Birth outcomes in pregnant women with epilepsy: A Nationwide multicenter study from Türkiye.

OBJECTIVE: The present study was aimed at investigating the effects of anti-seizure medications (ASMs), patient demographic characteristics, and the seizure type and frequency on the development of congenital malformations (CMs) in the infants of pregnant women with epilepsy (PWWE). METHODS: PWWE followed up at the neurology outpatient clinic of 21 centers between 2014 and 2019 were included in this prospective study. The follow-up of PWWE was conducted using structured, general pregnant follow-up forms prepared by the Pregnancy and Epilepsy Study Committee. The newborns were examined by a neonatologist after delivery and at 1 and 3 months postpartum. RESULTS: Of the infants of 759 PWWE, 7.2% had CMs, with 5.6% having major CMs. Polytherapy, monotherapy, and no medications were received by 168 (22.1%), 548 (72.2 %), and 43 (5.7 %) patients, respectively. CMs were detected at an incidence of 2.3% in infants of PWWE who did not receive medication, 5.7% in infants of PWWE who received monotherapy, and 13.7% in infants of PWWE who received polytherapy. The risk of malformation was 2.31-fold (95% confidence interval (CI): 1.48-4.61, p < .001) higher in infants of PWWE who received polytherapy. Levetiracetam was the most frequently used seizure medication as monotherapy, with the highest incidence of CMs occurring with valproic acid (VPA) use (8.5%) and the lowest with lamotrigine use (2.1%). The incidence of CMs was 5% at a carbamazepine dose <700 mg, 10% at a carbamazepine dose ≥700 mg, 5.5% at a VPA dose <750 mg, and 14.8% at a VPA dose ≥750 mg. Thus the risk of malformation increased 2.33 times (p = .041) in infants of PWWE receiving high-dose ASMs. SIGNIFICANCE: Birth outcomes of PWWE receiving and not receiving ASMs were evaluated. The risk of CMs occurrence was higher, particularly in infants of PWWE using VPA and receiving polytherapy. The incidence of CMs was found to be lower in infants of PWWE receiving lamotrigine.

The effect of taxifolin on oxidative sciatic nerve damage induced by cobalt chloride in rats: a biochemical and histopathological evaluation.

Cobalt is a trace element that increases lipid peroxidation and malondialdehyde levels and reduces the antioxidant defense mechanisms of nerve cells. High levels of cobalt exposure may cause peripheral neuropathy, but the mechanism behind this has not yet been elucidated. Taxifolin is a flavonoid whose antioxidant and anti­inflammatory properties are well­known. We aimed to investigate the effect of taxifolin on cobalt­induced oxidative sciatic nerve damage. Eighteen albino male Wistar rats were assigned to three groups: Control, Cobalt, and Taxifolin + Cobalt groups. Total oxidant and total antioxidant status and levels of malondialdehyde, total glutathione, and superoxide dismutase were measured to determine the effect of taxifolin on cobalt­induced sciatic nerve injury. The following statistically significant effect of taxifolin was observed: It prevented cobalt­induced oxidative sciatic nerve damage by reducing malondialdehyde levels and total oxidant status and increasing total antioxidant status, total glutathione levels, and superoxide dismutase levels. In a histopathological analysis, we observed similar findings in Control and Taxifolin + Cobalt groups. We determined that taxifolin is effective in preventing cobalt­induced oxidative damage in sciatic nerve injury.

Trigger Point Injection as a Rare Cause of Ischemic Stroke: A Case Report.

INTRODUCTION: Myofascial pain syndrome is a painful local or regional disease caused by myofascial trigger points. Trigger point injection (TPI) is a frequently used method for the treatment of myofascial pain. Major complications associated with TPI have rarely been reported in the literature. CASE REPORT: A 24-year-old woman, without medical history of any disease, was diagnosed with myofascial syndrome based on the presence of long-standing neck and right arm pain, and TPI with lidocaine was applied to the right trapezius region. During the procedure, blurred vision and loss of strength in the left arm occurred. Magnetic resonance and computed tomography imaging of the brain revealed findings that were consistent with an ischemic stroke in the right capsular interna and right occipital region. CONCLUSION: The reported patient is the first in the literature who suffered from ischemic stroke after TPI. The use of ultrasound for injections into the neck muscles could avoid serious complications.

The Effect of Anakinra on Acrylamide-induced Peripheral Neuropathy and Neuropathic Pain in Rats

Abstract Acrylamide is a neurotoxic compound. Moreover, anakinra is an interleukin-1 (IL-1) receptor antagonist used in rheumatoid arthritis treatment. This study investigated the effect of anakinra on acrylamide-related neuropathy and neuropathic pain. Acrylamide exposure caused a significant decrease in the pain threshold; an increase in malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1ß) levels; and a decrease in total glutathione (tGSH) values in the sciatic nerve. This indicates hyperalgesia presence, oxidative stress, and peripheral nerve tissue inflammation. Anakinra treatment significantly reduced the MDA, IL-1ß, and TNF-α levels, and increased the pain threshold and mean tGSH values. The analgesic effect of anakinra was 67.9% at the first hour, increasing to 74.9% and 76.7% at the second and third hours, respectively. The group receiving acrylamide exhibited histopathological changes (e.g., swollen and degenerated axons, hypertrophic and hyperplasic Schwann cells, and congested vessels). The use of anakinra significantly improved these morphological changes. Anakinra is concluded to reduce neuropathic pain and prevent neurotoxic effect of acrylamide on peripheral nerves due to its analgesic, antioxidant, and anti-inflammatory properties

The role of protein oxidation in the development of diabetic microvascular complications.

OBJECTIVE: The role of protein oxidation in the development of diabetic microvascular complications was investigated. METHODS: In total, 266 participants were split into five groups: Group 1; diabetes mellitus for at least 10 years without any complications, Group 2; diabetic nephropathy, Group 3; diabetic neuropathy, Group 4; diabetic retinopathy, and Group 5; control group. Thiol, disulfide, ferroxidase, and ischemia-modified albumin (IMA) levels were analyzed in the serum. RESULTS: Native thiol, total thiol, and native thiol/total thiol were lower in Group 4 than Groups 1, 3, and 5 (p<0.001). However, disulfide/native thiol and disulfide/total thiol were higher in Group 4 than all other groups (p<0.001). IMA was higher in Groups 3 and 4 than all other groups (p<0.001). Ferroxidase was lower in Groups 3 and 4 than Group 2 (p<0.001). CONCLUSION: Thiol-disulfide homeostasis impairment in favor of disulfide may have a function in the progress of diabetic retinopathy. Furthermore, the disruptions of IMA and ferroxidase levels involve in the development of diabetic retinopathy and neuropathy.

Altered Macular Vasculature in Migraine Patients without Aura: Is It Associated with Ocular Vasculature and White Matter Hyperintensities?

AIM: We aimed to determine the alterations in macular and optic nerve vasculature in patients with migraine without aura using optical coherence tomography-angiography (OCTA). We also aimed to determine whether there were clinical differences and alterations in ocular structures in migraine cases with white matter hyperintensities (WMH) using magnetic resonance imaging (MRI). Materials and Methods. The study group comprised patients with migraine without aura and age- and sex-matched healthy controls. Detailed histories of the patients with migraine were recorded including the disease duration, number of attacks in the last month, and attack durations. Visual evoked potentials (VEP) were recorded in all migraine patients. The migraine disability assessment (MIDAS) questionnaire was administered to all patients. The patients were divided into two groups as migraine with WMHs and migraine without WMHs. All subjects underwent a complete neurological and ophthalmological examination. Only the right eyes of the patients were included in the study. Retinal imaging was performed using OCT and OCTA. RESULTS: A total of 66 migraine patients (29 with WMH and 37 without WMH) and 43 healthy controls were included in this study. Among the migraine patients, disease duration, attack frequency in the last month, attack durations, and the visual analogue scale (VAS), MIDAS, and VEP scores were all similar between those with and without WMHs. There was no significant difference between the groups regarding the ganglion cell complex, foveal, and retinal nerve fiber layer thicknesses. The superficial or deep vascular perfusion densities of the optic disc were also similar between the groups. The foveal avascular zone (FAZ) was significantly larger (P=0.034), and both superficial and deep macular vascular densities were significantly lower in the migraine groups compared with the healthy controls (P=0.001). There was no significant difference concerning the FAZ size or vascular densities between the migraine groups with and without WMHs. In the correlation analysis performed between the migraine patients, the FAZ size was correlated with age and VAS and MIDAS scores while both superficial and deep macular vascular densities were negatively correlated with age and VAS and MIDAS scores. CONCLUSION: We suggest that for not only migraine with aura but also migraine without aura, neurovascular structures play an important role in pathogenesis, and novel studies are warranted to elucidate the alterations in these and determine the significance of WMHs in these patient groups.

Is ischemia associated with the formation of White matter lesions in migraine?

OBJECTIVE: White matter lesions (WMLs) are more common in migraine patients than in the normal population. Ischemia/hypoxia and oxidative stress are considered to play a role in WMLs formation. This study aimed to investigate ischemia-modified albumin (IMA), ferroxidase and thiol/disulfide homeostasis in migraineurs with and without WMLs. PATIENTS AND METHODS: Sixty-two migraineurs with WML, 59 migraineurs without WML and 61 controls were included in the study. All participants underwent brain MRI. WMLs was evaluated according to the Fazekas scale. IMA, ferroxidase, total thiol, native thiol and disulfide measurements were carried out in all participants. RESULTS: The IMA levels were higher in the migraine groups compared to the control group (p < 0.001) and in the WML group compared to non-WML (p < 0.001). The total and native thiol levels were higher in the non-WML group compared to the control and WML groups (p < 0.001 for both). The disulfide levels were similar between the control and non-WML groups, but they were significantly lower in the WML group compared to the control and non-WML groups. There was no significant difference between the groups in terms of the ferroxidase levels (p = 0.092). The thiol/disulfide, IMA and ferroxidase levels were not significantly correlated with the frequency and duration of attacks, severity of pain and disability due to migraine. CONCLUSION: Increased serum IMA levels in migraineurs point to the role of ischemia/hypoxia, and increased total thiol and decreased disulfide levels indicate an oxidant/antioxidant imbalance in migraine. Ischemia/hypoxia may play a role in WMLs formation in migraine.

Assessments of vessel density and foveal avascular zone metrics in multiple sclerosis: an optical coherence tomography angiography study.

BACKGROUND/OBJECTIVES: To investigate optical coherence tomography angiography (OCT-A) findings of foveal avascular zone (FAZ) metrics and macular & peripapillary vessel densities (VD) in subjects with multiple sclerosis (MS). METHODS: The study design was prospective and cross-sectional. FAZ metrics and VDs of the superficial capillary plexus (SCP), deep capillary plexus (DCP), retinal peripapillary capillary plexus (RPCP) along with the structural OCT measurements were scanned by using the Nidek's RS-3000 Advance in MS patients and healthy controls. All subject also underwent an assessment of visual evoked potentials (VEPs). The relationships between the OCT-A parameters with other clinical findings were analysed. RESULTS: Forty-seven MS patients (94 eyes) and 61 healthy volunteers (122 eyes) were included in this study. Thirty-five eyes of the MS patients had an ON history. The structural OCT measurements were significantly differed between the groups (P < 0.001). All FAZ metrics were inversely correlated with central foveal thickness (CFT) (P < 0.001). The FAZ area and perimeter were inversely correlated with the VD of both SCP and DCP (P < 0.05). The VDs of SCP and DCP were significantly differed between the study groups (P < 0.001). The VEP latency was inversely correlated with the retinal nerve fibre layer, macular and ganglion cell layer thicknesses, the VD of SCP, and the VD of the DCP (P < 0.001). CONCLUSIONS: Based on OCT angiography, VDs of macular and peripapillary area may be useful in detecting damage from ON in patients with MS.

Peripheral neurotoxic effects of cisplatin on rats and treatment with rutin.

BACKGROUND: Cisplatin, used in cancer treatment, has toxic and apoptotic effects on the peripheral nervous system. Rutin, also known as vitamin P, has antioxidant and antiapoptotic activity. OBJECTIVES: The purpose of this study was to investigate the biochemical and histopathologic efficacy of rutin on neurotoxic and apoptotic effects caused by cisplatin in the peripheral nervous system. MATERIAL AND METHODS: Twenty-four albino Wistar male rats were divided into the following 4 groups: control group (CG), only cisplatin-injected group (CIS), cisplatin and rutin 50 mg/kg (RG-50)-injected group, and cisplatin and rutin 100 mg/kg (RG-100)-injected group. Analyses were performed on sciatic nerve tissue of experimental animals. Analyses of malondialdehyde (MDA), total glutathione (tGSH), glutathione reductase (GSHRd), glutathione-s-transferase (GST), and superoxide dismutase (SOD) were performed. Caspase-3 expression in nerve tissue was also investigated. The analyzed groups were compared with CG. RESULTS: Biochemical investigation shows that there is a statistically significant difference between CG and only CIS and RG-50. Control group and RG-100 were found to be similar. Cisplatin-induced changes were observed in histopathological analysis of the nerve tissue. The RG-100 and CG were found to be similar. The caspase-3 expression in the neural tissue was compared between groups. Control group and CIS were found to be different. Control group and RG-100 were found to be similar. CONCLUSIONS: Antioxidant and antiapoptotic effectiveness of rutin was detected against the toxic effects caused by cisplatin in the peripheral nerve tissue.

Is rosuvastatin protective against on noise-induced oxidative stress in rat serum?

Noise, one of the main components of modern society, has become an important environmental problem. Noise is not only an irritating sound, but also a stress factor leading to serious health problems. In this study, we have investigated possible effects of rosuvastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, thought to have an antioxidant effect, on noise-induced oxidative stress in the serum of rat models. Thirty-two male Wistar albino rats were used. In order to ease their adaptation, 2 weeks before the experiment, the rats were divided into four groups (with eight rats per each group): Noise exposure plus rosuvastatin usage, only noise exposure, only rosuvastatin usage and control. After the data had been collected, oxidant (Malondialdehyde, nitric oxide [NO], protein carbonyl [PC]) and antioxidant (superoxide dismutase [SOD], glutathione peroxidase [GSH-PX], catalase [CAT]) parameters were analyzed in the serum. Results indicated that SOD values were found to be significantly lower, while PC values in serum were remarkably higher in the group that was exposed to only noise. GSH-Px values in serum dramatically increased in the group on which only rosuvastatin was used. During noise exposure, the use of rosuvastatin caused significantly increased CAT values, whereas it resulted in reduced PC and NO values in serum. In conclusion, our data show that noise exposure leads to oxidative stress in rat serum; however, rosuvastatin therapy decreases the oxidative stress caused by noise exposure.

Possible effects of rosuvastatin on noise-induced oxidative stress in rat brain.

The problem of noise has recently gained more attention as it has become an integral part of our daily lives. However, its influence has yet to be fully elucidated. Other than being an unpleasant stimulus, noise may cause health disorders through annoyance and stress, including oxidative stress. Rosuvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, may possess antioxidant properties. Based on rat models, our project investigates the effect of rosuvastatin on noise-induced oxidative stress in the brain tissue. Thirty-two male Wistar albino rats were used. The rats were divided into four groups: Noise exposure plus rosuvastatin usage, only noise exposure, only rosuvastatin usage, and control. After the data had been collected, oxidant and antioxidant parameters were analyzed in the cerebral cortex, brain stem, and cerebellum. Results indicated that superoxide dismutase values were significantly decreased in the cerebral cortex, while malondialdehyde values in the brainstem and cerebellum were significantly increased in the group with only noise exposure. Superoxide dismutase values in the brainstem were significantly increased, but nitric oxide values in the cerebellum and brainstem and malondialdehyde values in the cerebellum and cerebral cortex were significantly decreased in the group where only rosuvastatin was used. During noise exposure, the use of rosuvastatin caused significantly increased superoxide dismutase values in the cerebral cortex and brainstem, but significantly reduced malondialdehyde values in the brain stem. Consequently, our data show that brain tissue was affected by oxidative stress due to continued exposure to noise. This noise-induced stress decreases with rosuvastatin therapy.

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.

Cerebral blood flow evaluation during the hypnotic state with transcranial Doppler sonography.

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.

A patient with progressive headache and partial optic chiasm involvement.

A 69-year-old woman presented with a 2-month history of bilateral throbbing daily headaches and a 2-week history of progressive visual loss. Radiologic imaging, visual field test, and cerebrospinal fluid analysis findings are discussed. After treatment, the symptoms were resolved without deficit.