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 report one case of amicrobic pustulosis cured with Dedrogyl (25-hydroxycholecalciferol), active metabolite of the vitamin D. The importance of our case stems from the physiopathologic study of this cure. The patient is a 16-year-old boy suffering from a hypoparathyroidism since his younger days. Consequently, he shows a hypocalcemia and convulsive seizures due to the hypoparathyroidism. Those seizures had been wrongly attributed to a primary epilepsy of a neurologic origin and a treatment with Phenobarbital had been instituted. In fact, they were side-effects of the hypoparathyroidism and the Phenobarbital had only aggravated the hypoparathyroidal hypocalcemia as a result of its effect on the metabolism of the vitamin D (deviation of this metabolism by enzyme induction at the level of the liver). The Dedrogyl (25-hydroxycholecalciferol) has restored a normal phospho-calcium balance and the hypocalcemia has disappeared as well as the convulsive seizures which, one year later, had not reappeared while they had previously been continual. And above all, standing back one year, we have recorded a complete cure of the amicrobic pustulosis on account of the Dedrogyl.
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PMID:[Amicrobic pustulosis hypoparathyroidism epilepsy: treatment by 25-hydroxycholecalciferol]. 723 92

Although intravenous phenobarbital loading is effective in barbiturate withdrawal, controlled infusions of a drug are inconvenient. To develop a practical and more widely applicable method, oral loading doses of phenobarbital were given to 21 barbiturate addicts, whose estimated mean daily intake of barbiturates was 1 gm (range 0.5 to 4 gm). Twelve had a past or present history of barbiturate withdrawal seizures. Phenobarbital was given orally at a rate of 120 mg/hr until a predetermined clinical end point of phenobarbital effect was achieved. This end point was the presence of at least three of the following: nystagmus, drowsiness, ataxia, dysarthria, or emotional lability. The total phenobarbital loading dose (mean +/- SD) was 23.4 +/- 7.1 mg/kg, median phenobarbital concentration after loading was 35.9 mg/l (range 13.2 to 71.6 mg/l), and median half-life (t 1/2) of phenobarbital was 90 hr (range 38 to 240 hr). One patient with t 1/2 = 38 hr was given supplemental doses of phenobarbital. None developed seizures or other evidence of barbiturate withdrawal.
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PMID:Barbiturate and hypnosedative withdrawal by a multiple oral phenobarbital loading dose technique. 723 1

A post-mature female newborn with a history of birth trauma developed frequent apneic spells coincident with left posterior-quadrant alpha discharges on her electro-encephalogram. Except during apneic spells, clinical seizure activity was rare. The alpha discharges occurred at regular intervals and were associated with disrupted sleep cycles and a diminution in the proportion of quiet sleep. Phenobarbital apparently abolished the apnea and alpha discharges and resulted in normal sleep cycles and state proportions. At 20 months of age the patient is neurologically and developmentally normal. She has been free of apnea and seizures since the newborn period, despite withdrawal of the anticonvulsant at eight months of age. The authors relate her favorable course to the etiology, periodicity and therapeutic response of her clinical and electrical seizures.
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PMID:Periodic alpha seizures with apnea in a newborn. 738 Jan 21

The course of ischemic increase of extracellular potassium concentration ([K+]e) was studied in rat cerebral cortex with potassium selective microelectrodes and correlated to the preischemic functional and metabolic state. Complete cerebral ischemia was induced in artificially ventilated rats by cardiac arrest. Seven different functional states including conditions with cerebral hypermetabolism (seizures, amphetamine intoxication, hyperthermia) and hypometabolism (barbiturate anesthesia, hypothermia) were chosen in order to cover a wide range of cerebral metabolic rates (CMRO2 : 28.7--2.4 ml O2/(100 g)/min). The ischemic increase of [K+]e was delayed in conditions with low CMRO2 and accelerated in conditions with high CMRO2; the time interval to the terminal steep rise in extracellular potassium concentration varied within the extremes of 35 +/- 5 and 365 +/- 12 sec (means +/- S.E.M.), the control state (N2O-analgesia) being 116 +/- 5 sec. In groups with high CMRO2 electrocortical activity ceased within 15 sec and in groups with low CMRO2 within 22 sec. The rates of the ischemic [K+]e increase, measured as rate of change in the potassium electrode potential (mV/sec), remained high in conditions with high preischemic CMRO2 and low in conditions with low CMRO2, indicating a remaining influence of the preischemic metabolism on membrane ion permeability. These results support previous metabolic data indicating that the rate of consumption of high energy phosphates during ischemia mirrors the preischemic cerebral metabolic rate. Phenobarbital anesthesia did not change the initial rate of [K+]e increase but reduced the rate of [K+]e increase later during ischemia, suggesting a special effect of barbiturates on partly depolarized membranes.
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PMID:The increase in extracellular potassium concentration in the ischemic brain in relation to the preischemic functional activity and cerebral metabolic rate. 740 19

Clinico-pharmacological evaluation on Carbamazepine serum levels was performed in a group of epileptic patients. CBZ (Carbamazepine) blood levels have been detected in a heterogeneous group of epileptic patients taking several other antiepileptic drugs. Patients in which there was a good reduction of epileptic seizures after CBZ was added, had a mean blood level of 4.2 plus or minus 1.4 microgram/ml. When Dyphenilhydantoine (DPH) and/or Phenobarbital (PB) were associated with CBZ they both decreased CBZ blood levels; on the contrary CBZ did not appear to modify DPH and PB blood levels.
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PMID:[Clinicopharmacologic study of blood carbamazepine levels in a group of epileptic patients]. 746 20

The ED50 for abolition of generalized seizures and reduction of afterdischarges to 20% of the control duration was determined in kindled rats for phenobarbital, carbamazepine, phenytoin, valproic acid, clonazepam, and diazepam, both at a stimulation intensity of 200 microA and at 10 microA above the threshold for generalized seizures (threshold stimulation). Phenobarbital, carbamazepine, and valproic acid acted in a stimulus-dependent manner, i.e. the ED50 was higher at 200 microA than at threshold stimulation. Phenytoin had the same ED50 irrespective of the stimulus intensity. Generalized seizures and afterdischarges were suppressed by the same doses of the drugs mentioned. The benzodiazepines, clonazepam and diazepam, had a differential effect: they suppressed generalized seizures at low doses, whereas afterdischarges were only suppressed incompletely at relatively high doses. The ED50 of both benzodiazepines was independent of stimulus intensity. In order to avoid erroneous conclusions a standardization of kindling parameters, especially stimulation intensity, is proposed when drug effects are to be compared.
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PMID:Stimulation-dependent effect of antiepileptic drugs in amygdala kindled rats on both seizure score and duration of afterdischarges. 797 35

In this investigation a newly developed direct cortical stimulation technique was evaluated for measurement of anticonvulsant efficacy in rats. The kinetics of drug action for carbamazepine, phenytoin, valproate, phenobarbital, ethosuximide and oxazepam were studied in conjunction with their pharmacokinetics. Motor cortex stimulation with a ramp-shaped pulse train allowed successive determination of a threshold for localized seizure activity (TLS) and for generalized seizure activity (TGS). For each drug the time course of effect was followed in individual animals. Differential effects on the pharmacodynamic parameters were seen. Phenytoin and carbamazepine clearly elevated the TGS. However, phenytoin did not affect TLS and carbamazepine only marginally. Valproate increased both TLS and TGS to the same extent. Phenobarbital and oxazepam elevated both thresholds, but the effect on TGS was more pronounced. Ethosuximide had little effect on both thresholds. Comparison with other animal models suggested that elevation of TLS reflects an effect on seizure initiation, whereas elevation of TGS above TLS reflects an effect on seizure propagation. All drugs exhibited a nonlinear relationship between plasma concentration and anticonvulsant efficacy, without ceiling of anticonvulsant intensity at the highest concentrations. The effective concentration range of most compounds coincided with the "therapeutic" range in humans. The direct cortical stimulation technique is useful for preclinical monitoring of anticonvulsant efficacy with most antiepileptic drugs because it allows detection of both qualitative and quantitative differences. In addition the model is particularly useful for time course studies.
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PMID:Characterization of the pharmacodynamics of several antiepileptic drugs in a direct cortical stimulation model of anticonvulsant effect in the rat. 818 21

Phenobarbital (PB) (5, 25 and 50 mg/kg), which was administered intraperitoneally to evaluate the effect of it on El mice, inhibited convulsive seizures dose-dependently. On the other hand, microelectrodes were implanted continually into the hippocampus of El mice, after which changes in the neuronal activity caused by a seizure were studied, as well as the effect of PB (5, 25 and 50 mg/kg) on the neuronal activity. The neuronal activity increased during the convulsive seizure when compared to the neuronal activity as the mice moved about freely. Further, after the convulsive seizure, five or six groups of bursts were seen periodically. PB reduced the neuronal activity dose-dependently judging by the number of bursts in the initial group of bursts.
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PMID:The effect of phenobarbital on the multiple neuronal activity in the hippocampus of El mice. 841 83

The purpose of this investigation was to determine the effects of adrenalectomy and adrenalectomy with corticosterone replacement on pain sensitivity and on the pharmacodynamics of a central nervous system depressant, phenobarbital, and a central nervous system stimulant, theophylline. Male Sprague-Dawley rats, bilaterally adrenalectomized, were maintained on normal saline solution or normal saline solution with corticosterone, 160 micrograms/ml, as drinking water for 9 or 11 days. Sham-operated animals served as normal controls. They were then tested for pain sensitivity by the tail-flick method. Phenobarbital or theophylline was infused i.v. slowly until the onset of loss of righting reflex or of maximal seizures, respectively. Samples of cerebrospinal fluid (CSF), blood (for serum) and the brain were obtained at that time and assayed for phenobarbital or theophylline by high-performance liquid chromatography. Compared to the controls, the adrenalectomized rats required a smaller dose and lower concentrations of phenobarbital in serum, brain and CSF (12% decrease) to produce loss of righting reflex. The opposite effect was observed in adrenalectomized rats supplemented with corticosterone. Adrenalectomy had no apparent effect on the dose and the serum, brain and CSF concentrations of theophylline at the onset of maximal seizures whereas adrenalectomized, corticosterone-supplemented animals required a larger dose and higher concentrations (17% increase in CSF) of theophylline than controls to produce seizures. Tail-flick latency was slightly (19%) but statistically significantly reduced in adrenalectomized rats and lengthened (18%) in adrenalectomized, corticosterone-supplemented animals.
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PMID:Kinetics of drug action in disease states. XLI. Effect of adrenalectomy on the hypnotic activity of phenobarbital, the neurotoxicity of theophylline and pain sensitivity in rats. 843 30

A novel method for the assessment of the threshold for clonic seizures induced by excitatory amino acids based on continuous infusion of the glutamate agonists [alpha-amino-3-hydroxy-5-terbutyl-4-isoxazolepropionate (ATPA), kainate or N-methyl-D-aspartate (NMDA)] into the lateral brain ventricle of unrestrained mice is reported. Using this novel method of seizure threshold determination, it was found that systemically administered diphenylhydantoin and carbamazepine elevated the threshold for ATPA and had negligible effects on the threshold for kainate and NMDA. Phenobarbital and trimethadione elevated the threshold for all excitatory amino acids tested, whereas valproate elevated the threshold for ATPA and kainate seizures. Ethosuximide elevated the threshold for ATPA and kainate and decreased the threshold for NMDA seizures. The quisqualate antagonists [2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline and 1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine] elevated the threshold for ATPA and less so for kainate seizures, whereas the NMDA antagonist 3-((+-)2-carboxypiperazine-4-yl)-propyl-1-phosphonate elevated the threshold for NMDA seizures. 1-(4-Aminophenyl)4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine in higher doses was also active against NMDA seizures, whereas 3-((+-)2-carboxypiperazine-4-yl)-propyl-1-phosphonate did so with kainate seizures. Among seven different convulsants, pentylenetetrazol, picrotoxin and the beta-carboline methyl 6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate lowered the threshold for seizures induced by excitatory amino acids. Pentylenetetrazol and picrotoxin did so with kainate seizures, whereas methyl 6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate lowered ATPA thresholds. Bicuculline, 3-mercaptopropionate, strychnine and pilocarpine were inactive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of the seizure threshold for excitatory amino acids in mice by antiepileptic drugs and chemoconvulsants. 850 95


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