Search

Aims: To understand the different influences of statins on the incidence rate of each stroke subtype in association with low-density lipoprotein (LDL) cholesterol levels, we performed a post hoc analysis on the data from the Japan Statin Treatment Against Recurrent Stroke (J-STARS) study. Methods: Subjects (n = 1,578) were divided into three groups according to their mean postrandomized LDL cholesterol level (< 100, 100–120, and ≥ 120 mg/dL) until the last observation before the event or the end of follow-up. A Cox proportional hazard model for time to events was used for calculating adjusted hazard ratios, 95% confidence intervals, and the trend tests. Results: The event rates for atherothrombotic stroke did not decrease in accordance with the postrandomized LDL cholesterol level subgroups of either the control or the pravastatin group (p = 0.15 and 0.33 for the trend, respectively). In the control group, however, no atherothrombotic stroke event was observed in the subgroup of the low postrandomized LDL cholesterol level (less than 100 mg/dL). The event rates for atherothrombotic stroke were lower in the middle postrandomized LDL cholesterol level subgroup (100–120 mg/dL) of the pravastatin group than that of the control group. The event rates for lacunar stroke decreased in the lower postrandomized LDL cholesterol level subgroup of the control group but not of the pravastatin group (p = 0.004 and 0.06 for the trend, respectively). Conclusions: Statins showed different influences on the risks of atherothromobotic and lacunar stroke according to postrandomized LDL cholesterol levels.

Importance The Systolic Blood Pressure Intervention Trial (SPRINT) demonstrated that a systolic blood pressure (BP) target less than 120 mm Hg was superior to less than 140 mm Hg for preventing vascular events. This trial excluded patients with prior stroke; therefore, the ideal BP target for secondary stroke prevention remains unknown. Objective To assess whether intensive BP control would achieve fewer recurrent strokes vs standard BP control. Design, Setting, and Participants Randomized clinical trial (RCT) of standard vs intensive BP control in an intent-to-treat population of patients who had a history of stroke. Patients were enrolled between October 20, 2010, and December 7, 2016. For an updated meta-analysis, PubMed and the Cochrane Central Library database were searched through September 30, 2018, using the Medical Subject Headings and relevant search terms forcerebrovascular diseaseand forintensive BP lowering. This was a multicenter trial that included 140 hospitals in Japan; 1514 patients who had a history of stroke within the previous 3 years were approached, but 234 refused to give informed consent. Interventions In total, 1280 patients were randomized 1:1 to BP control to less than 140/90 mm Hg (standard treatment) (n = 640) or to less than 120/80 mm Hg (intensive treatment) (n = 640). However, 17 patients never received intervention; therefore, 1263 patients assigned to standard treatment (n = 630) or intensive treatment (n = 633) were analyzed. Main Outcomes and Measures The primary outcome was stroke recurrence. Results The trial was stopped early. Among 1263 analyzed patients (mean [SD] age, 67.2 [8.8] years; 69.4% male), 1257 of 1263 (99.5%) completed a mean (SD) of 3.9 (1.5) years of follow-up. The mean BP at baseline was 145.4/83.6 mm Hg. Throughout the overall follow-up period, the mean BP was 133.2/77.7 (95% CI, 132.5-133.8/77.1-78.4) mm Hg in the standard group and 126.7/77.4 (95% CI, 125.9-127.2/73.8-75.0) mm Hg in the intensive group. Ninety-one first recurrent strokes occurred. Nonsignificant rate reductions were seen for recurrent stroke in the intensive group compared with the standard group (hazard ratio [HR], 0.73; 95% CI, 0.49-1.11;P = .15). When this finding was pooled in 3 previous relevant RCTs in a meta-analysis, the risk ratio favored intensive BP control (relative risk, 0.78; 95% CI, 0.64-0.96;P = .02; absolute risk difference, −1.5%; 95% CI, −2.6% to −0.4%; number needed to treat, 67; 95% CI, 39-250). Conclusions and Relevance Intensive BP lowering tended to reduce stroke recurrence. The updated meta-analysis supports a target BP less than 130/80 mm Hg in secondary stroke prevention. Trial Registration ClinicalTrials.gov identifier:NCT01198496

Supplemental material, DS_10.1369_0022155418793600 for 4′,6-Diamidino-2-Phenylindole Distinctly Labels Tau Deposits by Chengyu Li, Tetsuya Takahashi, Tejashwi Shrestha, Eiji Kinoshita, Tomoyasu Matsubara, Masayasu Matsumoto and Hirofumi Maruyama in Journal of Histochemistry & Cytochemistry

The etiology of transient global amnesia (TGA) is not well understood. MR studies, including studies using diffusion-weighted imaging (DWI), have been used to investigate the pathophysiology of TGA, and focal hippocampal lesions have been detected in some studies. The aim of this study was to investigate serial changes in MR images from the patients with TGA. In seven TGA patients, serial MRI scans (from the same day of the・ onset to several days after the, onset of symptoms) using a 1.5-T MR unit were prospectively evaluated. Iri four patients, the duration of TGA was over 12 hr. Three of those patients showed small punctate hippocampal hypersensitivity with decreased ADC values on DW images. These lesions were detected in the postacute phase (a time window of 24 - 48 hr after the onset of symptoms). In follow-up studies performed several days after the onset of symptoms, DWI lesions had disappeared in the subacute phase (7-10 days after the TGA episode). The delayed hippocampal lesion on DW images with 1.5-T MRI in patients with TGA appears to be associated with longer duration of symptoms, to persist for several days and to disappear in the chronic phase.

Cerebral air embolism can be easily identified on computed tomography (CT) scans. However, changes in the distribution and amount of intracranial air are not well known. We report two patients with cerebral air embolism and present imaging findings on the serial changes in the intracranial air. We thought that the embolic source was venous in one patient because CT showed air inflow in cortical veins in the bilateral frontal areas, reflecting air buoyancy. In the other patient, CT showed air inflow into not only the cortical veins but also the bilateral cerebral hemispheres and we thought this to be a paradoxical cerebral air embolism. We found that intracranial air can be promptly absorbed and while cerebral infarcts due to air are clearly visualized on diffusion-weighted images (DWI), the air may rapidly disappear from images. In patients with suspected cerebral air embolism whose CT findings show no intracranial air, DWI should be performed because it may reveal cerebral infarction due to cerebral air embolism.

The aim of this study is to clarify the relationship between serum 3-O-methyldopa (3-OMD) and the clinical effects of entacapone. The 3-OMD and maximum serum concentration (Cmax) of levodopa were measured in 21 Parkinson's Disease patients who took 100 mg levodopa / dopa decarboxylase inhibitor. After the administration of entacapone, the 3-OMD concentration and percentage of "on" time during waking hours (% of "on" time) were studied for 8 weeks. The 3-OMD concentration was reduced by 34%, and the increase in % of "on" time was 28% at the 8th week compared with baseline. We defined the COMT-index as [baseline 3-OMD concentration] / [levodopa Cmax when 100 mg levodopa was administered alone]. The COMTindex was significantly correlated with the increase in % of "on" time at the 8th week. In conclusion, the measurement of baseline 3-OMD and levodopa pharmacokinetics is useful for predicting the clinical effects of entacapone.

BACKGROUND AND PURPOSE: Asymptomatic microbleeds shown by T2*-weighted MR imaging are associated with small-artery diseases, especially with intracerebral hemorrhage. Few studies have focused on the prevalence of microbleeds in patients with recurrent stroke. We investigated frequency of microbleeds in patients with recurrent stroke and association of presence of microbleeds with a combination of stroke subtypes and severity of leukoaraiosis. METHODS: The study population consisted of 102 patients with primary stroke and 54 patients with recurrent stroke. Microbleeds were counted and classified by using T2*-weighted MR imaging with a 1.0-T system. RESULTS: Patients with recurrent stroke showed a significantly higher prevalence of microbleeds (68.5%) than did patients with primary stroke (28.4%) (P < .0001). Among patients with recurrent stroke, the highest frequency of microbleeds occurred in those with intracerebral hemorrhage alone (92.3%), with the next highest frequency occurring in those with a combination of intracerebral hemorrhage and ischemic stroke (76.5%) and then those with ischemic stroke alone (50.0%) (P < .05). Leukoaraiosis was more severe in patients with recurrent stroke than in patients with primary stroke, and correlations between grade of microbleeds and severity of leukoaraiosis were found in patients with primary stroke (r = 0.367, P < .001) and in patients with recurrent stroke (r = 0.553, P < .0001). Logistic regression analysis identified recurrent stroke (odds ratio, 4.487; 95% confidence interval, 1.989−10.120) and leukoaraiosis (odds ratio, 5.079; 95% confidence interval, 2.125−12.143) as being significantly and independently associated with microbleeds. CONCLUSION: Asymptomatic microbleeds are observed to occur frequently in patients with recurrent stroke, either hemorrhagic or ischemic stroke, and are closely associated with the severity of leukoaraiosis.

Summary: We examined the cerebellar metabolism of a 61-year-old man with a small infarct in the left middle cerebellar peduncle and an intact cerebellum. Positron emission tomographic images obtained 28 days after onset showed prominent hypoperfusion and hypometabolism (almost 50% below the normal level) in the left cerebellar hemisphere. This case report shows that neural deafferentation may cause prominent hypometabolism without morphologic changes in the cerebellum. An arrest in synaptic activity may be the most important factor for the adaptive decrease in oxygen metabolism seen in ischemic brain.

A device for controlling a propagation direction of noise which is preferably associated with a sound insulating wall to significantly improve its sound reducing effect of alleviating noise emitted from a noise source such as a railroad, highway and the like on which an electric car and automobiles run. The device comprises a hollow structural body composed of a plurality of elongate hollow passages superimposed one upon the other and spaced apart from each other. The passages are arranged in a propagation direction of noise emitted from the noise source and serve to refract and lag in phase the noise passed therethrough, thereby producing a sound reducing region located intermediate between a direct propagation sound and the refraction propagation sound.