A common polymorphism decreases LRP1 mRNA stability and is associated with increased plasma factor VIII levels.

The low-density lipoprotein receptor-related protein 1 (LRP1) gene is associated with increased levels of plasma factor VIII (FVIII). We aimed to explore eight functional genetic LRP1 variants for their potential roles in regulating FVIII levels and acute ischemic stroke (AIS). This genetic association study enrolled 192 patients with AIS and 134 controls. There were no significant differences in the genetic frequency of the eight functional single-nucleotide polymorphisms (SNPs) between the control and AIS groups. However, while analyzing the association between the eight SNPs and plasma FVIII levels, subjects with T/T genotype of rs1800137 (vs. CC+CT) were found to be associated with higher FVIII levels (23.5IU/dL; 95% confidence interval, 7.4-39.5IU/dL; P=0.0044) after adjusting for age, gender, estimated glomerular filtration rate, O blood type, inflammatory state, and body mass index. An analysis of the mRNA stability and abundance was designed and performed using minigene system transfected into HepG2 cells to assess the possible differences in mRNA stabilities between rs1800137 CC (rs1800137C) and TT (rs1800137T) genotypes. Site-directed mutagenesis revealed that rs1800137T accounts for the observed decrease in mRNA stability. The SNP rs1800137, located in exon 8, has been identified as an exon-splicing enhancer in silico. However, alternative splicing of LRP1 without inclusion of exon 8 was not identified. In transfected HepG2 cells, cycloheximide slowed down the degradation of the rs1800137T-containing minigene. These results demonstrate that synonymous SNP rs1800137 can lead to increased plasma FVIII levels due to decreased mRNA stability via translation-dependent mRNA degradation associated with codon optimality.

Timing of Symptomatic Infarct Swelling Following Intravenous Thrombolysis in Acute Middle Cerebral Artery Infarction: A Case-Control Study.

BACKGROUND: The risk of symptomatic infarct swelling has been reported to be higher in patients treated with recombinant tissue plasminogen activator (rt-PA). The aim of this study was to evaluate the timing of symptomatic infarct swelling after rt-PA treatment. METHODS: We retrospectively analyzed 14 868 patients with acute ischemic stroke from a stroke registry databank. We recruited patients with massive middle cerebral artery (MCA) infarction and symptomatic infarct swelling and excluded those with parenchymal or symptomatic hemorrhage. Multiple linear regression and multivariate logistic regression analyses were used to estimate the impact of rt-PA on the timing of symptomatic infarct swelling. RESULTS: A total of 23 patients with rt-PA treatment and 117 patients without rt-PA treatment were included. The rt-PA treatment group had a lower rate of coronary artery disease (8.7% vs 32.5%; P = .023), lower severity of baseline National Institutes of Health Stroke Scale score (19 vs 23; P = .014), shorter duration of infarct swelling (27.6 vs 45.4 hours; P < .001), and higher rate of hemicraniectomy surgery (65.2% vs 28.2%; P =.001) than those without rt-PA treatment. After adjusting for variables in multiple linear regression analysis, rt-PA treatment and an elevated C-reactive protein level were associated with early symptomatic infarct swelling ( P = .014 and P = .041, respectively). The rt-PA treatment was an independent factor related to early symptomatic infarct swelling within 36 hours ( P = .005; odds ratio [OR]: 5.3; confidence interval [CI]: 1.65-17.0) or 48 hours ( P = .009; OR: 16.4; CI: 2.00-134). CONCLUSION: Intravenous rt-PA treatment may hasten the onset of cerebral edema and subsequent cerebral herniation in large MCA territory infarction.

Magnetic Resonance Perfusion Imaging Provides a Significant Tool for the Identification of Cardioembolic Stroke.

Despite advances in imaging techniques and detailed examinations to determine the etiology of a stroke, the cause still remains undetermined in about one fourth of all ischemic strokes. The aim of this prospective study was to determine whether perfusion magnetic resonance imaging (MRI) can differentiate cardioembolic stroke from large artery atherosclerosis (LAA). We recruited 17 cardioembolic stroke and 22 LAA stroke patients, who were classified according to the Trial of Org 10172 in Acute Stroke Treatment and underwent perfusion MRI within 24 hours after the onset of stroke. The patients with cardioembolic stroke had more severe initial stroke severity and larger volumes of initial and final infarct compared to those with LAA stroke. Receiver operating characteristic curve analysis showed that the ratio of time to maximum of the residual curve (Tmax) volume for a 2-, 3-, 4- or 5-s lag over Tmax volume for a 8s lag all had excellent area under the curve values (> 0.9) to predict cardioembolic stroke. After adjusting for initial National Institute of Health Stroke Scale scores, a threshold of 3.73 for (Tmax > 4s volume)/(Tmax > 8s volume) had the highest odds ratio to predict cardioembolic stroke (p=0.012; odds ratio: 58.5; 95% confident interval: 2.5-1391.1), with 87.5% sensitivity and 94.4% specificity. In conclusion, perfusion MRI could be a reliable tool to identify cardioembolic stroke with its lower collateral. This is important as it could be used to reveal the exact mechanism and provide supportive evidence to classify a stroke.

Comparisons of outcomes in stroke subtypes after intravenous thrombolysis.

The purpose of this study was to analyze the outcomes and complications between stroke subtypes after intravenous thrombolysis. A total of 471 patients with acute ischemic stroke after intravenous thrombolysis from January 2007 to April 2014 were enrolled and classified according to the Trial of Org 10172 in Acute Stroke Treatment. A multivariate logistic regression model was used to evaluate the outcomes and complications among stroke subtypes after adjusting for baseline variables. Of the 471 patients, 117 (25.1 %) had large-artery atherosclerosis (LAA), 148 (31.8 %) had cardioembolism (CE), 82 (17.6 %) had small vessel disease (SVD), 119 (25.5 %) had undetermined etiology, and 5 (1.1 %) had other determined etiology. The patients with SVD had the mildest initial stroke severity and highest ratio of good and favorable outcomes, whereas those with CE had a higher rate of symptomatic intracranial hemorrhage (sICH) than those with SVD. After adjusting for confounding factors, the ratio of favorable outcome in the patients with SVD stroke was higher than in those with LAA. SVD was associated with a significantly lower rate of any hemorrhage compared to other stroke subtypes, whereas there were no differences in sICH or mortality between stroke subtypes. A lower initial National Institutes of Health Stroke Scale score was associated with good and favorable outcomes, and lower rates of sICH and mortality. The patients with SVD after intravenous thrombolysis had better outcomes and a lower rate of hemorrhage even after adjusting for confounding factors. Stroke severity was an independent factor associated with better functional outcomes, sICH and mortality.

Shortened Activated Partial Thromboplastin Time Is Associated With Acute Ischemic Stroke, Stroke Severity, and Neurological Worsening.

BACKGROUND: The role played by hemostasis in the pathogenesis of ischemic strokes is still controversial. The activated partial thromboplastin time (APTT) measures the time necessary to generate fibrin from initiation of the intrinsic pathway. In the present study, we looked for a possible association of ischemic strokes with the shortened APTT. METHODS: The study population consisted of 154 patients with acute ischemic strokes who had been admitted from December 2013 to December 2014 to the Department of Neurology, Chiayi Chang Gung Memorial Hospital, and 71 control subjects with no history of stroke. RESULTS: In a univariate risk analysis, shortened APTT was associated with an odds ratio (OR) for acute ischemic strokes of up to 1.86 (95% confidence interval [CI], 1.06-3.29, P = .031). In a multivariate analysis using a logistic regression model including age, sex, hypertension, diabetes mellitus, and shortened APTT, shortened APTT was still found to significantly add to the risk of ischemic stroke (OR = 2.12 with 95% CI, 1.13-3.98, P = .020). Shortened APTT was also associated significantly with neurological worsening (OR = 3.72 with 95% CI 1.03-13.5, P = .046). As for stroke severity, shortened APTT was associated with an OR for moderate/severe stroke of up to 3.42 (95% CI, 1.53-7.61, P = .003). CONCLUSION: Shortened APTT is a prevalent and independent risk factor for ischemic stroke, stroke severity, and neurological worsening after acute stroke.

Perfusion-diffusion Mismatch Predicts Early Neurological Deterioration in Anterior Circulation Infarction without Thrombolysis.

Perfusion-diffusion mismatch in magnetic resonance imaging (MRI) represents the non-core hypoperfused area in acute ischemic stroke. The mismatch has been used to predict clinical response after thrombolysis in acute ischemic stroke, but its role for predicting early neurological deterioration (END) in acute ischemic stroke without thrombolysis has not been clarified yet. In this study, we prospectively recruited 54 patients with acute non-lacunar ischemic stroke in anterior circulation without thrombolysis. All patients received the first perfusion MRI within 24 hours from stroke onset. Target mismatch profile was defined as a perfusion-diffusion mismatch ratio ≥ 1.2. END was defined as an increase of ≥ 4 points in the National Institute of Health Stroke Scale (NIHSS) score within 72 hours. There were 13 (24.1%) patients developing END, which was associated with larger infarct growth (p = 0.002), worse modified Rankin Scale (p = 0.001) and higher mortality rate at 3 months (p = 0.025). Target mismatch profiles measured by T(max) ≥ 4, 5 and 6 seconds were independent predictors for END after correcting initial NIHSS score. Among the 3 T(max) thresholds, target mismatch measured by T(max) ≥ 6 seconds had the highest odd's ratio in predicting END (p < 0.01, odd's ratio = 17), with an 80% sensitivity and a 79.5% specificity. In conclusion, perfusion-diffusion mismatch could identify the patients at high risk of early clinical worsening in acute ischemic stroke without thrombolysis.

Factor VIII levels are associated with ischemic stroke, stroke subtypes and neurological worsening.

The role played by hemostasis in the pathogenesis of ischemic stroke is still controversial. In the present study, we looked for a possible association of ischemic stroke with the high clotting activity of factor VIII (FVIII). The study population consisted of 116 patients with acute ischemic stroke who had been admitted between September 2013 and September 2014 to the Department of Neurology, Chiayi Chang Gung Memorial Hospital, and 76 control subjects with no history of stroke. FVIII levels were higher in stroke patients as compared to controls (127.5 ± 52.5 vs. 108.4 ± 49.0 IU/dL; P = 0.012). In a univariate risk analysis, FVIII at levels above 150 IU/dL was associated with an odds ratio (OR) for ischemic stroke of up to 2.55 (95% CI, 1.20-5.42, P = 0.013). In a multivariate analysis using a logistic regression model including age, hypertension, low density lipoprotein cholesterol level, estimated glomerular filtration rate, and high FVIII (< 150 IU/dL), high FVIII was still found to significantly add to the risk of ischemic stroke (OR = 3.26 with 95% CI, 1.38-7.68, P = 0.007). As for the stroke subtypes, mean FVIII level was significantly higher in patients with cardioembolic stroke than patients with noncardioembolic stroke (156.0 ± 51.5 IU/dL vs. 124.3 ± 51.9 IU/dL). High levels of FVIII were also associated significantly with neurological worsening (OR = 3.66 with 95% CI, 1.24-10.82, P = 0.019). A high plasma level of FVIII is a prevalent and independent risk factor for ischemic stroke and neurological worsening after acute stroke.

Low baseline urine creatinine excretion rate predicts poor outcomes among critically ill acute stroke patients.

Urinary creatinine excretion rate (CER) is an established marker of muscle mass. Low CER has been linked to poor coronary artery disease outcomes, but a link between CER and acute stroke prognosis has not been previously explored. We prospectively collected data from patients with acute stroke (ischemic or hemorrhagic) within 24 hours from symptom onset in a Neurological and Neurosurgery Intensive Care Unit in Taiwan. Baseline CER (mg/d) was calculated by urine creatinine concentration in morning spot urine multiplies 24-hour urine volume on the second day of admission. Patients were divided into 3 tertiles with highest, middle, and lowest CER. Primary endpoint was poor outcome defined as modified Rankin Scale 3-6 at 6 months. Among 156 critically ill acute stroke patients meeting study entry criteria, average age was 67.9 years, and 83 (53.2%) patients had ischemic stroke. Patients with lowest CER (vs. highest CER) had a high risk of poor outcome at 6-month after adjustment (odds ratio 4.96, 95% confidence interval 1.22 to 20.15, p value = 0.025). In conclusion, low baseline CER, a marker of muscle mass, was independently associated with poor 6-month outcome among critically ill acute stroke patients. We speculate that preservation of muscle mass through exercise or protein-energy supplement might be helpful for improving prognosis in severe stroke patients.

Hemodynamic factors may play a critical role in neurological deterioration occurring within 72 hrs after lacunar stroke.

BACKGROUND: Whether a perfusion defect exists in lacunar infarct and whether it is related to early neurological deterioration (END) is still under debate. The aim of this study was to evaluate whether END in lacunar infarct is related to a perfusion defect using diffusion-weighted imaging (DWI), diffusion tensor imaging (DTI) and perfusion MR imaging. METHODS: One hundred and forty-one consecutive patients had an MRI scan within 30 hours after onset of symptoms and 43 patients with acute lacunar infarct and classic lacunar syndrome were recruited. The MRI sequences included DWI, DTI and cerebral blood flow (CBF) maps to respectively represent the topographic locations of acute infarcts, the corticospinal tract and perfusion defects. The END was defined in reference to the National Institute of Health Stroke Scale (NIHSS) as an increase ≧2 within 72 hours. Cohen's Kappa coefficient was used to examine the reliability between the 2 image readers. A multivariate logistic regression model was constructed adjusting for baseline variables. RESULTS: Ten out of the 43 patients had END. Patients having END was significantly associated with lower chances of favorable and good outcomes at 3 months (p = 0.01 and p = 0.002, respectively). END was predicted when the non-core hypoperfused area overlapped on the corticospinal tract, which is defined as the expected END profile. Cohen's Kappa coefficient between the 2 image readers to define images of expected END profiles was 0.74. In 15 patients with expected END profile, 9 had END clinically, whereas 28 patients had no expected END profile, and only 1 patient had END (p<0.0001). After adjusting for sex, the expected END profile was still associated with END (odds ratio, 42.2; p = 0.002). CONCLUSION: Our study demonstrated that the END in acute lacunar stroke is likely related to the transformation of non-core hypoperfused area into infarction in the anatomy of corticospinal tracts.

Mutual effect of rs688 and rs5925 in regulating low-density lipoprotein receptor splicing.

Analysis of the low-density lipoprotein receptor (LDLR) gene based on the rs688 and rs5925 genetic polymorphisms has provided evidence suggesting that haplotypes related to rs688 and rs5925 are associated with ischemic cerebrovascular diseases. Both rs688 and rs5925 have been empirically identified as exon-splicing enhancers in silico, and rs688 has been shown to be a functional polymorphism that modulates LDLR exon 12 splicing efficiency both in vitro and in vivo. The aim of this study was to evaluate whether rs688 and rs5925 and their haplotypes may alter the splicing efficiency of exons 12 and 13 both in vivo and in vitro. When the minigenes were evaluated for splicing efficiency, we found that converting rs688C to the T allele reduced exon 12 splicing efficiency. In parallel, converting rs688T to the C allele increased the efficiency of exon 12 inclusion. The apparent difference in splicing efficiency was 9.36%±2.58% between the C and T alleles. When rs688C existed in the minigene, the major and minor rs5925 alleles were also sufficient to account for the differences in splicing efficiency of LDLR involving exon 13. The apparent splicing efficiency difference was 5.43%±2.87%. Sequential mutations of rs688 and rs5925 were performed to generate four different haplotypes in the LDLR minigene system. The splicing efficiencies for the haplotypes CC, CT, TC, and TT were 79.60%±1.38%, 76.68%±0.85%, 69.02%±1.79%, and 68.54%±1.38%, respectively. The splicing efficiency of the four haplotype groups differed significantly. In vivo analysis of human leukocyte samples was also compatible with in vitro analysis, indicating a mutual effect between rs688 and rs5925 in regulating LDLR splicing efficiency.

Genetic polymorphism of LDLR (rs688) is associated with primary intracerebral hemorrhage.

Intracranial hemorrhage is the third most common cause of cerebrovascular disease. Some polymorphisms that affect clotting factors increase the risk of thrombosis. However, few reports have analyzed the effect of polymorphisms on the hemostatic state in bleeding disorders. The low-density lipoprotein receptor (LDLR) has been shown to contribute to factor VIII (FVIII) homeostasis, which represents a link between LDLR and hemostasis. FVIII plays a pivotal role in the coagulation cascade. Patients with high levels of FVIII are at an increased risk of arterial and venous thrombosis. On the other hand, patients with insufficient FVIII tend to bleed excessively, such as in hemophilia A. In a previous study, analysis of the genetic LDLR variant rs688 provided evidence suggesting that genetic polymorphisms of rs688 are associated with thrombotic cardiovascular diseases. The current study aimed to investigate the potential role of rs688 in primary intracerebral hemorrhage (PICH). This genetic association study was conducted within an isolated Taiwanese population (447 PICH patients and 430 controls). Genotypes C/C and C/T were used as the reference genotypes, and the genotype T/T was found to be associated with a 73% decreased risk of PICH. The preliminary evidence suggests that genetic polymorphisms of LDLR are associated with PICH.

Association of renal biomarkers with 3-month and 1-year outcomes among critically ill acute stroke patients.

BACKGROUND: The comparative relationships of widely recognized biomarkers of renal injury with short-term and long-term outcomes among critically ill acute stroke patients are unknown. We evaluated the impact of baseline albuminuria [urine albumin-creatinine ratio (UACR) ≥ 30 mg/g] or low estimated glomerular filtration rate (eGFR<60 ml/min per 1.73 m(2)) on stroke patients admitted to the intensive care unit (ICU). METHODS: We reviewed data on consecutive stroke patients admitted to a hospital ICU in Taiwan from September 2007 to August 2010 and followed-up for 1 year. Baseline UACR was categorized into <30 mg/g (normal), 30-299 mg/g (microalbuminuria), and ≥ 300 mg/g (macroalbuminuria), while eGFR was divided into ≥ 60, 45-59, and <45 ml/min per 1.73 m(2). The outcome measure was death or disability at 3-month and 1-year after stroke onset, assessed by dichotomizing the modified Rankin Scale at 3-6 versus 0-2. RESULTS: Of 184 consecutive patients, 153 (83%) met study entry criteria. Mean age was 67.9 years and median admission NIHSS score was 16. Among the renal biomarkers, only macroalbuminuria was associated with poorer 3-month outcome (OR 8.44, 95% CI 1.38 to 51.74, P = 0.021) and 1-year outcome (OR 18.06, 95% CI 2.59 to 125.94, P = 0.003) after adjustment of relevant covariates. When ischemic and hemorrhagic stroke were analyzed separately, macroalbuminuria was associated with poorer 1-year outcome among ischemic (OR 17.10, 95% CI 1.04 to 280.07, P = 0.047) and hemorrhagic stroke patients (OR 1951.57, 95% CI 1.07 to 3561662.85, P = 0.048), respectively, after adjustment of relevant covariates and hematoma volume. CONCLUSIONS: Presence of macroalbuminuria indicates poor 3-month and 1-year outcomes among critically ill acute stroke patients.

Clinical features and outcomes of spinal cord infarction following vertebral artery dissection: a systematic review of the literature.

OBJECTIVE: Spinal cord infarction (SCI) is a rare complication of vertebral artery dissection (VAD). Its clinical features and outcomes have not yet been well documented. METHODS: In addition to reporting a case with bilateral SCI caused by left VAD, we performed a systematic review of the literature conducted through a PubMed search. RESULTS: A total of 17 cases were reviewed (nine men and eight women). The average age was 40·5±14·6 years. In addition to neck pain or headache (88%), patients with VAD-associated SCI often presented with a sensory level (76%) or Brown-Séquard syndrome (53%). The most common regions of dissection were at the V1 or proximal V2 segments, and the infarcted area of SCI was mainly located at C2-C5 levels. Regarding the vascular territory, posterior spinal artery infarction was noted in 29% of patients, spinal sulcal artery infarction in 42%, and anterior spinal artery (ASA) watershed infarction in 29%. Eleven patients (65%) had a good outcome and six patients (35%) had a poor outcome (including one mortality; 6%). Smoking, age above 50 years, and ASA watershed infarction were associated with a poor outcome, while spinal sulcal artery infarction was associated with a good outcome. CONCLUSION: Neck pain or headache is an important warning symptom of VAD, and the presence of a concomitant sensory level or Brown-Séquard syndrome is helpful for the early diagnosis of SCI caused by VAD. One-third of patients had a poor outcome, and smoking, old age, and ASA watershed infarction represented important risk factors.

Polymorphisms at the LDLR locus may be associated with ischemic cerebrovascular disease independent of lipid profile.

The low-density lipoprotein receptor (LDLR) gene has been reported to be associated with cerebral infarction. This study aimed to explore 2 genetic LDLR variants, rs688 and rs5925, for their potential roles in cerebral infarction. This genetic association study was conducted within an isolated Taiwanese population; 815 ischemic stroke patients (431 with atherothrombotic stroke and 384 with lacunar infarction) and 430 normal controls were enrolled. There was no significant difference in the genetic frequency of rs688 and rs5925 between the control group and overall ischemic stroke, atherothrombotic stroke, or lacunar infarct groups. However, when analyzing the association between the haplotypes related to rs688 and rs5925 and cerebral ischemic stroke, the most common haplotype allele CT was used as the reference allele, and the haplotype TC associated with a 65% increased risk of overall ischemic stroke, 72% increased risk of atherothrombotic stroke, and 70% increased risk of lacunar infarction; this indicated a synergistic effect between these 2 single-nucleotide polymorphisms. The LDLR analysis based on the haplotypes rs688 and rs5925 was conducted in a Taiwanese population and provided preliminary evidence suggesting that genetic polymorphisms of LDLR are associated with cerebral infarction.

ALOX5AP genetic variants and risk of atherothrombotic stroke in the Taiwanese population.

We explored the role of variants of the arachidonate 5-lipoxygenase-activating protein (ALOX5AP) gene as factors for atherothrombotic stroke (ATS). A HapMap-based haplotype-tagging single nucleotide polymorphism (htSNP) association study was conducted in an isolated Taiwanese population. Multivariate logistic regression analyses revealed that patients with the GG/CG genotype of rs4293222 and the AA/AG genotype of rs4360791 had a 1.61-fold (odds ratio [OR]=1.61; 95% confidence interval [CI]=1.02-2.56, p=0.042) and a 1.69-fold (OR=1.69; 95% CI=1.00-2.86, p=0.047) increased risk of ATS, compared with patients with the CC/GG genotype, respectively. The most common haplotype allele, GTA, was used as a reference when analyzing the association between the haplotypes related to rs4293222, rs10507391, rs12429692 and ATS. The combined frequencies of all minor variant alleles of the three selected htSNP were associated with a 44% decreased risk of ATS (OR=0.56; 95% CI=0.37-0.84, p=0.005). This study provides preliminary evidence suggesting that genetic polymorphisms of ALOX5AP are associated with ATS.

Genetic polymorphisms of low density lipoprotein receptor can modify stroke presentation.

Low density lipoprotein is transcytosed across the blood-brain barrier mediated by low density lipoprotein receptor (LDLR). LDLR in the brain is mainly expressed on capillary endothelial cells and is therefore considered to be an important susceptibility gene in modifying the stroke presentation. A HapMap-based haplotype-tagging single nucleotide polymorphism association study was conducted in an isolated Taiwanese population. Two hundred and ninety-two unrelated patients with cerebral infarction, 76 patients with small vessel occlusion (SVO) disorder and 216 with non-SVO disorder were enrolled. For rs2738446, under the dominant model, the odds ratios (ORs) associated with the CC genotype were computed, with GG + CG carriers considered as the reference group. Homozygote CC carriers had a two-fold increased risk of SVO disorder [OR=2.0, 95% confidence interval (CI)=1.08-3.70, p=0.025). For rs2738450, under the dominant model, the ORs associated with the CC genotype were computed, with AA + AC carriers considered as the reference group. Homozygote CC carriers had a 1.85-fold increased risk of SVO disorder (OR=1.85, 95% CI=1.01-3.33, p=0.04). When analysing the association between the haplotype related to rs2738446 and rs2738450 and SVO disorder, the most common haplotype allele CC was used as the reference, and the GA haplotype allele was associated with a 48% decreased risk of SVO disorder (OR=0.52; 95% CI=0.29-0.93, p=0.029). Haplotype-based analysis of LDLR in Taiwanese patients with cerebral infarction provided preliminary evidence suggesting that genetic polymorphisms of LDLR can modify the stroke presentation.

Gouty arthritis in acute cerebrovascular disease.

BACKGROUND: Gouty arthritis is a metabolic disorder associated with several medical diseases and is considered as a high-risk factor of acute myocardial infarction and cardiovascular mortality. Since no study has assessed the frequency of gout attack in acute-stroke patients, a retrospective analysis of gouty arthritis in stroke patients was performed to identify the frequency and characteristics of gouty arthritis in hospitalized stroke patients. METHODS: We reviewed the data of 920 patients admitted to the neurology ward of the Chiayi Chang Gung Memorial Hospital between 2002 and 2005 with ischemic stroke. The frequency of gouty arthritis in these patients was evaluated. The severity of the risk factors was compared between the patients with gout and those without. RESULTS: The frequency of gouty arthritis in the stroke patients was 6.5%. Most patients had an attack of gout within 9 days of admission. History of gout, uric acid level and hypercholesterolemia were independent risk factors of gout attack during acute stroke. The duration of acute-ward stay was longer in patients with gout than in those without (17.17 vs. 14.01 days, p = 0.016). CONCLUSIONS: Our retrospective study demonstrated that gout attack is not uncommon in acute-stroke patients and may result in longer duration of acute-ward stay.

Gastrointestinal hemorrhage after acute ischemic stroke and its risk factors in Asians.

BACKGROUND: The aim of this study was to examine the frequency and risk factors of gastrointestinal (GI) hemorrhage in acute ischemic stroke patients in Taiwan. METHOD: 920 patients admitted for acute ischemic stroke from January 2001 to October 2005 were included in the study. We reviewed the available medical records for any episode of GI hemorrhage, possible precipitating factors and administration of ulcer prophylaxis. RESULTS: Seventy-two patients (7.8%) experienced GI hemorrhage; these patients were of an older age (74.7 vs. 69.0 years, p < 0.001), had a longer acute ward stay (30.4 vs. 12.9 days, p < 0.001) and higher mortality rate (odds ratio 9.61, CI 4.53-20.42) than patients without GI hemorrhage. In multivariate logistic regression analysis, the important risk factors of GI hemorrhage included sepsis, previous history of GI hemorrhage, severe stroke, renal insufficiency and abnormal liver function. Of the 779 patients who had a 0-1 risk factor, 26 (3.3%) experienced GI hemorrhage; of the 27 patients with more than 2 risk factors, 17 (63%) suffered GI hemorrhage. CONCLUSION: This study of Asians revealed a higher frequency of GI hemorrhage after acute ischemic stroke than that reported in previous studies, and the frequency of GI hemorrhage was positively correlated with the number of risk factors present. We suggest that identifying stroke patients with a high risk of hemorrhage may allow clinicians to set up ulcer prophylactic protocols for the patients most likely to benefit, especially in an Asian population.

Periictal magnetic resonance imaging in status epilepticus.

PURPOSE: To determine the changes of magnetic resonance imaging (MRI) during the periictal phase in status epilepticus (SE). PATIENTS AND METHODS: We identified 15 patients diagnosed of status epilepticus with corresponding MRI changes, including 11 patients with generalized convulsive status epilepticus (GCSE), 2 with complex partial status epilepticus (CPSE), and 2 with simple partial status epilepticus (SPSE). All MRI changes, corresponding electroencephalogram, and prognosis were evaluated. RESULTS: Regional cortical lesions were observed on MRI, including restricted diffusion in diffusion-weighted images (DWIs) (11 out of 15) and hyperintense signal change in fluid-attenuated inversion recovery (FLAIR) images (12 out of 15) with hypervascularity and parenchymal swelling. The remote lesions included crossed cerebellar diaschisis (3 patients), ipsilateral thalamic lesion (4 patients), and basal ganglia lesions (3 patients). Although the periictal MRI changes were usually reversible, irreversible changes were also found, especially in GCSE, such as focal brain atrophy, cortical laminar necrosis, and mesial temporal sclerosis. GCSE patients with periodic epileptic form discharges had higher possibilities of widespread MRI abnormalities and poor prognosis in the future. CONCLUSIONS: In this study, DWIs and FLAIR images were proved useful in determining the extent and severity of early neuronal damage caused by epileptic discharges in SE patients. Seizure-induced long-term injuries were also observed in the follow-up MRI.