Determination of oxidative stress level and some antioxidant activities in refractory epilepsy patients.

The aim of this study was to determine the levels of superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH) and malondialdehyde (MDA) in patients with refractory epilepsy. Serum superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH) and malondialdehyde (MDA) levels were determined using the spectrophotometer method. Refractory epilepsy patients' serum superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH) and malondialdehyde (MDA) levels were statistically significant compared to the healthy control group (p < 0.05). In conclusion, superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH) and malondialdehyde (MDA) levels may play an important role in the etiopathogenesis of refractory epilepsy. This study was the first to investigate some parameters in refractory epilepsy disease.

Is Childhood Trauma a Risk Factor for Resistant Epilepsy?

Childhood traumas have been considered risk factors for many psychiatric disorders. Recent studies demonstrated that childhood traumas can also be considered risk factors for neurological diseases. In this context, the objective of this study is to investigate the effects of childhood traumas on treatment resistance in patients with epilepsy. The study sample consisted of 85 epilepsy patients, 40 male and 45 female, who were diagnosed and followed up by a neurologist. Of these patients, 45 were being followed up with the diagnosis of refractory epilepsy, and 40 were being followed up with the diagnosis of treatment-responsive epilepsy. Cranial magnetic resonance imaging and electroencephalography were performed on all patients. In addition, all patients were administered childhood trauma questionnaire (CTQ) and Hamilton depression rating scale (HAM-D). Epilepsy patients included in the study were divided into refractory epilepsy and treatment-responsive epilepsy groups. There was no significant difference between the groups in sociodemographic characteristics. On the other hand, total CTQ and all CTQ subscale scores and HAM-D scores were significantly higher in the refractory epilepsy group than in the treatment-responsive epilepsy group. This study demonstrates that childhood traumas may contribute to treatment resistance in epilepsy patients. Therefore, it is recommended that a history of childhood traumas be routinely queried in the treatment of epilepsy patients.

Association Between Severe Chronic Obstructive Pulmonary Disease and Polyneuropathy.

BACKGROUND Chronic obstructive pulmonary disease (COPD) is a life-threatening and devastating disease associated with low-grade systemic inflammation. In adults, the most common disease of the peripheral nervous system is peripheral neuropathy. While most polyneuropathy has a mixed presentation, some cases are motor dominant and others are sensory dominant. We investigated polyneuropathy in patients with COPD and hypothesized that low-grade systemic inflammation and other pathologies in patients with COPD cause peripheral axonal polyneuropathy. MATERIAL AND METHODS We included 62 patients with COPD without any neurological signs or symptoms, and 30 healthy volunteers with no known neurological or pulmonary diseases as controls. There were 38 men in the COPD group and 17 men in the control group; the mean ages of the 2 groups were 64.88 and 62.7 years, respectively. According to the Global Initiative for Chronic Obstructive Lung Disease COPD report, all COPD patients were group D. After collecting demographic and clinical characteristics of the participants, we performed an electrophysiological examination to investigate polyneuropathy and pulmonary function test results. C-reactive protein, hemoglobin, creatinine, partial carbon dioxide pressure (pCO2) levels were recorded. Electrophysiological examination was performed with a Medelec Synergy device using standard neurographic procedures, and the results were assessed. RESULTS Significant differences were found for forced expiratory volume in 1 sec (FEV1), %FEV1, forced vital capacity (FVC), %FVC, pCO2, and hemoglobin and creatinine levels, but all participants had a creatinine level within the normal range. There was no difference in sensory neuropathy between the groups, but a significant difference was found in terms of motor neuropathy. CONCLUSIONS As noted in previous studies, systemic inflammation, increased oxidative stress, decreased oxygen pressure, and multiple comorbidities in patients with COPD may all contribute to the development of neuropathy.

Effects of omalizumab therapy on peripheral nerve functions: short observational study.

INTRODUCTION: Peripheral neuropathy (PN) is a common neurological condition causing symmetrical and diffuse damage in nerves. The etiology of PN includes systemic diseases, toxic exposure, medications, infections, and hereditary diseases. Omalizumab is a humanized monoclonal anti-IgE antibody that exerts its activity by binding to free IgE in circulation. AIM: To investigate the relationship between omalizumab and peripheral neuropathy. MATERIAL AND METHODS: The study included 30 patients who underwent omalizumab therapy (Xolair) due to the diagnosis of chronic urticaria. A detailed neurological and physical examination was performed in each patient both before and 3 months after the therapy. Electrophysiological examination was also performed using a Medelec Synergy instrument. RESULTS: The 30 patients included 8 (26.7%) men and 22 (73.3%) women with a mean age of 37.5 ±14.14 years. No serious side effect of the medication was detected in any patient although local wound irritation occurred in 3 (10%) patients. Moreover, no change occurred in the pre-treatment Neuropathy Symptom Score (NSS) or Neurological Disability Score (NDS) of the patients and no pathological values that could result in neuropathy were observed during motor/sensory nerve conduction. However, significant changes were detected in the sensory and motor components of the nerves with regards to pre- and post-treatment values. CONCLUSIONS: Omalizumab therapy caused no peripheral neuropathy in any of our patients but altered the latency, amplitude, and velocity values of the peripheral nerves.

The association between retinal nerve fibre layer thickness and corpus callosum index in different clinical subtypes of multiple sclerosis.

The objective of this paper is to evaluate the association between physical disability in multiple sclerosis (MS) patients, the thickness of the retinal nerve fibre layer (RNFL) and corpus callosum volumes, as expressed by the corpus callosum index (CCI). This study was based on a cohort of 212 MS patients and 52 healthy control subjects, who were age and gender matched. The MS patients included 144 women and 177 relapsing-remitting MS (RRMS) patients. Peripapillary and volumetric optical coherence tomography (OCT) scans of the macula were performed using spectral-domain OCT technology. All magnetic resonance imaging (MRI) scans were performed using 1.5-T systems. CCI and RNFL were lower in MS than healthy control subjects (0.341 versus 0.386, p < 0.01 and 92.1 versus 105.0, p < 0.01). In addition, CCI correlated with RNFL (r = 0.464, p < 0.01). This was also true for the subgroup of patients with no history of optic neuritis (ON). There is a correlation between the thickness of the RNFL and CCI values in MS patients with no history of ON, which suggests that OCT might be a suitable marker for neurodegeneration in MS clinical trials.