Clinical, Demographic, and Radiological Characteristics of Patients Demonstrating Antibodies Against Myelin Oligodendrocyte Glycoprotein

Background: Optic neuritis, myelitis, and neuromyelitis optica spectrum disorder (NMOSD) have been associated with antibodies against myelin oligodendrocyte glycoprotein-immunoglobulin G (anti-MOG-IgG). Furthermore, patients with radiological and demographic features atypical for multiple sclerosis (MS) with optic neuritis and myelitis also demonstrate antibodies against aquaporin-4 and anti-MOG-IgG. However, data on the diagnosis, treatment, follow-up, and prognosis in patients with anti-MOG-IgG are limited. Aims: To evaluate the clinical, radiological, and demographic characteristics of patients with anti-MOG-IgG. Study Design: Multicenter, retrospective, observational study. Methods: Patients with blood samples demonstrating anti-MOG-IgG that had been evaluated at the Neuroimmunology laboratory at Ondokuz Mayis University's Faculty of Medicine were included in the study. Results: Of the 104 patients with anti-MOG-IgG, 56.7% were women and 43.3% were men. Approximately 2.4% of the patients were diagnosed with MS, 15.8% with acute disseminated encephalomyelitis (ADEM), 39.4% with NMOSD, 31.3% with isolated optic neuritis, and 11.1% with isolated myelitis. Approximately 53.1% of patients with spinal involvement at clinical onset demonstrated a clinical course of NMOSD. Thereafter, 8.8% of these patients demonstrated a clinical course similar to MS and ADEM, and 28.1% demonstrated a clinical course of isolated myelitis. The response to acute attack treatment was lower and the disability was higher in patients aged > 40 years than patients aged < 40 years at clinical onset. Oligoclonal band was detected in 15.5% of the patients. Conclusion: For patients with NMOSD and without anti-NMO antibodies, the diagnosis is supported by the presence of anti-MOG-IgG. Furthermore, advanced age at clinical onset, Expanded Disability Status Scale (EDSS) score at clinical onset, spinal cord involvement, and number of attacks may be negative prognostic factors in patients with anti-MOG-IgG.

The prevalence of carpal tunnel syndrome in patients with epilepsy.

Objective: Carpal tunnel syndrome (CTS) is the most common type of entrapment neuropathy caused by compression of the median nerve in the carpal tunnel. Epilepsy is characterised by recurrent seizures caused by abnormal neuronal discharges in the brain.This study aimed to investigate whether there is a link between epilepsy and carpal tunnel and, if so, the underlying factors. Materials and methods: Two hundred patients with epilepsy were included in this study. The patients' history of epilepsy, seizure type, and seizure frequency were assessed. The Tinel, Phalen, and Flick physical examination tests were performed on patients with complaints that matched those of median nerve neuropathy. Patients with epilepsy and clinically diagnosed carpal tunnel syndrome completed the Boston Carpal Tunnel Syndrome Questionnaire, and nerve conduction studies were performed. The relationship between seizure type and frequency in patients with carpal tunnel syndrome was compared. Results: Compared to focal-aware motor-onset seizures, the risk of detecting carpal tunnel syndrome was 88.7 times higher in focal-onset bilateral tonic-clonic seizures. Patients with a seizure frequency of one per month or more had a 0.704 times lower risk of CTS than those with a frequency of one per week or more (p = 0.026). Discussion: Patients with epilepsy, especially those experiencing frequent seizures or specific seizure types, may be more susceptible to repetitive wrist flexion-extension postures. Therefore, during clinical follow-up, it is important to inquire about the presence of carpal tunnel syndrome in patients with epilepsy.

Positive effects of ocrelizumab in patients with familial mediterranean fever and coexistent multiple sclerosis.

OBJECTIVES: This study aims to evaluate the effects of ocrelizumab (OCZ) on familial Mediterranean fever (FMF) attacks in multiple sclerosis (MS) patients with FMF (MS+FMF patients). PATIENTS AND METHODS: This retrospective observational study included 11 patients (2 males, 9 females; mean age 46.6±9.2; range, 22 to 55 years) with MS+FMF hospitalized between January 2016 and July 2019. Demographic, clinical, and laboratory parameters and patient reported outcomes were analyzed in patients treated with OCZ for 18 months. RESULTS: Combining OCZ with colchicine in MS+FMF patients significantly reduced the frequency of FMF attacks (p=0.003) and the frequency of joint attacks (p=0.002). Consistent with the clinical improvement, the maximum serum C-reactive protein levels were significantly decreased after combination therapy compared to before combination therapy (p=0.003). MS+FMF patients reported that FMF disease activity improved after OCZ therapy (Visual Analog Scale [VAS] 74±9.6 vs. VAS 46.5±8.1 mm, p=0.003). CONCLUSION: Ocrelizumab therapy led to a prominent decrease in the frequency of FMF attacks, alleviated functional impairment, and improved quality of life in MS+FMF patients.

Bi-allelic variants in HOPS complex subunit VPS41 cause cerebellar ataxia and abnormal membrane trafficking.

Membrane trafficking is a complex, essential process in eukaryotic cells responsible for protein transport and processing. Deficiencies in vacuolar protein sorting (VPS) proteins, key regulators of trafficking, cause abnormal intracellular segregation of macromolecules and organelles and are linked to human disease. VPS proteins function as part of complexes such as the homotypic fusion and vacuole protein sorting (HOPS) tethering complex, composed of VPS11, VPS16, VPS18, VPS33A, VPS39 and VPS41. The HOPS-specific subunit VPS41 has been reported to promote viability of dopaminergic neurons in Parkinson's disease but to date has not been linked to human disease. Here, we describe five unrelated families with nine affected individuals, all carrying homozygous variants in VPS41 that we show impact protein function. All affected individuals presented with a progressive neurodevelopmental disorder consisting of cognitive impairment, cerebellar atrophy/hypoplasia, motor dysfunction with ataxia and dystonia, and nystagmus. Zebrafish disease modelling supports the involvement of VPS41 dysfunction in the disorder, indicating lysosomal dysregulation throughout the brain and providing support for cerebellar and microglial abnormalities when vps41 was mutated. This provides the first example of human disease linked to the HOPS-specific subunit VPS41 and suggests the importance of HOPS complex activity for cerebellar function.

The prevalence of restless legs syndrome in patients undergoing coronary angiography and its relationship with the severity of coronary artery stenosis.

PURPOSE: Results from studies on the relationship between restless legs syndrome (RLS) and coronary artery disease (CAD) are conflicting. Some studies associate RLS with CAD by heart rate variability, blood pressure variability, and other autonomic, neuronal reasons, while other studies do not support these observations. The aim of this study was to investigate the prevalence of RLS in patients undergoing coronary angiography for CAD and to assess RLS prevalence with severity of CAD. METHODS: After inclusion and exclusion criteria were applied, enrolled patients with less than 50% coronary artery stenosis by angiography (0-49%) were assigned to group 1, and patients with 50% or more coronary artery stenosis were assigned to group 2. Patients were diagnosed with RLS if they met all five essential criteria of the International RLS study group. RLS prevalence and other comorbidities were compared between the two groups. RESULTS: Of 126 patients, 74 men (59%), mean age 64.0 ± 8.7 years, mean BMI 29.6 kg/m2, 47 (37%) were assigned to group 1 (no or nonobstructive CAD) and 79 (63%) were assigned to group 2 (obstructive CAD). No significant differences were found between the groups in terms of mean age, BMI, gender, or prevalence of hypertension, hypercholesterolemia, and DM. The prevalence of RLS in group 2 (29%) was significantly higher than in group 1 (15%), p = 0.013. CONCLUSION: These results suggest that prevalence of RLS is associated with CAD and with CAD severity. We conjecture that RLS may be related to vascular endothelial dysfunction in cardiovascular disease.

Evaluation of the association between sexual dysfunction and demyelinating plaque location and number in female multiple sclerosis patients.

Purpose To investigate the frequency of sexual dysfunction (SD) in female multiple sclerosis (MS) patients and to explore its association with the location and number of demyelinating lesions. Material and Methods We evaluated 42 female patients and 41 healthy subjects. All patients underwent neurological examination and 1.5 T brain and full spinal MRI. All subjects completed the female sexual function index (FSFI), Beck Depression Inventory (BDI), Beck Anxiety Inventory (BAI), and Short-Form 36 Quality of Life Scale (SF-36). All participants were also evaluated for serum thyroid stimulating hormone (TSH), T4, estradiol, and total testosterone. Results No statistically significant differences between the MS and control groups were found for age, body mass index (BMI), serum TSH, T4, E2, and total testosterone level. MS patients had a statistically significantly lower FSFI and SF-36 scores and higher BDI and BAI scores compared with healthy subjects. The location and number of demyelinating lesions were not associated with SD. Conclusion In our cohort, this difference in SD appears unrelated to the location and number of demyelinating lesions. These findings highlight the importance of the assessment and treatment of psychiatric comorbidities, such as depression and anxiety, in MS patients reporting SD.

Characteristics of headache and its relationship with disease severity in patients with Crimean-Congo hemorrhagic fever.

OBJECTIVES: Crimean-Congo Hemorrhagic Fever (CCHF) is a fatal, tick-borne disease. The classic clinical presentation of CCHF is characterized by sudden onset of high fever, chills, and severe headache. There are no previous reports on the characteristics of headaches caused by CCHF. Therefore, we investigated the relationship between CCHF-induced headache and the clinical course of the disease. METHODS: We included 60 patients with headache diagnosed with CCHF; they were divided into two groups: group 1 included patients with hospital stay <7 days and group 2 included patients with hospital stay >7 days. The control group included 43 viral pneumonia patients with headache. Patients described the characteristics of headaches and also self-rated the severity with a numeric pain scale that classified headache as either mild or severe. RESULTS: In the group with CCHF, 66.7% of the reported headaches met criteria for diagnosis of migraine. This ratio was significantly higher than that in the control group (37.5%). The headache severity scores in group 1 were lower than those in group 2. The hospitalization length was shorter (p=0.004) and the platelet levels were higher in CCHF patients with mild headache compared with CCHF patients with severe headache (p=0.005). CONCLUSION: CCHF patients had more often and severe headaches than the controls. The severity of headache may be associated with the severity of vascular endothelial damage, vasodilatation, and abnormal release of inflammatory cytokines in CCHF similar in migraine. Most CCHF patients experienced migraine-like headaches, suggesting that cerebral vessel involvement might be important in both CCHF and migraine.

Neuroprotective Effects of Eexenatide in a Rotenone-Induced Rat Model of Parkinson's Disease.

BACKROUND: Several studies suggest an association between Parkinson's disease (PD) and type 2 diabetes mellitus; these 2 diseases are both known to affect the common molecular pathways. As a synthetic agonist for the glucagon-like peptide 1 receptor, exenatide has been evaluated as a neuroprotective agent in multiple animal models. Rotenone models of PD have great potential for the investigation of PD pathology and motor and nonmotor symptoms, as well as the role of gene-environment interactions in PD causation and pathogenesis. Therefore, in this study, the neurochemical, behavioral and histologic effects of exenatide on a rotenone-induced rat model of PD were examined. MATERIALS AND METHODS: Eighteen adult male rats were randomly divided into the following 3 groups (n = 6): 1 group received stereotaxical infusion of dimethyl sulfoxide (vehicle, group 1) and the others received stereotaxical infusion of rotenone (groups 2 and 3). Apomorphine-induced rotation test was applied to the rats after 10 days. Thereafter, group 2 was administered isotonic saline, whereas group 3 was administered exenatide for 28 days. RESULTS: Malondialdehyde and tumor necrosis factor alpha levels increased in the rats with PD induced by rotenone, whereas malondialdehyde and tumor necrosis factor alpha levels markedly decreased in the rats treated with exenatide. The apomorphine-induced rotation test scores of exenatide-treated rats were determined to be lower compared with the untreated group. Additionally, treatment with exenatide significantly reduced the loss of dopaminergic neurons in striatum. CONCLUSIONS: These results have shown that exenatide has neuroprotective, anti-inflammatory and antioxidant effects in a rotenone-induced rat model of PD.

Evaluation of Overactive Bladder in Male Antidepressant Users: A Prospective Study.

PURPOSE: In this study, we investigated overactive bladder (OAB) functions in male patients who used antidepressant drugs (ADs) that were previously examined in female patients, based on conflicting data in literature regarding the effects of AD on OAB and the differences between male and female urinary system physiologies (anatomical and hormonal). METHODS: The study included 202 male patients (a control group of 90 healthy subjects, and an experimental group of 112 patients taking ADs for different disorders). All the patients completed the overactive bladder-validated 8 (OAB-V8) questionnaire, the International Consultation on Incontinence Questionnaire-Short Form (ICIQ-SF), and the Beck Depression Inventory (BDS). RESULTS: The OAB-V8, ICIQ-SF, and BDS scores for the antidepressant users were significantly higher than those of the control group. The highest prevalence of OAB symptoms was observed in patients taking venlafaxine (68.2%), and the lowest prevalence was in patients taking sertraline (28.0%). Moreover, the frequency of OAB between the antidepressant groups was statistically significant. The univariate logistic regression analyses showed a significant relationship between the presence of OAB, antidepressant usage, BDS score, and the age of a patient. In the multivariate logistic regression analyses, the association between the presence of OAB and antidepressant usage was statistically significant. CONCLUSIONS: The present study showed that the incidence of OAB and the severity of OAB symptoms increased in males using antidepressants for various disorders. This may have been due to unique pharmacological effects, on a molecular or individual level, of serotonin-norepinephrine reuptake inhibitors.

Investigation of Nerve Conduction Studies of Carpal Tunnel Syndrome Cases With Different Risk Factors: An Electrodiagnostic Study.

PURPOSE: The aim of this study was to determine whether there are electrodiagnostic differences between carpal tunnel syndrome (CTS) patients with diabetes mellitus, CTS + hypothyroidism (HT), CTS + fibromyalgia syndrome, CTS + rheumatoid arthritis (RA), and idiopathic CTS cases, by comparing nerve conduction studies. METHODS: This research examined electrophysiologic studies of 47 untreated HT + CTS, 47 diabetes mellitus + CTS, 49 RA + CTS, 52 fibromyalgia syndrome + CTS, 50 idiopathic CTS cases, and a healthy control group of 50 individuals (a total of 293 patients and 433 hands with CTS). RESULTS: There were no significant differences between the groups in terms of sex and age. There was no significant difference between the CTS groups-in terms of numbers-with mild, moderate, and severe CTS. When the CTS groups were compared with the control group, in all CTS groups on both left and right hands, there was a significant prolongation in median motor latency and median sensory latency (in the 3rd finger); also a significant decrease in median sensory velocity in the 3rd finger. In diabetes mellitus, HT, and RA groups, the median motor amplitudes in both hands were significantly decreased compared with the idiopathic group. There was a moderate significant negative correlation between disease duration and median motor amplitudes (of both right and left sides) in RA (right; P = 0.028, r = 0.761, left; P = 0.041, r = 0.694) and HT groups (right; P = 0.035, r = 0.637, left; P = 0.049, r = 0.697). CONCLUSIONS: Electrodiagnostic results showed both demyelinating injury and axonal damage in diabetes mellitus, HT, and RA patients with CTS, in these patients during treatment for CTS. Early treatment planning should include the risk factor diseases.

Atypical Features in a Large Turkish Family Affected with Friedreich Ataxia.

Here, we describe the clinical features of several members of the same family diagnosed with Friedreich ataxia (FRDA) and cerebral lesions, demyelinating neuropathy, and late-age onset without a significant cardiac involvement and presenting with similar symptoms, although genetic testing was negative for the GAA repeat expansion in one patient of the family. The GAA repeat expansion in the frataxin gene was shown in all of the family members except in a young female patient. MRI revealed arachnoid cysts in two patients; MRI was consistent with both cavum septum pellucidum-cavum vergae and nodular signal intensity increase in one patient. EMG showed demyelinating sensorimotor polyneuropathy in another patient. The GAA expansion-negative 11-year-old female patient had mental-motor retardation, epilepsy, and ataxia. None of the patients had significant cardiac symptoms. Description of FRDA families with different ethnic backgrounds may assist in identifying possible phenotypic and genetic features of the disease. Furthermore, the genetic heterogeneity observed in this family draws attention to the difficulty of genetic counseling in an inbred population and to the need for genotyping all affected members before delivering comprehensive genetic counseling.

Analysis of MMP2-1306C/T and TIMP2G-418C polymorphisms with relapsing remitting multiple sclerosis.

AIMS: Multiple sclerosis (MS) is an autoimmune, inflammatory disease characterized by loss of myelin forming oligodendrocytes and changes in the blood-brain barrier. Matrix metalloproteinase (MMP) -2 and -9 are known to cause disruption of the blood-brain barrier, remodeling of the basal lamina, regeneration of axons, and remyelination in MS. The imbalance between MMPs and tissue inhibitor metalloproteinases (TIMPs) may lead to the emergence of pathological processes such as MS. The roles of MMP2-1306 C/T and TIMP2-418 G/C genetic variants in MS have not been studied before. We aimed to investigate whether MMP2-1306C/T and TIMP2-418 G/C gene variants are risk factors for patients with relapsing remitting multiple sclerosis (RRMS). METHODS: The study included 102 RRMS and 102 healthy controls. Genomic DNA was extracted from peripheral leukocytes from ethylenediaminetetraacetic acid anticoagulated blood. Genotyping of the MMP2-1306C/T and TIMP2G-418C polymorphisms was performed using real-time PCR. RESULTS: There were significant differences in terms of distribution of genotype (MMP2-1306- CT, TT) and T allele frequency between the patients with RRMS and the control group (p<0.0001; p<0.0001). The groups were not different in terms of TIMP2G-418C polymorphisms. CONCLUSIONS: In the RRMS group, the genotype and allele frequencies of MMP2-1306C/T polymorphism showed significant differences from the controls. These results indicate that MMP2 might play a role in the pathogenesis of MS even during the inflammation stage.

Assessment of overactive bladder in women antidepressant users.

PURPOSE: The aim of this study was to evaluate the relationship between overactive bladder (OAB) and use of antidepressants in women. METHODS: This is a prospective trial, and in total, 205 consecutive female (113 patient taking antidepressants for various disorders and 92 healthy controls) outpatients from our outpatients were enrolled in this study. The patients were also divided into those with OAB symptoms, OAB-Validated 8 (OAB-V8 score of ≥8), and without OAB symptoms <8. The prevalence of OAB in the antidepressant users and healthy controls was compared. In addition, the prevalence of OAB was compared according to antidepressant type. RESULTS: The mean age of the participants was 36 ± 13 years. The demographic data of the two groups (OAB-V8 ≥ 8 and OAB-V8 < 8) were similar. The Beck Depression Inventory, OAB-V8, and Incontinence Questionnaire--Short Form scores of the antidepressant users were significantly higher than those of the control group (p < 0.001, p < 0.001, and p = 0.001, respectively). The prevalence of OAB was significantly higher in antidepressant users (64 %) than in the control group (33 %) (p = 0.003). The highest prevalence of OAB was detected in patients taking fluoxetine (63.6 %), and the lowest was observed in those taking sertraline (42.3 %) (p = 0.038). CONCLUSION: There were more OAB symptoms in antidepressant users than in control group. Each SSRI and SNRI has a unique pharmacological profile, and this could explain the opposing reports in the literature. We recommend that patients taking antidepressants be carefully monitored for OAB symptoms.

Demonstration of ameliorative effect of lacosamide: in a rat model of sepsis-induced critical illness polyneuropathy.

OBJECTIVES: Critical illness neuropathy (CIN) is a condition that may occur in diseases with severe systemic response, particularly in sepsis. The aim of this study is to investigate the potential anti-inflammatory and lipid-peroxidation inhibiting activities of lacosamide by measuring tumour necrotizing factor-alpha (TNF-alpha), C-reactive protein (CRP), malondialdehyde (MDA) and white blood cells (WBC) using electroneuromyography (ENMG) in rats with sepsis-induced critical illness neuropathy (SICIN). METHODS: Cecal ligation and puncture (CLP) procedure was performed on 39 rats to induce a sepsis model. The study groups were designed as follows: Group 1: normal (nonoperative); Group 2: (sham-operated); Group 3: CLP (untreated group); Group 4: CLP and lacosamide 20 mg/kg; Group 5: CLP and lacosamide 40 mg/kg. TNF-alpha, C reactive protein, MDA and WBC levels was measured and compound muscle action potential (CMAP) distal latans, amplitudes were measured by using ENMG in rats with SICIN. RESULTS: When untreated sepsis group was compared with both control and sham groups, CMAP amplitudes and latans were significantly lower (P < 000.1). When CLP, CLP+lacosamide 20 mg/kg and CLP+lacosamide 40 mg/kg groups were compared, plasma levels of TNF-alpha and MDA were significantly higher in the untreated CLP group (F = 12.74, P < 0.0001), (F = 19.43, P < 0.05). In the CLP+lacosamide 40 mg/kg group, CRP levels were significantly lower only compared to the CLP group (P < 0.001). DISCUSSION: We have showed that lacosamide may have beneficial effects on early SICIN by its potential anti-inflammatory and lipid peroxidation inhibiting activities; however, further comprehensive studies are required to clarify these effects.

Montelukast inhibits pentylenetetrazol-induced seizures in rats.

BACKGROUND: Montelukast is an antiinflammatory drug with an antioxidant property. In this study, we aimed to reveal whether montelukast has a preventive effect against seizures and post-seizure oxidative stress in pentylenetetrazol (PTZ)-induced seizures in rats. MATERIAL AND METHODS: Of the 48 male Sprague-Dawley rats used in the study, 24 were assigned to EEG recordings (group A) and 24 were assigned to behavioral studies (group B). In group A, the electrodes were implanted on dura over the left frontal cortex for EEG recording. After 10 days, in group A, i.p. saline, 25, 50, or 100 mg/kg montelukast+35 mg/kg PTZ was administered to the rats. EEG was recorded and spike percentage was evaluated. In group B, i.p. saline, 25, 50, or 100 mg/kg montelukast+70 mg/kg PTZ was administered to the rats. Racine's Convulsion Scale (RCS) and onset times of first myoclonic jerk (FMJ) was used to evaluate the seizures. Malondialdehyde (MDA) and superoxide dismutase (SOD) levels were determined in the brain tissue of animals. RESULTS: Animals treated with 50 or 100 mg/kg montelukast had significantly lower RCS and significantly increased FMJ onset time compared to the saline-treated animals. Moreover, groups given 25, 50, or 100 mg/kg montelukast had significantly lower MDA and higher SOD levels compared to the saline-treated group. The differences were more pronounced in the 100 mg/kg montelukast-pretreated group (p<0.001). CONCLUSIONS: Montelukast showed anticonvulsant action and led to amelioration of oxidative stress markers in PTZ-induced seizures in rats.

Lack of association between MIF gene -173G>C polymorphism with multiple sclerosis.

AIM: The aim of the present study was to investigate a possible association between the MIF -173G>C polymorphism and MS in Turkish patients. MATERIALS AND METHODS: The study included 153 MS-patients and 210 controls. Genomic DNA was isolated and genotyped using PCR-RFLP assay for the MIF -173G>C promoter polymorphism (rs755622). RESULTS: There was no statistically significant difference in allele and genotype frequencies between MS-patients and controls (p=0.227 and p=0.157, respectively). Accordingly, no association was observed when the patients were compared against controls in terms of GG versus GC+CC genotypes and GG+GC versus CC genotypes (p=0.324 and p=0.179, respectively). Also, there was no statistically significant association between MIF-173G>C polymorphism and clinical and demographic characteristics of MS-patients. Conlusion: The results of the present study suggest no relation between MS susceptibility and MIF gene - 173G>C polymorphism in the examined Turkish population.

Inhibitor effect of dexketoprofen in rat model of pentylenetetrazol-induced seizures.

OBJECTIVES: The relationship between epilepsy and inflammation is known, and it has been reported that there is an increase in cyclooxygenase (COX) levels in epilepsy. We aim to reveal the anticonvulsant effects of dexketoprofen in pentylenetetrazol (PTZ)-induced seizures in rats. MATERIALS AND METHODS: Forty-eight male Sprague-Dawley rats, 24 of them for EEG recording and 24 of them are for behavioral studies, were randomly divided in two groups: Group A for EEG recordings and Group B for behavioral assessment. A weight of 70 mg/kg PTZ was used for behavioral studies after dexketoprofen administration. Thirty-five milligrams per kilogram PTZ were used for EEG recording after dexketoprofen administration. The electrodes were implanted on dura over the left frontal cortex and the reference electrode was implanted over the cerebellum for EEG recording. The Racine convulsion scale (RCS), first myoclonic jerk (FMJ) onset time, and spike percentages were evaluated between the two groups. RESULTS: There was a significant (P< 0·05) difference between the RCS, FMJ onset time (P< 0·001), and spike percentage (P< 0·05) between the groups (Group 2 compared with Groups 3 and 4). CONCLUSION: Dexketoprofen has an antiepileptic feature and this effect increases as the dosage increases, however it is currently unknown through which mechanism this drug shows its anticonvulsant effect. Dexketoprofen, in the group of NSAIDs, shows an anticonvulsant effect on PTZ-induced epilepsy model. This study suggests that dexketoprofen can preferably be used with NSAIDs for epileptic patients in clinical practice.

Association of methylenetetrahydrofolate reductase gene C677T polymorphism with multiple sclerosis in Turkish patients.

BACKGROUND AND AIM: Multiple sclerosis (MS) is a chronic neurodegenerative autoimmune disease of the central nervous system. Genetic risk factors are known to contribute to the etiology of MS. Methylenetetrahydrofolate reductase (MTHFR) gene C677T polymorphism has been associated with susceptibility to various autoimmune diseases. The aim of this study was to investigate a possible association between the MTHFR gene C677T polymorphism and MS in Turkish patients. METHODS: The study included 130 MS patients and 150 group-matched controls. Genomic DNA was isolated and genotyped using polymerase chain reaction-based restriction fragment length polymorphism assay for the MTHFR gene exon C677T polymorphism. RESULTS: The genotype and allele frequencies of C677T polymorphism showed statistically significant differences between MS patients and controls (P = 0.002 and P = 0.002; odds ratio, 1.79; 95% confidence interval, 1.23-2.63, respectively). A significant association was observed when the patients were compared with the controls according to CC genotype versus CT + TT genotypes (P = 0.0005; odds ratio, 2.35; 95% confidence interval, 1.45-3.82). There were no statistically significant association between MTHFR gene C677T polymorphism and baseline clinical and demographical characteristics of MS patients. CONCLUSIONS: These results showed that T allele of C677T polymorphism was associated with MS susceptibility in Turkish population.