Inhibition of fatty acid synthase leads to apoptosis in cancers, which leads to high levels of fatty acid synthesis. This indicates that cancer cells depend on fatty acid in order to survive. In this study, we investigated whether or not there was a relationship between the glial tumor grade and free fatty acid level of tumor tissue.

Twenty patients who had high grade glial tumors and 20 patients who had low grade glial tumors, were included in the study. Tumors samples were obtained intraoperatively in order to measure the fatty acid levels. The fatty acids were studied in three groups: saturated fatty acids, monounsaturated fatty acids and polyunsaturated fatty acids. They were analyzed with gas chromatography.

The oleic acid, linoleic acid, eicosadienoic acid, arachidonic acid, and docosadienoic acid levels were high in the tumor tissue of low grade tumors. The myristic acid, palmitic acid, stearic acid, alpha linoleic acid, eicosenoic acid, dihomo-gamma-linolenic acid, docosahexaenoic acid, and ceramide levels were high in the tumor tissue of high grade glial tumors. However, none of these high values were statistically significant. The high values of behenic acid, a saturated fatty acid, in low grade glial tumors were statistically significant.

High levels of behenic acid in patients with low grade glial tumor is important as it indicates persistence of the tissue integrity and tissue resistance. behenic acid levels can be a prognostic factor in glial tumors.

FOXJ1 is a member of the Forkhead/winged-helix (Fox) family of transcription factors, which is required for the differentiation of the cells acting as adult neural stem cells which participate in neurogenesis and give rise to neurons, astrocytes, oligodendrocytes. The expression pattern of FOXJ1 in the brain after cerebral ischemia has so far not been described. In the current study, we investigated the expression pattern of FOXJ1 in the rat brain after cerebral ischemia by animal model.

We performed a middle cerebral artery occlusion (MCAO) model in adult rats and investigated the expression of FOXJ1 in the brain by Western blotting and immunochemistry; double immunofluorescence staining was used to analyze FOXJ1's co-expression with Ki67.

Western blot analysis showed that the expression of FOXJ1 was lower than normal and sham-operated brain after cerebral ischemia, but the level of FOXJ1 gradually increased from Day 1 to Day 14. Immuohistochemical staining suggested that the immunostaining of FOXJ1 deposited strongly in the ipsilateral and contralateral hemisphere in the cortical penumbra (CP). There was no FOXJ1 expression in the ischemic core (IC). The positive cells in the cortical penumbra might migrat to the ischemic core. In addition, double immunofluorescence staining revealed that FOXJ1 was co-expressed with mAP-2 and gFAP, and Ki67 had the colocalization with NeuN, GFAP, and FOXJ1.

All our findings suggest that FOXJ1 plays an important role on neuronal production and neurogenesis in the adult brain after cerebral ischemia.

Subthalamic nucleus (STN) deep brain stimulation (DBS) is currently the main surgical procedure for medically refractory Parkinson's disease. The benefit of intra-operative microelectrode recording (MER) for the purpose of neurophysiological localization and mapping of the STN continues to be debated.

A retrospective review of the charts and operative reports of all patients receiving STN DBS implantation for Parkinson's disease at our institution from January 2004 to March 2011 was done.

Data from 43 of 44 patients with Parkinson's disease treated with STN DBS were reviewed. The average number of tracts on the left was 2.4, versus 2.3 on the right. The average dorsal and ventral anatomical boundaries of the STN based on Schaltenbrand's Stereotactic Atlas were estimated to be at -5.0 mm above and +1.4 mm below target respectively. The average dorsal and ventral boundaries of the STN using MER were -2.6 mm above and +2.0 mm below target respectively. The average dorsal-ventral distance of the STN as predicted by Stereotactic Atlas was 6.4 mm, compared to 4.6 mm as determined by MER. MER demonstrated the average dorsal and ventral boundaries on the left side were -2.6 mm and +2.2 mm from target respectively, while the average dorsal and ventral boundaries on the right side were -2.5 mm and +1.8 mm from target respectively with MER.

MER in STN DBS surgery demonstrated measurable difference between stereotactic atlas/MRI STN target and neurophysiologic STN localization.

Reactive oxygen species (ROS) are often associated with persistent pains such as neuropathic and inflammatory pain. Hydrogen gas can reduce ROS and alleviate cerebral, myocardial, and hepatic ischemia/reperfusion injuries. In the present study, we aim to investigate whether hydrogen-rich saline can reduce neuropathic pain in a rat model of chronic constriction injury (CCI).

Thirty SD rats were randomly divided into three groups: sham group was administered sodium chloride by intrathecal injection (n=10); control groups underwent CCI surgery and were administered sodium chloride by intrathecal injection (n=10); vehicle group underwent CCI surgery and was administered hydrogen-rich saline by intrathecal injection (n=10). Drugs were administered in the dose of 100ul/kg once a day at 0.5 hours before and 1-7 day after CCI surgery. The mechanical thresholds were tested at one day before and 3-14 day after CCI surgery.

We found that hydrogen-rich saline significantly elevated the mechanical thresholds of neuropathic pain compared to vehicle (physiologic saline) control in CCI rats (p<0.05); it also decreased the levels of myeloperoxidase, maleic dialdehyde, and protein carbonyl in spinal cord by 7 days post-chronic constriction injury(p<0.05). In addition, hydrogen-rich saline also suppressed the expression of p38-mitogen-activated protein kinase (p38MAPK) and brain-derived neurotrophic factor (BDNF) in the spinal cord by 7 days post-chronic constriction injury (p<0.01, p<0.01, respectively), but had no effect on P2X4R (p>0.05), an ATP receptor.

Intrathecal injection of hydrogen-rich saline can decrease oxidative stress and the expression of p38MAPK and BDNF that may contribute to the elevated threshold of neuropathic pain in rat CCI model.

Since a large proportion of multiple sclerosis (MS) patients exhibit cognitive deficits, it is important to have reliable and cost-effective screening measures that can be used to follow patients effectively. the objective of this study was to evaluate the clinical value of the Montreal Cognitive Assessment (MoCA) test in detecting cognitive deficits in MS patients.

Forty-one (70.1% women, mean age 44.51 ±7.43) mildly impaired (EDSS: 2.26 ±1.87) MS patients were recruited for this study. In addition to the MoCA, they were administered the MSNQ-P (patient version) and the MSNQ-I (informant version), the bDI-FS and a comprehensive neuropsychological test battery.

there were significant correlations between the MoCA test and the three factors derived from the neuropsychological evaluation (Executive/speed of processing, Learning, Delayed recall). the MoCA test was correlated with the MSNQ-I but only marginally with the MSNQ-P. In addition, there was no significant correlation between the MSNQ-P and the neuropsychological factors, whereas significant correlations were found between two of those factors (Learning and Delayed recall) and the MSNQ-I, suggesting that the informant version is more reliable than the patient version for the presence of cognitive deficits.

the results obtained in the present study support the value of the MoCA test as a screening tool for the presence of cognitive dysfunction in MS patients, even in patients with mild functional disability (EDSS).

Neurologic disorders represent a major burden of disease globally and the spectrum ranges from noncommunicable disorders like stroke and neurodegenerative disorders to central nervous system infections.

The purpose of the study is to assess the burden of neurological diseases in a tropical environment.

A one year retrospective survey of neurological diseases seen at the University of Calabar Teaching Hospital, Nigeria, was evaluated using patients' medical record.

Neurological diseases constituted 24.2% of all medical conditions seen over a one year period. Stroke was found to be the commonest cause of admissions accounting for 42.1% of the cases followed by peripheral neuropathy (13.8%) and meningoencephalitis (7.2%). The immediate case fatality rate was 33.6%. Fifty two percent were discharged home with various levels of recovery while 12.5% left against medical advice. About 2% were referred to other tertiary health institutions.

The pattern of neurologic diseases in the local medical wards was not remarkably different from those observed in Nigeria and elsewhere. Stroke remains the most frequent cause of neurologic admissions and mortality in this region is same as observed elsewhere.

To promote understandings about the pathogenesis of ischemic stroke (IS) through mining key genes, functions and pathways with microarray technology.

Differentially expressed genes (DEGs) in blood between patients with IS and healthy people were screened out through comparing microarray data obtained from Gene Expression Omnibus. Overrepresented functions in DEGs were revealed by Gene Ontology (GO) enrichment analysis. Interaction network was constructed for the top 24 DEGs with information from Human Protein Reference Database (HPRD). Relevant microRNAs (miRNAs) were retrieved from three databases: TargetScan, miRBase and miRanda.

A total of 503 DEGs were obtained. Functional enrichment analysis showed that immune response, signaling pathways and apoptosis were significantly over-represented. Six key genes with big degree, betweenness and clustering coefficient were then revealed, which might play important roles in the development of IS. In addition, 57 differentially expressed miRNAs targeting the 6 genes were retrieved.

Our study provides insights into the pathogenesis of IS and potential targets to treat the disease.

Infantile gratification phenomena are self-stimulatory behaviors that are often misdiagnosed as epilepsy. Although the prognosis is thought to be benign, limited long-term follow-up studies exist. This was the objective of our study in addition to exploring the risks of future developmental, behavioral, or neurological abnormalities.

Series of consecutive infants with gratification phenomena were identified both retrospectively and prospectively over an eight year period from a single pediatric neurology service. The diagnosis was based on descriptive history, review of videotaped events, lack of neurological or developmental abnormalities, and normal routine electroencephalogram.

Nineteen infants were followed for 3-11 years (mean 7.1). Their ages ranged between 4-13 months (mean 7) with 79% females. The diagnosis was not reached by the referring physician and 74% were misdiagnosed as epilepsy or movement disorder. The episodes recurred with variable frequency with gradual reduction in number and increase in length of attack-free periods with advancing age. Complete remission was noted in all patients by age 1-3 years (mean 1.9). However, 4 children (21%) developed features of attention deficit hyperactivity disorders (ADHD) on long-term follow up. In this group, the gratification phenomena appeared at a younger age with higher attack frequency.

Gratification phenomena in infants are benign and self-limited, often spontaneously disappearing by two years of age. A correlation with future ADHD was found; however, larger prospective studies are needed to further examine this possible association.

West Nile virus (WNV) is a virus of the family Flaviviridae. The main route of human infection is through the bite of an infected mosquito. Approximately 90% of WNV infections in humans are asymptomatic, but neurologic manifestations can be severe.

This study reviews the clinical profile of cases with neuroinvasive West Nile infection (NWNI) reported by the Surveillance program of the government of Saskatchewan in the Saskatoon Health Region (SHR). In 2007, 1456 cases of human West Nile cases were reported by the government of Saskatchewan in the whole province. One hundred and thirteen cases had severe symptoms of NWNI (8%), 1172 (80%) cases had mild symptoms of WNI and 171 (12%) had asymptomatic disease. Three hundred and fifty six cases were reported in the SHR, where 57 (16%) fulfilled criteria for NWNI.

From the 57 cases, 39 (68%) were females. Nine (16%) patients had a history of recent camping, two (4%) reported outdoor sports and four (8%) reported outdoor activities not otherwise specified. Twenty five patients had headache (43.9%), 25 confusion (42.1%), 23 meningitis (40.4%), 17 encephalitis (29.8%), 14 encephalopathy (24.6%), 11 meningoencephalitis (19.3%), 10 tremor (17.5%), acute flaccid paralysis 10 (17.5%), myoclonus 1 (1.8%), nystagmus 2 (3.5%), diplopia 2 (3.5%), dizziness 2 (3.5%). Three patients died related with comorbidities during admission.

During a year of high occurrence of WNI in Saskatchewan, 16% of cases developed NWNI. The recognition of neurological complications associated with WNI is important to improve their referral to tertiary centers.

Current recommendations for carotid endarterectomy (CEA) for symptomatic carotid stenosis state benefit is greatest when performed within two weeks of symptoms. However, only a minority of cases are operated on within this guideline, and no systematic examinations of reasons for these delays exist.

All CEA cases performed at our institution by vascular surgery for symptomatic carotid stenosis after neurologist referral in 2008-2009 were reviewed. Dates of symptom onset, initial presentation, referral to and evaluation by neurology and vascular surgery, vascular imaging, and CEA were collected, and the length of time between each analysed. Reasons for delays were noted where available.

Of 36 included patients, 34 had CEA more than two weeks after symptom onset. Median time to CEA from onset was 76 days (IQR, 38-105 days). Longest intervals were between surgeon assessment and CEA (14 days; IQR, 9-21 days), neurology referral and neurologist assessment (9 days; IQR, 2-26 days), vascular imaging and referral to vascular surgery (9 days; IQR, 2-35 days) and vascular surgery referral and assessment (8 days; IQR, 6-15 days). Few patients (44.1%) had reasons for delays identified; of these, process-related delays were related to delayed vascular imaging, delayed referral by primary care physicians, or multiple conflicting referrals.

There are significant delays between symptom onset and CEA in patients referred for CEA, with delay highest between specialist referral and evaluation. Strategies to reduce these delays may be effective in increasing the proportion of procedures performed within two weeks of symptom onset.