Fasciculation Health Dictionary

These drugs produce partial or complete paralysis of skeletal muscle (see under MUSCLE – Structure of muscle). Drugs in clinical use are all reversible and are used to help insert a breathing tube into the TRACHEA (endotracheal tube) during general ANAESTHESIA and ARTIFICIAL VENTILATION OF THE LUNGS. They may be broadly divided into depolarising and nondepolarising muscle relaxants. Depolarising muscle relaxants act by binding to acetylcholine receptors at the motor end-plate where nerves are attached to muscle cells, and producing a more prolonged depolarisation than acetylcholine, which results in initial muscle fasciculation (overactivity) and then ?accid paralysis of the muscle. The only commonly used depolarising drug is succinylcholine which has a rapid onset of action and lasts approximately three minutes. Non-depolarising muscle relaxants bind to the acetylcholine receptors, preventing acetylcholine from gaining access to them. They have a slower onset time and longer duration than depolarisers, although this varies widely between di?erent drugs. They are competitive antagonists and they may be reversed by increasing the concentration of acetylcholine at the motor end-plate using an anticholinesterase agent such as neostigmine. These drugs are broken down in the liver and excreted through the kidney, and their action will be prolonged in liver and renal failure. Other uses include the relief of skeletal muscle spasms in TETANUS, PARKINSONISM and spastic disorders. The drugs dantrolene and diazepam are used in these circumstances.... muscle relaxants

In clinical practice, the transmission of impulses at the NEUROMUSCULAR JUNCTION may be blocked to paralyse temporarily a patient for a surgical procedure, or to assist treatment on the intensive care unit. There are two main types of drug, both of which competitively block the ACETYLCHOLINE receptors on the motor end plates. (1) Depolarising neuromuscular blocking agents: these act by ?rst producing stimulation at the receptor, and then by blocking it. There are characteristic muscle fasciculations before the rapid onset of paralysis which is of short duration (less than ?ve minutes with the commonly used drug, suxamethonium). The drug is removed from the receptor by the enzyme, CHOLINESTERASE.

(2) Non-depolarising neuromuscular blocking agents: these drugs occupy the receptor and prevent acetylcholine from becoming attached to it. However, in su?ciently high concentrations, acetylcholine will compete with the drug and dislodge it from the receptor; the e?ect of these drugs is reversed by giving an anticholinesterase, which allows the amount of acetylcholine at the neuromuscular junction to build up. These drugs have varying durations of action, but all are slower in onset and of longer duration than the depolarisers.... neuromuscular blockade

Localized spontaneous, rapid contractions of individual muscle fibres. Unlike fasciculation (muscular quivering), fibrillation cannot be seen through the skin. In skeletal muscles, fibrillation is detected by an EMG. In heart muscle, it is detected by an ECG.Fibrillation usually occurs once a nerve supplying a muscle is destroyed, which causes the affected muscle to become weak and waste away.

Fibrillation of the heart muscle is caused by disruption to the spread of nerve impulses through the muscle wall of a heart chamber (see atrial fibrillation; ventricular fibrillation).... fibrillation

See fasciculation; tic.... twitch

n. prominent quivering of a few muscle fibres, not associated with any other abnormal features. It is usually a benign condition. See also fasciculation.... myokymia