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Background and aims Renal dysfunction is a potent risk factor for cardiovascular diseases, including stroke. This study aimed to evaluate the impact of admission estimated glomerular filtration rate (eGFR) levels on short-term (1-month) and long-term (1-year) mortality in patients with acute ischemic stroke. Methods From the Taiwan Stroke Registry data, we classified ischemic stroke patients, identified from April 2006 to December 2015, into 5 groups by eGFR at admission: ≥ 90, 60–89, 30–59, 15–29, and Results Among 52,732 ischemic stroke patients, 1480 died within one month. The 1-month mortality rate was over 5-fold greater in patients with eGFR Conclusions After acute ischemic stroke, patients with reduced eGFR are at elevated risks of short-term and long-term deaths in a graded relationship.

We investigated the impact of serum cholesterol levels on 30-day mortality after ischemic stroke in dialysis patients.From the Taiwan Stroke Registry data, we identified 46,770 ischemic stroke cases, including 1101 dialysis patients and 45,669 nondialysis patients from 2006 to 2013.Overall, the 30-day mortality was 1.46-fold greater in the dialysis group than in the nondialysis group (1.75 versus 1.20 per 1000 person-days). The mortality rates were 1.64, .62, 2.82, and 2.23 per 1000 person-days in dialysis patients with serum total cholesterol levels of 120 mg/dL, 120-159 mg/dL, 160-199 mg/dL, and ≥200 mg/dL, respectively. Compared to dialysis patients with serum total cholesterol levels of 120-159 mg/dL, the corresponding adjusted hazard ratios of mortality were 4.20 (95% confidence interval [CI] = 1.01-17.4), 8.06 (95% CI = 2.02-32.2), and 6.89 (95% CI = 1.59-29.8) for those with cholesterol levels of 120 mg/dL, 160-199 mg/dL, and ≥200 mg/dL, respectively.Dialysis patients with serum total cholesterol levels of ≥160 mg/dL or 120 mg/dL on admission are at an elevated hazard of 30-day mortality after ischemic stroke.

Objective: To examine psychometric properties of four stroke-specific health-related quality of life (HRQoL) measures, including original Stroke-Specific Quality of Life Scale (12-domain SSQoL), modified 8-domain SSQoL, Stroke Impact Scale (SIS 3.0), and modified SIS-16 focused on physical domains. Design and Setting: Prospective repeated measures study conducted in rehabilitation and wards in hospitals. Subjects: Study cohort was recruited with 263 patients in the first administration and 121 in the second administration, an average of two weeks later. To investigate discriminant validity, the same number of patients (i.e., 52) was grouped for each of 3 levels of stroke severity. Main measures: Outcome measures, including National Institutes of Health Stroke Scale, Mini-Mental State Examination, and Barthel Index. Patients completed HRQoL self-reports. Results: Domains of four measures showed (1) good reliability, except 12-domainSSQoL family roles (Cronbach’s α = 0.68) and personality domains (Cronbach’s α = 0.65) and SIS 3.0 social participation (ICC=0.67) domain; (2) acceptable precision, except 12-domain SSQoL family role domain and SIS 3.0 social participation domain; (3) good convergent validity, except 12-domain SSQoL/8-domain SSQoL vision domain (r = 0.19), (4) good discriminant validity, except 12-domain SSQoL and 8-domain SSQoL thinking domains ( P = 0.365); and (5) acceptable floor effects and strong ceiling effects. The 12-domain SSQoL and 8-domain SSQoL met scaling assumptions better than SIS 3.0 and SIS-16. Conclusions: Four measures showed acceptable psychometric properties with some domains slightly less satisfactory. Overall, use of 8-domain SSQoL and SIS 3.0 are feasible for clinical practice to monitor HRQoL of stroke survivors.

Background Asians have higher frequency of intracranial arterial stenosis. The present study aimed to compare the clinical features and outcomes of ischemic stroke patients with and without middle cerebral artery (MCA) stenosis, assessed by transcranial sonography (TCS), based on the Taiwan Stroke Registry (TSR). Methods Patients with acute ischemic stroke or transient ischemic attack registered in the TSR, and received both carotid duplex and TCS assessment were categorized into those with stenosis (≥50%) and without (

Background Discharge disposition planning is vital for poststroke patients. We investigated clinical factors associated with discharging patients to nursing homes, using the Taiwan Stroke Registry data collected from 39 major hospitals. Methods We randomly assigned 21,575 stroke inpatients registered from 2006 to 2008 into derivation and validation groups at a 3-to-1 ratio. We used the derivation group to develop a prediction model by measuring cumulative risk scores associated with potential predictors: age, sex, hypertension, diabetes mellitus, heart diseases, stroke history, snoring, main caregivers, stroke types, and National Institutes of Health Stroke Scale (NIHSS). Probability of nursing home care and odds ratio (OR) of nursing home care relative to home care by cumulative risk scores were measured for the prediction. The area under the receiver operating characteristic curve (AUROC) was used to assess the model discrimination against the validation group. Results Except for hypertension, all remaining potential predictors were significant independent predictors associated with stroke patient disposition to nursing home care after discharge from hospitals. The risk sharply increased with age and NIHSS. Patients with a cumulative risk score of 15 or more had an OR of 86.4 for the nursing home disposition. The AUROC plots showed similar areas under curves for the derivation group (.86, 95% confidence interval [CI], .85-.87) and for the validation group (.84, 95% CI, .83-.86). Conclusions The cumulative risk score is an easy-to-estimate tool for preparing stroke patients and their family for disposition on discharge.

We prospectively studied the role of somatosensory evoked potentials (SEPs) and psychometric tests in the assessment of subclinical portosystemic encephalopathy (PSE) in 61 cirrhotic patients with grade 0 PSE and 20 controls. Six additional uneducated controls underwent only psychometric tests. Median nerve-evoked cortical responses were recorded for N20-N65 interpeak latencies (IPLs). Psychometric tests were conducted within 4 hours of SEP testing. Seven (26.9%) controls and 30 (49.2%) cirrhotic patients had abnormal psychometric test results (writing sample tests, 20; five-point star tests, 17; number-connection tests, 19; and following-a-track tests, 18); seven controls and 25 cirrhotic patients had 6 or fewer years of education; 7 controls and 28 cirrhotics were older than 50 years of age. Cirrhotic patients (47.6 +/- 8.3 milliseconds) had higher N20-N65 IPLs than controls (40.2 +/- 3.0 milliseconds; P < .001). Twenty-nine (47.5%) cirrhotic patients had abnormal N20-N65 IPLs. Of the 26 cirrhotic patients with more than 6 years of education, 15 (57.7%) had abnormal N20-N65 IPLs and 5 (19.2%) had abnormal psychometric test results (P = .005). Our data show that N20-N65 IPLs of SEPs are helpful in the assessment of subclinical PSE; 47.5% of cirrhotic patients had subclinical PSE. Poorly educated and older subjects tended to have abnormal psychometric test results. SEPs were not affected by education and age and were more sensitive than psychometric tests in the assessment of subclinical PSE in better-educated cirrhotic patients.

Although nerve injury-induced long-term postsynaptic changes have been investigated, less is known regarding the molecular mechanisms within presynaptic axonal terminals. We investigated the molecular changes in presynaptic nerve terminals underlying chronic pain-induced plastic changes in the medial prefrontal cortex (mPFC). After neuropathic pain was induced by spared nerve injury (SNI) in rats, we assessed the release of the excitatory neurotransmitter glutamate by using in vitro synaptosomal preparations from the mPFC. We also measured the levels of synaptic proteins and protein kinases in synaptosomes using Western blotting. The results showed that unilateral long-term SNI augmented depolarization-evoked glutamate release from synaptosomes of the bilateral mPFC. This result was confirmed by a rapid destaining rate of FM1-43 dye in SNI-operated rats. Unilateral long-term nerve injury also significantly increased synaptic proteins (including synaptophysin, synaptotagmin, synaptobrevin, syntaxin, and 25-kDa synaptosome-associated protein) in synaptosomal fractions from the bilateral mPFC, and ultrastructure images demonstrated increased synaptic vesicular profiles in synaptosomes from SNI animals. Chronic pain upregulated the phosphorylation of endogenous protein kinases, including extracellular signal-regulated kinases 1 and 2 (ERK1/2) and Ca(2+)/calmodulin-dependent kinase II (CaMKII), and synapsin I, the primary presynaptic target of ERK1/2 and CaMKII. Both presynaptic proteins and protein kinases were upregulated after SNI in a time-dependent manner. These results indicate that the long-term neuropathic pain-induced enhancement of glutamate release in the mPFC is linked to increased synaptic vesicle proteins and the activation of the ERK1/2- and CaMKII-synapsin signaling cascade in presynaptic axonal terminals.

Churg-Strauss syndrome (CSS) is a rare autoimmune disease with small-vessel vasculitis. Neurological manifestation of CSS is common. Central nervous system is less frequently involved than that of peripheral nervous system.We report a case of 60-year-old man who presented with acute onset of right hemiparesis and impaired cognition. The presence of hypereosinophilia, asthma, sinusitis and extravascular eosinophil accumulation led to the diagnosis of Churg-Strauss syndrome. Brain magnetic resonance imaging (MRI) revealed multiple infarcts in bilateral cerebral and cerebellar hemispheres. The neurophysiology study did not reveal peripheral neuropathy. The patient was effectively treated with methylprednisolone, cyclophosphamide and warfarin.Symptoms and signs of central nervous system can be the initial neurological manifestation of CSS patients. CSS should be considered while patients have stroke and hypereosinophilia. In our patient, there is a good response to timely steroid, immunosuppressant and anticoagulant therapies.

Twenty-two patients with ischemic stroke, as a single event, in the territory of basilar artery (BA) are reported. On the basis of the findings from computerized tomography (CT) and clinico-radiologic features, the authors propose that this heterogeneous entity—the basilar artery (BA) syndrome—can be divided into five subtypes. Type 1 (complete type), characterized by infarctions in the whole territory of BA, is incompatible with life; type 2, with extensive brain stem infarct, may result in a locked-in state; and type 3, with infarctions in part of the BA territory (incomplete form or "partial syndrome") may have a more variable clinical outcome. However, type 4, with a top of the BA syndrome, and type 5, with negative CT BA syndrome (angiographically verified), are often more benign. Although initial CT scanning may infrequently be unrevealing, serial and follow-up CT scannings have proven their usefulness in the majority of cases as a noninvasive tool, in contrast to cerebral angiography, for predicting the short-term prognosis of BA syndrome.

Genetic C677T and A1298C polymorphisms in 5,10-methylenetetrahydrofolate reductase (MTHFR) and levodopa therapy in Parkinson's disease (PD) may increase homocysteine (Hcy) level. We examined whether connecting both polymorphisms influences the effect of levodopa on Hcy. MTHFR genotypes and Hcy, vitamin B(12), and folate levels were determined in 48 levodopa-treated PD patients (PD-L), 28 non-treated PD patients (PD-N) and 110 controls. Hcy was remarkably higher in PD-L than in PD-N and controls (p0.001); similarly, the differences were seen in different age subgroups and in both genders. Furthermore, Hcy differences between PD-L and PD-N were evident in 677C/T, T/T, C/T + A/A, T/T + A/A (all p0.05), and 1298A/A (p0.001), but not in others such as 677C/C, and C/C + A/A. Hcy in PD-N and controls was comparable for all genotypes. In PD-L, Hcy was the highest in 677T/T, then in C/T, and in C/C with a significant difference from T/T (p=0.014), but was not different among A1298C genotypes. Likewise, Hcy was the highest in 677T/T+1298A/A, intermediate in C/T+A/A, and the lowest in C/C+A/A. In PD-N, Hcy was similar among all genotypes. In conclusion, Hcy elevation may be caused by levodopa administration, and further promoted by 677C/T and T/T, but not by A1298C genotypes. The promoting elevation in 1298A/A is attributed to combining the 677T allele. Neither C677T nor A1298C genotypes contribute to elevating Hcy in PD-N.

Involvement of the central nervous system (CNS) by tuberculosis is rare; it can affect either immunocompromised or immunocompetent people.Here, we report a case of tuberculosis with CNS involvement. We present the case of an immunocompetent young man who developed fever, subacute headache, disturbance of consciousness, paraparesis, sphincter dysfunction, and hypoesthesia. The final diagnosis was tuberculous meningitis, myeloradiculitis and arachnoiditis based on clinical signs, imaging studies, and cerebrospinal fluid culture. The patient received antituberculosis medication with adjunct intravenous steroid therapy. Although his clinical condition improved significantly, some neurological sequelae persisted.Methods for detection of CNS TB and treatment protocols should be constantly re-evaluated to improve treatment outcome and reduce likelihood and severity of neurological sequelae.

BACKGROUND AND AIM The purpose of the present paper was to determine the role of zinc in subclinical portosystemic encephalopathy (SPSE). METHODS The serum zinc levels were studied for 10 cirrhotic patients who did not suffer SPSE and for 10 patients who did, and the results compared with those deriving from 10 healthy volunteers. The nutritional evaluation included serum prealbumin, albumin, and transferrin levels, body mass index (BMI), mid-arm muscle circumference (MAMC), and tricep skin-fold (TSF). The occurrence of SPSE was defined as a situation when the N20-N65 interpeak latencies of median nerve-stimulated somatosensory-evoked potentials (SEP) exceeded 2.5 SD of the control mean value. RESULTS Cirrhotic patients suffering SPSE (57.5 +/- 10.5 microg/dL) had lower serum zinc levels than those not experiencing SPSE (69.5 +/- 16.6 microg/dL, P = 0.03) and controls (77.7 +/- 6.8 microg/dL, P < 0.001). Four of the non-SPSE and nine SPSE patients had zinc levels less than the lower normal limit. Cirrhotic patients suffering SPSE had lower levels of albumin (2.8 +/- 0.4 g/dL vs 3.8 +/- 0.4 g/dL, P < 0.001), prealbumin (9.0 +/- 4.3 mg/dL vs 14.3 +/- 6.0 mg/dL, P = 0.02), and transferrin (158 +/- 56 g/L vs 218 +/- 50 g/L, P = 0.01), but a greater total bilirubin level (1.2 +/- 1.5 mg/dL vs 0.9 +/- 0.4 mg/dL, P = 0.005) than those not suffering SPSE. The serum zinc levels correlated with N20-N65 interpeak latencies (P = 0.03), serum albumin (P = 0.006), prealbumin (P < 0.001), and total bilirubin (P = 0.02) levels. CONCLUSIONS The data show that zinc deficiency is common in cases of non-alcoholic cirrhosis with SPSE. The early assessment of malnutrition and zinc deficiency are important.