strychnine has been researched along with Intellectual-Disability* in 3 studies
3 other study(ies) available for strychnine and Intellectual-Disability
| Article | Year |
|---|---|
Difficulties in assessing the effect of strychnine on the outcome of non-ketotic hyperglycinaemia. Observations on sisters with a mild T-protein defect.
Sisters with a mild variant of non-ketotic hyperglycinaemia resulting from a defect in the T-protein of the glycine cleavage system had different clinical outcomes. The older sister was ascertained at 6 months of age because of mental retardation. She received only brief treatment with sodium benzoate from 11-15 months and at 15 years of age is profoundly retarded and has epilepsy. The younger sister was diagnosed 36 h after birth, was treated with strychnine, sodium benzoate and arginine from the neonatal period and at 27 months of age is only moderately retarded and free of seizures. The possible role of strychnine in the improved outcome is discussed. Topics: Adolescent; Aminomethyltransferase; Arginine; Benzoates; Benzoic Acid; Child, Preschool; Drug Evaluation; Drug Therapy, Combination; Female; Glycine; Humans; Hydroxymethyl and Formyl Transferases; Intellectual Disability; Strychnine; Time Factors; Transferases | 1986 |
Attempts at use of strychnine sulfate in the treatment of nonketotic hyperglycinemia.
In two cases of nonketotic hyperglycinemia treated from early ages with strychnine sulphate, the patients demonstrated persistent severe psychomotor retardation and seizures. Strychnine therapy improved tone and feeding, but did not seem to alter fundamentally the course of the disease in either patient. Topics: Amino Acid Metabolism, Inborn Errors; Brain; Glycine; Humans; Infant; Infant, Newborn; Intellectual Disability; Male; Psychomotor Disorders; Strychnine | 1980 |
Strychnine therapy in nonketotic hyperglycinemia.
Nonketotic hyperglycinemia is an inborn error of metabolism resulting from a defect in the glycine cleavage enzyme system. It is characterized biochemically by elevated concentrations of glycine in blood, spinal fluid, and urine. Previous therapies which have been directed toward reducing the glycine concentration in plasma and CSF have not been successful in preventing neurological deterioration, which may be the result of the role of glycine as an inhibitory neurotransmitter. Strychnine treatment was initiated because it is a specific antagonist of glycine at postsynaptic membranes. The patient reported here has shown clinical and EEG improvement while taking strychnine in conjunction with sodium benzoate. Topics: Benzoates; Clonazepam; Drug Therapy, Combination; Electroencephalography; Enzymes; Female; Glycine; Humans; Infant; Intellectual Disability; Liver; Spasms, Infantile; Strychnine | 1979 |