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Biomedical subjects

J Bruni

Publications and source records attributed to J Bruni.

At least 37 records · Page 2Linked to original sources
PubMed1984

Pharmacokinetics of enteric-coated valproic acid.

Five adult epileptic patients received 1,000 mg of valproic acid (Depakene) in both the regular and the enteric-coated form. Serum valproic acid levels were determined at suitable intervals after drug administration. Pharmacokinetic parameters were equivalent for both preparations except for an absorption lag with the enteric-coated form. The relative bioavailability of the two compounds was similar across the group of patients, although there were marked differences between individual subjects. Close supervision of valproic acid serum levels is suggested after a change in drug formulation.

Adult↗
PubMed1984

Effects of carbamazepine and its epoxide metabolite on amygdala-kindled seizures in rats.

Fourteen animals with stable generalized kindled seizures received three doses of carbamazepine and its epoxide (12.5 to 50 mg/kg IP) in a crossover design. Both compounds suppressed the secondarily generalized convulsion but only affected the partial seizure from the amygdala to a limited extent. The parent drug and the metabolite were equipotent against both seizure types. The results confirm the belief that carbamazepine epoxide has anticonvulsant properties and suggest that it may exert a major therapeutic effect in humans.

Amygdala↗
PubMed1984

Neurological manifestations in systemic sclerosis (scleroderma).

One hundred and twenty-five patients with systemic sclerosis were surveyed for neurological manifestations in a prospective study. Seven (5.6%) were found to have a defined neurologic lesion: 4 with carpal tunnel syndrome and one each with trigeminal neuralgia, mononeuritis multiplex and peripheral neuropathy. Neurological involvement occurs but is uncommon in this connective tissue disorder.

Adult↗
PubMed1983

Treatment of status epilepticus in adults.

Status epilepticus is a medical emergency requiring immediate treatment. General treatment is aimed at restoring physiologic homeostasis, and drug therapy is aimed at arresting the convulsive activity and preventing its recurrence. Concurrent administration of diazepam and either phenytoin or phenobarbital will be effective in most cases. After the status epilepticus has been treated the underlying cause should be investigated and, if possible, treated.

Acid-Base Equilibrium↗
PubMed1983

Valproic acid therapy for complex partial seizures. Its efficacy and toxic effects.

Twenty-four adult outpatients with poorly controlled complex partial seizures were treated with valproic acid. Previous therapy with antiepileptic agents was continued to maintain stable plasma drug levels. Initially 12 patients experienced greater than 50% seizure reduction. Only five patients maintained longterm benefit. In the other seven patients a tolerance developed to valproic acid's efficacy. Duration of seizure control seemed to be a function of initial seizure frequency. Toxic effects were generally mild. No hepatotoxic effect was noted and no hematological abnormalities developed. Weight changes occurred in 17 patients (14 gained weight) and five patients experienced a postural tremor. Eighteen patients experienced nausea.

Adolescent↗
PubMed1983

Tonic status epilepticus presenting as confusional state.

A 17-year-old epileptic was admitted to the hospital in a confused state. Electroencephalography (EEG) with polygraphic recording revealed tonic status epilepticus. Therapy with phenytoin, phenobarbital, valproic acid, and methylphenidate was unsuccessful. Intravenous diazepam exacerbated the seizures. EEG with polygraphic recording may detect clinically inapparent tonic seizures in epileptics with unexplained confusion, and when generalized paroxysmal fast activity occurs during EEG recording.

Adolescent↗
PubMed1983

A double-blind crossover study of cinromide versus placebo in epileptic outpatients with partial seizures.

Cinromide was evaluated versus placebo as add-on therapy in a double-blind crossover study in epileptic outpatients with partial seizures at three sites. Four-week base lines were used before, between, and after the two 12-week treatment periods of the crossover. An operational definition was used to classify each partial seizure as Type A, B, or C. Doses of concurrent antiepileptic drugs were adjusted to maintain pretreatment therapeutic plasma levels. Doses of cinromide ranged from 1,200 to 4,800 mg/day, depending on patient response. Seven patients were withdrawn from the study because of adverse experiences (two receiving placebo and five receiving cinromide). Twenty-eight patients completed the entire 36-week study. A decrease in the average frequency of seizures/week was observed in 12 patients receiving cinromide and in 16 patients receiving placebo. The median frequencies with cinromide and placebo were 3.3 and 2.9 seizures/week, respectively (median initial base-line frequency 3.5 seizures/week for all 28 patients). Although patients were randomly assigned to receive either cinromide or placebo first, the median base-line seizure frequency was greater at the start of the first treatment period in the cinromide group (4.3 versus 2.5 seizures/week) and greater at the start of the second treatment period in the placebo group (3.8 versus 1.4). The median seizure frequency in each higher group decreased with treatment, whereas it increased in each of the lower groups. This study did not demonstrate a beneficial effect of cinromide over placebo for Type A, B, or C partial seizures. The data suggested the presence of an oscillation of seizure frequency in our population of epileptic patients having partial seizures, as well as a placebo effect. No significant carry-over effects were observed. Cinromide has previously been shown to have significant antiepileptic activity in various animal models of epilepsy. The lack of an antiepileptic response to cinromide in humans may have been due to factors other than species differences but indicates that a positive results of a drug in animal models is not the sole factor necessary to predict beneficial antiepileptic activity in humans.

Adolescent↗
PubMed1983

A double-blind study comparing carbamazepine with phenytoin as initial seizure therapy in adults.

Carbamazepine was compared with phenytoin in a double-blind study. Of 87 patients, data on 70 patients were complete and used for analysis. Thirty-five patients were treated with each drug. The incidence of major side effects, minor side effects, and complete control (85%) was the same in both groups. A mild but significant elevation of WBC count was found before initiation of drug treatment in the patients presenting with generalized convulsive seizures. Sporadically, elevations in SGOT and LDH were seen; WBC counts below 4,000 were reported, but these were not clinically significant.

Adolescent↗
PubMed1982

The effect of cinromide on "kindled" seizures in the rat.

Cinromide, an experimental anticonvulsant (Burroughs Wellcome Co.) was tested against focal cortical (simple partial analog), focal amygdala (complex partial analog), and generalized convulsive (tonic-clonic analog) seizures in the "kindled" rat. The toxicity in the CNS was measured by the ataxia scale devised by Desmedt, Niemegeers, Lewi and Janssen (Arzneimittel-Forsch, 26: 1592-1602, 1976). Cinromide was found to suppress generalized convulsions in small, subtoxic doses, whereas larger, sometimes toxic doses were required to suppress focal seizure activity. The general pattern of response resembles that of the standard clinical anticonvulsants which the present authors have previously investigated. Cinromide, however, was relatively more potent against focal amygdala (complex partial analog) seizures than any drug previously tested, except carbamazepine. These data suggest that cinromide should be clinically effective, not only against tonic-clonic seizures, but also, toxicity permitting, against complex partial attacks as well.

Animals↗
PubMed1981

Valproic acid and plasma levels of primidone and derived phenobarbital.

Five patients were studied to determine whether kinetic interaction occurs between valproic acid and primidone. During concurrent administration of primidone and valproic acid no significant interaction was observed. Primidone and derived phenobarbital levels did not change significantly. No adjustment of primidone dose was required when valproic acid was used as adjunctive therapy.

Adult↗
PubMed1981

Clinical utility of six methods of predicting phenytoin doses and plasma concentrations.

The usefulness of six reported methods of predicting phenytoin doses or plasma concentrations in epileptic patients is compared. Forty adult epileptic outpatients who were taking phenytoin sodium orally were followed prospectively for nine months; 16 met requirements for inclusion in the study. Six methods of predicting phenytoin dosage or plasma concentrations--one equation, two nomograms, and three graphs--were compared to actual phenytoin doses and corresponding steady-state serum levels. Criteria establishing good, high, and low predictions were specified for each method. No method produced consistently accurate results. Good dosage predictions occurred in 42-60% of the predictions with the six methods. Low predictions occurred in 0-50% of the estimates; 8-53% of the predictions were high. It is concluded that certain methods are clinically useful under some conditions if recommended cautions are observed.

Adult↗
PubMed1980

Clinical efficacy and long-term effects of valproic acid therapy on spike-and-wave discharges.

Twenty-two patients with absence seizures and other seizure types were treated with valproic acid and followed up for 1 year. Results were excellent with more than 75% improvement in 80% of patients with absence seizures, in 40% of those with tonic-clonic seizures, in all of those with myoclonic seizures, and in 43% of those with partial seizures. Fifty-seven percent of the patients had more than a 75% reduction in the total number of paroxysmal spike-wave discharges, and 62% had more than a 75% reduction in the number of spike-wave discharges lasting longer than 3 seconds. Photosensitivity and activation by hyperventilation decreased. More patients achieved good EEG control in 1 year than in 10 weeks.

Clinical Trials as Topic↗
PubMed1980

Valproic acid and plasma levels of phenobarbital.

During concurrent administration of phenobarbital and valproic acid, phenobarbital plasma concentrations often increase. This often requires a reduction of phenobarbital dosage. In normal cats and patients with epilepsy, we found no evidence of decreased renal excretion of phenobarbital. Metabolic studies in four patients revealed a decrease in the conversion of phenobarbital to hydroxyphenylphenobarbital and decreased urinary ratios of hydroxyphenylphenobarbital to phenobarbital. These data suggest that phenobarbital metabolism is inhibited by therapeutic plasma levels of valproic acid.

Adult↗
PubMed1980

Interactions of valproic acid with phenytoin.

The interaction of phenytoin and valproic acid was studied in four adults. We studied serial changes in total phenytoin concentrations, protein binding, urinary hydroxyphenylphenylhydantoin (HPPH) excretion, and half-life. In all four patients valproic acid caused an increase in the free fraction of phenytoin. Total phenytoin plasma concentrations decreased transiently in three patients and remained low throughout the study period in one patient. HPPH excretion increased transiently and then decreased, corresponding to changes in total phenytoin plasma concentrations. Biologic half-life transiently decreased in three patients (not statistically significant) and subsequently increased significantly in all four patients. The data suggest that valproic acid displaced phenytoin from protein-binding sites in all four patients and subsequently inhibited phenytoin metabolism in three patients.

Adult↗