Everyday Abilities Scale for India in Screening for Poststroke Dementia Among Young Stroke Survivors.

INTRODUCTION: Cognitive dysfunction after stroke is an important concern. We explored the utility of everyday abilities scale for India (EASI) for screening for dementia among young stroke survivors. METHODS: We interviewed 150 young stroke survivors and caregivers. Vascular dementia was diagnosed according to American Heart Association-American Stroke Association (ASA-AHA) criteria. EASI was administered to all caregivers. Receiver operating characteristic curve analysis was used to determine the area under the curve and optimum cut-points for EASI for the identification of dementia. RESULTS: Median EASI scores among subjects with dementia (n=35; 23.3%) was 2 (interquartile range: 0-4) and significantly different from those without (median: 0; interquartile range: 0-1; P<0.001). The area under the curve was 0.768 (95% confidence interval: 0.674-0.863), and at the optimum cut-point of 2 on EASI, a sensitivity of 60% and specificity of 91.3% was achieved for the identification of dementia. CONCLUSION: EASI appears to be a promising tool to screen for dementia among young stroke survivors.

Patterns of Transcranial Doppler Flow Velocities in Recent Ischemic Stroke Patients.

CONTEXT: Intracranial atherosclerosis is a common cause of stroke in India. Transcranial Doppler (TCD) provides a noninvasive way to study basal intracranial blood vessels. The Oxfordshire Community Stroke Project (OCSP) classification is a simple clinical stroke classification system that has prognostic significance and has been associated with size and location of the infarct. AIM: This study was undertaken to identify patterns of TCD abnormalities in our stroke population particularly in relation to the OCSP classification. SETTING AND DESIGN: A cross-sectional study was conducted at a tertiary care center in South India. METHODS: Recent nondisabling ischemic stroke patients were studied. TCD was used to insonate bilateral middle cerebral, bilateral anterior cerebral, bilateral vertebral, and basilar arteries. Mean flow velocity was used to define normal or abnormal flow as per standard criteria. STATISTICAL METHODS: Association between abnormal flow velocities and OCSP classification was studied using Chi-square tests. Univariate and multivariate analysis was performed to determine factors associated with abnormal flow velocities. RESULTS: Of the 59 participants studied, 42 (71%; 95% confidence interval [CI]: 57.3-84.7%) had abnormal flow velocities in one or more vessels and this was significantly associated with smoking (odds ratio = 5; 95% CI: 1.2-21.8). All abnormal flow velocities were blunted flow velocities. Anterior circulation flow velocity abnormalities were seen among all OCSP stroke subtypes, but posterior circulation flow abnormalities were associated with posterior circulation infarcts (P = 0.03). CONCLUSION: Intracranial flow velocity abnormalities are frequent among Indian stroke population. Further studies are needed to characterize these abnormalities fully.

Genetic polymorphisms in cyclin H gene are associated with oxaliplatin-induced acute peripheral neuropathy in South Indian digestive tract cancer patients.

PURPOSE: Digestive tract cancer patients treated with oxaliplatin are often associated with the development of peripheral neuropathy. The aim of the present study is to identify the influence of single-nucleotide polymorphisms (SNPs) in genes involved in oxaliplatin metabolism, cell cycle control, detoxification or excretion pathways with the development of oxaliplatin-induced acute peripheral neuropathy (acute OXAIPN) and its severity among digestive tract cancer patients treated with oxaliplatin-based chemotherapy. PATIENTS AND METHODS: A total of 228 digestive tract cancer patients undergoing with the oxaliplatin-based chemotherapy between November 2014 and December 2016 were included in the current study. Genomic DNA was extracted from peripheral blood by standard phenol-chloroform method. Genotyping of five SNPs in four genes [GSTP1 (rs1965), ABCG2 (rs3114018), CCNH (rs2230641, rs3093816), AGXT (rs4426527)] was carried out by Real-Time TaqMan SNP genotyping assay. RESULTS: We found that the two genetic variants rs2230641 and rs3093816 in cyclin H (CCNH) gene were significantly associated with both the incidence and severity of acute OXAIPN. For CCNH-rs2230641 (AA vs AG+GG; dominant model) Incidence: OR 2.62, 95% CI 1.44-4.75, p = 0.001, severity; OR 4.64, 95% CI 1.58-13.62, p = 0.002. For CCNH-rs3093816 (AA vs AG+GG; dominant model); incidence: OR 3.43, 95% CI 1.57-7.50, p = 0.001; severity: OR 2.36, 95% CI 1.05-5.30, p = 0.033. CONCLUSIONS: The results of the present study found significant association between CCNH polymorphisms and acute OXAIPN development. However, further studies are warranted from independent groups to validate our study results.

Progressive multifocal leukoencephalopathy in idiopathic CD4+ lymphocytopenia.

Progressive multifocal leukoencephalopathy is a central nervous system demyelinating disease caused by infection with John Cunningham virus. It affects predominantly the subcortical white matter, producing progressive neurological deficits and large confluent white matter lesions on imaging. It is usually seen in immunodeficient individuals, such as those suffering from acquired immunodeficiency syndrome, those on treatment with monoclonal antibodies, and those following therapeutic bone marrow suppression. Here, we report a rare case of progressive multifocal leukoencephalopathy in an apparently immunocompetent adult, who was found to have idiopathic CD4 lymphocytopenia upon further investigation.

Association of Voltage-Gated Sodium Channel Genetic Polymorphisms with Oxaliplatin-Induced Chronic Peripheral Neuropathy in South Indian Cancer Patients

Oxaliplatin is a platinum drug active against digestive tract cancers. Among its side effects, peripheral neuropathy is one of the dose-limiting toxicities. This affects around 50 to 70% of patients but the pathophysiology of development of oxaliplatin-induced peripheral neuropathy (OXAIPN) remains unclear. Sodium channels (SCNAs) play major role in neuronal electrical signaling processes and mutations in SCNAs lead to various neuronal diseases involving the central and peripheral nervous systems. In this study, we evaluated whether SCNA genetic variants might be associated with risk of chronic OXAIPN in patients with digestive tract cancers treated with oxaliplatin. Methodology: Blood samples from 228 digestive tract cancer patients who had received oxaliplatin in adjuvant and neoadjuvant or metastatic settings were obtained and genomic DNA was extracted by phenol-chloroform extraction. Genotyping was performed with the real-time polymerase chain reaction (RT-PCR) using validated real-time TaqMan single nucleotide polymorphism (SNP) genotyping assays. Neuropathy was evaluated and graded according to National Cancer Institute Common Toxicity Criteria (NCI-CTC) version 4.03. Results: We found that the rs6746030 polymorphic variant of SCN9A was significantly associated with a higher incidence of chronic OXAIPN (GA+AA vs GG: OR=1.8, 95% CI=1.04-3.4, P=0.04; dominant model) while the rs6754031 variant was linked with a lower incidence (OR=0.45, 95% CI=0.22-0.77, P=0.005; dominant model). The SCN 10A polymorphic variant was associated with severity of chronic OXAIPN (P=0.006, OR=2.0, 95% CI=1.2 - 3.3). Conclusion: The results of the present prospective study provide evidence in support of a causal relationship between chronic OXAIPN and voltage gated sodium channel polymorphisms. However, further studies from independent groups are required to validate these results.

Oxaliplatin-induced Peripheral Neuropathy in South Indian Cancer Patients: A Prospective Study in Digestive Tract Cancer Patients.

PURPOSE: The aim of the current study is to report our prospective experience on the prevalence of oxaliplatin-induced peripheral neuropathy (OXAIPN) in patients with digestive tract cancers treated with oxaliplatin-based combination therapy. MATERIALS AND METHODS: A total of 219 patients scheduled to be treated with oxaliplatin-based combination therapy were prospectively examined at baseline and follow-up during the therapy between November 2014 and December 2016. The incidence of acute OXAIPN was measured using a descriptive questionnaire (yes/no question) based on sum of number of symptoms present and NCI-CTCAE version 4.03 was applied to clinically grade the severity of chronic OXAIPN. RESULTS: Acute and chronic OXAIPN was found in 108 of 219 (49.3%) and 127 of 219 (58%) patients, respectively. Out of 11 acute OXAIPN symptoms, the vast majority of patients manifested cold-induced pharyngolaryngeal (63.8%) dysesthesias or perioral (61.1%) paresthesias. Development of acute OXAIPN was predictive of subsequent development of chronic OXAIPN (P = 0.0001). All the patients received a median cumulative dose of 780 mg/m2 (range: 130-1040 mg/m2). There was a significant correlation between the patients who received the median cumulative dose and the development of chronic OXAIPN. The incidences of OXAIPN in patients with median cumulative dose of ≤780 mg/m2 was 51/120 (42.5%) and >780 mg/m2 was OXAIPN 76/99 (76.7%) (P = 0.0001). CONCLUSION: The current study results demonstrate that the vast majority of patients who receive oxaliplatin-based combination chemotherapy will manifest acute OXAIPN that may contribute to the development of chronic peripheral neuropathy on repeated courses of drug administration.

Tethered Cord Syndrome-A Study of the Short-Term Effects of Surgical Detethering on Markers of Neuronal Injury and Electrophysiologic Parameters.

OBJECTIVE: Several studies have assessed clinical and radiologic outcomes after detethering of the cord for tethered cord syndrome (TCS). However, no data regarding the impact of detethering on the metabolism or electrophysiologic functioning of the cord are available. The aim of this study was to assess the changes in the cerebrospinal fluid (CSF) levels of markers of neuronal injury and alterations in the electrophysiologic functioning of the spinal cord after detethering. METHODS: This prospective study included patients with congenital TCS. Patients underwent clinical assessment, magnetic resonance imaging, somatosensory evoked potentials (SSEP) study, and CSF biochemical analysis (to estimate lactate, glial fibrillary acidic protein, and S100B levels), before and 3 months after surgery. Clinical and radiologic outcomes were assessed. We studied changes in biochemical and electrophysiologic parameters before and after detethering as surrogate markers for the effects of this intervention. RESULTS: Twenty-one patients were recruited over 2 years. Detethering led to clinical improvement in 75% of patients with motor deficits, 60% of patients with bladder symptoms, and 50% of patients with gait problems. At 3 months follow-up, 43% (median) of the preoperative vertical tethering was found to be corrected. There was significant reduction in CSF lactate, glial fibrillary acidic protein, and S100B levels as well as a significant decrease in the latencies of the SSEP waves 3 months after surgery. CONCLUSIONS: Surgical detethering led to a reduction in the CSF levels of the markers of anaerobic metabolism and neuronal injury. There was also a reduction in the latencies of the SSEP waves, indicating better electrophysiologic functioning of the cord.

Etiology and outcome determinants of intracerebral hemorrhage in a south Indian population, A hospital-based study.

BACKGROUND: There is paucity of methodologically sound published studies on intracerebral hemorrhage (ICH) from India, on pub med/embase search. AIMS: To explore etiology of ICH and correlate the causes, location, and size of hemorrhage to clinical outcome. MATERIALS AND METHODS: A hospital-based descriptive study from South Indian eastern coastal town of Puducherry; 60 consecutive subjects aged > 12 years, predominantly of inbred Tamil population, with head CT evidence of intracerebral hemorrhage not associated with trauma and brain tumors, were recruited. Outcome at three months was measured using Glasgow Outcome scale, NIHSS and mortality. SPSS v 19 was used for statistical analysis. RESULTS: Commonest etiological factor was hypertension, followed by bleeding diathesis, thrombolysis for myocardial infarction, and cortical vein thrombosis. Most frequent locations of hematoma were basal ganglia, thalamus, internal capsule, and cerebral and cerebellar parenchyma. Hematoma volume correlated significantly with systolic and mean arterial pressure but not with diastolic blood pressure. Poor outcome was correlated to size (P < 0.05) and intraventricular extension of hematoma (P < 0.05), and to systolic, diastolic and mean arterial pressure, but not to age, gender, smoking, alcoholism, ischemic heart disease, and blood sugar level. Among diabetic patients with ICH, the size of hematoma (P = 0.04) and severity of coma (P = 0.01) at admission were significantly worse compared to the non-diabetic, but not the outcome at three months [Glasgow outcome scale or mortality (P = 0.94 and 0.14)]. CONCLUSIONS: The location of hemorrhage and correlation with outcome agreed with the patterns described for the non-white races in prior reports. Independence of outcome to diabetic status despite a more severe initial presentation may indicate importance of good care, even in high risk groups.

Evaluation of an IgG-ELISA strategy using Taenia solium metacestode somatic and excretory-secretory antigens for diagnosis of neurocysticercosis revealing biological stage of the larvae.

Diagnosis of neurocysticercosis (NCC) is complicated because of the variability in clinical presentations and course of the disease where viability of parasite is a major determinant. The present study describes evaluation of ELISAs using Taenia solium metacestode somatic and excretory-secretory (ES) antigens for detection of anti-T. solium metacestode IgG antibodies in serum and cerebrospinal fluid (CSF). And results of the ELISAs in cases with a definitive diagnosis of NCC are correlated with the biological stages of the parasite such as live vesicular or degenerated stage. The sensitivity of the IgG-ELISA using ES antigen is observed to be much higher in serum (88.2%) than in CSF (64.28%) although it is only marginally higher in serum (76.4%) than in CSF (75%) when somatic antigen is used in the ELISA. Whereas, the specificities of the ELISA using either somatic or ES antigen for detection of IgG antibodies in serum (97.97%; 96.96%) and CSF (96.42%; 97.61%) are comparable. A strong association is observed between live stage of the parasite and detection of antibodies in sera and CSF from more number of NCC patients by ELISA using ES antigens. Similarly, detection of antibodies by ELISA using somatic antigens could be associated with the dead or degenerated stage of the parasite in brain. The IgG-ELISA strategy developed in the present study opens up an avenue for diagnosis of NCC in hospitals or in population prevalence studies. The use of crude extracts of ES proteins might improve the serodiagnosis of the cases of NCC carrying live vesicular stage of the parasite larvae.