Charcot-Marie-Tooth disease: Difference between revisions

From Citizendium
Jump to navigation Jump to search
imported>Howard C. Berkowitz
(New page: {{subpages}} <!-- Text is transcluded from the BASEPAGENAME/Definition subpage-->)
 
imported>Howard C. Berkowitz
No edit summary
Line 1: Line 1:
{{subpages}}
{{subpages}}
<!-- Text is transcluded from the BASEPAGENAME/Definition subpage-->
'''Charcot-Marie-Tooth disease (CMT)''' is part of a family of genetically-defined [[neurology|neurologic]] diseases characterized by progressive distal wasting and loss of reflexes in the muscles of the legs (and occasionally involving the arms). Onset is usually in the second to fourth decade of life.
 
This condition has been divided into two subtypes, hereditary motor and sensory neuropathy ( HMSN) types I and II. HMSN I is associated with abnormal nerve conduction velocities and nerve hypertrophy, features not seen in HMSN II. <ref>Adams et al., ''Principles of Neurology'', 6th ed, p1343</ref>
 
The genetic abnormality is associated with the coding for [[peripheral myelin protein 22]]. It is most an autosomal dominant trait.

Revision as of 12:28, 12 June 2010

This article is a stub and thus not approved.
Main Article
Discussion
Related Articles  [?]
Bibliography  [?]
External Links  [?]
Citable Version  [?]
 
This editable Main Article is under development and subject to a disclaimer.

Charcot-Marie-Tooth disease (CMT) is part of a family of genetically-defined neurologic diseases characterized by progressive distal wasting and loss of reflexes in the muscles of the legs (and occasionally involving the arms). Onset is usually in the second to fourth decade of life.

This condition has been divided into two subtypes, hereditary motor and sensory neuropathy ( HMSN) types I and II. HMSN I is associated with abnormal nerve conduction velocities and nerve hypertrophy, features not seen in HMSN II. [1]

The genetic abnormality is associated with the coding for peripheral myelin protein 22. It is most an autosomal dominant trait.

  1. Adams et al., Principles of Neurology, 6th ed, p1343