clonazepam has been researched along with Leigh Disease in 1 studies
Clonazepam: An anticonvulsant used for several types of seizures, including myotonic or atonic seizures, photosensitive epilepsy, and absence seizures, although tolerance may develop. It is seldom effective in generalized tonic-clonic or partial seizures. The mechanism of action appears to involve the enhancement of GAMMA-AMINOBUTYRIC ACID receptor responses.
clonazepam : 1,3-Dihydro-2H-1,4-benzodiazepin-2-one in which the hydrogens at positions 5 and 7 are substituted by 2-chlorophenyl and nitro groups, respectively. It is used in the treatment of all types of epilepsy and seizures, as well as myoclonus and associated abnormal movements, and panic disorders. However, its use can be limited by the development of tolerance and by sedation.
Leigh Disease: A group of metabolic disorders primarily of infancy characterized by the subacute onset of psychomotor retardation, hypotonia, ataxia, weakness, vision loss, eye movement abnormalities, seizures, dysphagia, and lactic acidosis. Pathological features include spongy degeneration of the neuropile of the basal ganglia, thalamus, brain stem, and spinal cord. Patterns of inheritance include X-linked recessive, autosomal recessive, and mitochondrial. Leigh disease has been associated with mutations in genes for the PYRUVATE DEHYDROGENASE COMPLEX; CYTOCHROME-C OXIDASE; ATP synthase subunit 6; and subunits of mitochondrial complex I. (From Menkes, Textbook of Child Neurology, 5th ed, p850).
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 0 (0.00) | 18.7374 |
1990's | 0 (0.00) | 18.2507 |
2000's | 1 (100.00) | 29.6817 |
2010's | 0 (0.00) | 24.3611 |
2020's | 0 (0.00) | 2.80 |
Authors | Studies |
---|---|
Visch, HJ | 1 |
Rutter, GA | 1 |
Koopman, WJ | 1 |
Koenderink, JB | 1 |
Verkaart, S | 1 |
de Groot, T | 1 |
Varadi, A | 1 |
Mitchell, KJ | 1 |
van den Heuvel, LP | 1 |
Smeitink, JA | 1 |
Willems, PH | 1 |
1 other study available for clonazepam and Leigh Disease
Article | Year |
---|---|
Inhibition of mitochondrial Na+-Ca2+ exchange restores agonist-induced ATP production and Ca2+ handling in human complex I deficiency.
Topics: Adenosine Triphosphate; Bradykinin; Calcium; Cell Nucleus; Clonazepam; Cytosol; Electron Transport C | 2004 |