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.