Impact of MCA stenosis on the early outcome in acute ischemic stroke patients.

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 (<50%) in the extracranial internal carotid artery (ICA) and MCA, respectively. Logistic regression analysis, Kaplan-Meier method and Cox proportional hazard model were applied to assess relevant variables between groups. RESULTS: Of 6003 patients, 23.3% had MCA stenosis, 10.1% ICA stenosis, and 3.9% both MCA and ICA stenosis. Patients with MCA stenosis had greater initial NIHSS, higher likelihood of stroke-in-evolution, and more severe disability than those without (all p<0.001). Patients with MCA stenosis had higher prevalence of hypertension, diabetes and hypercholesterolemia. Patients with combined MCA and extracranial ICA stenosis had even higher NIHSS, worse functional outcome, higher risk of stroke recurrence or death (hazard ratio, 2.204; 95% confidence intervals, 1.440-3.374; p<0.001) at 3 months after stroke than those without MCA stenosis. CONCLUSIONS: In conclusion, MCA stenosis was more prevalent than extracranial ICA stenosis in ischemic stroke patients in Taiwan. Patients with MCA stenosis, especially combined extracranial ICA stenosis, had more severe neurological deficit and worse outcome.

Cholesterol Levels Are Associated with 30-day Mortality from Ischemic Stroke in Dialysis Patients.

BACKGROUND: We investigated the impact of serum cholesterol levels on 30-day mortality after ischemic stroke in dialysis patients. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Psychometric comparisons of four disease-specific health-related quality of life measures for stroke survivors.

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.

Upregulation of presynaptic proteins and protein kinases associated with enhanced glutamate release from axonal terminals (synaptosomes) of the medial prefrontal cortex in rats with neuropathic pain.

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.

Age-changed normative auditory event-related potential value in children in Taiwan.

BACKGROUND/PURPOSE: Event-related potentials (ERPs) reflect higher cortical function and the P3 (P300) wave has been associated with various sensory, cognitive, and attention processes. The aims of this study were to understand the age-related change in ERPs in children between the ages of 6 and 13 years and to establish a normal reference value for Taiwanese children for use in future study of neurocognitive dysfunction in children. METHODS: Using an auditory oddball paradigm, ERPs were recorded in 63 mentally and physically normal children ages 6 to 13 years. Parietal, central, and frontal ERP long-latency components (N1, P2, N2, P3) were measured in each test participant. RESULTS: Linear regression analysis demonstrated a significant linear decrease in P3, P2, N2, and N1 latencies and a significant linear increase in P3, P2, and N1 amplitudes in children between the ages of 6 and 13 years. P3 latency was significantly longer in children ages 6-7 years than in older children. The parietal P3 latency decreases 6.7 msec per year from ages 6 to 13 years. A wide variation in P3 latency in the children ages 6-7 years and a significant increase in P3 amplitude in those ages 12-13 years were observed from our data. A significant increase in P2 amplitude was also observed in children older than 10 years. CONCLUSION: The authors conclude that there exists an age-related change in ERP latency and amplitude during childhood. A negative correlation between ERP latencies and age and a positive correlation between ERP amplitude and age were found in this study. The authors emphasize that the auditory ERP value in children is not equal to that of adults. A normative auditory ERP value in children should be established prior to clinical application.

Multiple cerebral and cerebellar infarcts as the first clinical manifestation in a patient with Churg-Strauss syndrome: case report and literature review.

PURPOSE: 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. CASE REPORT: 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. CONCLUSION: 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.

Tuberculosis with meningitis, myeloradiculitis, arachnoiditis and hydrocephalus: a case report.

PURPOSE: Involvement of the central nervous system (CNS) by tuberculosis is rare; it can affect either immunocompromised or immunocompetent people. CASE REPORT: 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. CONCLUSION: 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.

Methylenetetrahydrofolate reductase polymorphisms and plasma homocysteine in levodopa-treated and non-treated Parkinson's disease patients.

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 (p<0.001); 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 p<0.05), and 1298A/A (p<0.001), 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.

Role of zinc in subclinical hepatic encephalopathy: comparison with somatosensory-evoked potentials.

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.