Atilla Ilhan

Pentylenetetrazol-induced kindling seizure attenuated by Ginkgo biloba extract (EGb 761) in mice

Ginkgo biloba extract (EGb 761) has been used therapeutically for centuries. It has attracted great attention as agents for improving circulation, particularly cerebral circulation, which may lead to improved mental function. Many researches hypothesized on the role of the extract in the treatment of diseases involving free radicals and oxidative damage. In the present study, anticonvulsant and antioxidant effects of EGb 761 were investigated in pentylenetetrazol (PTZ)-kindled mice. Valproic acid (VA), a major antiepileptic drug, was also tested for comparison. EGb 761-treated mice displayed a significant attenuated response to PTZ on the test day (day 26) compared with saline-treated and VA-treated animals. Valproic acid significantly increased seizure latency. Pretreatments with EGb 761 significantly protected against PTZ-induced convulsive behaviors (seizure latency, seizure score). EGb 761 and VA significantly decreased PTZ-induced oxidative injury in brain tissue. EGb 761 was found to be the most effective in preventing PTZ-induced oxidative damage among both substances studied. The data obtained support our speculation that neuroprotective action of EGb 761 may correlate with its ability to inhibit not only excessive reactive oxygen species (ROS) formation but also seizure generation. Taken together, the results of the present study show that the effect of EGb 761 on ROS production contributes to their neuroprotective action. It might be concluded that the suppression of seizure-induced ROS generation may be involved in the mechanism of action of antiepileptic drugs.

IL-6 Levels in Migraine Patients Receiving Topiramate

There is considerable evidence suggesting that cytokines play important roles in pain and in mediating neurovascular inflammation associated with migraine headaches. Although consensus exists to recommend topiramate (TPM) for migraine prevention, the mechanism of action in this regard is unknown. We measured serum interleukin‐6 (IL‐6) levels in 66 migraine patients. Of these patients, 23 (34.9%) were taking TPM for migraine, and 43 (65.1%) were not. The IL‐6 levels were compared with those of healthy controls without migraine, from the population living in the same region. The mean IL‐6 levels in migraine patients taking TPM and patients who did not were 67.06 ± 92.09 pg/mL and 44.09 ± 59.19 pg/mL, respectively (P > 0.05). The IL‐6 levels were higher in the patients taking TPM. The IL‐6 level in the controls was 8.60 ± 7.36 pg/mL, which was significantly lower than the patient group using TPM (P = 0.001). Our results show that, although IL‐6 may be involved in pain induction or inflammatory mechanisms of migraine attacks, the serum IL‐6 level was not reduced in migraine patients receiving TPM therapy. In conclusion, we found high IL‐6 levels in migraine patients both with and without TPM therapy, suggesting that high IL‐6 levels during pain‐free periods could be a conditioning factor, making patients more vulnerable to pain attacks in chronic migraine. Further studies investigating the possible mechanism of TPM in migraine are needed.

The anti-oxidant and anti-apoptotic effects of nebivolol and zofenopril in a model of cerebral ischemia/reperfusion in rats.

The aim of this experiment was to investigate whether nebivolol and zofenopril have protective effects against oxidative damage and apoptosis induced by cerebral ischemia/reperfusion (I/R). There were seven groups of rats, with each containing eight rats. The groups were: the control group, I/R group, I/R plus zofenopril, I/R plus nebivolol, I/R plus nebivolol and zofenopril, zofenopril only and nebivolol only. Cerebral I/R was induced by clamping the bilateral common carotid artery and through hypotension. The rats were sacrificed 1h after ischemia, and histopathological and biochemical analyses were carried out on their brains. The total antioxidant capacity was evaluated by using an automated and colorimetric measurement method developed by Erel. I/R produced a significant increase in the levels of total oxidant status and malondialdehyde levels, the number of caspase-3 immunopositive cells and activities of prolidase and paraoxonase in brain when compared with the control group (p<0.05). A significant decrease in brain total antioxidant capacity and nitric oxide levels were found in I/R group when compared with the control group (p<0.05). Both nebivolol and zofenopril treatment prevented decreasing of the total antioxidant capacity and nitric oxide levels, produced by I/R in the brain (p<0.05). Both nebivolol and zofenopril treatment prevented the total oxidant status, malondialdehyde levels, activities of paraoxonase and prolidase from increasing in brains of rats exposed to I/R (p<0.05). In conclusion, both nebivolol and zofenopril protected rats from ischemia-induced brain injury. The protection may be due to the indirect prevention of oxidative stress and apoptosis.

The protective effect of erdosteine on short-term global brain ischemia/reperfusion injury in rats.

Experimental studies have demonstrated that free radicals play a major role on neuronal injury during ischemia/reperfusion (I/R) in rats. Erdosteine is a thioderivative endowed with mucokinetic, mucolytic and free-radical-scavenging properties. The aim of the present study was to investigate the effect of erdosteine treatment against short-term global brain ischemia/reperfusion injury in rats. The study was carried out on Wistar rats divided into four groups. (i) Control group, (ii) ischemia/reperfusion group, (iii) ischemia/reperfusion+erdosteine group, and (iv) erdosteine group. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities as well as thiobarbituric acid reactive substances (TBARSs) and nitric oxide (NO) levels were analysed in erythrocyte and plasma of rats. Plasma NO levels were significantly higher in the ischemia/reperfusion group than the other groups. The activities of SOD and GSH-Px were decreased, while TBARS levels increased in the ischemia/reperfusion group compared to other groups in both plasma and erythrocyte. The erythrocyte CAT activity was higher in erdosteine group and there was a statistically significant increase, when compared with the erdosteine plus ischemia/reperfusion group. By treating the rats with erdosteine, the depletion of endogenous antioxidant enzymes (SOD, CAT, GSH-Px) and increase of TBARS and NO levels were prevented. This study, therefore, suggests that erdosteine reduces parameters of oxidative stress is well supported by the data.

Cerebral Blood Flow Evaluation During the Hypnotic State With Transcranial Doppler Sonography

Abstract Cerebral blood flow was measured in normal waking (alert relaxed mental imagery) and hypnotic states. Mean flow velocity (Vm) in the middle cerebral artery (MCA) was significantly increased in hypnosis (Condition II) from Condition I (5 minutes before hypnotic induction). Vm decreased in Condition III (hypnotic imagination). After hypnosis, Vm values returned to baseline. Pulsatility index values and resistive index values showed significant variations during sonographic monitoring between Conditions I and IV (5 minutes after the completion of hypnosis). Both values were significantly higher in Condition I than IV. These findings show that hypnotic status can modulate cerebral blood flow.

Possible Pathogenic Link Between Migraine and Urotensin-II

Our aim was to determine the levels of human urotensin-II (hU-II) in the plasma of migraine patients and controls, to ascertain if there were a difference in the pathogenesis of migraine. A total of 27 patients who suffer from migraines and 27 controls were included in the study. Venous blood samples were drawn twice both from migraine patients and controls to measure hU-II plasma levels. The average levels of hU-II during migraine episode, between episodes, and controls were found to be 0.483, 0.493, and 0.737 pg/mL, respectively. The levels of hU-II in the controls were higher significantly. When comparisons were made according to sex, age groups, and types and durations of migraine, there was no significant difference in the levels of hU-II in the patients. The low levels of hU-II in the plasma of migraine patients compared with controls may be an indicator of its role in the pathogenesis.

Neuromyelitis optica: atipic clinic presentation.

We present a patient with neuromyelitis optica who exhibited longitudinally extensive transverse myelitis and aquaporin-4 IgG positivity. Patient did not have optic neuritis clinically, but we detected it with examination of visual evoked potentials (prolonged P100 wave latans), subclinically. We argue that neuromyelitis optica may also be considered in elderly patients with isolated involvement of the longitudinally extensive transverse myelitis, and visually evoked potential evaluation is important to determine of subclinic optic neuritis and anti-AQP-4 is also important to support to determination.

Median and Ulnar Neuropathy Assessment in Parkinson’s Disease regarding Symptom Severity and Asymmetry

Background. While increasing evidence suggests comorbidity of peripheral neuropathy (PNP) and Parkinsons disease (PD), the pathogenesis of PNP in PD is still a debate. The aim of this article is to search the core PD symptoms such as rigidity and tremor as contributing factors to mononeuropathy development while emphasizing each individual patients asymmetric symptom severity. Methods. We studied 62 wrists and 62 elbows of 31 patients (mean age 66.48 ± 10.67) and 64 wrists and 64 elbows of 32 age-gender matched healthy controls (mean age 62.03 ± 10.40, p = 0.145). The Hoehn and Yahr disability scale and Unified Parkinsons Disease Rated Scale were used to determine the severity of the disease. Results. According to electrodiagnostic criteria, we confirmed median neuropathy in 16.12% (bilateral in two-thirds of the patients) and ulnar neuropathy in 3.22% of the PD group. While mean age (p = 0.003), age at PD onset (p = 0.019), and H&Y scores (p = 0.016) were significant, tremor and rigidity scores were not. The comparison of the mean indices of electrophysiologic parameters indicated subclinical median and ulnar nerve demyelination both at the wrist and at the elbow in the patient groups where a longer disease duration and mild tremor and rigidity scores are prominent, remarkably. Conclusion. A disease related peripheral neurodegeneration beyond symptom severity occurs in PD.

Anterior interosseous nerve involvement in a patient due to weight lifting: MRI and EMG finding.

Received: 23-07-2012 Review completed: 26-07-2012 Accepted: 01-09-2012 simplex virus and usually presents with new lesions on imaging. On the other hand, immune-mediated relapse will be CSF HSV PCR-negative with no new lesions on imaging.[6] The distinction between active re-infection and post-infectious inflammatory encephalopathy is crucial, because the former would be managed with a repeat course of acyclovir, and the latter with corticosteroids and, possibly, intravenous immunoglobulin or plasmapheresis.[6] The presence of gliotic lesions in the medial thalami in our patient ruled out re-infection and aided in the management with corticosteroids.

Cryptogenic Isolated Cortical Venous Infarct: A Report of Three Cases

Cortical vein infarction without dural sinus involvement is extremely rare. Herein, we present three patients with headache, partial seizure and rightsided numbness. On neurological examination, focal neurologic deficit was not observed in our patients. Magnetic resonance imaging revealed cerebral ischemia which showed as hypointense on T1-weighted images and hyperintense on T2-weighted images that do not follow the boundary of arterial territories, indicating cortical venous infarct. Cortical venous infarct should be suspected in patients who present with sudden onset headache and/or focal epileptic seizures even if there is no neurologic deficit. The diagnosis and treatment of cortical venous infarct should be considered as an emergency because of the high potential for full recovery with anticoagulant treatment.