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)

Previous studies have shown that potassium-evoked, calcium-dependent, endogenous aspartate release is greater from hippocampal slices of adult epileptic (EL) mice than from nonepileptic control C57BL/6J (B6) mice. To examine further the association between epilepsy and enhanced aspartate release in EL mice, endogenous neurotransmitter release from hippocampal slices was studied in young, seizure-free EL mice and in two nonseizure control mouse strains, DDY and B6. DDY is the parental strain from which EL arose, and it has a genetic background similar to EL. Released amino acid neurotransmitters were quantitated by HPLC with fluorescent detection and were expressed as picomoles of amino acid released per minute of incubation per slice +/- SEM. Aspartate release was significantly higher in EL mice (15.8 +/- 0.8) than in either the control B6 or DDY mice (8.5 +/- 1.4 and 8.4 +/- 1.7, respectively). No significant differences were found among the B6, DDY, and EL mice for the release of glutamate (23.0 +/- 2.0, 32.3 +/- 5.8, and 25.9 +/- 2.6, respectively) or GABA (23.5 +/- 0.7, 19.5 +/- 3.2, and 21.8 +/- 3.2, respectively). Thus, enhanced aspartate release precedes the onset of EL seizures and may be related to the cause rather than to the effects of seizure activity.
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PMID:Enhanced aspartate release related to epilepsy in (EL) mice. 791 88

Progesterone increases cocaine's cardiovascular toxicity in sheep and rats. To determine whether progesterone enhances the lethality of cocaine, nonpregnant female rats were treated with either IM progesterone (P4) or vehicle, and pregnant rats (Preg) were untreated. The rats received one IP injection of cocaine at a dose between 25-75 mg/kg and were observed for seizures and/or death. All 62 rats that died did so within 17 min, preceded by seizures in 90.3%. Mean times-to-seizure and times-to-death, and mean lethal serum cocaine concentrations did not differ among groups. Serum progesterone levels (ng/ml +/- SEM) at the time of death were different among groups: 24 +/- 1.7 (C), 102 +/- 6.4 (P4), and 139 +/- 5.2 (Preg). Logistic regression dose/fatality curves, LD50s, and LD10s for the pregnant, progesterone, and control groups were not significantly different from one another. Though progesterone has enhanced cocaine's cardiac toxicity in some studies, it does not increase the risk of death from acute cocaine exposure in rats.
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PMID:Cocaine LD50 in Long-Evans rats is not altered by pregnancy or progesterone. 793 64

A study of 72 alcoholics, hospitalized for alcohol withdrawal syndrome, was undertaken to determine the incidence of seizures, their relationship with other withdrawal symptoms, the presence of brain atrophy and the relationship of this last with withdrawal intensity severity. Sixty-seven (93%) were male and the mean age was 44.9 +/- 1.3 (mean +/- SEM) years. Thirty-three (46%) of the 72 patients had seizures at admission, 10 of these developed minor withdrawal symptoms, in 18 delirium tremens ensued and 5 showed no symptoms of withdrawal. Thirty-nine (54%) had withdrawal syndrome without seizures. Twenty-one of these developed minor withdrawal syndrome and 18 delirium tremens. Seizures showed no relationship with the other withdrawal manifestations, and in all the cases preceded them. Our findings also show that alcoholics with seizures due to withdrawal are more prone to suffer seizures in their future withdrawal episodes, and that alcoholics who suffer morning withdrawal symptoms are prone to develop delirium tremens. In 46 patients a CT scan was performed. Though the alcoholics showed ventricular and sulcal enlargement, brain atrophy was similar when the seizure and non-seizure groups or those with and without delirium tremens were compared. However, cortical and ventricular atrophy were related to the existence of previous episodes of withdrawal syndrome [corrected].
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PMID:Alcoholic withdrawal syndrome and seizures. 794 73

The influence of methohexital and propofol on seizure activity and recovery profiles was assessed in a randomized, crossover study involving 13 adult outpatients undergoing electroconvulsive therapy (ECT). Arterial blood pressure, heart rate, hemoglobin oxygen saturation, and electroencephalogram (EEG) activity were monitored during the ECT procedure. After premedication with glycopyrrolate, 0.2 mg intravenously (i.v.), and labetalol 20-30 mg i.v. hypnosis was induced with a bolus injection of either methohexital or propofol, 0.75 mg/kg. Muscle paralysis was achieved by administering succinylcholine, 1.4 mg/kg i.v. Ventilation was assisted using a face mask while administering 100% oxygen. Thereafter, an electrical stimulus was administered and the length of the resulting motor and EEG seizures was measured. Mood level and cognitive function were assessed prior to induction of anesthesia and after ECT. A total of 72 treatment sessions were evaluated. Each patient underwent a minimum of four treatments and received both induction drugs equally. Although the use of propofol was associated with significantly shorter motor and EEG seizure durations (mean +/- SEM) compared with methohexital (34 +/- 1.6 s and 52 +/- 2.9 s vs 39 +/- 1.5 s and 61 +/- 3.0 s, respectively), this difference was not clinically significant because the durations exceeded 30 s in both groups. Although awakening times were similar, both hemodynamic stability and cognitive recovery were more favorable after propofol. Compared with methohexital, the use of propofol was associated with a clinically insignificant decrease in seizure duration. However, propofol was associated with improved hemodynamic stability and an earlier return of cognitive function after ECT.
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PMID:Anesthesia for electroconvulsive therapy: effects of propofol and methohexital on seizure activity and recovery. 801 Apr 57

Plasminogen activator inhibitor-1 (PAI-1) is a serpin proteinase inhibitor which regulates fibrinolysis and the proteinase cascade of tumour invasion. In this study, PAI-1 was identified in the cerebrospinal fluid (CSF) from patients without neurological disease and patients with various neurological disorders. The mean level of PAI-1 in the CSF of 28 patients without central nervous system (CNS) disease was 0.28 +/- 0.03 (SEM) ng/ml. CSF PAI-1 was significantly increased in the following diagnostic categories:dementia (Alzheimer's disease), cerebral infarction, CNS infection, alcohol withdrawal seizures and CNS neoplasia. In all these disorders, with the exception of CNS infection, PAI-1 was also increased as a fraction of total CSF protein. CSF PAI-1 was not increased in patients with hydrocephalus or idiopathic seizure disorders. Complementary plasma samples were available for 18 of the 128 CSF specimens studied. For these cases, there was no correlation between plasma PAI-1 and CSF PAI-1 levels. PAI-1 may represent a non-specific marker of disease in the central nervous system.
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PMID:Plasminogen activator inhibitor-1 in the cerebrospinal fluid as an index of neurological disease. 805 48

Antiepileptic drug (AED)-related chronic leukopenia [white blood cell (WBC) count < 4,000/microliters] is a dilemma, especially when the AED is effective in controlling seizures. We evaluated the possible mechanisms of leukopenia in 7 patients. Mean WBC count was 3,000/microliters with a mean of 42% polymorphonuclear leukocytes (PMN). The AEDs were carbamazepine (CBZ) alone in 1 patient or CBZ combined with phenytoin (PHT), primidone (PRM), phenobarbital (PB) and/or valproate (VPA) in 5 patients; one patient was receiving PHT only. Bone marrow (BM) aspirates and PMN antibody studies using chemiluminescence were normal. Two liver-spleen scans showed mild relative splenomegaly. After exercise, WBC count (n = 7) increased by 54% (SEM 12%), while the WBC counts in controls (n = 5) increased by 52 +/- 16%. Antinuclear antibodies (Hep-2) were absent in 6 patients and positive (1:160) in 1. PMN adhesion to nylon wool was decreased (54 +/- 10% in patients vs. 80 +/- 5% in controls: n = 13, p < 0.005). Our data, particularly the appropriate WBC response to the stress of exercise, and normal BM examinations suggest that continuation of AED therapy when leukopenia is stable and the percentage of PMN is normal is probably safe. Caution should be used if the absolute PMN count is consistently < 1,000/microliters. BM examinations need not be performed routinely for every patient with neutropenia due to AEDs, especially if the leukopenia fluctuates in the range of 2,000-4,000 cells/microliters.
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PMID:Evaluation of the mechanisms of antiepileptic drug-related chronic leukopenia. 811 38

Resting metabolic rate (RMR) and the thermic effect of a meal (TEM) were compared among women of three levels of aerobic fitness. Twenty-three euthyroid, eumenorrheic women (aged 18-35 years) were divided into three groups based on VO2 max standardized for fat-free weight (FFW), as determined from a graded exercise test: High Fit (HF): n = 7, VO2 max > 70 ml*kg FFW-1*min-1; Moderately Fit (MF): n = 8, VO2 max = 55-70 ml*kg FFW-1*min-1; and Low Fit (LF): n = 8, VO2 max < 55 ml*kg FFW-1*min-1). At 0700h RMR was measured for 1 h by indirect calorimetry with subjects in a fasted, preovulatory state, having refrained from exercise on the preceding day. The subject then consumed a liquid meal (12 kcal*kg FFW-1) and indirect calorimetry was continued for 3 h to determine the TEM. RMR adjusted for FFW using analysis of covariance was significantly higher (P < 0.05) in the HF group (mean +/- SEM = 1.08 +/- 0.03 kcal*min-1) compared to the MF (0.99 +/- 0.04) and LF (0.90 +/- 0.04) groups. Group differences in the thermic response did not reach statistical significance, although there was a trend for a high TEM in the HF group. There was a positive relationship between RMR and energy flux (average daily kcalorie intake + daily kcaloric expenditure in physical activity). These results suggest that women who exhibit high levels of exercise and aerobic fitness may be less energy efficient during the non-exercise portion of the day then their less active counterparts.
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PMID:Resting metabolic rate and postprandial thermogenesis by level of aerobic fitness in young women. 840 94

In febrile convulsions glucose concentrations are known to increase both in the blood and cerebrospinal fluid (CSF). The reason behind this increase is, however, incompletely understood. We have studied the effects of convulsion and fever on the CSF and blood glucose concentrations in four different groups of children: febrile and non-febrile children, with and without convulsions. The concentration of glucose in the CSF was significantly higher in febrile children with (4.4 +/- 0.1 mmol/l, mean +/- SEM n = 35, p < 0.01. ANOVA, Duncan's test) and without convulsions (3.9 +/- 0.2 mmol/l, n = 22, p < 0.05) than in non-febrile, non-convulsive children (3.3 +/- 0.1 mmol/l, n = 21). In non-febrile convulsive children, the CSF glucose concentration was 3.7 +/- 0.2 mmol/l (n = 10). Both fever and seizures increased the CSF glucose levels (p < 0.0001) and p = 0.028, respectively, analysis of covariance). There was a linear correlation between the body temperature and concentration of glucose in the CSF (r = 0.454, p < 0.0001, n = 88, Pearson's correlation analysis). The changes in blood glucose concentrations between the groups paralleled those found in the CSF. Our results show that hyperglycaemia and an increase in the CSF glucose concentration in febrile convulsions is not explained just by a stress reaction, evoked by the seizure, as has been hypothesized earlier, but by the influence of increased body temperature as well.
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PMID:The role of fever on cerebrospinal fluid glucose concentration of children with and without convulsions. 858 Jun 26

Patients with cortical myoclonus may have purely focal or multifocal jerks, or they may have additional bilateral or generalized jerks, suggesting the spread of excitatory myoclonic activity between the cerebral hemispheres and across the sensorimotor cortex. The factors contributing to this spread of activity were investigated in 10 patients with multifocal cortical myoclonus and eight patients with multifocal and bilateral or generalized cortical myoclonus. The two groups were termed 'non- spreaders' and 'spreaders' respectively. Eight of the patients were also epileptic. Motor thresholds to single transcranial magnetic shocks at rest were higher in 'non- spreaders' (median 88%, range 45-100% of stimulator output) than either 'spreaders' (50%, range 26-90%, P=0.023) or health controls (38%, range 28-53%, P<0.001). This pathological elevation in motor threshold was not simply an effect of treatment with antiepileptic drugs. Paired transcranial magnetic stimuli were used to investigate ipsilateral cortico-cortical and transcallosal inhibition, There was less (MANOVA, P<0.05) ipsilateral inhibition at interstimulus intervals (ISIs) of 1-6 ms in 'spreaders' (mean 107+/-SEM 23% of control) compared with 'non- spreaders' (75+/-15%) or healthy subjects (59+/-10%). There was also less (P<0.05) transcallosal inhibition across inhibitory timings (10, 12 and 14 ms) in the 'spreaders' (98+/-6% of control) compared with the 'non-spreaders' (64+/-8%) or healthy subjects (59+/-6%). There was no relationship between ipsilateral cortico-cortical and transcallosal inhibition and the presence or absence of epilepsy, although non-epileptic patients did have higher motor thresholds (median 85%, range 32-100% of stimulator output) than either epileptic patients (50%, range 26-90%, P<0.001) or healthy controls (38%, range 28-53%, P=0.002). Abnormalities in ipsilateral and transcallosal inhibition appear to facilitate the spread of the cortical myoclonic activity responsible for bilateral and generalized jerks. However, these abnormalities in inhibition do not play a major role in the development of generalized seizures in patients with cortical myoclonus.
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PMID:Abnormalities of the balance between inhibition and excitation in the motor cortex of patients with cortical myoclonus. 862 91

Immaturity in water and electrolyte balance in the brain has been considered to increase the susceptibility of young animals and children to febrile convulsions (FCs). Arginine-vasopressin (AVP) is involved in the regulation of several centrally mediated events such as modulation of fever and the ease with which water permeates into and out of the brain. To evaluate the possible role of AVP in the control of water balance and susceptibility to convulsions during fever we measured the AVP concentration in the cerebrospinal fluid (CSF) and plasma of febrile children with or without convulsions. The febrile population consisted of 47 children, of whom 29 experienced seizures during fever. Seven children with epileptic symptoms and 18 children without seizures were included as nonfebrile controls. The CSF AVP concentration in febrile children without seizures and in nonfebrile convulsive children was significantly lower (0.60 +/- 0.07 pmol/l, mean +/- SEM, P < 0.01 and 0.65 +/- 0.19 pmol/l, P < 0.05, respectively) than in nonfebrile children without convulsions (0.83 +/- 0.06 pmol/l). However, the levels of CSF AVP were not significantly different in children with FCs (0.71 +/- 0.06 pmol/l) compared with other groups. CSF AVP correlated with the CSF osmolality (r = 0.33, P = 0.02). No statistical differences in plasma AVP levels between the groups could be found. The present data provide support for the hypothesis of synchronous regulation of osmolality and AVP concentration in CSF. During fever the concentration of CSF AVP was lower in nonconvulsive children compared with nonfebrile nonconvulsive children. CSF AVP levels were not affected in febrile children by convulsions.
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PMID:Vasopressin in the cerebrospinal fluid of febrile children with or without seizures. 873


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