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Charcot-Marie-Tooth disease type 1 (CMT1, hereditary sensorimotor polyneuropathy type-1, HSMN1)

Demyelinating polyneuropathy. Epidemiology: - most common hereditary neuropathy [1] Pathology: 1) abnormal myelin formation 2) Schwann cell proliferation Genetics: 1) autosomal dominant 2) most kindreds have a duplication at 17p11.2 Clinical manifestations: (also see Charcot-Marie-Tooth disease) 1) slowly progressive distal muscle atrophy & weakness 2) absent deep tendon reflexes 3) high arched feet & palate may be present 4) hammer toes 5) palpably enlarged peripheral nerves Laboratory: - CMT1 gene mutation [1] Special laboratory: 1) nerve conduction studies: a) decreased nerve conduction velocity characteristic of demyelinating neuropathy (50% of normal conduction velocity) (< 38 m/s) b) diagnostic test of choice c) few other disorders show this degree of nerve conduction velocity slowing 2) electromyography: a) enlarged motor unit potential b) reduced recruitment c) fibrillation potentials not prominent 3) muscle biopsy shows chronic denervation, a non-specific finding

Specific

Charcot-Marie-Tooth disease type 1A; hereditary motor & sensory neuropathy 1A (CMT1A) Charcot-Marie-Tooth disease type 1B (CMT1B) Charcot-Marie-Tooth disease type 1C (CMT1C) Charcot-Marie-Tooth disease type 1D (CMT1D) Charcot-Marie-Tooth disease type 1E (CMT1E) Charcot-Marie-Tooth disease type 1F (CMT1F) Charcot-Marie-Tooth disease type 1X (CMTX)

General

Charcot-Marie-Tooth disease (peroneal muscle atrophy, hereditary sensorimotor polyneuropathy (HSMN))

References

  1. Medical Knowledge Self Assessment Program (MKSAP) 11, 17, 18. American College of Physicians, Philadelphia 1998, 2015, 2018