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A 63-year-old man was found with confusion and right limb monoparesis. He was taken to the emergency center under suspicion of stroke. Head computed tomography and magnetic resonance (MR) imaging and MR angiography were immediately conducted, which revealed no abnormality, but diffusion-weighted imaging showed increased intensity areas in the splenium of the corpus callosum and the left posterior limb of the internal capsule with decreased apparent diffusion coefficient (ADC) in the same areas. Immediately after the head scan, blood sugar level was measured, which revealed hypoglycemia (23 mg/dl). He quickly became lucid after intravenous administration of 20 ml of 50% glucose solution, and the paresis disappeared. Follow-up brain MR imaging was conducted 3 days later, but no clearly abnormal findings were seen on T(2)-weighted, fluid-attenuated inversion recovery, diffusion-weighted, or ADC images. Reports of reversible high intensity area in the splenium of the corpus callosum on diffusion-weighted imaging due to transient hypoglycemia are rare. Hemiparesis is one of the manifestations of hypoglycemia, so verifying the blood sugar level is important. Since MR imaging can be conducted easily now, we may need to consider the imaging findings in the differential diagnosis of hypoglycemia.

Objective: The aim of this investigation was to determine the factors influencing acute intracerebral hemorrhage severity on admission and clinical outcomes at discharge. Methods: Sixty acute stroke hospitals throughout Japan participated in the Japan Standard Stroke Registry Study (JSSRS), documenting the in-hospital course of 16,630 consecutive patients with acute stroke from January 2001 to March 2004. We identified 2,840 adult patients from the JSSRS who had intracerebral hemorrhage. Results: Intracerebral hemorrhage severity on admission was strongly related to age, previous stroke history, and hemorrhage size in a monotone fashion [χ2(9) = 374.5, p < 0.0001]. Drinking history was also predictive of intracerebral hemorrhage severity on admission, but the association was not monotone. Interestingly, intracerebral hemorrhage severity on admission was increased in nondrinking and heavy drinking compared to mild drinking (p < 0.05). Unsuccessful outcome (modified Rankin scale score = 3–6) was related to age, previous stroke history, hemorrhage size, and intracerebral hemorrhage severity on admission [χ2(9) = 830.4, p < 0.0001]. Mortality was related to hemorrhage size, intraventricular hemorrhage, intracerebral hemorrhage severity on admission, and surgical operation [χ2(7) = 540.4, p < 0.0001]. Conclusion: We could find four varied factors associated with intracerebral hemorrhage severity and its outcomes. Interestingly, intracerebral hemorrhage severity tended to be greater in nondrinking and heavy drinking than mild drinking. Additionally, surgical operation decreased intracerebral hemorrhage mortality.

Argatroban, which is a thrombin inhibitor, has an indication as a treatment in the acute phase on atherosclerotic ischemic stroke in Japan. Howeve, in cardioembolic stroke, argatroban is considered to be contraindicated with the side effect of hemorrhage, though there is no clear clinical evidence to show that argatroban increases hemorrhagic compared with heparin. The efficacy of anticoagulant treatment with argatroban on cardioembolic stroke was evaluated retrospectively in this study. We identified 3,113 patients from the Japan Standard Stroke Registry Study who had had a cardioembolic ischemic stroke. We excluded patients with the anti-platelet treatment or the combination therapy of anticoagulation. Our analyses are therefore based on a cohort of 2,529 patients who were treated either with heparin, and argatroban, or with no anti-coagulation treatment. With multivariable regression, hemorrhagic it was shown that hemorrhage was significantly reduced in heparin and argatroban treatments in the patients with mild severity. There was no significant difference in the recurrence of ischemic stroke between the treatments. Both argatroban and heparin showed dramatic improvement compared with the no treatment standard, but only heparin achieved statistical significance for mortality and change in NIHSS score (admission to discharge) in the moderate stroke subgroup [NIHSS 11-22]. Both heparin and argatroban [more so than heparin alone] have a significantly reduced mortality risk. From the present study, it is suggested that argatroban may be useful on cardioembolic stroke, increasing the improvement of recovery of stroke severity without increasing the risk of hemorrhage. Further prospective studies are awaited for evaluating better the efficacy of argatroban on cardioembolic stroke.

After focal cerebral ischemia, tumor necrosis factor-α deteriorates cerebral edema and survival rate. Therefore, tumor necrosis factor-α neutralization could reduce cerebral microvascular permeability in acute cerebral ischemia. Left middle cerebral artery occlusion for 120 mins followed by reperfusion was performed with the thread method under halothane anesthesia in Sprague-Dawley rats. Antirat tumor necrosis factor-α neutralizing monoclonal antibody with a rat IgG Fc portion (15 mg/kg) was infused intravenously right after reperfusion. Stroke index score, infarct volume, cerebral specific gravity, and the endogenous expression of tumor necrosis factor-α, matrix metalloproteinase (MMP)-2, MMP-9, and membrane type 1-MMP in the brain tissue were quantified in the ischemic and matched contralateral nonischemic hemisphere. In the antitumor necrosis factor-α neutralizing antibody-treated rats, infarct volume was significantly reduced ( P = 0.014, n = 7; respectively), and cerebral specific gravity was dramatically increased in the cortex and caudate putamen ( P

In order to explore candidates for proteins required in exocytosis, we used two anti-allergic drugs, amlexanox and cromolyn, which inhibit IgE mediated degranulation of mast cells and basophils, as molecular probes in affinity chromatography. These two drugs chiefly bound to the same kinds of calcium binding proteins in bovine lung. These proteins were as follows: bovine calgranulin C homolog, an 8-kDa unknown protein, S-100L, calgranulin B, calcyphosine, and annexins I–V. The homologous affinity of the two drugs to these proteins is in accord with the similar anti-allergic property of both drugs. From these findings it is presumed that these drugs interact with these proteins and affect pharmacologically the degranulation.

A 63-year-old man was found with confusion and right limb monoparesis. He was taken to the emergency center under suspicion of stroke. Head computed tomography and magnetic resonance (MR) imaging and MR angiography were immediately conducted, which revealed no abnormality, but diffusion-weighted imaging showed increased intensity areas in the splenium of the corpus callosum and the left posterior limb of the internal capsule with decreased apparent diffusion coefficient (ADC) in the same areas. Immediately after the head scan, blood sugar level was measured, which revealed hypoglycemia (23 mg/dl). He quickly became lucid after intravenous administration of 20 ml of 50% glucose solution, and the paresis disappeared. Follow-up brain MR imaging was conducted 3 days later, but no clearly abnormal findings were seen on T(2)-weighted, fluid-attenuated inversion recovery, diffusion-weighted, or ADC images. Reports of reversible high intensity area in the splenium of the corpus callosum on diffusion-weighted imaging due to transient hypoglycemia are rare. Hemiparesis is one of the manifestations of hypoglycemia, so verifying the blood sugar level is important. Since MR imaging can be conducted easily now, we may need to consider the imaging findings in the differential diagnosis of hypoglycemia.

Background Cardioembolic stroke generally results in more severe disability, since it typically has a larger ischemic area than the other types of ischemic stroke. However, it is difficult to differentiate cardioembolic stroke from non-cardioembolic stroke (atherothrombotic stroke and lacunar stroke). In this study, we evaluated the levels of plasma brain natriuretic peptide in acute ischemic stroke patients with cardioembolic stroke or non-cardioembolic stroke, and assessed the prediction factors of plasma brain natriuretic peptide and whether we could differentiate between stroke subtypes on the basis of plasma brain natriuretic peptide concentrations in addition to patient's clinical variables. Methods Our patient cohort consisted of 131 consecutive patients with acute cerebral infarction who were admitted to Kagawa University School of Medicine Hospital from January 1, 2005 to December 31, 2007. The mean age of patients (43 females, 88 males) was 69.6 ± 10.1 years. Sixty-two patients had cardioembolic stroke; the remaining 69 patients had non-cardioembolic stroke (including atherothrombotic stroke, lacunar stroke, or the other). Clinical variables and the plasma brain natriuretic peptide were evaluated in all patients. Results Plasma brain natriuretic peptide was linearly associated with atrial fibrillation, heart failure, chronic renal failure, and left atrial diameter, independently (F4,126 = 27.6, p < 0.0001; adjusted R2 = 0.45). Furthermore, atrial fibrillation, mitral regurgitation, plasma brain natriuretic peptide (> 77 pg/ml), and left atrial diameter (> 36 mm) were statistically significant independent predictors of cardioembolic stroke in the multivariable setting (Χ2 = 127.5, p < 0.001). Conclusion It was suggested that cardioembolic stroke was strongly predicted with atrial fibrillation and plasma brain natriuretic peptide. Plasma brain natriuretic peptide can be a surrogate marker for cardioembolic stroke.

The purpose of this study was to identify predictors of atherosclerosis in a healthy young cohort comprised of 241 subjects who underwent a regular employee medical check-up at Ohshima National Sanatorium over a 9-month period. All subjects underwent carotid ultrasound examinations to determine maximal common carotid artery intima media thickness. In addition, serum total cholesterol, triglycerides, high-density lipoprotein cholesterol, blood urea nitrogen, creatinine, glucose, and insulin were evaluated. The subjects were relatively young (mean age, 44 years; range, 18 to 62 years), with 130 females (54%) and 111 males (46%). Maximal common carotid artery intima media thickness was predicted by smoking habit, body mass index, fasting blood sugar, fasting serum insulin, and systolic blood pressure (F5,235 = 52.8, P < 10-5). There was clear separation in common carotid artery intima media thickness values based on body mass index, smoking, and fasting serum insulin, and somewhat more overlap with systolic blood pressure and fasting blood sugar. These findings suggest that smoking and high values of body mass index, fasting serum insulin, systolic blood pressure, and fasting blood sugar are warning factors for early atherosclerosis development, and could conceivably serve as the basis of diagnostic screening. Smoking is particularly deleterious, as smokers with high body mass index, high fasting serum insulin, or high systolic blood pressure tend to have larger common carotid artery intima media thickness values than would have been predicted by consideration solely of the individual risk factors.

Background: Cardioembolic stroke generally results in severer disability, since it typically has a larger ischemic area than the other types of ischemic stroke. However, it is difficult to differentiate cardioembolic from noncardioembolic stroke (atherothrombotic and lacunar stroke), whenever ischemic stroke patients have sinus rhythm at the time of presentation. Methods: In this study, we evaluated the levels of plasma brain natriuretic peptide in acute ischemic stroke patients with cardioembolic or noncardioembolic stroke and assessed whether this could provide a basis for differentiating cardioembolic stroke (especially due to paroxysmal atrial fibrillation) from noncardioembolic stroke. Our patient cohort consisted of 99 consecutive patients with acute cerebral infarction who were admitted to Kagawa University School of Medicine Hospital from January 1, 2005, to December 31, 2006. We excluded 23 patients with valve disease, heart failure, myocardial infarction or chronic renal failure. The mean age of the remaining 76 patients (51 males, 25 females) was 70.0 ± 10.1 years. Results: Thirty-six patients had cardioembolic stroke with atrial fibrillation (including permanent and paroxysmal atrial fibrillation); the remaining 40 had noncardioembolic stroke. The plasma brain natriuretic peptide was evaluated on the first morning after admission in all patients. In cardioembolic stroke with atrial fibrillation (permanent and paroxysmal atrial fibrillation), the plasma brain natriuretic peptide, ratio of peak early filling velocity to peak atrial systolic velocity (E/A) and left atrial diameter were significantly increased (p < 0.001), and the left atrial appendage flow was significantly decreased (p < 0.001), compared with noncardioembolic stroke. Analyzed in those 4 factors, cardioembolic stroke was strongly predicted with >95% accuracy assessed by plasma brain natriuretic peptide and left atrial appendage flow. Conclusion: From our results, it was suggested that the first-day brain natriuretic peptide and left atrial appendage flow measurements would be helpful in differentiating cardioembolic stroke with atrial fibrillation from noncardioembolic stroke.

Postischemic delayed hypoperfusion (PDH) is based on the imbalance between local vasodilators and vasoconstrictors. We evaluated the time course of cerebral blood flow and cerebral specific gravity representing cerebral edema after transient forebrain ischemia induced by bilateral occlusion of the common carotid arteries in anesthetized gerbils to determine whether PDH is a significant factor in development of cerebral edema. PDH appeared 45 minutes after reperfusion followed by the increase of cerebral edema. Thereafter, the local cerebral blood flow recovered from PDH 24 hours after reperfusion in spite of the stable cerebral specific gravity. Furthermore, cerebral specific gravity established a linear correlation with the local cerebral blood flow 120 minutes after reperfusion in the 3 different durations of cerebral ischemia (30, 60, and 90 minutes). It is suggested that cerebral edema is not the cause in PDH development, but PDH may cause cerebral edema.

Following cerebral ischemia, i.v. infusion of angiotensin II increases cerebral edema and mortality. Angiotensin type 1 receptor blockage should therefore improve acute cerebral ischemia. Left middle cerebral artery occlusion (120 min) followed by reperfusion was performed with the thread method under halothane anesthesia in Sprague-Dawley rats. Olmesartan (angiotensin type 1 receptor blocker; 0.01 or 0.1μmol/kg/h) was infused i.p. for 7 days following middle cerebral artery occlusion followed by reperfusion. Stroke index score, infarct volume, specific gravity, and brain angiotensin II and matrix metalloproteinases were quantified in the ischemic and non-ischemic hemispheres. Olmesartan treatment improved stroke index score, infarct volume, and cerebral edema in our cerebral ischemia model. In particular, stroke index score, infarct volume, and cerebral edema were reduced even with a low dose of olmesartan that did not decrease blood pressure. Paralleling these effects on cerebral ischemia, olmesartan treatment also reduced the reactive upregulation in brain angiotensin II, matrix metalloproteinase-2, matrix metalloproteinase-9, and membrane type 1-matrix metalloproteinase in the ischemic area. Angiotensin type 1 receptor stimulation may be one of the important factors that cause cerebral edema following cerebral ischemia, and that its inhibition may be of therapeutic advantage in cerebral ischemia.

Following focal cerebral ischemia, tumor necrosis factor-alpha deteriorates cerebral edema and survival rate. Therefore, tumor necrosis factor-alpha neutralization could reduce cerebral microvascular permeability in acute cerebral ischemia. Left middle cerebral artery occlusion for 120 min followed by reperfusion was performed with the thread method under halothane anesthesia in Sprague-Dawley rats. Anti-rat tumor necrosis factor-alpha neutralizing monoclonal antibody with a rat IgG Fc portion (15 mg/kg) was infused intravenously right after reperfusion. Stroke index score, infarct volume, cerebral specific gravity, and the endogenous expression of tumor necrosis factor-a, matrix metalloproteinase-2, matrix metalloproteinase-9, and membrane type 1- matrix metalloproteinase in the brain tissue were quantified in the ischemic and matched contralateral non-ischemic hemisphere. In the anti-tumor necrosis factor-alpha neutralizing antibody treated rats, infarct volume was significantly reduced (p = 0.014, n = 7; respectively), and cerebral specific gravity was dramatically increased in cortex and caudate putamen (p < 0.001, n = 7; respectively) in association with a reduction in matrix metalloproteinase-9 and membrane type 1- matrix metalloproteinase upregulation. Tumor necrosis factor-alpha in the brain tissue was significantly elevated in the ischemic hemisphere 6 hours after reperfusion in the non-specific IgG treated rats (p = 0.021, n = 7) and was decreased in the anti-tumor necrosis factor-alpha neutralizing antibody treated rats (p = 0.001, n = 7). Post-reperfusion treatment with anti-rat tumor necrosis factor-alpha neutralizing antibody reduced brain infarct volume and cerebral edema, which is likely mediated by a reduction in matrix metalloproteinases upregulation. (See Figure 1).