Physical Medicine and Rehabilitation for Charcot-Marie-Tooth Disease 

  • Author: Divakara Kedlaya, MBBS; Chief Editor: Robert H Meier III, MD   more...
 
Updated: May 1, 2012
 

Background

Charcot-Marie-Tooth disease (CMT) is the most common inherited neurologic disorder. CMT is characterized by inherited neuropathies without known metabolic derangements. In 1886, Professor Jean Martin Charcot of France (1825-1893) and his student Pierre Marie (1853-1940) published the first description of distal muscle weakness and wasting beginning in the legs, calling it peroneal muscular atrophy.

Howard Henry Tooth (1856-1926) described the same disease in his Cambridge dissertation in 1886, calling the condition peroneal progressive muscular atrophy. Tooth was the first to correctly attribute the disorder's symptoms to neuropathy rather than to myelopathy, as physicians had done before him. In 1912, Hoffman identified a case of peroneal muscular atrophy with thickened nerves. This disease was referred to as Hoffman disease and later was known as Charcot-Marie-Tooth-Hoffman disease.

In 1968, CMT was subdivided into 2 types, CMT-1 and CMT-2, based on pathologic and physiologic criteria. CMT has been further subdivided, based on the genetic cause of the disease. With the advent of genetic testing, all of the different diseases that fall under the heading of CMT syndrome eventually are likely to become distinguishable.

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Pathophysiology

Charcot-Marie-Tooth disease (CMT) is actually a heterogeneous group of genetically distinct disorders with a similar clinical presentation. CMT-1 is a disorder of peripheral myelination resulting from a mutation in the peripheral myelin protein-22 (PMP-22) gene. Mutations in the gene encoding the major peripheral nervous system myelin protein, myelin protein zero (MPZ), account for 5% of patients with CMT. The mutation results in abnormal myelin that is unstable and spontaneously breaks down. This process results in demyelination, leading to uniform slowing of conduction velocity.

Slowing of conduction in motor and sensory nerves was believed to cause weakness and numbness. A study by Krajewski and colleagues suggested that neurologic dysfunction and clinical disability in CMT-1A are caused by loss or damage to large-diameter motor and sensory axons.[1] Pain and temperature sensations usually are not affected, because they are carried by unmyelinated (type C) nerve fibers.

In response to demyelination, Schwann cells proliferate and form concentric arrays of remyelination. Repeated cycles of demyelination and remyelination result in a thick layer of abnormal myelin around the peripheral axons. These changes cause what is referred to as an onion bulb appearance.

CMT-2 is primarily a neuronal (ie, axonal) disorder, not a demyelinating disorder. Type 2 results in peripheral neuropathy through direct axonal death and wallerian degeneration. CMT-3 (also known as Dejerine-Sottas disease) is characterized by infantile onset. Type 3 results in severe demyelination with delayed motor skills and is a much more severe form than type 1. Marked segmental demyelination with thinning of the myelin around the nerve is observed on histologic examination. CMT-X (X-linked CMT) and CMT-4 are also demyelinating neuropathies.

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Epidemiology

Frequency

United States

The prevalence of Charcot-Marie-Tooth disease (CMT) is 1 person per 2500 population, or about 125,000 patients in the US. CMT-1 incidence is 15 persons per 100,000 population. CMT-1A incidence is 10.5 persons per 100,000 population, or 70% of CMT-1 cases. CMT-2 incidence is 7 persons per 100,000 population. CMT-X represents at least 10-20% of persons with the CMT syndrome.

International

In Japan, the prevalence of Charcot-Marie-Tooth disease is reportedly 10.8 cases per 100,000 population. In Italy, the prevalence is reported to be 17.5 cases per 100,000 population, and in Spain, it is 28.2 cases per 100,000 population.

Mortality/Morbidity

Morbidity in Charcot-Marie-Tooth disease is mainly secondary to distal muscle weakness and foot deformities.[2, 3] In rare cases, phrenic nerve involvement of the diaphragm can cause ventilatory difficulties.

Race

No race predilection is recognized in Charcot-Marie-Tooth disease.

Sex

There is no known sex predilection in Charcot-Marie-Tooth disease.

Age

The age of presentation for Charcot-Marie-Tooth disease (CMT) varies depending on the type of CMT. Please refer to the table under Causes.

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Contributor Information and Disclosures
Author

Divakara Kedlaya, MBBS  Clinical Associate Professor, Department of Physical Medicine and Rehabilitation, Loma Linda University School of Medicine; Medical Director, Physical Medicine and Rehabilitation and Pain Management, St Mary Corwin Medical Center

Divakara Kedlaya, MBBS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, and Colorado Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Milton J Klein, DO, MBA  Consulting Physiatrist, Heritage Valley Health System-Sewickley Hospital and Ohio Valley General Hospital

Milton J Klein, DO, MBA is a member of the following medical societies: American Academy of Disability Evaluating Physicians, American Academy of Medical Acupuncture, American Academy of Osteopathy, American Academy of Physical Medicine and Rehabilitation, American Medical Association, American Osteopathic Association, American Osteopathic College of Physical Medicine and Rehabilitation, American Pain Society, and Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Michael T Andary, MD, MS  Professor, Residency Program Director, Department of Physical Medicine and Rehabilitation, Michigan State University College of Osteopathic Medicine

Michael T Andary, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, and Association of Academic Physiatrists

Disclosure: Allergan Honoraria Speaking and teaching

Kelly L Allen, MD  Medical Director, Medevals

Disclosure: Nothing to disclose.

Chief Editor

Robert H Meier III, MD  Director, Amputee Services of America; Active Medical Staff, Presbyterian/St Luke's Hospital, Spalding Rehabilitation Hospital, Select Specialty Hospital; Consulting Staff, Kindred Hospital

Robert H Meier III, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Association of Academic Physiatrists

Disclosure: Nothing to disclose.

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Foot deformities in a 16-year-old boy with Charcot-Marie-Tooth disease type 1A.
Charcot-Marie-Tooth disease type 1A DNA test showing duplication in the short arm of chromosome 17 (A) compared with normal (B).
Nerve conduction study showing decreased nerve conduction velocity in the median nerve in an 18-year-old woman with Charcot-Marie-Tooth disease type 1.
Table. Charcot-Marie-Tooth Disorders: Genetic and Clinical Feature Comparison
CMT TypeChromosome; Inheritance PatternAge of OnsetClinical FeaturesAverage NCVs§
CMT-1A (PMP-22 dupl.)17p11; AD*First decadeDistal weakness15-20 m/s
CMT-1B (P0 -MPZ)**1q22; ADFirst decadeDistal weakness< 20 m/s
CMT-1C (non-A, non-B)16p13;ADSecond decadeDistal weakness26-42 m/s
CMT-1D (EGR-2)#10q21; ADFirst decadeDistal weakness15-20 m/s
CMT-1E17p11; ADFirst decadeDistal weakness, deafness15-20 m/s
CMT-1F8p21; ADFirst decadeDistal weakness15-20 m/s
CMT-X (connexin-32)Xq13; XD‡Second decadeDistal weakness25-40 m/s
CMT-2A1p36; AD10 yDistal weakness>38 m/s
CMT-2B3q; ADSecond decadeDistal weakness,



sensory loss, skin ulcers



Axon loss; Normal
CMT-2C12q23-q24, ADFirst decadeVocal cord, diaphragm, and



distal weakness



>50 m/s
CMT-2D7p14; AD16-30 yDistal weakness, upper limb predominantlyAxon loss; N††
CMT-2E8p21; AD10-30 yDistal weakness, lower limb predominantlyAxon loss; N
CMT-2F7q11-q21; AD15-25 yDistal weaknessAxon loss; N
CMT-2G12q12-q13; ?AD9-76 yDistal weaknessAxon loss; N
CMT-2H?; AR†15-25 yDistal weakness, pyramidal featuresAxon loss; N
CMT-2I1q22; AD47-60 yDistal weaknessAxon loss; N
CMT-2J1q22; AD40-50 yDistal weakness, hearing lossAxon loss; N
CMT-2K8q13-q21; AR< 4 yDistal weaknessAxon loss; N
CMT-2L12q24; AD15-25 yDistal weaknessAxon loss; N
CMT – R-Ax (Ouvrier)ARFirst decadeDistal weaknessAxon loss; N
CMT – R-Ax (Moroccan)1q21; ARSecond decadeDistal weaknessAxon loss; N
Cowchock syndromeXq24-q26First decadeDistal weakness, deafness, mental retardationAxon loss; N
HNPP|| (PMP-22)



or tomaculous neuropathy



17p11; ADAll agesEpisodic weakness and numbnessConduction Blocks
Dejerine-Sottas-syndrome (DSS) or HMSN-3P0; AR



PMP-22; AD



8q23; AD



2 ySevere weakness< 10 m/s
Congenital



hypomyelination (CH)



P0, EGR-2 or PMP-22



AR



BirthSevere weakness< 10 m/s
CMT-4A8q13; ARChildhoodDistal weaknessSlow
CMT-4B



(myotubularin- related



protein 2)



11q23; AR2-4 yDistal and proximal



weakness



Slow
CMT-4C5q23; AR5-15 yDelayed walking14-32 m/s
CMT-4D (Lom)



(N-myc downstream-



regulated gene 1)



8q24; AR1-10 yDistal muscle wasting, foot and hand deformities10-20 m/s
CMT-4E (EGR-2)10q21; ARBirthInfant hypotonia9-20 m/s
CMT-4G10q23.2; AR8-16 yearsDistal weakness9-20 m/s
CMT-4H12p11.21-q13.11; AR0-2 yearsDelayed walking9-20 m/s
CMT-4F19q13; AR1-3 yMotor delayAbsent
*Autosomal dominant



†Autosomal recessive



‡X-linked dominant



§Nerve conduction velocities



||Hereditary neuropathy with liability to pressure palsy



¶Peripheral myelin protein



#Early growth response



**Myelin protein zero



††Normal



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