Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Valproic acid is a branched-chained fatty acid, structurally unrelated to any other antiepileptic drug. Since publication of the original review in the Journal in 1977, several clinical trials have documented its efficacy and safety in adults and children for the treatment of generalised seizures (absence, tonic-clonic, myoclonic), partial seizures (simple, complex, secondarily generalised) and compound/combination seizures (including those refractory to treatment with other antiepileptic drugs). Valproic acid monotherapy has demonstrated efficacy equivalent to that of carbamazepine, phenytoin, and phenobarbital in the treatment of both generalised and partial seizures and ethosuximide in the treatment of absence seizures. Adverse effects associated with the drug are primarily gastrointestinal (nausea, vomiting, dyspepsia) in nature, although the use of enteric-coated formulations has reduced the incidence of abdominal discomfort. Weight gain, tremor and transient hair loss are commonly reported. Importantly, valproic acid has minimal neurological adverse effects (sedation, ataxia, impairment of cognitive function) compared with other antiepileptic drugs, a finding that may be of particular relevance in many patients with epilepsy. The incidence of rare, fatal liver failure has been greatly reduced by identifying and avoiding administration of valproic acid to high risk patient populations. An estimated risk of 1 to 2% for neural tube defects, predominantly spina bifida aperta, with maternal use of valproic acid therapy has been reported. Valproic acid inhibits hepatic drug metabolism and displaces other highly bound drugs from their plasma protein binding sites. Therefore, coadministered drugs which are highly protein bound or hepatically metabolised may require dosage adjustment. Enzyme-inducing antiepileptic drugs may increase valproic acid metabolism and necessitate increasing its dosage. Thus, comparative trials and extensive clinical experience have demonstrated the efficacy and tolerability of valproic acid and support its role as a valuable and well established first-line treatment for patients with a broad range of seizure types.
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PMID:Valproic acid. A reappraisal of its pharmacological properties and clinical efficacy in epilepsy. 751 5

This multicenter, open-label trial was designed to study the safety of intravenous (IV) sodium valproate in patients with epilepsy. All 318 patients (previously treated with antiepileptic drugs) were hospitalized for seizure control or anticipated seizures. The protocol allowed physicians to set the number of infusions and treatment duration. Adverse events, laboratory studies performed, and seizure activity were documented on case report forms. The patients' mean age was 34.4 years (range, 2-87 years). The most common reason for admission was lack of seizure control (235 patients, 185 of whom were admitted for video-electroencephalographic monitoring). The median dosage of valproate was 375 mg infused over 1 hour. The median number of doses was four, given over 2 days. In 54 patients (17%), transient adverse events were reported. The most frequent were headache, reaction at the injection site, and nausea (2.2% each); somnolence (1.9%); vomiting (1.6%); and dizziness and taste perversion (1.3% each). No persistent or severe hematologic or serum chemistry abnormalities were found. Vital signs were not significantly affected by the IV infusion of valproate. At the dosages and rates of administration studied, intravenous valproate appears to be safe and well tolerated.
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PMID:Safety of intravenous valproate. 757 66

Vomiting in infants can be caused by a wide variety of neurological disorders. All involve stimulation of a central pattern generator for vomiting located in the brainstem, the nucleus tractus solitarius. This, in turn, projects to multiple motor nuclei involved in the vomiting reflex. The chemoreceptor trigger zone (the area postrema) in the floor of the fourth ventricle is a major afferent to the nucleus tractus solitarius that can be stimulated by pressure from hydrocephalus, closed head injuries, or tumors. Other neurological causes of vomiting discussed include migraine, epilepsy, and dysautonomia. The treatment of vomiting associated with nervous system disease may be very difficult unless the condition is acute and readily reversible.
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PMID:Disorders of the central and autonomic nervous systems as a cause for emesis in infants. 758 85

We studied 10 neurologically normal patients (8 females, 2 males) aged 8-30 years (mean 17 years) who had recurrent episodes if visually induced occipital seizures. Television and computer screens were the main triggers. Seizure onset occurred between the ages of 5 and 17 years (mean 11 years). All seizures were stimulus related and began with elementary visual symptoms, followed in most patients by a slow clustering of cephalic pain, epigastric discomfort, and vomiting, with either normal of only mildly impaired responsiveness. EEG features included normal background activity, occipital spikes and waves, and a photoparoxysmal response which could be occipital, generalized, or both. Four patients also showed spontaneous generalized epileptiform abnormalities, and 3 had rolandic spikes. An Oz electrode was critical in identifying epileptiform activity in some patients. Complete seizure control was achieved in most patients with monotherapy, although occasional stimulus-related seizures occurred in 3 patients who showed a wider range of photosensitivity. These patients have an idiopathic localization-related epilepsy with age-related onset and specific mode of precipitation. Although this type of epilepsy has been reported previously, it has remained underrecognized, probably because it is difficult to differentiate clinically from migraine or from nonreflex childhood idiopathic occipital epilepsy.
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PMID:Idiopathic photosensitive occipital lobe epilepsy. 764 27

Felbamate is currently being developed as an antiepileptic agent. Although its mechanism of action has yet to be fully elucidated, felbamate appears to inhibit both the spread of seizures and increase seizure threshold in animal models. Data available in the clinical setting provide evidence that, at doses of up to 3600 mg/day as an adjunct to existing antiepileptic therapy or as monotherapy following substitution for other medications, the drug reduces the frequency of partial onset seizures in adult patients refractory to conventional antiepileptic treatments. Felbamate is also effective in the treatment of Lennox-Gastaut syndrome in children, a severe epilepsy which is usually refractory to antiepileptic agents. The effect of felbamate in the treatment of generalised tonic-clonic seizures in adults with partial onset seizures which are secondarily generalised is promising but requires clarification in large-scale trials. The most common adverse effects occurring during administration of felbamate are mild to moderate gastrointestinal (nausea, vomiting and anorexia) and central nervous system (headache, somnolence, diplopia, dizziness and insomnia) disturbances. Drug interactions with other antiepileptic agents may prove problematic in terms of adverse effects. Thus, at this stage of its development, the antiepileptic efficacy of felbamate in treatment-refractory patients with partial onset seizures and Lennox-Gastaut syndrome has been proven but efficacy in generalised tonic-clonic seizures requires further substantiation in large well controlled and well designed clinical trials. In addition, a more comprehensive base of comparative clinical trials data is necessary to further clarify issues of relative efficacy and tolerability compared with other antiepileptic agents. The clinical implications of the drug interactions associated with felbamate also require more detailed investigation. These data will be awaited with interest and when available will help to place felbamate in perspective in the management of epilepsy.
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PMID:Felbamate. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy in epilepsy. 769 93

Abdominal epilepsy is a rare cause of abdominal pain. We report an adult patient with intermittent, paroxysmal epigastric abdominal pain, accompanied by nausea, vomiting, restlessness and anxiety. Physical examination was normal. Blood analysis disclosed only leucocytosis with neutrophilia. X ray examinations, ultrasound and CT abdominal scan, mesenteric arteriography and exploratory laparotomy did not show evidence of pathology. The electroencephalogram (EEG) showed bilateral theta slow activity during hyperventilation. We started treatment with carbamazepine and the patient remained asymptomatic for nine months. However he had a relapse because he did'nt take his medication regularly. At that time the serum levels of carbamazepine were low. The EEG showed bursts of diffuse paroxysmal acute waves. Once therapeutic serum levels of carbamazepine were achieved the pain disappeared. He has remained asymptomatic during the last twelve months, while taking his treatment regularly.
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PMID:[Abdominal epilepsy in the adult]. 770 24

We analyzed 91 psychomotor seizures from 31 patients seizure free at least one year after temporal lobectomy (implying temporal lobe onset). Fifty symptoms were looked for in every seizure and their time of onset and ending noted. Statistical analysis was used to define symptom clusters and the order of appearance of symptoms. Of the eighteen most common symptoms examined, all of these symptoms form a tight cluster showing a high degree of correlation. Within this cluster, there was a tendency towards the following subclusters: (a) epigastric aura, ictal vomiting, alimentary and hand automatisms; (b) behavioral arrest, complete loss of consciousness, staring and bilateral facial contraction; (c) unilateral dystonic posturing of an arm, mimetic automatisms, complex gestures, ictal speech and partial loss of consciousness; (d) looking around, agitation, vocalizations and whole body movements. We also found a strong correlation between epigastric sensation and ictal vomiting in psychomotor seizures arising from the right but not the left temporal lobe. The commonest sequence of symptoms was: behavioral arrest followed by alimentary and hand automatisms, looking around and whole body movements, in that order.
Epilepsy Res 1995 Jan
PMID:Psychomotor seizures of temporal lobe onset: analysis of symptom clusters and sequences. 771 60

A suppository for rectal administration of carbamazepine has been developed for situations in which it is unsuitable to use the oral route of administration. In an open, controlled, within-patient study, the pharmacokinetics, clinical efficacy, and tolerability of carbamazepine slow-release tablets were compared with those of carbamazepine suppositories in children with epilepsy. The pharmacokinetic part of the study comprised 22 children, and an additional nine children were included in the clinical part of the study. Treatment with slow-release tablets was replaced for 7 days with carbamazepine suppositories in bioequivalent dosage. Clinical factors such as the rate of seizures and the local tolerability were studied, and an overall assessment of efficacy was made. In the pharmacokinetic part, 24-hour plasma concentration curves for carbamazepine and carbamazepine-10,11-epoxide were recorded. The plasma concentration profiles (minimum, maximum, and mean concentrations, fluctuation index, and area under the curve) for carbamazepine and the other metabolites did not show any significant differences between oral and rectal administration when the suppository dose was increased by 25% compared to the tablets. No increase in seizure frequency was detected, and the overall assessment was very good to good in 25 of the 29 epileptic children. Increased flatulence during treatment with suppositories was noted in two children, one had anal irritation, and one had nausea/vomiting. Treatment with carbamazepine slow-release tablets in children with epilepsy can be replaced by carbamazepine suppositories in 25% higher dosage, with good clinical effect and appropriate pharmacokinetic values, when it is unsuitable to use the common oral route of administration.
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PMID:Replacing carbamazepine slow-release tablets with carbamazepine suppositories: a pharmacokinetic and clinical study in children with epilepsy. 778

We describe the development of temporal lobe epilepsy in an 84-year-old man who had suffered domoic acid intoxication. Following intoxication he had nausea, vomiting, confusion, and coma. Generalized convulsions and complex partial status epilepticus progressively developed. After 3 weeks he improved and was seizure free with severe residual memory deficit. Electroencephalograms initially showed periodic epileptiform discharges, later evolving to epileptic abnormalities over frontotemporal regions with diffuse slow waves. Eight months after the intoxication the electroencephalogram was normal. One year after the acute episode, complex partial seizures developed. Electroencephalograms showed epileptic discharges independently over both temporal lobes, with left-sided predominance. Magnetic resonance imaging revealed a hyperintense T2-weighted signal and atrophy of both hippocampi; a positron emission tomographic scan showed bitemporal decreased glucose metabolism. Pneumonia developed and the patient died 3 1/4 years after the intoxication. Autopsy disclosed severe bilateral hippocampal sclerosis. The seizures following acute domoic acid intoxication, the postmortem pathology, and the fact that temporal lobe epilepsy developed 1 year after intoxication indicate that the human hippocampus is also vulnerable to kainate receptor excitotoxicity, and provide strong evidence supporting the role of excitotoxic injury in epileptogenesis. This report provides a unique human parallel to, and validates the animal model of, kainate-induced epilepsy as an important tool for studying temporal lobe epilepsy.
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PMID:Temporal lobe epilepsy caused by domoic acid intoxication: evidence for glutamate receptor-mediated excitotoxicity in humans. 781 46

Sixty-one refractory epileptic patients (46 with partial epilepsy) were treated with intravenous immunoglobulins in a controlled double-blind/dose finding clinical trial; 18 (7 females, mean age 18.5 years) received placebo, while 14 (3 females, mean age 26.2 years, 2 excluded), 14 (4 females, mean age 24.6 years, 1 excluded) and 15 (5 females, mean age 24.4 years) patients received 100, 250 and 400 mg/kg per infusion of intravenous immunoglobulins, respectively. Seven perfusions were scheduled, four the 1st week, and thereafter one during the 2nd, 3rd and 6th week. The patients were followed for 6 months. An optional infusion was given at the end of the study. A comparison of the mean number of seizures per day was made between the baseline (4 weeks before the first infusion) and the 6th month after the first infusion. Patients were considered responders if they had a decrease of at least 50% in daily seizure frequency at the end of the study compared with the baseline. We did not find severe adverse events. One patient had to stop infusions for possible related side effects (vomiting). When all patients were analyzed together, we found a positive trend in favor of intravenous immunoglobulin treatment, but this was not significant (P = 0.095). There was no relationship between dose and efficacy (P = 0.31). When the largest group with partial epilepsy was analyzed separately, we noted 19 responders in the test group, compared with 2 in the placebo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of refractory epilepsy with intravenous immunoglobulins. Results of the first double-blind/dose finding clinical study. 781 96


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