Results 171 to 180 of about 21,834 (203)
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An Electroencephalographic Study of 4-Aminopyridine
Anesthesia & Analgesia, 1982The electroencephalographic (EEG) effects of 4-aminopyridine (4-AP) given intravenously in therapeutic doses were studied in four conscious human volunteers. 4-AP (0.2 mg/kg) caused an increase of the occipital alpha peak frequency of 0.4 to 1.0 Hz. In the dose range of 0.2 to 0.3 mg/kg there was neither evidence for epileptic activity in the EEG nor ...
R L, Sia +4 more
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4-Aminopyridine Hydrochloride (Pymadin)
1986Some of the pharmacological actions of aminopyridines have been known for many years (Dohrn 1924; Dingemanse and Wibaut 1928; von Haxthansen 1955; Fastier and MacDowall 1958 a), but it is only since Bulgarian pharmacologists and anaesthetists, on the basis of their experimental and clinical studies, advocated the use of 4-aminopyridine hydrochloride ...
D. S. Paskov, S. Agoston, W. C. Bowman
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4-Aminopyridine derivatives with antiamnesic activity
European Journal of Medicinal Chemistry, 2000Acetylcholine (Ach) enhancement, useful in the treatment of Alzheimer's disease (AD), may be obtained by means of ion channel modulators such as 4-aminopyridine (4-AP). 4-AP is also the central ring of tacrine, the first drug approved for the treatment of AD. The synthesis and pharmacological activity of three 4-AP derivatives, prepared with the aim of
A, Andreani +6 more
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Atypical Presentation of 4-Aminopyridine Overdose
Annals of Emergency Medicine, 19964-Aminopyridine (4-AP) is an investigational drug for the treatment of neurologic disorders including multiple sclerosis (MS). Until recently, relatively little was known about 4-AP toxicity in overdose; the only recorded cases involved neurologic symptoms ranging from mild parasthesias to tonic-clonic seizures.
T A, Pickett, R, Enns
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Effects of 4-aminopyridine on saxitoxin intoxication
Toxicology and Applied Pharmacology, 1996Effects of 4-aminopyridine (4-AP) on neurotoxicity induced by saxitoxin (STX) are investigated in this study. In vitro, twitch tension evoked by nerve stimulation was depressed by STX (1.35 nM) in rat phrenic nerve-diaphragm preparations, and this inhibition was antagonized by 4-AP (0.1 mM).
H M, Chen, C H, Lin, T M, Wang
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Pharmacokinetics of 4‐aminopyridine derivatives in dogs
Journal of Veterinary Pharmacology and Therapeutics, 2009Blockade of potassium channels with 4‐aminopryidine (4‐AP) restores conduction to demyelinated axons and improves function. Unfortunately, 4‐AP causes adverse effects and its clinical effects are unpredictable and limited. Derivatives of 4‐AP have been tested in models of spinal cord injury in guinea pigs; three derivatives (methyl‐, ethyl‐ and t‐butyl
N J, Olby +7 more
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An unusual case of 4-aminopyridine toxicity
The Journal of Emergency Medicine, 20064-aminopyridine (4-AP) is an orphan drug in the United States. It enhances neuronal conduction at synapses and is indicated in the treatment of selected neuromuscular disorders, including multiple sclerosis and myasthenia gravis, among others. Its documented toxicity generally has been limited to central nervous system (CNS) hyperexcitation and ...
Nicholas C, Johnson, Matthew W, Morgan
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Determination of 4-aminopyridine in plasma
Analytical Biochemistry, 1981Abstract Gas-liquid chromatographic procedures for the determination of 4-aminopyridine in human and animal plasma are reported. The procedures involve the addition of an internal standard 3-methyl-4-aminopyridine to plasma followed by extraction into methylene chloride/isopropranol under alkaline conditions.
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Distribution of the 4-aminopyridine derivative 3-methoxy-4-aminopyridime in mice
Neuropharmacology, 1989The tissue distribution of [14C]3-Methoxy-4-aminopyridine was studied after intravenous administration in mice using whole body and microautoradiography. Dense accumulation was found in cholinergically innervated, secretory organs. High radioactivity was detected in the adrenal medulla suggesting that the observed excitement and hyperglycemia are due ...
S G, Berger +2 more
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Does 4-aminopyridine “beat” downbeat nystagmus?
Journal of Neurology, Neurosurgery & Psychiatry, 2013The flocculus of cerebellum inhibits the vestibular nuclei and keeps the eyes steady during downward gaze. Disinhibition of the flocculus leads to slow upward drift of the eyes, followed by corrective downward saccade—the ‘downbeat’—hence the name ‘downbeat’ nystagmus. Asymmetry in the vertical smooth pursuit pathway or, imbalance in the neural tone of
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