Centrally acting muscle relaxants: These drugs inhibit transmission in polyneuronal pathways controlling muscle tone. Thus, they inhibit spinal interneurones and promote inhibitory influences of the brain stem reticular formation on spinal motor neurones. They reduce spasm of skeletal muscles without affecting voluntary movement.
Ach is rapidly inactivated by ChE and endplate returns to its resting potential. However, if there is prolonged depolarization induced by these drugs, there is no further generation of action potential after the initial twitch and there is loss of electrical excitability at the motor endplate.
Directly acting muscle relaxant: They exert direct action on the skeletal muscle, by interfering with the release of Ca2+ from the sarcoplasmic reticulum, they interfere with the excitation-contraction coupling (Bhattacharya 2003).
Treatment of respiratory paralysis arising from an adverse reaction or overdose of a neuromuscular blocking agent should be by positive pressure artificial respiration with oxygen and maintenance of a patient airway until the recovery of normal respiration is assured. With the competitive blocking agents, this may be hastened by the administration of neostigmine methyl sulphate (0.5 to 2mg, intravenously) or edrophonium (10mg intravenously, repeated as required.) (Hardman 1996).
Neostigmine is a quaternary ammonium compound that inhibits cholinesterase activity and thus prolongs and intensifies the physiological actions of acetylcholine. It probably also has direct effects on skeletal muscle fibres. ...