ascorbic-acid and Epilepsy

Migraine is the most common form of headache disorder globally. The etiology of migraine is multifactorial, with genetic components and environmental interactions considered to be the main causal factors. Some researchers postulate that deficits in mitochondrial energy reserves can cause migraine or an increase in homocysteine levels can lead to migraine attacks; therefore, vitamins could play a vital role in migraine prevention. For instance, riboflavin influences mitochondrial dysfunction and prevents migraine. Genes such as flavoenzyme 5,10-methylenetetrahydrofolate reductase (MTHFR), especially the C677T variant, have been associated with elevated plasma levels of homocysteine and migraine with aura. Homocysteine catalyzation requires the presence of vitamins B6, B12, and folic acid, which can decrease the severity of migraine with aura, making these vitamins potentially useful prophylactic agents for treating migraine with aura. Menstrual migraine, on the other hand, is associated with increased prostaglandin (PG) levels in the endometrium, indicating a role for vitamin E, which is an anti-PG. Vitamin C can also be used as a scavenger of reactive oxygen species for treating neurogenic inflammation in migraine patients. This paper reviews possible therapies based on vitamin supplementation for migraine prophylaxis, focusing on migraine with aura and menstrual migraine.

Topics: Adult; Ascorbic Acid; Epilepsy; Female; Folic Acid; Genotype; Homocysteine; Humans; Menstruation; Migraine Disorders; Migraine with Aura; Vitamin B 12; Vitamin B 6; Vitamin E

NMDA receptors play a central role in neuronal plasticity and in several pathological situations. Transient activation of this receptor triggers long-term potentiation, whereas sustained activation leads to cell death. Evidence for control of this activity by a redox site in cell cultures, brain tissues and in recombinant NMDA receptors are discussed by Henri Gozlan and Yehezkel Ben-Ari. The characteristics of this modulation and the consequences of redox state modifications on NMDA-mediated events are examined in vitro under physiological and pathological conditions. Since metabolic disorders enhance NMDA receptor function, the redox site could constitute a new target for selectively preventing in vivo the deleterious consequences of overactivation without blocking neuronal plasticity mediated by NMDA receptors.

Topics: Alkylation; Animals; Ascorbic Acid; Brain; Cells, Cultured; Epilepsy; Free Radicals; In Vitro Techniques; Ischemia; Neuronal Plasticity; Oxidation-Reduction; Receptors, N-Methyl-D-Aspartate; Recombinant Proteins; Sulfhydryl Compounds; Sulfhydryl Reagents; Synaptic Transmission; Xenopus laevis

In animal experiments, neuroprotective, anticonvulsive and antidepressant-like properties have been increasingly attributed to administrations of ascorbic acid (AA, vitamin C) in at least medium (low millimolar) doses, which however await validation in well controlled clinical studies. In mammalian cortical and subcortical neurons, small to modest acidification (<0.4-0.5 pH-units) is belonging to the key strategies for controlling local excitability and is associated with neuroprotection, e.g. by limiting excitotoxicity. Such acidifications are furthermore involved in the mechanisms of some anticonvulsants and antidepressants. As AA-transport and regulation of intracellular pH (pHi) are closely interwoven on the level of special transmembrane solute carriers, I suppose that the aforementioned beneficial AA-effects might be based upon a discrete "hormetic" acidification of cortical and or subcortical neurons via an AA-mediated weakening of their pHi-regulation. This assumption is supported by findings in non-neuronal cells suggesting both, intracellular acidification and inhibition of a core-element of the pHi-regulation apparatus by millimolar AA. In mammalian subcortical neurons, there is already first evidence of a modest acidification after adding low millimolar AA.

Topics: Alzheimer Disease; Animals; Anticonvulsants; Antidepressive Agents; Antioxidants; Ascorbic Acid; Brain; Carrier Proteins; Cations; Dehydroascorbic Acid; Depressive Disorder; Epilepsy; Humans; Hydrogen-Ion Concentration; Intracellular Fluid; Mammals; Mechanistic Target of Rapamycin Complex 1; Nerve Tissue Proteins; Neurons; Neuroprotective Agents; Oxidation-Reduction

Epilepsy is one of the chronic and heterogeneous epidemic neurological disorders leading to substantial mortality. The aim of the present study was to investigate the serum levels of malondialdehyde (MDA), vitamin C, and trace elements namely zinc (Zn), copper (Cu), and manganese (Mn) in epileptic patients of Bangladesh and to establish if there are any pathophysiological correlations.. This was a case-control study with 40 generalized epileptic patients and 40 healthy subjects as controls. Epilepsy was determined by the presence of seizure events with an abnormal electroencephalography and magnetic resonance imaging report of brain.. Anthropometric parameters highlighted that age is a major risk factor of epilepsy and men are more prone to epilepsy than women. Blood serum analysis demonstrated significantly ( P < .001) higher values of MDA and lower level of vitamin C in the patient group (4.41 ± 0.76 μmol/mL and 18.31 ± 0.84 μmol/L, respectively) compared with control (1.81 ± 0.70 μmol/mL and 29.72 ± 1.06 μmol/L, respectively). Pearson's correlation analysis revealed a negative correlation between the serum level of MDA and vitamin C for both patient ( r = -0.023, P = .887) and control group ( r = -0.142, P = .383). This study also revealed that the trace elements (Zn, Cu) were significantly ( P < .05) lower in epileptics (68.32 ± 4.59 and 50.81 ± 2.54 μg/dL, respectively) where the level of Mn in patients (187.71 ± 9.04 μg/dL) was almost similar to that of the control group ( P > .05). The univariate analysis demonstrated that zinc <70 μg/dL (odds ratio = 3.56, P < .05) and copper <50 μg/dL were associated (odds ratio = 14.73, P < .001) with an increased risk of epilepsy. Establishment of interelement relationship strongly supported that there was a disturbance in the element homeostasis of epileptic patients.. The study results strengthen the role of lipid peroxidation, antioxidants and trace elements in the pathogenesis and warrant larger studies to investigate the association of these biochemical parameters with epilepsy.

Topics: Adult; Ascorbic Acid; Bangladesh; Copper; Epilepsy; Female; Humans; Lipid Peroxidation; Male; Malondialdehyde; Manganese; Risk Factors; Trace Elements; Young Adult; Zinc

The benefits of regular exercise on brain health are undeniable. Long-term exercise increases the production of reactive oxygen species in brain. Therefore, athletes often consume antioxidant supplements to remedy exercise-related damage and fatigue during exercise. The aim of this study is to evaluate the role of ascorbic acid in the effects of different intensities of swimming exercise on the brain susceptibility to experimental epilepsy in rats. Ascorbic acid was administered intraperitoneally (ip) during three different swimming exercise programme for 90 days (15 min, 30 min, 90 min/day). The anticonvulsant activity regarding the frequency of epileptiform activity appeared in the 80 min after 500 units intracortical penicillin injection in 30 min and 90 min/day exercise groups. The administration of ascorbic acid (100 mg/kg, ip) did not alter the anticonvulsant properties seen in the in short-duration (15 min/day) swimming exercise group. The amplitude of epileptiform activity also became significant in the 110 and 120 min after penicillin injection in the moderate (30 min/day) and long duration (60 min/day) groups, respectively. The results of the present study provide electrophysiologic evidence that long-term administration of ascorbic acid causes anticonvulsant activities in the moderate and long-duration swimming exercise. Antioxidant supplementation such as ascorbic acid might be suggested for moderate and long-duration swimming exercise in epilepsy.

Topics: Animals; Anticonvulsants; Ascorbic Acid; Brain; Disease Models, Animal; Electroencephalography; Epilepsy; Exercise Therapy; Male; Physical Conditioning, Animal; Rats, Wistar; Swimming; Time Factors

Much evidence supports the idea that oxidative stress is involved in the pathogenesis of epilepsy, and therapeutic interventions with antioxidants are expected as adjunct antiepileptic therapy. The aims of this study were to non-invasively obtain spatially resolved redox data from control and pentylenetetrazole (PTZ)-induced kindled mouse brains by electron paramagnetic resonance (EPR) imaging and to visualize the brain regions that are sensitive to oxidative damage. After infusion of the redox-sensitive imaging probe 3-methoxycarbonyl-2,2,5,5-tetramethyl-piperidine-1-oxyl (MCP), a series of EPR images of PTZ-induced mouse heads were measured. Based on the pharmacokinetics of the reduction reaction of MCP in the mouse heads, the pixel-based rate constant of its reduction reaction was calculated as an index of redox status in vivo and mapped as a redox map. The obtained redox map showed heterogeneity in the redox status in PTZ-induced mouse brains compared with control. The co-registered image of the redox map and magnetic resonance imaging (MRI) for both control and PTZ-induced mice showed a clear change in the redox status around the hippocampus after PTZ. To examine the role of antioxidants on the brain redox status, the levels of antioxidants were measured in brain tissues of control and PTZ-induced mice. Significantly lower concentrations of glutathione in the hippocampus of PTZ-kindled mice were detected compared with control. From the results of both EPR imaging and the biochemical assay, the hippocampus was found to be susceptible to oxidative damage in the PTZ-induced animal model of epilepsy.

Topics: Animals; Ascorbic Acid; Brain; Cyclic N-Oxides; Electron Spin Resonance Spectroscopy; Epilepsy; Glutathione; Hippocampus; Kindling, Neurologic; Male; Mice, Inbred C57BL; Nitrogen Oxides; Oxidation-Reduction; Pentylenetetrazole

Although many approaches to the therapy of epilepsy exist, most of antiepileptic drugs, beside certain and unquestioned benefits, have convinced disadvantages. That is the reason for looking for new methods of treatment. Ascorbic acid, as an antioxidant and electron donor accumulated in central nervous system, seems to take part in diminishing reactions of oxidative stress in brain and cooperate with other antioxidants like alpha-tocoferol. Vitamin C, easily transported through the blood-brain barrier, is proved to reduce injury in the hippocampus during seizures. Depending on type of seizures, it has mostly inhibitory activity and even decreases mortality. Moreover, vitamin C acts as a neuroprotective factor by consolidating cell membranes and decreasing lipid peroxidation. A possible adjunctive role of vitamin C in epileptic patients needs to be considered.

Topics: Animals; Antioxidants; Ascorbic Acid; Brain; Cognition; Epilepsy; Humans; Motor Activity; Oxidative Stress

In this case presentation, a woman with high serum levels of aluminum was treated with chelation therapy with deferoxamine and ascorbic acid. This patient was initially bedridden and the clinical situation was complicated by epileptic seizures. After the chelation therapy, the clinical condition was ameliorated and the therapy continued without the correlation to aluminum serum levels. The role of metals in neurodegenerative disorders and the correlation between iron metabolism and amyloid beta peptide are described. This case suggests chelation therapy could represent a promising therapeutic option for this dramatic disease.

Topics: Aged; Aluminum; Alzheimer Disease; Antioxidants; Ascorbic Acid; Chelation Therapy; Deferoxamine; Epilepsy; Fatal Outcome; Female; Humans; Iron; Siderophores

It is well known that oxidative stress plays an important role in the etiology of epilepsy. We investigated effects of selenium (Se) and topiramate (TPM) combination supplementation on antioxidant and oxidant values in control and patients with epilepsy and refractory epilepsy. For the aim, we used control (n = 19), epilepsy + TPM (n = 19), epilepsy + TPM + Se (n = 15) groups. We also used control (n = 15), refractory epilepsy (n = 15), and refractory epilepsy + Se (n = 8) groups. TPM (0.2 mg/daily) and Se, as sodium selenite (twice daily with 0.1 mg doses), were orally supplemented to the patients for 45 days. Erythrocyte lipid peroxidation levels were higher in refractory epilepsy groups than in control although its level and seizure numbers were decreased in TPM and TPM + Se supplemented groups of the patients. The erythrocyte reduced glutathione (GSH), glutathione peroxidase (GSH-Px), plasma total antioxidant status (TAS), and vitamin E concentration in refractory epilepsy group were lower than in control. However, the erythrocyte and plasma TAS, erythrocyte GSH and GSH-Px, and plasma vitamins A and C values were increased either by Se or Se + TPM in epilepsy and refractory epilepsy groups. There were no effects of TPM and Se on plasma β-carotene values in the groups. In conclusion, TPM and selenium caused protective effects on the epilepsy and refractory epilepsy-induced oxidative injury by inhibiting free radical production and supporting antioxidant redox system.

Topics: Adult; Antioxidants; Ascorbic Acid; beta Carotene; Case-Control Studies; Epilepsy; Female; Fructose; Glutathione; Glutathione Peroxidase; Humans; Lipid Peroxidation; Male; Oxidative Stress; Pilot Projects; Selenium; Topiramate; Vitamin A; Vitamin E; Young Adult

The effects of ascorbic acid and α-tocopherol pre-treatment on hypoxia induced changes in brain cortex excitability were tested in immature rats exposed chronically to simulated altitude of 7 000 m.. Rat pups were kept together with their mothers for 8 hours a day in hypobaric chamber since the day of the birth till the postnatal day 11 or 17. Each day immediately before placing to hypobaric chamber pups were pretreated intraperitoneally either with ascorbic acid (100 mg/kg) or α-tocopherol (1 500 mg/kg). Cortical afterdischarges were elicited by repeated stimulation of the right sensorimotor cortex. The duration of evoked cortical afterdischarges was analyzed.. Duration of cortical afterdischarges progressively declines with age. Hypoxia prolonged the duration of afterdischarges in 12-, 18- and 25-day-old animals. Pretratment with ascorbic acid or α-tocopherol shorted afterdischarges duration in youngest experimental group when compared with animals exposed to hypoxia only.. Hypoxia significantly affects the brain cortex excitability by prolonging afterdischarges duration. This effect differs with age. Antioxidant pre-treatment brought about shorter duration of cortical afterdischarges only in the youngest experimental group. The antioxidant effect is therefore age dependent.

Topics: Age Factors; alpha-Tocopherol; Animals; Animals, Newborn; Antioxidants; Ascorbic Acid; Cerebral Cortex; Epilepsy; Evoked Potentials; Female; Hypoxia, Brain; Male; Oxidative Stress; Pregnancy; Rats

The present study was designed to observe the effect of PTZ on expression of caspsae-3, and to evaluate the neuroprotective role of vitamin C (vit-C) against PTZ-induced apoptotic neurodegeneration in adult rat brain. We observed that administration of a single conclusive dose of pentylenetetrazol (PTZ 50mg/kg) in adults rats induced epileptic seizure and increased activation of caspase-3 and caused neuronal death. Further, rats were injected with vit-C (250 mg/kg) 30 min before PTZ injection. The protective effect of vit-C against PTZ-induced apoptotic neurodegeneration in adult rat brain was observed using Western blot analysis and Nissl staining. The results showed that conclusive dose of PTZ-induced seizure, increased expression of caspase-3 and neuronal apoptosis in adult rat brain. Whereas, the pretreatment of vit-C along with PTZ showed significantly decreased expression of caspase-3 as compare to control group. Finally, our results indicated that vit-C can prevent some of the deleterious effect of seizure and neuronal degeneration induced by PTZ in adult rat brain.

Topics: Animals; Apoptosis; Ascorbic Acid; Brain; Caspase 3; Disease Models, Animal; Epilepsy; Male; Nerve Degeneration; Neuroprotective Agents; Pentylenetetrazole; Rats; Rats, Sprague-Dawley

Ascorbic acid and nitric oxide are known to play important roles in epilepsy. The aim of present study was to identify the involvement of nitric oxide (NO) in the anticonvulsant effects of ascorbic acid on penicillin-induced epileptiform activity in rats. Intracortical injection of penicillin (500, International Units (IU)) into the left sensorimotor cortex induced epileptiform activity within 2-5 min. Thirty minutes after penicillin injection, nitric oxide synthase (NOS) inhibitor, N(G)-nitro-l-arginine methyl ester (l-NAME, 100mg/kg), neuronal nitric oxide synthase (nNOS) inhibitor 7-nitroindazole (7-NI, 40 mg/kg), NO substrate, l-arginine (500 mg/kg) were administered with the most effective dose of ascorbic acid (100 mg/kg) intraperitoneally (i.p.). The administration of l-arginine significantly decreased the frequency of epileptiform activity while administration of l-NAME did not influence the mean frequency of epileptiform activity. Injection of 7-NI decreased the mean frequency of epileptiform activity but did not influence amplitude. Ascorbic acid decreased both the mean frequency and amplitude of penicillin-induced epileptiform activity in rats. The application of l-NAME partially and temporarily reversed the anticonvulsant effects of ascorbic acid. The results support the hypothesis of neuro-protective role for NO and ascorbic acid. The protective effect of ascorbic acid against epileptiform activity was partially and temporarily reversed by nonspecific nitric oxide synthase inhibitor l-NAME, but not selective neuronal nitric oxide synthase inhibitor 7-NI, indicating that ascorbic acid needs endothelial-NOS/NO route to decrease penicillin-induced epileptiform activity.

Topics: Analysis of Variance; Animals; Antioxidants; Arginine; Ascorbic Acid; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Administration Schedule; Drug Interactions; Electroencephalography; Enzyme Inhibitors; Epilepsy; Free Radical Scavengers; Indazoles; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Synthase Type III; Penicillins; Rats; Rats, Wistar

The objective of the present study was to evaluate the neuroprotective effects of ascorbic acid (AA) in rats, against the neuronal damage and memory deficit caused by seizures. Wistar rats were treated with 0.9% saline (i.p., control group), ascorbic acid (500 mg/kg, i.p., AA group), pilocarpine (400 mg/kg, i.p., pilocarpine group), and the association of ascorbic acid (500 mg/kg, i.p.) plus pilocarpine (400 mg/kg, i.p.), 30 min before of administration of ascorbic acid (AA plus pilocarpine group). After the treatments all groups were observed for 24 h. Pilocarpine group presented seizures which progressed to status epilepticus in 75% of the animals. Pretreatment with AA led to a reduction of 50% of this rate. Results showed that pretreatment with AA did not alter reference memory when compared to a control group. In the working memory task, we observed a significant day's effect with important differences between control, pilocarpine and AA plus pilocarpine groups. Pilocarpine and AA plus pilocarpine groups had 81 and 16% of animals with brain injury, respectively. In the hippocampus of pilocarpine animals, it was detected an injury of 60%. As for the animals tested with AA plus pilocarpine, the hippocampal region of the group had a reduction of 43% in hippocampal lesion. Our findings suggest that seizures caused cognitive dysfunction and neuronal damage that might be related, at least in part, to the neurological problems presented by epileptic patients. AA can reverse cognitive dysfunction observed in rats with seizures as well as decrease neuronal injury in rat hippocampus.

Topics: Animals; Antioxidants; Ascorbic Acid; Epilepsy; Hippocampus; Male; Memory Disorders; Neurons; Pilocarpine; Rats; Rats, Wistar

Epilepsy is a symptom of cerebral dysfunction, where there is a sudden and disorganised discharge of electrical activity from a group of neurones, producing symptoms that range from sensory absences to convulsive movements and unconsciousness. Fasting is recognised as reducing the frequency of epileptic seizures in difficult to control patients. The ketogenic diet is a high fat, low carbohydrate and adequate protein diet that mimics the biochemical effects of fasting. It is deficient in some essential elements that require supplementation.. A 9-year old girl with learning difficulties, developmental delay and refractory epilepsy was placed on the ketogenic diet in 2003. Prior to starting the diet she had had as many as 12 tonic seizures/day, with prolonged periods of non-convulsive status epilepticus. Subsequent to being placed on the diet, the frequency of her seizures reduced markedly; there were long periods during which she had none. In late 2006, the patient inhaled a primary molar. This was retrieved by emergency bronchoscopy and at the same time the remaining primary teeth were extracted. Three weeks later she was admitted to hospital with low-grade fever, persistently bleeding sockets, oedema of her hands and feet, a petechial rash and bruising. A differential diagnosis included: liver disease, bleeding dyscrasia, oncological pathology or scurvy. The most striking finding amongst a number of investigations was a vitamin C level of 0.7 micromol/l (Deficiency: < 11 micromol/l). Accordingly a diagnosis of scurvy was made.. The patient was prescribed ascorbic acid 500 mg twice/day. Three weeks later the patient's vitamin C level was 141.5 micromol/l; the dose was therefore reduced to 250 mg once/day.. At two-month review, the signs and symptoms of scurvy had resolved.. Inhaling a tooth and scurvy are both rare occurrences. Paediatric dentists should be aware of the possible implications of a ketogenic diet.

Topics: Ascorbic Acid; Child; Diet, Ketogenic; Epilepsy; Female; Gingival Hemorrhage; Humans; Scurvy; Tooth Loss; Treatment Outcome

Epileptic seizure results from excessive discharge in a population of hyperexcitable neurons. A number of studies help to document the effects of active oxygen free radical scavengers such as alpha-tocopherol or ascorbic acid (vitamin C). In the present study, we examined the effects of ascorbic acid, at the six different doses, on penicillin-induced epileptiform activity.. A single microinjection of penicillin (2.5 microl, 500 units, intracortically) into the left sensorimotor cortex induced epileptiform activity within 2-5 min, progressing to full seizure activity lasting approximately 3-5 h. In the first set of experiments, 30 min after penicillin injection, six different doses of ascorbic acid (25, 50, 100, 200, 400, or 800 mg/kg) were administered intraperitoneally (IP). The other group of animals received the effective dose of ascorbic acid (100 mg/kg, IP) for 7 days. Ascorbic acid administration was stopped 24 h before penicillin treatment. Another group of rats received the effective dose of ascorbic acid (100 mg/kg, IP) 30 min before penicillin treatment. In the second set of experiments, the lipid peroxidation (MDA) and reduced glutathione (GSH) levels of brain were measured in the control, control + ascorbic acid, penicillin, and penicillin + ascorbic acid groups.. Ascorbic acid, at the low dose (50, 100 mg/kg, 30 min after penicillin injection), decreased both the frequency and amplitude of penicillin-induced epileptiform activity in rats. Ascorbic acid, at intermediate doses (200, 400 mg/kg, 30 min after penicillin injection), decreased the frequency of epileptiform activity without changing the amplitude. Ascorbic acid, at the lowest dose (25 mg/kg) and highest dose (800 mg/kg) (30 min after penicillin injection), did not change either the frequency or amplitude of epileptiform activity. Ascorbic acid, at the low dose (100 mg/kg) was the most effective dose in changing the frequency and amplitude of penicillin-induced epileptiform activity. Pretreatment with ascorbic acid (100 mg/kg) 30 min before penicillin treatment caused a significant delay in the onset of penicillin-induced epileptiform activity. Pretreatment with ascorbic acid (100 mg/kg) for 7 days did not change the latency of epileptiform activity. The most effective dose of ascorbic acid (100 mg/kg) prevented both the decrease in GSH level and the increase in lipid peroxidation level (MDA) occurring after penicillin-induced epileptiform activity.. These data indicate that ascorbic acid has neuroprotective activity against penicillin-induced epileptiform electrocorticogram activity.

Topics: Animals; Ascorbic Acid; Brain; Disease Models, Animal; Dose-Response Relationship, Drug; Electroencephalography; Epilepsy; Free Radical Scavengers; Glutathione; Injections, Intraperitoneal; Lipid Peroxidation; Male; Penicillins; Rats; Rats, Wistar

The aim of the study was to estimate the activity of chosen antioxidants in blood serum and saliva in patients with periodontal disease treated due to epilepsy.. Twenty-five epileptics and fifteen control persons were involved in the study. The activity of selected endogenous antioxidants were determined by spectrophotometric assay. Concentrations of vitamin A and vitamin E were measured using liquid chromatography.. The analysis of the serum and saliva from patients with overgrown gingiva revealed: reduced activity of superoxide dismutase, glutathione peroxidase and glutathione reductase, elevated lipid peroxides, and decreased concentration of ascorbic acid and alpha-tocopherol. All values were statistically significant.. Our results indicate on the oxidant-antioxidant disturbances in epileptic patients, which can play an important role in the pathomechanism of periodontal disease in these persons. Further studies on the role of antioxidants in patients with epilepsy treated with antiepileptic drugs and afflicted with gingival hyperplasia will be continued.

Topics: Adolescent; Adult; Aged; Antioxidants; Ascorbic Acid; Child; Epilepsy; Humans; Lipid Peroxides; Middle Aged; Periodontal Diseases; Saliva; Vitamin E

The specific role of endogenous glutathione in response to neuronal degeneration induced by trimethyltin (TMT) in the hippocampus was examined in rats. A single injection of TMT (8 mg/kg, i.p.) produced a rapid increase in the formation of hydroxyl radical and in the levels of malondialdehyde (MDA) and protein carbonyl. TMT-induced seizure activity significantly increased after this initial oxidative stress, and remained elevated for up to 2 weeks post-TMT. Although a significant loss of hippocampal Cornus Ammonis CA1, CA3 and CA4 neurons was observed at 3 weeks post-TMT, the elevation in the level of hydroxyl radicals, MDA, and protein carbonyl had returned to near-control levels at that time. In contrast, the ratio of reduced to oxidized glutathione remained significantly decreased at 3 weeks post-TMT, and the glutathione-like immunoreactivity of the pyramidal neurons was decreased. However glutathione-positive glia-like cells proliferated mainly in the CA1, CA3, and CA4 sectors and were intensely immunoreactive. Double labeling demonstrated the co-localization of glutathione-immunoreactive glia-like cells and reactive astrocytes, as indicated by immunostaining for glial fibrillary acidic protein. This suggests that astroglial cells were mobilized to synthesize glutathione in response to the TMT insult. The TMT-induced changes in glutathione-like immunoreactivity appear to be concurrent with changes in the expression levels of glutathione peroxidase and glutathione reductase. Ascorbate treatment significantly attenuated TMT-induced seizures, as well as the initial oxidative stress, impaired glutathione homeostasis, and neuronal degeneration in a dose-dependent manner. These results suggest that ascorbate is an effective neuroprotectant against TMT. The initial oxidative burden induced by TMT may be a causal factor in the generation of seizures, prolonged disturbance of endogenous glutathione homeostasis, and consequent neuronal degeneration.

Topics: Animals; Antioxidants; Ascorbic Acid; Astrocytes; Dose-Response Relationship, Drug; Drug Interactions; Epilepsy; Glial Fibrillary Acidic Protein; Glutathione; Glutathione Disulfide; Hippocampus; Homeostasis; Hydroxyl Radical; Malondialdehyde; Nerve Degeneration; Neurons; Oxidative Stress; Rats; Rats, Sprague-Dawley; Trimethyltin Compounds

Magne-B6 was used, together with anticonvulsive therapy, in the treatment of 25 patients with different forms of epilepsy. In all cases, psychiatric status of patients featured by depression, anxiety and some psychotic sighs. The drug was prescribed in the mean therapeutic dose during 28 days. Along with psychopathologic examination, a psychometric method, using self-rating scales for Zung anxiety and depression scale, SCL-90 and Global clinical impression (CGI) scale, was administered. Magne-B6 exerted a positive non-specific influence on patient's mental state, especially with regard to affective disorders. The positive effect of the drug emerged on 14th day of the treatment and achieved a statistically significant level to 28th day. The medication was more effective in asthenic and subdepressive syndromes, in encephalopathic syndrome the efficacy was lower. The drug was well tolerated and did not cause any side effects.

Topics: Adult; Anxiety Disorders; Ascorbic Acid; Data Interpretation, Statistical; Depression; Drug Combinations; Epilepsy; Female; Humans; Magnesium; Male; Middle Aged; Time Factors; Treatment Outcome; Vitamin B 6

Scurvy has been known since ancient times, but the discovery of the link between the dietary deficiency of ascorbic acid and scurvy has dramatically reduced its incidence over the past half-century. Sporadic reports of scurvy still occur, primarily in elderly, isolated individuals with alcoholism. The incidence of scurvy in the pediatric population is very uncommon, and it is usually seen in children with severely restricted diets attributable to psychiatric or developmental problems. The condition is characterized by perifollicular petechiae and bruising, gingival inflammation and bleeding, and, in children, bone disease. We describe a case of scurvy in a 9-year-old developmentally delayed girl who had a diet markedly deficient in vitamin C resulting from extremely limited food preferences. She presented with debilitating bone pain, inflammatory gingival disease, perifollicular hyperkeratosis, and purpura. Severe hypertension without another apparent secondary cause was also present, which has been previously undescribed. The signs of scurvy and hypertension resolved after treatment with vitamin C. The diagnosis of scurvy is made on clinical and radiographic grounds, and may be supported by finding reduced levels of vitamin C in serum or buffy-coat leukocytes. The response to vitamin C is dramatic. Clinicians should be aware of this potentially fatal but easily curable condition that is still occasionally encountered among children.

Topics: Ascorbic Acid; Ascorbic Acid Deficiency; Child; Developmental Disabilities; Diet; Epilepsy; Female; Fruit; Humans; Knee Joint; Magnetic Resonance Imaging; Radiography; Scurvy

Penfield proposed that the meningocerebral scar that forms following trauma to the brain plays an important role in the development of posttraumatic epilepsy. Although the epileptogenic scar has come to be widely accepted as a cause of epilepsy, there is no direct evidence that scar formation contributes to epileptogenesis. This current study showed that procedures that control the development of collagen in a fibroblastic scar may modify the development of epilepsy. Epilepsy induced in the guinea pig by injection of metallic aluminum powder into the cerebral cortex was used as a model of posttraumatic epilepsy. Following application of aluminum and implantation of epidural electrodes, animals received either daily injections of prednisolone or an ascorbic acid-deficient diet to block scar formation. Control animals also had an injection of aluminum, but afterward received saline injections or a normal diet. Control animals developed epileptic spikes and often exhibited focal seizures. All manifestations of epileptogenesis were markedly reduced in animals treated with prednisolone or the ascorbic acid-deficient diet. The reduction in epileptiform activity corresponded to reduced collagenous scar formation in the treated animals. Although effective when given prophylactically, prednisolone did not inhibit the activity of an already established epileptic focus whether induced by aluminum or by amygdala kindling, nor did it block pentylenetetrazol-induced seizures. The finding that epileptogenesis is blocked by two procedures that inhibit scar formation but show no evidence of a direct anticonvulsant effect, suggests that scar formation is a significant factor in epileptogenesis induced by metallic aluminum. The collagenous component appears to be more significant than the glial component of the scar.

Topics: Action Potentials; Aluminum Oxide; Animals; Ascorbic Acid; Brain; Cicatrix; Collagen; Electroencephalography; Epilepsy; Fibroblasts; Glial Fibrillary Acidic Protein; Guinea Pigs; Kindling, Neurologic; Male; Prednisolone

Topics: Ascorbic Acid; Epilepsy; Humans; Phenobarbital; Phenytoin; Primidone

1. Forty-eight children, who were long-term hospital patients, were investigated to assess their leucocyte ascorbic acid status. 2. Twenty-nine children had been receiving long-term anticonvulsants therapy, and these children did not have a significantly lower level of ascorbic acid than the untreated group, which did not have epilepsy. 3. The ascorbic levels of all subjects were low and seventeen had levels between 7-3 and 16-o mug/10-8 white blood cells.

Topics: Adolescent; Anticonvulsants; Ascorbic Acid; Child; Child, Preschool; Diet; Epilepsy; Humans; Leukocytes; Time Factors

Topics: Ascorbic Acid; Epilepsy; Vitamins