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At least 919 records · Page 51Linked to original sources
PubMed1975

Seizure activity and anticonvulsant drug concentration.

Current methods permit frequent, accurate serum anticonvulsant drug concentration measurements and continuous, 24-hour electroencephalographic recording with minimal environmental restriction. These techniques were used to perform longitudinal, 24-hour recordings of electroencephalographic paroxysmal activity and sleep-wake state concurrently with frequent measurements of serum anticonvulsant drug concentrations in two patients with poorly controlled convulsions. Drug administration was designed with the intent of producing high serum concentrations at times of maximum electroencephalographic paroxysmal activity. The suppression of clinical seizures coincided with decreased numbers of paroxysmal bursts in the electroencephalogram and increased serum anticonvulsant drug concentration.

Anticonvulsants↗
PubMed1975

A primate model for testing anticonvulsant drugs.

Senegalese baboons (Papio papio), with a natural syndrome of photosensitive epilepsy, consistently show generalized myoclonic jerks if stimulated stroboscopically at hourly intervals, two to eight hours after the intravenous administration of allylglycine, 200 mg/kg. This provides a model for testing the acute antiepileptic effects of established or new drugs. The relationship between concentration of drug, antiepileptic action, and acute neurological toxic effects can be studied. Pnehobarbital (15 mg/kg) and diazepam (0;5 to 1.5 mg/kg) were highly effective in the absence of signs of toxic reaction (plasma levels: phenobarbital sodium, 0.7 to 1.7 mg/100 ml; diazepam, greater than 0.5 mug/ml). After administration of carbamazepine (30 to 40 mg/kg) and diphenylhydantoin sodium (40 to 50 mg/kg), antiepileptic action was seen, but was accompanied by severe toxic signs (nystagmus and ataxia). Sulthiame (20 to 125 mg/kg) and ethosuximide (50 to 100 mg/kg) had little antiepileptic activity and no acute toxic effects. This primate model may aid the identification of new drugs that are active against grand mal seizures and status epilepticus.

Allyl Compounds↗
PubMed1999

A new twist for stopping the shakes? Revisiting GABAergic therapy for essential tremor.

Aside from physiological tremor, essential tremor (ET) is by far the most common cause of tremor in humans, affecting large numbers of individuals in every human population. The crude prevalence of ET has been conservatively estimated to be between 0.4% and 3.9%, although some estimates of the prevalence of ET among the elderly are higher than 20%. Essential tremor is the most prevalent adult-onset movement disorder, and is also regarded as one of the most common neurological disorders of adults, with a prevalence that is similar to or greater than that of stroke, Alzheimer disease, migraine headache, and lumbosacral pain syndromes. Essential tremor is as much as 20 times more prevalent than Parkinson disease.

Acetates↗
PubMed1965

Histidinemia.

Explore the source record for details and available documents.

Amino Acid Metabolism, Inborn Errors↗
PubMed1976

Congenital malformations in four siblings of a mother taking anticonvulsant drugs.

Four siblings have various congenital malformations attributable to the teratogenic effect of anticonvulsant drugs. Their mother has 23-year history of continuous medication for seizures. Since the malformations noted in her four offspring are more extensive and severe in each subsequent child, the question arises as to the possible cumulative effect of antiepileptic drugs in producing congenital malformations. The observations in this family strongly support the need to carefully evaluate all offspring of mothers receiving anticonvulsant drugs.

Abnormalities, Drug-Induced↗
PubMed1981

Drugs in the treatment of tinnitus.

Many drugs and some foods can cause or aggravate tinnitus in some patients. These substances should be identified and withdrawn. Tinnitus may be improved by the treatment of associated conditions, infections, or hearing loss with appropriate drugs--hypotensives, antibiotics, vasodilators, fluoride or thyroxine. Intravenous lignocaine can temporarily reduce or abolish tinnitus in many patients but can aggravate existing tinnitus in some and may have no effect on others. Analogy with pain of central origin suggests that the beneficial effects of lignocaine (lidocaine) may be due to its anticonvulsant action. Lignocaine is used as a test to distinguish between different mechanisms of tinnitus and to predict responses to oral anticonvulsants. Dramatic responses with lignocaine are usually associated with cochlear hearing loss and often with comparable though less marked responses to oral anticonvulsants. Patients who do not benefit from lignocaine do not respond to oral anticonvulsants. The action of anticonvulsants is often potentiated by tricyclic antidepressants. The majority of patients who respond to lignocaine can also have their tinnitus effectively masked, as predicted, on a tinnitus synthesizer. A small proportion respond to masking and not to lignocaine and a small proportion to lignocaine and not to masking. Beneficial effects of masking and anticonvulsants are cumulative. Anticonvulsants may also produce subjective improvement in clarity, improved tolerance of hearing aids and increased masking benefit when a hearing aid is worn.

Amobarbital↗
PubMed1978

Downbeat nystagmus due to anticonvulsant toxicity.

Isolated downbeat nystagmus was observed in 2 patients on multiple anticonvulsant regimens. The nystagmus disappeared when phenytoin dosage was reduced. Electrooculographic analysis revealed impaired downward tracking, supporting the concept of "pursuit" nystagmus.

Adult↗
PubMed1979

Mucocutaneous eruptions due to antiepileptic drug therapy in children.

Three children with bullous erythema multiforme and 1 with toxic epidermal necrolysis associated with antiepileptic drug therapy are described. One patient is unique because of seven mucocutaneous eruptions caused by three classes of antiepileptic drugs. Lymphocyte stimulation by antiepileptic drugs could not be demonstrated in the 2 patients in whom appropriate studies were performed, and no precipitating antibodies to antiepileptic drugs were found. Observation of four diagnostic and therapeutic principles, which are illustrated by the course of our patients, may reduce the incidence of life-threatening mucocutaneous eruptions and simplify the long-term management of individuals in whom such reactions occur.

Anticonvulsants↗