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)

Clinical effects at three different serum levels of sodium valproate (VPA) were compared in a triple-blind, multiple crossover trial comprising 13 epileptic inpatients. Patients were selected regardless of seizure type, and all were in concomitant antiepileptic treatment, which was kept constant throughout the study. A significant relationship between the decrease in number of seizures and increasing VPA serum level was demonstrated. The relationship between VPA dose and serum level was curvilinear. Statistical evaluation of patients by seizure type in relation to clinical effect of VPA was only possible for secondary generalized seizures. Between phenytoin, phenobarbital, and carbamazepine and the different VPA serum levels no interactions could be demonstrated. Recorded side effects were always mild and transient. No obvious correlation between side effects and VPA serum level was established.
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PMID:Sodium valproate, serum level and clinical effect in epilepsy: a controlled study. 37 7

In this two-phase study, 21 pediatric patients with epilepsy and spasticity were initially treated with dantrolene sodium suspension and, after a washout period, began a double-blind portion where one half received dantrolene sodium suspension and the other half received a placebo suspension. The frequency of seizures, serum anticonvulsant levels and electroencephalograms were compared with control values. On dantrolene sodium suspension, there was no persistent change in these parameters. Therefore, it is concluded that dantrolene sodium does not adversely affect the frequency of seizures in children with epilepsy and spasticity, who are being maintained on anticonvulsant medications.
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PMID:Effect of dantrolene sodium on the incidence of seizures in children with spasticity. 37 80

The clinical and electroencephalographic (EEG) effects of sodium valproate were studied in four patients by means of serial 24-hour EEG recordings and simultaneous hourly determinations of serum drug concentrations. The patients all had frequent clinical seizures and generalized spike-wave discharges. Valproate appeared to reduce diurnal paroxysmal discharges (PD) and clinical seizures, but the effect on nocturnal PD was less marked. The extent and duration of the depression of PD and seizures varied. Altering the distribution of the total daily dose may change the pattern of clinical seizures and PD. Valproate concentrations fluctuated widely over 24 hours, and the significance of single estimations often cited in the literature appears dubious. Peak serum concentrations above 100 micrograms per milliliter may be necessary in some patients to achieve clinical and EEG improvement.
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PMID:Sodium valproate: serial monitoring of EEG and serum levels. 38 50

A total of 142 patients (84 per cent aged less than 20 years) with various forms of generalized epilepsy have been treated with sodium valproate alone or in combination with other drugs. The mean duration of symptoms was six years, and half the patients had daily seizures. Nine patients had typical absences, 33 had absences with automatisms, 28 had tonic-clonic seizures with or without photosensitivity, and 72 had various forms of myoclonic epilepsy. Dosage varied from 23 to 54mg/kg and twice-daily administration was usual. Estimation of serum levels did not assist in management. Fits ceased in 63 per cent of all cases and a further 18 per cent showed improvement greater than 50 per cent. Of the 69 with 3c/sec spike-and-wave discharges, 81 per cent became free from all fits, as did 77 percent of those with myoclonic jerks. Fits ceased in eight of the 32 patients with myoclonic astatic epilepsy and there was improvement greater than 50 per cent in a further eight patients. Other anticonvulsants were often withdrawn and always reduced. 21 patients received sodium valproate alone from the start of treatment and all other drugs were withdrawn in another 38. Sodium valproate alone controlled all fits in four children with absences, in 18 with absences with automatisms, 10 with tonic-clonic seizures and 22 with myoclonic epilepsy. Side-effects were rare, mild and often temporary. Potentiation of barbiturates and benzodiazepines occurred, especially clonazepam, which should be avoided. Many patients were more alert. Sodium valproate appears to be the drug of choice for epilepsies associated with generalized spike-and-wave discharges, myoclonic epilepsies or photosensitive epilepsies, and is of especial value in children and mentally retarded patients because it lacks sedating effects and often induces liveliness.
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PMID:Treatment of generalized epilepsies of childhood and adolescence with sodium valproate ("epilim"). 40 4

An uncontrolled trial of sodium valproate in 25 severe epileptics uncontrollable by conventional antiepileptic drugs is presented. Excellent control was achieved in petit mal, myoclonic and minor motor seizures. No serious side effects were encountered, but hyperactivity may be aggravated and interaction with other anticonvulsants does occur.
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PMID:Sodium valproate for the treatment of childhood epilepsies. 40 93

The effect of electrically induced seizures on the permeability of the rat blood-brain barrier was investigated. The small radioactive tracers sodium (24Na+), chloride (36Cl-) carbon labelled thiourea (14C-thiourea) and glucose (14C-D-glucose) were studied in indicator dilution experiments with indium labelled diethylenetriaminepenta-acetic acid (113mIn-DTPA) as reference substance. This method allows a quantitative estimate of the transcapillary loss of solutes, the extraction (E), during a single passage through the brain. Passage of macromolecules was studied using as marker substance Evans Blue which binds to plasma albumin. In the resting state ENa, ECl, Ethiourea and Eglucose were 2.9, 4.8, 9.3 and 12.5%, respectively. During seizures and during shortlasting hypercapnia E glucose decreased while E for the other tracers was unchanged. As cerebral blood flow increased, there must be an increased transfer of test substances into the brain. This finding is in agreement with recent human studies [15]. When Evans Blue was injected intravenously prior to electroshock, there was no staining of brain tissue after one electroshock but following repeated electroshocks some staining was observed. In an attempt quantify this transcapillary loss of albumin by means of indicator dilution, 51Cr-labelled erythrocytes were used as intravascular reference substance against 113mIn-DTPA (a plasma tracer). However, the albumin loss (by pinocytosis or otherwise) occurring after ten electroshocks could not be detected during a single passage through the brain.
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PMID:Blood-brain barrier during electroshock seizures in the rat. 40 65

A 12-week study of clinical response, EEG changes and serum antiepileptic drug (AED) levels using sodium valproate (VAL) was undertaken. The study showed that VAL is a powerful adjunct in the treatment of intractable epilepsy. It was most effective in patients with generalized seizures, but no seizure type was totally resistant. No serious adverse effects were encountered; nausea was easily overcome by readjusting the drug dosage. In most cases the only EEG change was decrease of epileptiform activity, and this correlated well with decreased frequency of clinical seizures. These two features in turn were most often seen with a serum VAL level of 40 microgram per milliliter or greater. Intoxication with VAL was accompanied by marked slowing of the background rhythms, but no increase in beta activity. Other modifications of the EEG were probably due to changes in the plasma levels of other drugs. Interactions between VAL and conventional antiepileptic drugs occur, so that serum concentrations of all drugs must be monitored in patients receiving VAL.
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PMID:Sodium valproate in the treatment of intractable seizure disorders: a clinical and electroencephalographic study. 41 51

1. Starting with published data derived mainly from hippocampal slice preparations, we have used computer-modeling techniques to study hippocampal pyramidal cells (HPCs). 2. The dendrites of the HPC apparently have a short electrotonic length. Calcium spikes are apparently generated by a voltage-dependent mechanism whose kinetics are slow in comparison with those generating sodium spikes of the soma. Inward calcium currents are assumed to trigger a long-lasting potassium conductance. This slow calcium-potassium system, which in our model is located predominantly on the dendrites, provides a heuristic model to describe the mechanism for a) the after-depolarization following an HPC soma (sodium) spike, b) the long afterhyperpolarization following repetitive firing, c) bursts of spikes that sometimes occur after orthodromic or antidromic stimulation, and d) the buildup of the "depolarizing shift" during the strong synaptic input presumed to occur during seizures. 3. Fast prepotentials or d-spikes are shown to arise most probably from dendritic "hot spots" of sodium-regenerative membrane. The limited amplitude and short duration of these prepotentials imply that the hot spots are located on small dendrites. 4. Dendritic electroresponsiveness, first postulated for the HPC by Spencer and Kandel (52), is analyzed quantitatively here and is shown to provide rich integrative possibilities for this cell. Our model suggests that, for these nerve cells, alterations in specific membrane properties, particularly calcium electroresponsiveness, can lead to bursting behavior that resembles epileptogenic neuronal responses.
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PMID:Hippocampal pyramidal cells: significance of dendritic ionic conductances for neuronal function and epileptogenesis. 42 74

Acute renal failure secondary to interstitial nephritis caused by therapeutic ingestion of sodium diphenylhydantoins has been reported recently. The interference of sodium diphenylhydantoins on Vitamin D metabolism causing or aggravating ricketts has also been reported. This communication deals with an infant girl who was admitted to the hospital due to seizures. Four months before, she had convulsions and she was treated with diphenylhydantoins until admission. She was found to have renal failure and ricketts. Histological diagnosis of interstitial nephritis was established by means of percutaneous renal biopsy. Clinical and radiological improvement of ricketts was observed after dehydrotachysterol treatment. Clinical and biochemical alterations of renal failure slowly subsided. She had a clear-cut history of vitamin D defficiency ricketts. Seizures were due to hypocalcemia tetany but was erroneusly treated as "grand mal" epilepsy, with diphenylhydantoins. Interstitial nephritis complicated with acute renal failure was probably caused by diphenylhydantoins administration.
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PMID:[Renal failure and rickets]. 46 92

Since the causes of toxemia of pregnancy are unknown, therapy is still symptomatic and is now determined by the most recent knowledge of the pathophysiology of the disease. Rest, a balanced, predominantly protein-rich diet and avoidance of stress are recommended as prophylactic treatment of toxemia of pregnancy in patients with a predisposition of the condition. Early recognition of the symptoms of toxemia of pregnancy is of great importance. Treatment of mild cases consists of bed rest, possibly supplemented by sedatives and a preponderantly proteinrich diet. Administration of diuretics is obsolete and sodium restriction is no longer recommended. Antihypertensives are seldom indicated. Overweight women are no longer maintained on specially low calorie diets. Severe cases of toxemia of pregnancy must be trated as inpatients under intensive care. Principles of treatment are: 1. Prevention of seizures (by sedation). 2. Improvement of the general condition of the women (especially circulation and renal function). 3. Delivery at an opportune time for mother and child. Treatment of eclampsia follows largely the same principles. In these cases, immediate delivery is required regardless of the condition of the fetus.
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PMID:[Present day status in therapy of toxemia of pregnancy (author's transl)]. 47 58


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