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

Acute and abrupt fetal bradycardia are considered to be vagal in origin. In addition to head compression and funis compression bradycardias, we will report on those acute fetal bradycardias occurring during maternal seizures and maternal voiding, during aortocaval compression, during terminal labor, and during the immediate postpartum period. While certain mechanisms are known which can explain some or parts of these bradycardias, we conclude that in the clinical setting information is insufficient to determine their etiology with precision. Instead of labeling abrupt fetal heart rate pattern as resulting from either head or funis compression, it is suggested that the patterns be described according to their severity and duration. Such acute fetal bradycardias can be detrimental in terms of reduced umbilical flow. Administration of atropine may be indicated in the otherwise healthy fetus with acute bradycardia.
Am J Obstet Gynecol 1977 Dec 15
PMID:Fetal reacting bradycardia. 2 47

The existence of specific receptor sites for benzodiazepines has been well documented by in vitro binding studies. In this study, using a highly radiolabelled [3H]-flunitrazepam, we investigated the binding of benzodiazepines to their receptor sites under in vivo conditions. Tracer doses of [3H]flunitrazepam (0.001 mg/kg) were injected i.v. into mice and the concentration of the drug in the brain was monitored. The accumulation of [3H]flunitrazepam 20 min after injection was found to be highest in the hippocampus, cortex, hypothalamus; to be intermediate in the striatum, medulla oblongata/pons and midbrain and to be lowest in the cerebellum. This corresponds well with the different densities of benzodiazepine receptors which we found in in vitro studies, with the exception of medulla oblongata/pons and cerebellum. When increasing doses (0.01--10 mg/kg) of non-labelled benzodiazepine derivatives (flunitrazepam, clonazepam, the 3S and 3R enantiomers of 5-(o-fluorophenyl)-1,3-dihyrdo-1,3-dimethyl-7-nitro-2H-1,4-benzodiazepine-2-one, and chlordiazepoxide) were injected simultaneously with [3H]flunitrazepam, a dose-dependant, saturable and and stereo-specific decrease of [3H]flunitrazepam concentration in the mouse hippocampus was observed. The dose range in which the unlabelled benzodiazepines decreases the levels of [3H]flunitrazepam in the hippocampus corresponds closely to that which inhibited pentylenetetrazol- or picrotoxin-induced seizures, indicating that this in vivo method determines the occupation of pharmacologically relevant receptors.
Brain Res 1979 Dec 21
PMID:In vivo receptor occupation by benzodiazepines and correlation with the pharmacological effect. 4 15

The ability of midbrain homogenates from two strains of mice to accumulate several putative neurotransmitters, or their precursor in the case of acetylcholine, has been examined. The high-affinity transport mechanisms toward glutamate, GABA, dopamine, and glycine were similar in both strains. The seizure-prone DBA21BG strain had a significantly higher capacity to transport choline than did the relatively seizure-resistant C57BL/6 IBC mice. Howaver, no difference in the density of muscarinic binding sites in the two mouse strains was found.
Neurochem Res 1979 Dec
PMID:Seizure proneness and neurotransmitter uptake. 4 44

303 patients underwent brain biopsy; 20 patients were available for a follow-up EEG examination, up to 16 years after the biopsy. 4 patients (20%) had focal fits starting within 6 months after the intervention. In the EEG of 15 patients (75%) 2 varieties of focal abnormalities appeared: "trepanation activity" which, for reasons discussed below should be regarded as an abnormality; and other focal features, including spikes, more often seen in patients with epilepsy. It is concluded that irritative brain lesions appear in a considerable number of patients after brain biopsy. The decision of performing this diagnostic procedure should be made after taking in consideration that: by enhancing the possibility of a correct diagnosis we may induce focal seizures in every fifth patient and irritative phenomena in three fourths of their EEG'S.
J Neurol 1975 Dec 02
PMID:Late effects of brain biopsy. 5 35

1. Epileptiform after-discharges (EADSs) induced by electrical stimulation of the isolated suprasylvian gyrus were studied in cats with chronically implanted electrodes. 2. In a given region and at a certain time after stimulation, the following events took place: (a) a slow radial spread of the zone of maximal depolarization, from the cortical surface downward, as evidenced by a laminar study; (b) a massive cellular discharge preceded by a period during which few unit activities were detected, followed by bursts of spike activity timed with the surface-positive waves of the ECoG; (c) a surface-negative DC shift with maximal amplitude around 1000 mum below the surface; (d) the occurrence of a synchronizing focus from which the paraoxysmal waves propagated to the whole gyrus. 3. All these phenomena spread across the surface of the gyrus with a velocity (7-20 mm/min) similar to that of focal seizures in man.
Electroencephalogr Clin Neurophysiol 1976 Dec
PMID:Temporo-spatial propagation of epileptoform after-discharges in the isolated cat suprasylvian gyrus. 6 56

Self-sustained, 3-4/sec spike-wave ADs were elicited in lateralis intermedius-lateralis posterior thalamic bursting neurons following incremental responses elicited by 10/sec shock-trains applied to the anterior suprasylvian cortex. The pattern of cortically elicited thalamic spike-wave complexes, with brief depolarizing components and a long-lasting hyperpolarizing wave, resembles that of previously described spike-wave seizures elicited in cortical interneurons following specific thalamo-cortical augmenting responses.
Electroencephalogr Clin Neurophysiol 1976 Dec
PMID:Cortically elicited spike-wave after discharges in thalamic neurons. 6 58

A 10-year-old boy with idiopathic epilepsy refractory to treatment from age 4 and with clinical signs of hyperandrogenism was treated with chlormadinone acetate (24 mg/day) during two alternate periods of 3 months. The administration of chlormadinone was associated with a marked clinical and electroencephalographic improvement as well as a concomitant decrease in the levels of plasma testosterone and delta4 androstenedione. No changes in plasma gonadotropins were observed. Placebo had no effect neither in seizures nor in the concentration of hormones in the plasma. Since chlormadinone acetate is not a very potent gonadotropin inhibitor in males, it is suggested that the clinical and electroencephalographic improvement associated with the use of this compound, might be the consequence of a decrease in the plasma levels of androgens, mainly testosterone.
Helv Paediatr Acta 1976 Dec
PMID:Improvement of intractable idiopathic epilepsy with chlormadinone acetate. A case report. 6 43

Serotonin was determined in platelets of 140 patients with idiopathic mal seizures. According to anticonvulsive therapy these patients were divided into the following five groups: no medication, Diphenylhydantoin, Diphenylhydantoin calcium, Primidon, and combination of various of the anticonvulsants mentioned. The results obtained in the entire group of patients as well as in the various subgroups were compared with those of a group of healthy persons without therapy. In addition the various subgroups were compared to each other. There were significantly reduced serotonin values in the patients with idiopathic grand mal seizures as well as in each of its various groups as compared with the values obtained in healthy persons. Furthermore, significantly higher values were observed in the patients receiving primidone as compared with those receiving no anticonvulsants, Diphenylhydantoin, and a combination of various anticonvulsants. Our results taken together with those reported in the literature point to the possibility that a special imbalance in the cerebral neurotransmitter system, including a deficiency of serotonin, may represent a pathogenetic factor for idiopathic grand mal seizures. In addition, this investigation indicates that primidone elevates serotonin in platelets of patients with grand mal seizures.
J Neurol 1978 Dec 22
PMID:Serotonin metabolism with idiopathic grand mal seizures. 8 62

To evaluate the clinical efficacy and mechanisms underlying EEG feedback training of epileptic patients, 5 adult patients with poorly controlled seizures were studied for 4--10 months during which quantitative analysis of seizures, the EEG, and serum anticonvulsant levels was conducted. Sustained seizure reduction did not occur during the first 4--5 weeks in which feedback signals were presented randomly in relation to the EEG. When feedback was then made contingent upon central 9--14 c/sec activity, seizures declined by 60% in 3 patients. Power spectral analysis showed upward shifts in EEG frequency, decreases in abnormal slow activity, and enhancement of alpha rhythm activity as a function of contingent training, but no specific EEG change was associated with seizure reduction in all patients. No evidence was obtained for the hypothesized involvement of a 'sensorimotor rhythm' or motor inhibition in the training effects. The lack of effect in two patients could not be attributed to insufficient training, lack of motivation, or to differences in seizure classification. A second phase of research showed that continued laboratory training was both sufficient and necessary for maintaining clinical and EEG effects. Results indicate that: (1) significant seizure reductions can occur with EEG feedback training which are not related to placebo effects, non-specific factors or to changes in medication; (2) EEG changes associated with such training can best be described as 'normalization'; (3) continued clinical investigation of EEG feedback training as a non-pharmacological adjunct to conventional therapy appears justified.
Electroencephalogr Clin Neurophysiol 1978 Dec
PMID:EEG feedback training of epileptic patients: clinical and electroencephalographic analysis. 8 38

Intravenous procaine HCl given at low doses (0.5-2.5 mg/kg) to two monkeys with bilateral alumina hippocampal foci depressed interictal spiking or had little effect. At 5.0 mg/kg unilateral limbic activation occurred. At 10.0 mg/kg unilateral or bilateral limbic activation and generalized seizures could be evoked within 3-10 min. At higher doses (15 and 20 mg/kg) bilateral limbic activation or brief (one min) generalized seizures occurred. The unilateral-onset psychomotor seizures were not identical to spontaneous psychomotor seizures, and the generalized seizures never occurred spontaneously in these monkeys. However, these results do indicate that procaine challenges may selectively activate limbic epileptogenic areas without activation of debilitating generalized tonic-clonic seizures.
Electroencephalogr Clin Neurophysiol 1979 Dec
PMID:Procaine-induced seizures in epileptic monkeys with bilateral hippocampal foci. 9 2


1 2 3 4 5 6 7 8 9 10 Next >>