7.2:
Classification of Skeletal Muscle Relaxants
Skeletal muscle relaxants are a group of drugs that can reduce muscle stiffness and induce temporary paralysis to relieve pain. There are two types.
Spasmolytic drugs relieve involuntary and painful muscle contractions arising from hyper-excited motor neurons found in the brain or spinal diseases or injuries.
Baclofen, a common spasmolytic, acts on spinal nerves and activates the receptors of the inhibitory neurotransmitter GABA. This prevents the excitatory neurotransmitters from firing off the motor neurons.
On the contrary, neuromuscular blockers inhibit transmission at the neuromuscular junction to induce muscle paralysis during surgical anesthesia. They can be non-depolarizing or depolarizing.
Non-depolarizing agents, such as rocuronium, prevent the action of the neurotransmitter acetylcholine by blocking the binding site on its receptor. As a result, the muscles relax.
Depolarizing agents like succinylcholine mimic acetylcholine's action by binding to its receptors and opening sodium channels in muscle cells. The influx of sodium ions extends membrane depolarization, producing repeated muscle contractions and temporary muscle paralysis.
7.2:
Classification of Skeletal Muscle Relaxants
Skeletal muscle relaxants are a group of drugs that can reduce muscle stiffness and induce temporary paralysis to relieve pain. These agents can act centrally to reduce muscle tone or spasms in painful conditions such as multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), or spinal injuries; they are called antispasmodics or spasmolytics.
Peripherally acting skeletal muscle relaxants interfere with the neurotransmission at the neuromuscular end plate to induce paralysis during surgical procedures and are called neuromuscular blockers.
Centrally acting agents do not alter consciousness. However, they do have some sedative actions. They do not interfere with neuromuscular transmission and help reduce rigidity, spasticity, and hyperreflexia. Antispasmodics include baclofen, mephenesin, chlormezanone, chlorzoxazone, diazepam, thiocolchicoside and tizanidine.
The peripherally acting neuromuscular blockers include nondepolarizing (competitive) blockers such as mivacurium, vecuronium, rocuronium, pancuronium, and d-tubocurarine, and depolarizing blockers such as succinylcholine and decamethonium. Decamethonium and tubocurarine are no longer utilized clinically.
Neuromuscular blockers act at the skeletal muscle end plate.
Nondepolarizing blockers prevent acetylcholine actions by blocking the acetylcholine binding sites of the receptor, causing muscle relaxation. On the other hand, depolarizing blockers mimic the actions of acetylcholine by binding to the acetylcholine receptors and opening the Na+ channels of the muscle, promoting Na+ influx. This ion influx extends membrane depolarization leading to repeated contraction of the muscles and induction of flaccid paralysis.