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Muscle relaxing drugs

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This article refers to skeletal muscle relaxants. For information on smooth muscle relaxants, see Antispasmodic drugs.

A muscle relaxant is a drug which decreases the tone of a muscle. See also Neuromuscular-blocking drugs.

A muscle relaxant is a drug which affects skeletal muscle function and decreases the muscle tone. It may be used to alleviate symptoms such as muscle spasms, pain, and hyperreflexia. The term "muscle relaxant" is used to refer to two major therapeutic groups: neuromuscular blockers and spasmolytics. Neuromuscular blockers act by interfering with transmission at the neuromuscular end plate and have no CNS activity. They are often used during surgical procedures and in intensive care and emergency medicine to cause paralysis. Spasmolytics, also known as "centrally-acting" muscle relaxants, are used to alleviate musculoskeletal pain and spasms and to reduce spasticity in a variety of neurological conditions. While both neuromuscular blockers and spasmolytics are often grouped together as muscle relaxants,[1][2] the term is commonly used to refer to spasmolytics only.[3][4]


The earliest known use of muscle relaxant drugs dates back to the 16th century, when European explorers encountered natives of the Amazon Basin in South America using poison-tipped arrows that produced death by skeletal muscle paralysis. This poison, known today as curare, led to some of the earliest scientific studies in pharmacology. Its active ingredient, tubocurarine, as well as many synthetic derivatives, played a significant role in scientific experiments to determine the function of acetylcholine in neuromuscular transmission.[5] By 1943, neuromuscular blocking drugs became established as muscle relaxants in the practice of anesthesia and surgery.[6] f

Neuromuscular-blocking drugsEdit

Synapse diag4

Detailed view of a neuromuscular junction:
1. Presynaptic terminal
2. Sarcolemma
3. Synaptic vesicle
4. Nicotinic acetylcholine receptor
5. Mitochondrion

Main article: Neuromuscular-blocking drugs

Muscle relaxation and paralysis can theoretically occur by interrupting function at several sites, including the central nervous system, myelinated somatic nerves, unmyelinated motor nerve terminals, nicotinic acetylcholine receptors, the motor end plate, and the muscle membrane or contractile apparatus. Most neuromuscular blockers function by blocking transmission at the end plate of the neuromuscular junction. Normally, a nerve impulse arrives at the motor nerve terminal, initiating an influx of calcium ions which causes the exocytosis of synaptic vesicles containing acetylcholine. Acetylcholine then diffuses across the synaptic cleft. It may be hydrolysed by Acetylcholine esterase (AchE) or bind to the nicotinic receptors located on the motor end plate. The binding of two acetylcholine molecules results in a conformational change in the receptor that opens the sodium-potassium channel of the nicotinic receptor. This allows Na+ and Ca2+ ions to enter the cell and K+ ions to leave the cell causing a depolarization of the end plate, resulting in muscle contraction.[7] Following depolarization, the acetylcholine molecules are then removed from the end plate region and enzymatically hydrolysed by acetylcholinesterase.[5]

Normal end plate function can be blocked by two mechanisms. Nondepolarizing agents like tubocurarine block the agonist, acetylcholine, from binding nicotinic receptors and activating them, thereby preventing depolarization. Alternatively, depolarizing agents such as succinylcholine are nicotinic receptor agonists which mimic Ach, block muscle contraction by depolarizing to such an extent that it desensitizes the receptor and it can no longer initiate an action potential and cause muscle contraction.[5] These neuromuscular blocking drugs are structurally similar to acetylcholine, the endogenous ligand, in many cases containing two acetylcholine molecules linked end-to-end by a rigid carbon ring system, as in pancuronium.[5].



The generation of the neuronal signals in motor neurons that cause muscle contractions are dependent on the balance of synaptic excitation and inhibition that the motor neuron receives. Spasmolytic agents generally work by either enhancing the level of inhibition, or reducing the level of excitation. Inhibition is enhanced by mimicking or enhancing the actions of endogenous inhibitory substances, such as GABA.


Because they may act at the level of the cortex, brain stem or spinal cord, or all three areas, they have traditionally been referred to as "centrally-acting" muscle relaxants. However, it is now known that not every agent in this class has CNS activity (e.g. dantrolene), so this name is inaccurate.[5]

Most sources still use the term "centrally acting muscle relaxant". According to MeSH, dantrolene is usually classified as a centrally acting muscle relaxant.[8] The World Health Organization, in its ATC, uses the term "centrally acting agents",[9] but adds a distinct category of "directly acting agents", for dantrolene.[10] Use of this terminology dates back to at least 1973.[11]

The term "spasmolytic" is also considered a synonym for antispasmodic.[12]

Clinical useEdit

Spasmolytics like carisoprodol, cyclobenzaprine, metaxalone, and methocarbamol are commonly prescribed for low back pain or neck pain, fibromyalgia, tension headaches and myofascial pain syndrome.[13] However, they are not recommended as first-line agents; in acute low back pain, they are not more effective than paracetamol or non-steroidal anti-inflammatory drugs (NSAIDs),[14][15] and in fibromyalgia they are not more effective than antidepressants.[13] Nevertheless, there is some (low quality) evidence suggesting that muscle relaxants can add benefit to treatment with NSAIDs.[16] In general, there is no high quality evidence to support their use.[13] No drug has been shown to be better than another, and all of them have adverse effects, particularly dizziness and drowsiness.[13][15] Concerns about possible abuse and interaction with other drugs, especially if increased sedation is a risk, further limit their use.[13]

Agents like dantrolene and baclofen are not advised for orthopedic conditions, but rather for neurological conditions such as spasticity in cerebral palsy and multiple sclerosis.[13] Dantrolene, although thought of primarily as a peripherally acting agent, is associated with CNS effects, whereas baclofen activity is strictly associated with the CNS.

Muscle relaxants are thought to be useful in painful disorders based on the theory that pain induces spasm and spasm causes pain. However, there is considerable evidence to contradict this theory.[16]


Because of the enhancement of inhibition in the CNS, most spasmolytic agents have the side-effects of sedation, drowsiness and may cause dependence with long term use. Several of these agents also have abuse potential, and their prescription is strictly controlled.[17][18][19]

The benzodiazepines, such as diazepam, interact with the GABAA receptor in the central nervous system. While it can be used in patients with muscle spasm of almost any origin, it produces sedation in most individuals at the doses required to reduce muscle tone.[5]

Baclofen is considered to be at least as effective as diazepam in reducing spasticity, and causes much less sedation. It acts as a GABA agonist at GABAB receptors in the brain and spinal cord, resulting in hyperpolarization of neurons expressing this receptor, most likely due to increased potassium ion conductance. Baclofen also inhibits neural function presynaptically, by reducing calcium ion influx, and thereby reducing the release of excitatory neurotransmitters in both the brain and spinal cord. It may also reduce pain in patients by inhibiting the release of substance P in the spinal cord as well.[5][20]

Clonidine and other imidazoline compounds have also been shown to reduce muscle spasms by their central nervous system activity. Tizanidine is perhaps the most thoroughly studied clonidine analog, and is an agonist at α2-adrenergic receptors, but reduces spasticity at doses that result in significantly less hypotension than clonidine.[21] Neurophysiologic studies show that it depresses excitatory feedback from muscles that would normally increase muscle tone, therefore minimizing spasticity.[22][23] Furthermore, several clinical trials indicate that tizanidine has a similar efficacy to other spasmolytic agents, such as diazepam and baclofen, with a different spectrum of adverse effects.[24]

The hydantoin-derivative dantrolene is a spasmolytic agent with a unique mechanism of action outside of the CNS. Dantrolene reduces skeletal muscle strength by inhibiting the excitation-contraction coupling in the muscle fiber. In normal muscle contraction, calcium is released from the sarcoplasmic reticulum through the ryanodine receptor channel, which causes the tension-generating interaction of actin and myosin. Dantrolene interferes with the release of calcium by binding to the ryanodine receptor and blocking the endogenous ligand ryanodine by competitive inhibition. Muscle that contracts more rapidly is more sensitive to dantrolene than muscle that contracts slowly, although cardiac muscle and smooth muscle are depressed only slightly, most likely because the release of calcium by their sarcoplasmic reticulum involves a slightly different process. Major adverse effects of dantrolene include general muscle weakness, sedation, and occasionally hepatitis.[5]

Central acting muscle relaxants Edit

Unclassified Edit

Here are several other skeletal muscle relaxants somr of which may belong in the above categories:

Acting on smooth muscle Edit

Other Edit

Drugs from classes other than the muscle relaxant class are also used to treat spasticity:

See also Edit


  1. "Definition of Muscle relaxant." (c) 1996-2007. Retrieved on September 19, 2007.
  2. "muscle relaxant." mediLexicon. (c) 2007. Retrieved on September 19, 2007.
  3. "Muscle relaxants." WebMD. Last Updated: February 15, 2006. Retrieved on September 19, 2007.
  4. "Skeletal Muscle Relaxant (Oral Route, Parenteral Route)." Mayo Clinic. Last Updated: April 1, 2007. Retrieved on September 19, 2007.
  5. 5.0 5.1 5.2 5.3 5.4 5.5 5.6 5.7 Miller, R.D. "Skeletal Muscle Relaxants," in, "Basic & Clinical Pharmacology: Seventh Edition," by Bertram G. Katzung. Published by Appleton & Lange, 1998, p.434-449. ISBN 0838505651
  6. Bowman, W.C. "Neuromuscular block." Br. J. Pharmacol. January 2006. Vol. 147, Suppl. S277-86. PMID: 16402115
  7. C.R. Craig , R. E. Stitzel (2003) Modern Pharmacology with clinical applications Lippincott Williams & Wilkins ISBN 0781737621 p339
  8. MeSH Dantrolene
  9. ATC/DDD Index.
  10. ATC/DDD Index.
  11. Ellis KO, Castellion AW, Honkomp LJ, Wessels FL, Carpenter JE, Halliday RP (June 1973). Dantrolene, a direct acting skeletal muscle relaxant. J Pharm Sci 62 (6): 948–51.
  12. Dorlands Medical Dictionary:antispasmodic.
  13. 13.0 13.1 13.2 13.3 13.4 13.5 See S, Ginzburg R (2008). Choosing a skeletal muscle relaxant. Am Fam Physician 78 (3): 365–370.
  14. Chou R, Qaseem A, Snow V, et al. (October 2007). Diagnosis and treatment of low back pain: a joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann. Intern. Med. 147 (7): 478–91.
  15. 15.0 15.1 van Tulder MW, Touray T, Furlan AD, Solway S, Bouter LM (2003). Muscle relaxants for non-specific low back pain. Cochrane Database Syst Rev (2): CD004252.
  16. 16.0 16.1 Beebe FA, Barkin RL, Barkin S (2005). A clinical and pharmacologic review of skeletal muscle relaxants for musculoskeletal conditions. Am J Ther 12 (2): 151–71.
  17. Rang, H.P. & Dale, M. M "Drugs Used in Treating Motor Disorders" in, "Pharmacology 2nd Edition" Published by Churchill Livingston London, 1991, p.684-705.
  18. Standaert, D.G. & Young, A. B "Treatment Of Central Nervous System Degerative Disorders" in, "Goodman & Gilman's The Pharmacological Basis of Therapeutics 10th Edition" by Hardman, J.G. & Limbird, L.E. Published by McGraw Hill, 2001, p.550-568.
  19. Charney, D.S., Mihic, J. & Harris, R.A. "Hypnotics and Sedatives" in, "Goodman & Gilman's The Pharmacological Basis of Therapeutics 10th Edition" by Hardman, J.G. & Limbird, L.E. Published by McGraw Hill, 2001, p.399-427.
  20. Cazalets JR, Bertrand S, Sqalli-Houssaini Y, Clarac F (1998). GABAergic control of spinal locomotor networks in the neonatal rat. Ann. N. Y. Acad. Sci. 860: 168–80.
  21. Young, R.R. (editor). "Symposium: Role of tizanidine in the treatment of spasticity." Neurology. 1994, Vol. 44 (Suppl. 9), p. 1.
  22. Bras H, Jankowska E, Noga B, Skoog B (1990). Comparison of Effects of Various Types of NA and 5-HT Agonists on Transmission from Group II Muscle Afferents in the Cat 2 (12): 1029–1039.
  23. Jankowska E, Hammar I, Chojnicka B, Hedén CH (2000). Effects of monoamines on interneurons in four spinal reflex pathways from group I and/or group II muscle afferents. Eur. J. Neurosci. 12 (2): 701–14.
  24. Young, R.R; Weigner, A.W. "Spasticity." Clin. Orthop. 1987, Vol. 219, p. 50.

External references Edit


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