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Neuromuscular-blocking drugs, or Neuromuscular blocking agents (NMBAs), block transmission at the neuromuscular junction, [1] causing paralysis of the affected skeletal muscles. This is accomplished via their action on the post-synaptic acetylcholine (Nm) receptors.
Flaccid paralysis resulting from cholinergic crisis can be distinguished from myasthenia gravis by the use of the drug edrophonium (Tensilon), as it only worsens the paralysis caused by cholinergic crisis but strengthens the muscle response in the case of myasthenia gravis. Edrophonium is a cholinesterase inhibitor, hence it increases the ...
The toxicity of curare alkaloids in humans has not been systematically established, but it is considered highly toxic and slow-acting, with a lowest reported lethal dose of 375 μg/kg (unknown route of administration). [35] For animals, the median lethal dose of tubocurarine is: [35] 1200 μg/kg (dog, intravenous) 140 μg/kg (mouse, intravenous)
Drugs that interfere with nerve function, such as curare, can also cause paralysis. Pseudoparalysis ( pseudo- meaning "false, not genuine", from Greek ψεῦδος [ 7 ] ) is voluntary restriction or inhibition of motion because of pain, incoordination, orgasm, or other cause, and is not due to actual muscular paralysis. [ 8 ]
The drug has a relatively intermediate duration of action when compared to other non-depolarizing agents. [2] The drug has an onset of 2 to 3 minutes in adults and an expected peak effect at 3 to 5 minutes. [2] Recovery is expected to begin within 20 to 35 minutes of the initial dose, but it may take up to 70 minutes to achieve 95% recovery. [2]
Medications for gastroparesis aim to manage symptoms and may include what are called prokinetic agents. These work by inducing stomach contractions to move food through your digestive tract.
Some reports say Ozempic and Mounjaro cause gastroparesis—but clinical trials do not. Doctors explain a potential link between weight loss drugs and stomach paralysis.
The available research seems to suggest that the concurrent prophylactic use of a neuroleptic and an antiparkinsonian drug is useless to avoid early extrapyramidal side-effects and may render the person more sensitive to tardive dyskinesia. Since 1973 the use of these drugs has been found to be associated with the development of tardive dyskinesia.