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Review Article

J Korean Dysphagia Soc 2015; 5(1): 14-17

Published online January 1, 2015

Copyright © The Korean Dysphagia Society.

Botulinum Toxin Injection for Achalasia and Non-achalasia Esophageal Motility Disorders

Jung Ho Park, M.D.

Department of Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea

Abstract

Botulinum toxin is one of the deadliest nerve poisons known throughout human history. Among seven different biological substances, only subtypes A, B and E have been implicated in human botulinum intoxication. Botulinum toxin A is synthesized intracellularly as an inactive, single-chain polypeptide that is converted to a dichain molecule by proteolysis. The dichain molecule is composed of a heavy chain (molecular weight 100 KDa) and a light chain (50 KDa) linked by a disulfide bond. Light chain of botulinum toxin A irreversibly interferes with acetylcholine (Ach) release by destroying the synaptosome-associated protein of 25 KDa (SNAP-25) and its effect begins 3-5 hours after injection and peak effect appears 2 weeks later. However, neuromuscular blockade by botulinum toxin A is rapidly reversed by axonal sprouting that emerge over 2 to 6 months for a gradual return of neuromuscular function, thereby limiting the duration of efficacy of botulinum toxin A. Recently botulinum toxin A is used therapeutically for a variety of spastic disorders, including strabismus, hemifacial spasm, skin wrinklers and disorders of GI smooth muscle. This review summarized the current state of knowledge concerning the use botulinum toxin in the achalasia and non-achalasia esophageal motility disorder.

Keywords: Botulinum toxin, Achalasia, Esophageal motility disorder

Article

Review Article

J Korean Dysphagia Soc 2015; 5(1): 14-17

Published online January 1, 2015

Copyright © The Korean Dysphagia Society.

Botulinum Toxin Injection for Achalasia and Non-achalasia Esophageal Motility Disorders

Jung Ho Park, M.D.

Department of Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea

Abstract

Botulinum toxin is one of the deadliest nerve poisons known throughout human history. Among seven different biological substances, only subtypes A, B and E have been implicated in human botulinum intoxication. Botulinum toxin A is synthesized intracellularly as an inactive, single-chain polypeptide that is converted to a dichain molecule by proteolysis. The dichain molecule is composed of a heavy chain (molecular weight 100 KDa) and a light chain (50 KDa) linked by a disulfide bond. Light chain of botulinum toxin A irreversibly interferes with acetylcholine (Ach) release by destroying the synaptosome-associated protein of 25 KDa (SNAP-25) and its effect begins 3-5 hours after injection and peak effect appears 2 weeks later. However, neuromuscular blockade by botulinum toxin A is rapidly reversed by axonal sprouting that emerge over 2 to 6 months for a gradual return of neuromuscular function, thereby limiting the duration of efficacy of botulinum toxin A. Recently botulinum toxin A is used therapeutically for a variety of spastic disorders, including strabismus, hemifacial spasm, skin wrinklers and disorders of GI smooth muscle. This review summarized the current state of knowledge concerning the use botulinum toxin in the achalasia and non-achalasia esophageal motility disorder.

Keywords: Botulinum toxin, Achalasia, Esophageal motility disorder

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