnoid hemorrhage due to the rupture of the aneurysm, conservative treatment was continued and re-attack was prevented. In the follow-up examinations, stenosis and aneurysmal outpouching were repaired and the patient was discharged with no sequela on the 47th day. This case suggests that repetitive morphologic evaluation using MR images and prudent medical treatment are necessary to prevent recurrence of ischemic stroke due to intracranial arterial dissection combined with aneurysmal outpouching.

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A 52-year-old man presented with a non-traumatic arterial dissection of bilateral anterior cerebral arteries (ACAs) manifesting as headache and left-sided hemiparesis, followed by consciousness disturbance and paraparesis of lower extremities. Magnetic resonance imaging (MRI) revealed cerebral infarction in his bilateral frontal lobes. MRI angiography (MRA), CT angiography (CTA) and digital subtraction angiography (DSA) revealed arterial dissection of bilateral A2 and A3 portions that progressed in two days. He has recovered well with conservative treatment and rehabilitation for several months. We discuss the mechanism by which the arterial dissection occurred simultaneously in the bilateral A2 portions.

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A 79-year-old female had medication for diabetes mellitus. She presented with dysarthria and right hemiplegia suddenly after supper. Diffusion weighted imaging (DWI) revealed a hyper-intensity lesion in the left internal capsule, and acute ischemic stroke was suspected. However, these symptoms disappeared rapidly after glucose infusion because plasma glucose level was 35 mg/dl. DWI obtained 24 hours later showed complete resolution of the hyper-intensity lesion in the left internal capsule.
Recently, tissue type plasminogen activator (tPA) was approved for acute ischemic stroke within 3 hours from onset, and was thought to be more effective if tPA is administrated as early as possible. Generally, in the case of glucose level under 50 mg/dl, administration of tPA is a contraindication. Hypoglycemic symptoms can be classified as autonomic and neuroglycopenic. Hypoglycemic hemiparesis is well-defined, ranging from reversible focal deficits to irreversible coma and death, but these cases are very rare. For the emerging patients presenting with focal neurological signs, hypoglycemic hemiparesis may be misdiagnosed as transient ischemic attack or acute cerebral infarction.
For the administration of tPA, we must never overlook hypoglycemia. For patients presenting with focal neurological signs, we should always take hypoglycemic hemiparesis into consideration, and early treatment must be started because the patients may have permanent disability if not treated promptly with glucose intake.

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Intravascular large B-cell lymphoma (IVLBCL) is a rare fatal neoplasm characterized by intravascular proliferation of lymphoma cells that commonly affects the central nervous system and skin. A 66-year-old woman, with a prior history of sudden onset of right hearing loss, developed transient monoplegia in the left arm in November 2008. Warfarin was started because of the patent foramen oval and stagnation in the deep vein of her legs. Since then, she developed various neurological episodes including brain stem, cranial nerves, and myelopathic abnormalities as well as skin rash, fever and hematologic abnormalities with a high serum LDH, monocytosis, anemia, thrombocytopenia, and splenomegaly. A skin biopsy and bone marrow aspiration revealed no atypical cells. Because she presented with high fever and body weight loss, low-dose prednisolone was started and warfarin was stopped. But even with steroid initiation, she became confused. Then, diffusion and FLAIR MR images showed multiple small hyperintense lesions in the cortical and subcortical regions. A stereotactic open brain biopsy of the left frontal cortex revealed large atypical intravascular tumor cells occluding the lumen of small cortical and meningeal vessels, and immunohistochemical staining demonstrated tumor cells as B cell-origin. She received R-CHOP chemotherapy and achieved a partial remission. IVL should be considered as an important differential diagnosis for patients presenting with a variety of neurological disorders and skin lesions accompanied by a high serum LDH. While brain biopsy is a rather invasive measure, in some cases, it can be only a diagnostic clue.

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