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Charcot-Marie-Tooth Disease Treatment & Management

  • Author: Divakara Kedlaya, MBBS; Chief Editor: Vinod K Panchbhavi, MD, FACS  more...
 
Updated: Mar 14, 2016
 

Approach Considerations

Charcot-Marie-Tooth (CMT) disease continues to be an incurable condition. Patients should be evaluated and treated symptomatically in a multidisciplinary approach by a team that includes the following[41] :

  • Neurologist
  • Physiatrist
  • Orthopedic surgeon
  • Physical therapist
  • Occupational therapist
  • Orthotists
  • Mental health provider
  • Genetic counselor

This approach is crucial for improving the quality of life of CMT patients.[42]  Specialists in neurogenetics may be consulted to order specific genetic tests and proper genetic counseling.

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Medical Therapy

Currently, no medical treatment exists to reverse or slow the natural disease process for the underlying disorder. Nothing can correct the abnormal myelin, prevent its degeneration, or prevent axonal degeneration.[43] Improved understanding of the genetics and biochemistry of the disorder offers hope for an eventual treatment.

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Surgical Therapy

Orthopedic surgery is required to correct severe pes cavus deformities, scoliosis, and other joint deformities. Treatment is determined by the age of the patient and the cause and severity of the deformity.

Surgical procedures consist of the following three types:

  • Soft-tissue procedures (plantar fascia release, tendon release or transfer)
  • Osteotomy (metatarsal, midfoot, calcaneal)
  • Joint-stabilizing procedures (triple arthrodesis)

Procedures are usually staged. The initial procedure is a radical plantar or plantar-medial release-plantar fasciotomy, with a dorsal closing-wedge osteotomy of the first metatarsal base if necessary. Tendo calcaneus lengthening should not be performed as part of the initial procedure, because the force used to dorsiflex the forefoot causes the calcaneus to dorsiflex into an unacceptable position.

If the hindfoot is flexible and a posterior release is not necessary, posterior tibial tendon transfer can be done as part of the initial procedure for severe anterior tibial weakness.[44] . In a prospective study of 14 patients with CMT disease who had cavovarus foot deformity, Dreher et al found that tibialis posterior tendon transfer was effective at correcting the foot-drop component of cavovarus foot deformity; the transfer apparently worked as an active substitution.[45]

When the hindfoot is flexible, early aggressive treatment with soft-tissue releases can delay the need for more extensive reconstructive procedures. The Jones procedure includes transfer of the extensor hallucis longus tendon to the first metatarsal head and arthrodesis of the interphalangeal joint of the great toe.

A review paper by Faldini et al concluded that plantar fasciotomy, midtarsal osteotomy, the Jones procedure, and dorsiflexion osteotomy of the first metatarsal yielded adequate correction of flexible cavus feet in patients with CMT disease in the absence of fixed hindfoot deformity.[46]  

The Coleman block test is sometimes used to help decide what type of surgery is best. In cases of cavovarus deformity, this test evaluates hindfoot flexibility.[47] The Coleman block test is performed by placing the patient's foot on a wood block that is 2.5-4 cm thick, with the heel and lateral border of the foot on the block and bearing full weight while the first, second, and third metatarsals are allowed to hang freely into plantarflexion and pronation.

If heel varus corrects while the patient is standing on the block, the hindfoot is considered flexible. If the subtalar joint is supple and corrects with the block test, then surgical procedures may be directed at correcting forefoot pronation, which is usually due to plantarflexion of the first metatarsal. If the hindfoot is rigid, then surgical correction of the forefoot and hindfoot is required.

Triple arthrodesis serves as a salvage procedure for patients in whom other procedures have been unsuccessful, as well as in patients with untreated fixed deformities.

Children younger than 8 years with supple hindfeet usually respond to plantar releases and appropriate tendon transfers. A first metatarsal osteotomy may be needed in some cases.

Children younger than 12 years with rigid hindfoot deformities may need radical plantar-medial release, first metatarsal osteotomy, and Dwyer lateral closing-wedge osteotomy of the calcaneus to correct the deformities.

In the early 1970s, the Akron dome osteotomy was developed as a salvage surgical option to manage rigid cavus deformity of the foot. In a retrospective study, Weiner et al showed that this operation is a valuable salvage procedure in the management of the rigid cavus deformity in children with CMT disease.[48]

Wukich and Bowen reported that only 14% of patients with CMT disease required triple arthrodesis.[49] They also reported hindfoot stability with triple arthrodesis, and when the posterior tibial tendon was transferred anteriorly, this eliminated the need for a postoperative drop-foot brace. They reported good or excellent results in 88% of patients who were treated with this method.

Ward et al studied the long-term results of surgical reconstruction procedures for cavovarus foot deformity in 25 patients with CMT disease who had undergone the procedure between 1970 and 1994 and were evaluated at a mean follow-up of 26.1 years.[50] The authors found that the use of soft-tissue procedures and first metatarsal osteotomy resulted in lower rates of degenerative changes and reoperations in comparison with results obtained with triple arthrodesis.

Generally, spinal deformities in children with CMT disease can be treated with the same techniques used for idiopathic scoliosis.

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Prevention

Regular and proper follow-up and therapeutic interventions are necessary to avoid joint contractures and deformities.

Proper genetic counseling helps parents to understand the risk of having children with this disorder and gives them a chance to make informed decisions regarding pregnancy.[19, 32]

A study of mitochondrial data from 442 patients suggested that MT-ATP6 mutations are an important cause of CMT disease and can be evaluated with a simple blood test.[51]

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Long-Term Monitoring

Patients should have regular follow-up visits to check for deterioration in function and the development of contractures. This follow-up allows early detection of complications. Proper interventions early in the disease course help to avoid significant and permanent functional limitations.[33]

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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, Colorado Medical Society, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Vinod K Panchbhavi, MD, FACS Professor of Orthopedic Surgery, Chief, Division of Foot and Ankle Surgery, Director, Foot and Ankle Fellowship Program, Department of Orthopedics, University of Texas Medical Branch School of Medicine

Vinod K Panchbhavi, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Surgeons, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, Orthopaedic Trauma Association, Texas Orthopaedic Association

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Styker.

Additional Contributors

James K DeOrio, MD Associate Professor of Orthopedic Surgery, Duke University School of Medicine

James K DeOrio, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Foot and Ankle Society

Disclosure: Received royalty from Merete for other; Received royalty from SBi for other; Received royalty from BioPro for other; Received honoraria from Acumed, LLC for speaking and teaching; Received honoraria from Wright Medical Technology, Inc for speaking and teaching; Received honoraria from SBI for speaking and teaching; Received honoraria from Integra for speaking and teaching; Received honoraria from Datatrace Publishing for speaking and teaching; Received honoraria from Exactech, Inc for speaking a.

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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 1. Charcot-Marie-Tooth Disorders: Genetic and Clinical Feature Comparison
CMT Type Chromosome; Inheritance Pattern Age of Onset Clinical Features Average NCVs§
CMT 1A (PMP-22 dupl.) 17p11; AD* First decade Distal weakness 15-20 m/s
CMT 1B (P0 -MPZ)** 1q22; AD First decade Distal weakness <20 m/s
CMT 1C (non A, non B) 16p13;AD Second decade Distal weakness 26-42 m/s
CMT 1D (early growth response [EGR]–2)#[[22] 24] 10q21; AD First decade Distal weakness 15-20 m/s
CMT 1E 17p11; AD First decade Distal weakness, deafness 15-20 m/s
CMT 1F 8p21; AD First decade Distal weakness 15-20 m/s
CMT X (Connexin-32)[23, 24, 25, 26, 27] Xq13; XD Second decade Distal weakness 25-40 m/s
CMT 2A 1p36; AD 10 y Distal weakness >38 m/s
CMT 2B 3q; AD Second decade Distal weakness,



sensory loss, skin ulcers



Axon loss; Normal
CMT 2C 12q23-q24, AD First decade Vocal cord, diaphragm, and



distal weakness



>50 m/s
CMT 2D 7p14; AD 16-30 y Distal weakness, upper limb predominantly Axon loss; N††
CMT 2E 8p21; AD 10-30 y Distal weakness, lower limb predominantly Axon loss; N
CMT 2F 7q11-q21; AD 15-25 y Distal weakness Axon loss; N
CMT 2G 12q12-q13; ?AD 9-76 y Distal weakness Axon loss; N
CMT 2H ?; AR 15-25 y Distal weakness, Pyramidal features Axon loss; N
CMT 2I 1q22; AD 47-60 y Distal weakness Axon loss; N
CMT 2J 1q22; AD 40-50 y Distal weakness, hearing loss Axon loss; N
CMT 2K 8q13-q21; AR <4 y Distal weakness Axon loss; N
CMT 2L 12q24; AD 15-25 y Distal weakness Axon loss; N
CMT R-Ax (Ouvrier) AR First decade Distal weakness Axon loss; N
CMT R-Ax (Moroccan) 1q21; AR Second decade Distal weakness Axon loss; N
Cowchock syndrome Xq24-q26 First decade Distal weakness, deafness, mental retardation Axon loss; N
HNPP|| (PMP-22)



Or tomaculous neuropathy



17p11; AD All ages Episodic weakness and numbness Conduction Blocks
Dejerine-Sottas syndrome (DSS) or hereditary motor and sensory neuropathy (HMSN) 3 P0; AR



PMP-22; AD



8q23; AD



2 y Severe weakness <10 m/s
Congenital



hypomyelination (CH)



P0, EGR2 or PMP-22



AR



Birth Severe weakness < 10 m/s
CMT 4A 8q13; AR Childhood Distal weakness Slow
CMT 4B



(Myotubular in-related



protein-2)[17]



11q23; AR 2-4 y Distal and proximal



weakness



Slow
CMT 4C 5q23; AR 5-15 y Delayed walking 14-32 m/s
CMT 4D (Lom)



(N-myc Downstream-



Regulated Gene 1)



8q24; AR 1-10 y Distal muscle wasting, foot and hand deformities 10-20 m/s
CMT 4E (EGR2) 10q21; AR Birth Infant hypotonia 9-20 m/s
CMT 4G 10q23.2; AR 8-16 years Distal weakness 9-20 m/s
CMT 4H 12p11.21-q13.11; AR 0-2 years Delayed walking 9-20 m/s
CMT 4F 19q13; AR 1-3 y Motor delay Absent
*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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