Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied 10 patients with intractable epilepsy being evaluated for epilepsy surgery for preictal changes in spiking. All patients were implanted with intracranial electrodes and underwent continuous EEG/audiovisual monitoring. Interictal spikes were detected and recorded continuously by a dedicated computerized system. Edited spikes were counted during 0-5, 5-10, and 0-60 min epochs before each seizure, during epochs of unvarying state of arousal (awake or sleep stage II). When comparing by repeated measures, 1-way ANOVA, total spiking (in all recording channels) did not differ among the different preictal epochs (0-5, 5-10, 0-60 min) in 45 seizures (F = 0.88, P = 0.40, using the Geisser-Greenhouse adjustment--GGA). Likewise, no significant differences were obtained during those same epochs when comparing spiking originating from the channel of seizure onset in 5 patients with 28 seizures of localized onset (F = 1.19, P = 0.38 using the GGA). Our findings indicate that in patients with intractable epilepsy, no changes in spiking occur in the 5 min prior to seizures, when compared to more distant preictal epochs.
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PMID:Does interictal spiking change prior to seizures? 171 30

Seventy patients aged from one month to 18 years with seizure disorders were classified into three groups: I. Patients who had hard control seizure attacks even under medication; II. those who had occasional seizure attacks (less than 6 times per year) and III. those who had no seizure attacks after receiving medication for at least one year. Blood samples were taken for somatostatin, substance P, prolactin and vasoactive intestinal peptide (VIP) assays. Lumbar puncture was made in 32 children and CSF samples were also assayed for neuropeptides. Somatostatin levels in serum were significantly elevated in group I and group II (P = 0.05, ANOVA) but not in group III and control group. Similar observations were made in substance P, prolactin and VIP studies. In CSF, the somatostation can better indicate the difference between epileptic and normal children (comparison with group I, P greater than 0.001; with group II, P less than 0.001; even with those who were seizure free after medication, P less than 0.05). In conclusion, the levels of several neuropeptides (somatostatin, substance P. prolactin, VIP) were elevated in children with seizure disorders both in serum and CSF. The present investigation provides a new category for the understanding of the pathogenesis, treatment as well as prognosis of seizure disorders.
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PMID:Somatostatin, substance P, prolactin and vasoactive intestinal peptide levels in serum and cerebrospinal fluid of children with seizure disorders. 171 68

Electroencephalographic (EEG) seizures were measured in rats after intrahippocampal injection of 120 nmol quinolinic acid into the stratum radiatum CA1 or 0.19 nmol kainic acid in the dentate gyrus or in the stratum radiatum. Injection of 5 micrograms SMS 201-995, a peptidase-resistant cyclic octapeptide analogue of somatostatin, into the stratum radiatum, 15 min before quinolinic acid, did not significantly modify the number of seizures and the total time in seizures. Five micrograms SMS 201-995 injected into the stratum radiatum reduced the number of seizures induced by kainic acid in the same area and the total time spent in seizures by 58% and 75%, respectively (Student's t-test; P less than 0.01). In both instances the latency to the first ictal episode was not significantly modified. Lesions of the medial septum, which reduced the activity of choline-o-acetyl-transferase (CAT) in the dorsal hippocampus by greater than 90% after one week did not significantly affect seizures induced by quinolinic acid. In rats lesioned in the medial septum, 5 micrograms SMS 201-995 reduced the total time spent in seizures by 43%, without changing the number of ictal episodes and raised the latency to the first quinolinic acid-induced seizure by 53% (ANOVA 2 x 2, P less than 0.05) but had no effect on these measures in the corresponding sham-operated group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A peptidase-resistant cyclic octapeptide analogue of somatostatin (SMS 201-995) modulates seizures induced by quinolinic and kainic acids differently in the rat hippocampus. 183 Jan 35

An animal model with four well defined endpoints for studying the cardiotoxicity and neurotoxicity of bupivacaine is described. Five male Wistar rats (264-324 g) were anesthetized, tracheostomized and ventilated, and ECG and EEG leads were placed. Femoral arteries and veins were then cannulated. Twenty minutes before bupivacaine infusion, 0.1 mg/kg pancuronium was given intravenously, and anesthesia was adjusted to halothane 0.5%, 30% O2 and 70% N2O. Bupivacaine infusion was then begun at 2 mg/kg/minute. Bupivacaine doses producing the following endpoints were then determined: (1) first ventricular arrhythmia (ARR), (2) seizures (SZ), (3) isoelectric EEG (ISO EEG), and (4) asystole (ASYS). The doses of bupivacaine (in mg/kg +/- SD) precipitating AAR, SZ, ISO EEG and ASYS were 4.22 +/- 1.87, 7.08 +/- 1.55, 11.05 +/- 5.15 and 20.4 +/- 6.49 mg/kg, respectively. These endpoints were present and readily determined in all animals. The doses of bupivacaine producing ARR and SZ were not significantly different (p greater than 0.05). The doses producing SZ, ISO EEG and ASYS were significantly different from each other (p greater than 0.05, ANOVA and the Duncan test). These results indicate that it is possible to study, in the anesthetized and paralyzed rat that is intensely monitored, many of the variables associated with local anesthetic toxicity currently of clinical interest. The use of a constant local anesthetic infusion allows ready observation of the progression of toxic signs.
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PMID:A rodent model for studying four well defined toxic endpoints during bupivacaine infusion. 191 99

Avoidance of homologous blood products and patients' demand for preoperative autologous blood donation programs are increasing. As many of these patients are older, with a compromised cardiovascular system and a slow response of the erythropoietic system when anemia occurs, the feasibility and benefit of autologous blood donation is often limited. Augmentation of preoperative blood donation by therapy with recombinant human erythropoietin (rHuEPO) has been described in animal models and in patients. METHODS. In a multicenter, controlled, randomized trial, 49 patients scheduled for orthopaedic or vascular surgery received 0 (control group, n = 9), 200 (n = 10), 300 (n = 11), 400 (n = 10) or 500 (n = 9) U/kg rHuEPO (Erypo, Cilag, Sulzbach, distributor Fresenius, Oberursel, Germany) subcutaneously twice a week for 3 weeks while every week 450 ml blood was collected. Iron sulphate 100 mg was prescribed orally twice a day. Patients were ineligible if they had uncontrolled hypertension, recent myocardial infarction, haematological disorders or a history of seizures. Blood donation had to be cancelled if the haematocrit was below 30%. RESULTS. There was a significant (ANOVA) drop of the haematocrit value only in the control group, and end-point values for haematocrit and haemoglobin were significantly elevated in the 400 and 500 U/kg groups compared with the control group (Table 9). DISCUSSION. The erythropoietic stimulus of phlebotomy for autologous blood donations is often not efficient enough to guarantee a constant haematocrit. Lowering of the preoperative haematocrit jeopardizes the aim of avoidance of homologous blood transfusions. rHuEPO increased the efficiency of autologous blood collections, as predonation haematocrit values could be preserved in the high-dosage groups. As a consequence, homologous transfusions could be avoided. However, there were broad interindividual differences in the erythropoietic response, possibly due to limitations in iron availability. Adverse effects of rHuEPO therapy, such as hypertension, thrombosis or neurologic disorders, are mostly reported in patients with terminal kidney failure. No such disturbances were observed in the present study. CONCLUSION. rHuEPO ameliorates the preoperative decrease of haemoglobin and haematocrit values due to autologous blood donations in a dose-related fashion. The individually adjusted dosage of rHuEPO and iron supplementation merits further investigation.
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PMID:[Erythropoietin therapy during frequent autologous blood donations. Dose-finding study]. 748 23

Having a seizure in public is a concern to people with epilepsy and can represent a barrier to psychosocial adjustment. Seeing his or her own seizures might help the patient deal with seizures more realistically, but also could be emotionally detrimental. We therefore showed patients videos of their own seizures before their discharge from our inpatient epilepsy monitoring unit. One of the investigators was present to answer questions. The Spielberger State Trait Anxiety Scale (SSTAS) was administered before and after viewing and 1 month later together with a questionnaire related to the patients' feelings and attitudes about viewing their own seizures. Results using one-way repeated-measures multivariate analysis of variance (MANOVA) showed no differences for the items in the pre- and posttest questionnaire. For the SSTAS, no significant differences were detected among the pretest and the two posttests by one-way repeated ANOVA (p = 0.10). These results suggest that it is not harmful to view one's own seizures in a controlled setting.
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PMID:It is not harmful for patients with epilepsy to view their own seizures. 758 59

Febrile convulsions (FC) are frequent acute neurologic disturbances of childhood. The cellular and neurochemical mechanisms causing FC are unclear. Among other mechanisms, the CNS histamine (HA) has been suggested to participate in seizure control and thermoregulation. We evaluated the possible role of HA in regulation of FC by measuring HA and tele-methylhistamine (t-MH) concentrations in the cerebrospinal fluid (CSF) of children with FC. The study group consisted of 35 children treated for acute FC in the hospital. The control groups consisted of (a) feverish children without seizures (n = 23), (b) convulsive children without fever (n = 7), and (c) children with neither fever nor convulsions (n = 21). HA was assayed by high-performance liquid chromatography (HPLC) with fluorescence detection, and t-MH was measured by gas chromatography-mass spectrometry. CSF HA concentration in the group of febrile children without seizures was significantly higher (0.69 +/- 0.16 pmol/ml, mean +/- SE) than in children with FC (0.36 +/- 0.07 pmol/ml, p < 0.05, analysis of variance, ANOVA). HA concentration was 0.37 +/- 0.18 pmol/ml in the group of nonfebrile convulsive children and 0.36 +/- 0.08 pmol/ml in the nonfebrile nonconvulsive group. No statistical differences in t-MH were detected between groups. The increased susceptibility to seizures during fever may be connected to the lack of increase in CSF HA in the FC group. The data support the hypothesis that the central histaminergic neuron system may be involved in inhibition of seizures associated with febrile illnesses in childhood.
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PMID:Histamine in cerebrospinal fluid of children with febrile convulsions. 761 12

The potency of S-(+)-ketamine is approximately double that of the racemic ketamine. This study was carried out to investigate the recovery of cerebral electrical function after a bolus of 1.3 mg/kg ketamine or 0.65 mg/kg S-(+)-ketamine and subsequent continuous application of 4 mg/kg h ketamine per h or 2 mg/kg S-(+)-ketamine, per h for 15 min. Furthermore, the centrally acting, cholinergic agonist physostigmine has been reported to antagonize ketamine and to shorten the recovery period. Therefore, after S-(+)-ketamine 0.012 mg/kg physostigmine was tested against saline placebo. METHODS. With their own informed consent and the approval of the ethics committee 12 healthy volunteers were enrolled in a double-blind cross-over study. All drugs were dissolved in identical volumes. On three dates with intervals of at least 1 week between, ketamine/NaCl, S-(+)-ketamine/physostigmine or S-(+)-ketamine/NaCl was administered (Table 1). The sequence was randomized. The EEG was recorded from 20 sites according to the 10/20 system and after Fast-Fourier transformation computed into amplitudes within the delta, theta, alpha, and beta bands and within the total spectrum. The median, the spectral edge frequency and the dominant frequency (dF) were also determined. Mean values of all electrodes before and at 10, 15, 30, 45 and 195 min after the bolus injection were compared using two-dimensional analysis of variance (ANOVA, significance level P < 0.05). RESULTS. The characteristic increase in theta-amplitude and decrease of alpha-amplitude were observed after ketamine and S-(+)-ketamine. Median and dF dropped from the alpha to the theta frequency range. Ketamine led to a greater increase in total, delta, theta and beta amplitude during anaesthesia. 3 hours after ketamine/S-(+)-ketamine anaesthesia a significant decrease in the median and dominant frequency and in total, delta, theta, alpha and beta amplitudes confirmed residual impairment of cerebral function after all study drugs. No differences were found between physostigmine and placebo. DISCUSSION. The EEG changes during ketamine/S-(+)-ketamine administration suggest a slightly deeper anaesthetic level after ketamine. The course of recovery was not different after ketamine and after S-(+)-ketamine. The spectral edge frequency did not differ between measurement points, and is therefore not suitable for assessment of the depth of anaesthesia reached with ketamine/S-(+)-ketamine. The dose of physostigmine tested was probably too low to produce antagonism of S-(+)-ketamine. An increased dosage of physostigmine has yet to be studied, but is likely to cause a higher rate of side effects, such as nausea, vomiting and bradycardia, and possibly even tonic-clonic seizures.
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PMID:[Ketamine racemate versus S-(+)-ketamine with or without antagonism with physostigmine. A quantitative EEG study on volunteers]. 784 Apr 18

A retrospective study was carried out to determine whether a prior cerebral injury or medical illness was associated with hippocampal sclerosis in intractable, surgically treated temporal lobe epilepsy (TLE), or whether there was evidence for progressive hippocampal neuron damage from repeated seizures. Temporal lobe epilepsy patients (n = 162) from one epilepsy centre were retrospectively and blindly catalogued into groups based on the presence or absence of an initial precipitating injury (IPI) and whether, when an IPI was present, it had involved seizures (independent variables). Patients were catalogued into four groups: (i) non-seizure IPIs (Group A; n = 54); (ii) IPIs with a prolonged seizure (Group B; n = 66); (iii) IPIs with repetitive non-prolonged seizures (Group C; n = 20); (iv) or no IPIs and idiopathic TLE (Group D; n = 22). The dependent variables were: the differences in the time course of clinical seizures, and quantified hippocampal neuron counts and seizure outcomes. Statistically significant (ANOVA at least P < 0.05) results showed the following. (i) Patients with IPIs (Groups A, B and C) had hippocampal sclerosis, while those with idiopathic TLE (Group D) showed fewer neuron losses and worse post-resection seizure relief. (ii) Patients with non-seizure IPIs (Group A) were on average older at injury; had a longer latent period; showed less neuron losses in Ammon's horn, CA1 and prosubiculum than seizure associated IPIs (Groups B and/or C). (iii) Initial precipitating injury patients with repetitive non-prolonged seizures (Group C) showed the shortest latent period, earliest age of TLE onset, and less CA2 damage than the other IPI groups. Other findings that were statistically significant by analysis of covariance along with the IPI category included the following. (i) CA1 (P = 0.0097) and prosubiculum (P = 0.0089) neuron losses were greater in patients when their TLE was longer than 22 years. (ii) IPIs after age 4 years were associated with latent periods shorter than 10 years compared with variable and longer latent periods of IPIs before age 4 years (P = 0.0015). These results indicate that in surgically treated TLE, hippocampal sclerosis and good seizure outcomes are associated with IPIs. Most of the hippocampal damage found at surgery and the clinical time course of the habitual TLE are influenced by the pathogenic IPI mechanism. However, some secondary neuron losses were associated with longer TLE seizure histories.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The clinical-pathogenic mechanisms of hippocampal neuron loss and surgical outcomes in temporal lobe epilepsy. 789 97

We assessed the relationship between temporal lobe metabolism measured quantitatively and qualitatively with PET using [18F]-fluorodeoxyglucose (FDG) and postoperative seizure frequency after anterior temporal lobectomy. Forty-three patients with refractory partial epilepsy had anterior temporal lobectomy and preoperative assessment with PET-FDG. Qualitative PET analysis was performed visually by two blinded observers, and quantitative PET analysis was performed using an anatomic template for six control and six temporal lobe subregions, deriving an asymmetry index for each region. Seizure outcome was assessed 1 year after surgery; patients were classified as being seizure-free or as having persistent seizures. Qualitative data were analyzed using Fisher's exact test and the t test, and quantitative data were analyzed using a repeated-measures ANOVA. Thirty-two patients (74%) were seizure-free at follow-up, and 11 had persistent seizures, although most improved. Twenty-nine of 35 patients (83%) with restricted temporal lobe hypometabolism by visual analysis were seizure-free, compared with three of eight patients (37.5%) with normal scans or multilobar hypometabolism. Quantitative analysis revealed that an asymmetry of mesial temporal lobe glucose consumption (uncal region) correlated with improved surgical outcome (p < 0.02). We developed a logistic regression model to predict individual outcome based on the asymmetry in uncal metabolism. Lateral temporal metabolism did not correlate with outcome. We conclude that both visual PET analysis and quantitative PET analysis predict outcome after temporal lobectomy, although quantitative measures offer more precise information.
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PMID:Predictors of outcome after anterior temporal lobectomy: positron emission tomography. 799 Nov 21


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