Effects of preceding antiplatelet agents on severity of ischemic stroke in patients with a history of stroke.

INTRODUCTION: Antiplatelet agents are effective for secondary prevention of ischemic stroke and can reduce the severity of first-ever ischemic stroke. However, it is uncertain if prophylactic antiplatelet therapy reduces the severity of recurrent ischemic stroke. The aim of this study was to determine the effect of preceding antiplatelet treatment on the severity of thrombotic stroke (TS) in patients with a prior history of stroke. METHODS: From a prospective hospital registry of 1338 consecutive patients with acute ischemic stroke, we identified patients with a prior history of stroke who were admitted for cardioembolic stroke (CE); TS including large-artery atherosclerosis, small vessel occlusion, and branch atheromatous disease; or other cause or cryptogenic stroke (OCS). Cases in each subtype were categorized based on preceding medication: antiplatelet agents (AP) and none (N). Severity of stroke (National Institutes of Health Stroke Scale: NIHSS) on admission was compared between AP and N cases. RESULTS: The total cohort of 252 patients included 83 with CE, 102 with TS, and 67 with OCS. After excluding those with prior anticoagulants, the median NIHSS on admission was lower in AP cases than in N cases (3 vs. 5, p = 0.002). In multivariate analysis, preceding AP treatment was independently associated with minor stroke (NIHSS ≤4) on admission in CE group (OR 8.48, 95% CI 1.71-62.9, p = 0.008) and TS group (OR 4.24, 95% CI 1.44-13.4, p = 0.009). CONCLUSION: Preceding antiplatelet treatment in patients with a prior history of stroke may reduce the severity of subsequent thrombotic and cardiogenic stroke.

Clinical characteristics and intracranial arterial lesions of non-young adult ischemic stroke patients with RNF213 p.R4810K variant.

BACKGROUND: Although RNF213 p.R4810K, a genetic susceptibility variant for moyamoya disease (MMD), is associated with intracranial artery stenosis/occlusion (ICASO), the impact of this variant on ischemic stroke patients in non-young adults is unclear. We aimed to determine the characteristics of non-young adult stroke patients with RNF213 p.R4810K. METHODS: We retrospectively identified acute ischemic stroke patients ≥50 years who were admitted to our hospital and underwent intracranial vascular imaging. We reviewed the patients with RNF213 p.R4810K and compared stroke characteristics and the frequency and location of ICASO between patients with and without the variant. RESULTS: Among 341 patients, RNF213 p.R4810K was identified in 7 patients (2.1%). Five of the 7 patients with the variant (71%) had multiple ICASO without any finding of MMD and remaining 2 patients had no ICASO. The presumed etiologies of ICASO were atherosclerosis in 3 cases, vasculitis in 1, and undetermined vasculopathy in 1. ICASO in the anterior circulation was more common in patients with the variant than in those without (71% vs. 25%). The internal carotid artery, the M1 segment of the middle cerebral artery, the A1 segment of the anterior cerebral artery, and the P1 segment of the posterior cerebral artery, which were the most frequently affected arteries in MMD, were more often affected in the variant group. CONCLUSIONS: Non-young adult stroke patients with RNF213 p.R4810K are more likely to have ICASO in arterial segments commonly affected in MMD. The etiology of their ICASO exhibited diverse mechanisms, possibly depending on vascular risk and other environmental factors.

Early Recurrence in Patients with Symptomatic, Non-Cardioembolic, Internal Carotid Artery Occlusion.

INTRODUCTION: There are limited data on the clinical course of patients with non-cardioembolic, mostly atherosclerotic, internal carotid artery occlusion (ICAO). The purpose of this study was to elucidate the frequency and underlying pathogenesis of early recurrent ischemic stroke in symptomatic non-cardioembolic ICAO. MATERIALS AND METHODS: Consecutive patients with symptomatic non-cardioembolic ICAO were retrospectively reviewed. Those who had a tandem occlusion of the proximal middle cerebral artery (MCA) or underwent endovascular thrombectomy were excluded. Early recurrent stroke was defined as deterioration of the NIHSS score by ≥1 point with new lesions on magnetic resonance (MR) diffusion-weighted imaging (DWI) in the ipsilateral territory of the ICAO within 30 days of the index stroke onset. Patients were classified into two groups on carotid ultrasonography: cervical occlusion and intracranial occlusion. The presumed pathogenesis of recurrent stroke was categorized as embolic or hemodynamic according to the topographical features of subsequent lesions on DWI. RESULTS: Of 36 consecutive medically treated patients with symptomatic non-cardioembolic ICAO without tandem MCA occlusion, 23 patients had cervical occlusion, and 13 had intracranial occlusion. Early recurrent stroke occurred in 16 patients (44.4%), which happened much more with intracranial occlusion than with cervical occlusion (69.2% vs 30.4%, p<0.02). Focusing on the presumed pathogenesis, hemodynamic was more common than embolic (68.8% vs 31.2%), especially with intracranial occlusion (77.8%). CONCLUSIONS: Early recurrent stroke occurs at a high frequency in symptomatic non-cardioembolic ICAO, and intracranial occlusion may be a risk factor for early recurrent stroke. The pathogenesis of recurrence is more often hemodynamic than embolic.

Long-term effectiveness of anticoagulants in oldest-old stroke survivors with atrial fibrillation.

BACKGROUND: Long-term anticoagulant therapy in oldest-old persons poses the risk of bleeding complications. The aim of this study was to evaluate the long-term benefits of anticoagulant therapy for oldest-old stroke survivors with AF. METHODS: Patients with atrial fibrillation (AF) who were 90 years of age or older and were prescribed an anticoagulant on discharge were identified from a set of data from a prospective follow-up registry of 1,484 consecutive patients admitted for ischemic stroke or transient ischemic attack over a 4-year period beginning in 2014. The outcome measures were stroke and death following discharge. RESULTS: Of the 77 identified patients with AF who were 90 years of age or older, 71 were prescribed an anticoagulant (median age 93 years, 73% women). Thirty-nine patients were given a direct oral anticoagulant (DOAC) (median age 92 years, 69% women), and 32 were given warfarin (median age 93 years, 78% women). During the follow-up period (median 466 days), 9 patients (13%) had stroke recurrence (recurrence rate: 14%/year), and 25 patients (35%) died (mortality rate: 33%/year). The type of all recurrent strokes was ischemic, and no fatal bleeding occurred. There was no difference in the incidence of recurrent strokes according to anticoagulant type (DOAC 15%/year, warfarin 13%/year, P = 0.743), but a higher proportion of patients on warfarin died (21% vs. 47%, P = 0.002). CONCLUSIONS: Given that a higher proportion of oldest-old stroke survivors with AF on anticoagulant therapy have recurrent ischemic stroke rather than hemorrhagic stroke, long-term anticoagulant therapy may be justified for secondary stroke prevention.

[Brain infarction and cerebral venous thrombosis in paroxysmal nocturnal hemoglobinuria: case report].

A 65-year-old woman with a six-year history of paroxysmal nocturnal hemoglobinuria (PNH) was admitted due to weakness in the right leg following a seven-day history of fever and upper respiratory infection. MRI revealed several high-intensity areas in bilateral frontal lobe cortices and the left cerebellum on diffusion-weighted imaging, and signal hypointensity along the course of the cortical vein in the left frontal lobe on T2*-weighted imaging. We diagnosed cerebral venous thrombosis and brain infarction, and commenced heparin infusion. She developed right-sided dens hemiparesis on hospital day 6, when brain CT showed subcortical hemorrhage in the left frontal lobe. Despite eculizumab administration and decompressive craniectomy for hematoma, she died on hospital day 26. Thrombosis in PNH has been recognized as a life-threating complication, and intensive treatment including emergent administration of eculizumab is warranted if this situation arises.

Attack Interval Is the Key to the Likely Pathogenesis of Multiple Transient Ischemic Attacks.

INTRODUCTION: The aim of this study was to test the hypothesis that the attack interval of multiple transient ischemic attacks (TIAs) is correlated with the underlying pathogenesis of ischemia. METHODS: Patients with multiple TIAs, defined as 2 or more motor deficits within 7 days, were studied. The attack interval between the last 2 episodes was classified into 3 groups: 2 episodes within an hour (Hour group), over hours within a day (Day group), and over days within a week (Week group). Patients with a lacunar syndrome, no cortical lesions, and no embolic sources were recognized as having a small vessel disease (SVD) etiology for their multiple events. RESULTS: Of 312 TIA patients admitted over a 9-year period, 50 (37 males, 13 females, mean 67.6 years) had multiple TIAs. Twelve patients were classified as being within the Hour group, 23 within the Day group, and 15 within the Week group. Lacunar syndromes were observed in 30 (75%, 35%, and 67%), embolic sources were detected in 28 (25%, 65%, and 67%), and a high signal lesion on diffusion-weighted imaging was depicted in 30 (75%, 48%, and 67%) patients (18 cortical, 11 subcortical, and one cerebellar). Patients in the Hour group had a significantly higher prevalence of SVD etiology (75%) than those in the Day and Week groups (30%, p = 0.0165; 27%, p = 0.0213, respectively). Four patients had a subsequent stroke within 7 days. CONCLUSION: Attack intervals of multiple TIAs may be correlated with the underlying pathogenesis of ischemia. Two motor deficits within an hour are more likely to suggest a SVD etiology.

Elevated CA125 is Related to Stroke Due to Cancer- Associated Hypercoagulation.

BACKGROUND: Cancer-associated hypercoagulation is one of the major pathophysiological mechanisms of stroke in cancer patients. Carcinomatous mucins are considered to play an important role in cancer-associated hypercoagulation. Therefore, carbohydrate antigen-125 (CA125), which is a typical mucin molecule and mucin-producing tumor marker, may be related to stroke due to cancer-associated hypercoagulation. AIMS: We aimed to clarify the association of CA125 with a hypercoagulable state in acute stroke patients with active cancer. METHODS: We studied 77 acute ischemic stroke patients with active cancer who had undergone CA125 measurement. The study patients were categorized into hypercoagulation or non-hypercoagulation groups. The hypercoagulation group was defined as stroke patients with a D-dimer value exceeding 3 µg/mL and multiple vascular territory infarcts. Elevation of tumor markers was defined as values more than twice the upper limit of the normal range. RESULTS: Forty-five (58%) and 32 (42%) patients were classified into hypercoagulation and non-hypercoagulation groups, respectively. The hypercoagulation group showed elevated CA125 and CEA levels, no history of hypertension, and pancreatic cancer more frequently, and higher CRP values, lower hemoglobin values, longer prothrombin time and lower platelet counts than the non-hypercoagulation group. In multivariable analysis, only elevation of CA125 was independently associated with the hypercoagulation group (adjusted odds ratio: 5.59 [95% confidence interval]: 1.33-26.41). CONCLUSIONS: CA125, a tumor marker for mucin-producing tumors, was related to stroke due to cancer- associated hypercoagulation. CA125 may be a potential biomarker for cancer-associated hypercoagulation.

A Japanese case of oculopharyngeal muscular dystrophy (OPMD) with PABPN1 c.35G > C; p.Gly12Ala point mutation.

BACKGROUND: Oculopharyngeal muscular dystrophy (OPMD) is a late-onset muscular dystrophy characterised by slowly progressive ptosis, dysphagia, and proximal limb muscle weakness. A common cause of OPMD is the short expansion of a GCG or GCA trinucleotide repeat in PABPN1 gene. CASE PRESENTATION: A 78-year-old woman presented with ptosis and gradually progressive dysphagia. Her son had the same symptoms. A physical examination and muscle imaging (MRI and ultrasound) showed impairment of the tongue, proximal muscles of the upper limbs, and flexor muscles of the lower limbs. Needle-electromyography (EMG) of bulbar and facial muscles revealed a myopathic pattern. Based on the characteristic muscle involvement pattern and needle-EMG findings, we suspected that the patient had OPMD. Gene analysis revealed PABPN1 c.35G > C point mutation, which mimicked the effect of a common causative repeat expansion mutation of OPMD. CONCLUSION: We herein describe the first reported Japanese case of OPMD with PABPN1 point mutation, suggesting that this mutation is causative in Asians as well as in Europeans, in whom it was originally reported.

[Utility of transesophageal echocardiography for etiologic diagnosis of centrum ovale infarcts].

A small centrum ovale infarct in the territory of the white matter medullary artery can be caused not only by embolism but also small-vessel disease. In our study, thorough screening for emboligenic diseases was performed, including the modality of transesophageal echocardiography (TEE), in patients with an acute, isolated, small (less than 1.5 cm) infarct in the centrum ovale. Of 79 patients enrolled in this study, 45 had emboligenic diseases, in whom a patent foramen ovale was detected in 29 patients, complicated aortic arch lesion in 15, atrial fibrillation in 6, occlusive carotid disease in 2, and others in 2. The majority (80%) of the emboligenic diseases were diagnosed by TEE. Therefore, TEE may be mandatory for the etiologic diagnosis of centrum ovale infarcts.

[Recurrent cerebral embolism due to the disseminated carcinomatosis of bone marrow with early gastric cancer].

A 67-year-old woman who had undergone laparoscopic proximal gastrectomy for early gastric cancer 10 months previously was admitted to our hospital due to dysarthria. Brain MRI demonstrated acute multiple small infarcts in the right middle cerebral artery (MCA) and the right posterior inferior cerebellar artery (PICA) territory, and she was diagnosed as embolic stroke. Anticoagulant therapy did not prevent further ischemic stroke. No embolic sources were detected by MR angiography, carotid duplex sonography, transthoracic and transesophageal echocardiography, and Holter electrocardiography. We also performed upper gastrointestinal endoscopy and contrast-enhanced CT of the thoracoabdominal area, but there was no evidence of local recurrence or lymph node metastases of gastric cancer. As the ALP and D-dimer levels were gradually increasing, we performed PET/CT, which revealed fluorodeoxyglucose (FDG) uptake in the vertebra bone, and disseminated carcinomatosis of bone marrow with early gastric cancer was diagnosed after bone marrow biopsy on Day 41. After undergoing chemotherapy, she had no further stroke and died on Day 207.

[Vertebrobasilar territory embolisms due to the ununited fracture of the right clavicle from 35 years ago].

A 61-year-old man, with a history of right clavicular fracture 35 years prior, visited our hospital due to the sudden onset of vertigo and tinnitus following weakness and numbness in his left arm and leg. He also had a 6-month history of right arm pain with overuse. Brain MRI showed acute brain infarcts in the right posterior cerebral artery territory. Intravenous alteplase was administered 188 minutes after onset. Although heparin infusion was commenced on day 2, he had vertigo again on day 9, and MRI showed a recurrent brain infarct in the right posterior inferior cerebellar artery territory. Ultrasound examination revealed occlusion of his right subclavian artery beneath the old right clavicular fracture as well as mobile thrombus in the proximal portion of the right subclavian artery. We speculated that a pseudarthrosis at the site of the old right clavicular fracture had repetitively pressed the right subclavian artery. Subsequently, we considered thrombi, which had developed in the proximal portion of the right subclavian artery, migrated into the right vertebral artery, causing recurrent emboli in the vertebrobasilar artery territory.

[Safety of Dual Antiplatelet Therapy with Argatroban in Patients with Acute Ischemic Stroke].

To prevent early neurological worsening or recurrence in stroke patients with intracranial arterial stenosis or branch atheromatous disease, aggressive antithrombotic therapy, such as dual antiplatelet therapy (DAPT) with or without anticoagulant therapy, is warranted. Such an aggressive antithrombotic therapy, however, may increase the bleeding risk. We studied the risks of DAPT with the anticoagulant argatroban in patients with acute ischemic stroke or transient ischemic attack (TIA). Between October 2011 and September 2015, 341 patients with stroke or TIA, who received DAPT with argatroban within 48 hours after onset, were retrospectively studied. The endpoint was any bleeding event during hospitalization or 30 days after admission. Median duration of DAPT was 12 days, and 66% of the patients received intravenous heparin (median duration, 5 days) following argatroban. No symptomatic intracerebral hemorrhages were observed, while severe, moderate, and mild extracranial hemorrhages occured in one (0.3%), three (0.9%), and four (1.2%) patients, respectively. In conclusion, DAPT with argatroban can be safely administered to patients with acute ischemic stroke or TIA. (Received July 24, 2017; Accepted January 15, 2018; Published May 1, 2018).

Rapid Identification of Type A Aortic Dissection as a Cause of Acute Ischemic Stroke.

BACKGROUND AND PURPOSE: Patients with acute aortic dissection (AAD) sometimes present predominantly with neurological symptoms from cerebral ischemia. Such stroke patients must not receive thrombolysis therapy, which can be fatal. However, patients remain at risk if there is a failure to notice concurrent AAD. We aimed to clarify the characteristics of AAD patients with stroke to identify markers for early AAD detection before thrombolysis. METHODS: Using the single-center database of Stanford type A-AAD patients between 2007 and 2013, we selected those presenting with acute focal neurological deficits, presumably due to cerebral ischemia. Results of physical, radiological, and blood examinations were assessed in AAD patients with stroke. RESULTS: Of 226 AAD patients, 23 (10%) had stroke secondary to AAD. Of the 23 patients, 21 (91%) were primarily examined by stroke physicians and 2 (9%) by cardiologists. Thirteen patients (57%) were potential candidates for intravenous thrombolysis. Only 11 patients (48%) complained of chest/back pain. Positive findings indicating AAD included occlusion or intimal flap of the common carotid artery on carotid ultrasound in 18 (90%) of 20 patients, elevated serum d-dimer values (≥6.9 µg/mL) in 18 (78%) of 23, left hemiparesis as a neurological symptom in 17 (74%) of 23, systolic blood pressure differential above 20 mmHg between the arms in 15 (71%) of 21 patients, and mediastinal widening on chest radiograph in 10 (67%) of 15 patients. All 14 patients who underwent complete evaluation showed 2 or more positive diagnostic findings. CONCLUSIONS: The combination of physical, radiological, and laboratory findings may be a useful rapid-screening method for AAD as a cause of acute ischemic stroke.

Factors Associated with Early Hospital Arrival in Patients with Acute Ischemic Stroke.

BACKGROUND AND PURPOSE: Factors associated with early arrival may vary according to the characteristics of the hospital. We investigated the factors associated with early hospital arrival in two different stroke centers located in Korea and Japan. METHODS: Consecutive patients with ischemic stroke arrived hospital within 48 hours of onset between January 2011 and December 2012 were identified and the clinical and time variables were retrieved from the prospective stroke registries of Severance Hospital of Yonsei University Health System (YUHS; Seoul, Korea) and National Cerebral and Cardiovascular Center (NCVC; Osaka, Japan). Subjects were dichotomized into early (time from onset to arrival ≤4.5 hours) and late (>4.5 hours) arrival groups. Univariate and multivariate analyses were performed to evaluate factors associated with early hospital arrival. RESULTS: A total of 1,966 subjects (992 from YUHS; 974 from NCVC) were included in this study. The median time from onset to arrival was 6.1 hours [interquartile range, 1.7-17.8 hours]. In multivariate analysis, the factors associated with early arrival were atrial fibrillation (Odds ratio [OR], 1.505; 95% confidence interval [CI], [1.168-1.939]), higher initial National Institute of Health Stroke Scale scores (OR, 1.037; 95% CI [1.023-1.051]), onset during daytime (OR, 2.799; 95% CI [2.173-3.605]), and transport by an emergency medical service (OR, 2.127; 95% CI [1.700-2.661]). These factors were consistently associated with early arrival in both hospitals. CONCLUSIONS: Despite differences between the hospitals, there were common factors related to early arrival. Efforts to identify and modify these factors may promote early hospital arrival and improve stroke outcome.

Relative systolic blood pressure reduction and clinical outcomes in hyperacute intracerebral hemorrhage: the SAMURAI-ICH observational study.

BACKGROUND AND PURPOSE: Blood pressure lowering is often performed as a part of general acute management in acute intracerebral hemorrhage (ICH) patients. The relationship between relative blood pressure reduction and clinical outcomes is not fully known. METHODS: Hyperacute (<3 h from onset) ICH patients with initial SBP more than 180 mmHg were included in the observational study. All patients received intravenous antihypertensive treatment based on a predefined protocol to lower and maintain SBP between 120 and 160 mmHg. The relative SBP reduction was defined as the ratio of SBP reduction to the admission SBP in the first 24 h, and associations between the relative SBP reduction and neurological deterioration (≥2 points decrease in the Glasgow Coma Scale score or ≥4 increase in the National Institutes of Health Stroke Scale score), hematoma expansion (>33% increase), and unfavorable outcome (modified Rankin scale score 4-6 at 3 months) were assessed with multivariate logistic regression analyses. RESULTS: Of the 211 patients [81 women, median age 65 (interquartile range 58-74) years, and median initial National Institutes of Health Stroke Scale score 13 (8-17)] enrolled, 17 (8%) showed neurological deterioration, 36 (17%) showed hematoma expansion, and 87 (41%) had an unfavorable outcome. On multivariate regression analyses, relative SBP reduction was independently and inversely associated with neurological deterioration (odds ratio 0.053, 95% confidence interval 0.011-0.254 per 10% increment), hematoma expansion (0.289, 0.099-0.841), and unfavorable outcome (0.254, 0.095-0.680) after adjusting for known predictive factors. CONCLUSION: Insufficient relative SBP reduction after standardized antihypertensive therapy in hyperacute ICH was independently associated with poor clinical outcomes. Aggressive antihypertensive treatment may improve clinical outcomes.

Blood pressure variability on antihypertensive therapy in acute intracerebral hemorrhage: the Stroke Acute Management with Urgent Risk-factor Assessment and Improvement-intracerebral hemorrhage study.

BACKGROUND AND PURPOSE: The associations between early blood pressure (BP) variability and clinical outcomes in patients with intracerebral hemorrhage after antihypertensive therapy, recently clarified by a post hoc analysis of Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial 2 (INTERACT2), were confirmed using the Stroke Acute Management with Urgent Risk-factor Assessment and Improvement (SAMURAI)-intracerebral hemorrhage study cohort. METHODS: Patients with hyperacute (<3 hours from onset) intracerebral hemorrhage with initial systolic BP (SBP) >180 mm Hg were registered in a prospective, multicenter, observational study. All patients received antihypertensive therapy based on a predefined standardized protocol to lower and maintain SBP between 120 and 160 mm Hg using intravenous nicardipine. BPs were measured hourly during the initial 24 hours. BP variability was determined as SD and successive variation. The associations between BP variability and hematoma expansion (>33%), neurological deterioration within 72 hours, and unfavorable outcome (modified Rankin Scale, 4-6) at 3 months were assessed. RESULTS: Of the 205 patients, 33 (16%) showed hematoma expansion, 14 (7%) showed neurological deterioration, and 81 (39%) had unfavorable outcomes. The SD and successive variation of SBP were 13.8 (interquartile range, 11.5-16.8) and 14.9 (11.7-17.7) mm Hg, respectively, and those of diastolic BP were 9.4 (7.5-11.2) and 13.1 (11.2-15.9) mm Hg, respectively. On multivariate regression analyses, neurological deterioration was associated with the SD of SBP (odds ratio, 2.75; 95% confidence interval, 1.45-6.12 per quartile) and the successive variation of SBP (2.37; 1.32-4.83), and unfavorable outcome was associated with successive variation of SBP (1.42; 1.04-1.97). Hematoma expansion was not associated with any BP variability. CONCLUSIONS: SBP variability during the initial 24 hours of acute intracerebral hemorrhage was independently associated with neurological deterioration and unfavorable outcomes. Stability of antihypertensive therapy may improve clinical outcomes.

Continuous antihypertensive therapy throughout the initial 24 hours of intracerebral hemorrhage: the stroke acute management with urgent risk-factor assessment and improvement-intracerebral hemorrhage study.

BACKGROUND AND PURPOSE: A short duration (<24 hours) of antihypertensive therapy (AHT) after acute intracerebral hemorrhage (ICH) may be sufficient because active bleeding generally ceases within several hours. We aimed to determine the association between sequential systolic blood pressure (SBP) levels during AHT and outcomes in ICH patients. METHODS: In 211 hyperacute ICH patients who underwent AHT based on predefined protocol, the mean of hourly SBP (mSBP) measurements was calculated over 1 to 8 hours (first mSBP), 9 to 16 hours (second mSBP), and 17 to 24 hours (third mSBP) after the initiation of AHT. Outcomes included neurological deterioration (72-hour Glasgow Coma Scale decrease ≥2 or National Instititutes of Health Stroke Scale increase ≥4), hematoma expansion (>33%), and unfavorable outcome (3-month modified Rankin Scale score 4-6). RESULTS: The median first, second, and third mSBPs were 132, 131, and 137 mm Hg, respectively. A higher first mSBP (odds ratio [OR], 2.41; 95% confidence interval [CI], 1.34-4.69 per 10 mm Hg) or second mSBP (OR, 2.08; 95% CI, 1.20-3.80) was independently associated with neurological deterioration, and a higher second mSBP (OR, 1.40; 95% CI, 1.02-2.00) or third mSBP (OR, 1.45; 95% CI, 1.05-2.05) was associated with unfavorable outcome. None of the mSBPs was associated with hematoma expansion. CONCLUSIONS: The continuation of AHT throughout the initial 24 hours after ICH may improve outcomes.

Systolic blood pressure after intravenous antihypertensive treatment and clinical outcomes in hyperacute intracerebral hemorrhage: the stroke acute management with urgent risk-factor assessment and improvement-intracerebral hemorrhage study.

BACKGROUND AND PURPOSE: Blood pressure (BP) lowering is often conducted as part of general acute management in patients with acute intracerebral hemorrhage. However, the relationship between BP after antihypertensive therapy and clinical outcomes is not fully known. METHODS: Hyperacute (<3 hours from onset) intracerebral hemorrhage patients with initial systolic BP (SBP) >180 mm Hg were included. All patients received intravenous antihypertensive treatment, based on predefined protocol to lower and maintain SBP between 120 and 160 mm Hg. BPs were measured every 15 minutes during the initial 2 hours and every 60 minutes in the next 22 hours (a total of 30 measurements). The mean achieved SBP was defined as the mean of 30 SBPs, and associations between the mean achieved SBP and neurological deterioration (≥2 points' decrease in Glasgow Coma Score or ≥4 points' increase in National Institutes of Health Stroke Scale score), hematoma expansion (>33% increase), and unfavorable outcome (modified Rankin Scale score 4-6 at 3 months) were assessed with multivariate logistic regression analyses. RESULTS: Of the 211 patients (81 women, median age 65 [interquartile range, 58-74] years, and median initial National Institutes of Health Stroke Scale score 13 [8-17]) enrolled, 17 (8%) showed neurological deterioration, 36 (17%) showed hematoma expansion, and 87 (41%) had an unfavorable outcome. On multivariate regression analyses, mean achieved SBP was independently associated with neurological deterioration (odds ratio, 4.45; 95% confidence interval, 2.03-9.74 per 10 mm Hg increment), hematoma expansion (1.86; 1.09-3.16), and unfavorable outcome (2.03; 1.24-3.33) after adjusting for known predictive factors. CONCLUSIONS: High achieved SBP after standardized antihypertensive therapy in hyperacute intracerebral hemorrhage was independently associated with poor clinical outcomes. Aggressive antihypertensive treatment may ameliorate clinical outcomes.

[A rare complication of dysarthria in a patient with inclusion body myositis: a case report].

We reported a 71-year-old man with inclusion body myositis with clinically overt dysarthria. He had been suffering from gradual progression of weakness in the hand muscles and lower extremities as well as dysarthria three years before admission. His neurological examination revealed muscle atrophy and weakness in the tongue, the forearm flexors, and the vastus medialis muscles. He had dysarthria to a moderate degree, while he denied any dysphasia. A biopsy from vastus lateralis muscle showed variation in fiber size, infiltration of mononucleated cells, and numerous fibers with rimmed vacuoles, leading to the diagnosis of definite inclusion body myositis. The EMG findings of the tongue demonstrated low amplitude motor unit potentials during voluntary contraction, abundant fibrillation potentials at rest, and preserved interference pattern at maximal contraction, implying myogenic changes. We surmised the dysarthria seen in this patient, an atypical clinical feature in IBM, presumably caused by muscle involvement in the tongue muscle. Dysphasia is common symptom in IBM patient and has been much reported previously. But dysarthria in IBM patient has not been aware, for this reason this report should be the rare case.