Muscle relaxant



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

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 spasm and pain, and hyperreflexia. The term "muscle relaxant" is used to refer to two major therapeutic groups: 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]

History

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 acetylcholine in neuromuscular transmission.[5] By 1943, neuromuscular blocking drugs became established as muscle relaxants in the practice of anesthesia and surgery.[6]

Neuromuscular-blocking drugs

 

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, 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 pancuronium.[5].

 

Spasmolytics

  The generation of the dantrolene), so this name is inaccurate.[5]

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.[8][9][10]

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]

substance P in the spinal cord as well.[11][5]

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.[12] Neurophysiologic studies show that it depresses excitatory feedback from muscles that would normally increase muscle tone, therefore minimizing spasticity.[13][14] 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.[15]

The 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]

Other common spasmolytic agents include: methocarbamol, orphenadrine.

See also

  • Paralysis
  • quaternary ammonium muscle relaxants

References

  1. ^ "Definition of Muscle relaxant." MedicineNet.com. (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. ^ a b c d e f g h 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. ^ 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.
  9. ^ 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.
  10. ^ 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.
  11. ^ 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. PMID 9928310.
  12. ^ Young, R.R. (editor). "Symposium: Role of tizanidine in the treatment of spasticity." Neurology. 1994, Vol. 44 (Suppl. 9), p. 1.
  13. ^ 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. PMID 12106064.
  14. ^ 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. PMID 10712650.
  15. ^ Young, R.R; Weigner, A.W. "Spasticity." Clin. Orthop. 1987, Vol. 219, p. 50.
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Muscle relaxants (Dantrolene
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Antihistamines
 
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