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DNM2-Related Intermediate Charcot-Marie-Tooth Neuropathy

Synonym: Dominant Intermediate Charcot-Marie-Tooth Neuropathy Type B (DI-CMTB)

, MD, PhD and , MS.

Author Information

Initial Posting: ; Last Update: June 25, 2015.

Estimated reading time: 11 minutes

Summary

Clinical characteristics.

DNM2-related intermediate Charcot-Marie-Tooth neuropathy (DI-CMTB) has a classic, mild to moderately severe Charcot-Marie-Tooth hereditary neuropathy phenotype that often includes pes cavus foot deformity, depressed tendon reflexes, distal muscle weakness and atrophy, and sensory loss. Age of onset varies greatly among affected individuals and ranges from age two to 50 years. It is unusual for individuals with DI-CMTB to become wheelchair bound. Other findings include asymptomatic neutropenia and early-onset cataracts (often noted in childhood before age 15 years).

Diagnosis/testing.

The diagnosis is suspected in individuals with typical findings of CMT hereditary neuropathy and intermediate or axonal motor median nerve conduction velocities (NCV) ranging from 26 m/s to normal. Diagnosis requires identification of a heterozygous pathogenic variant in DNM2, the only gene known to be associated with DI-CMTB.

Management.

Treatment of manifestations: Treatment of DI-CMTB is symptomatic and involves evaluation and management by a multidisciplinary team that includes neurologists, orthopedic surgeons, and physical and occupational therapists. Treatment may include ankle/foot orthoses, orthopedic surgery, forearm crutches or canes, wheelchairs, acetaminophen or nonsteroidal anti-inflammatory agents (NSAIDs) for musculoskeletal pain, and career and employment counseling.

Prevention of secondary complications: Physical therapy to prevent foot contractures, acquired foot deformities, and difficulty walking.

Surveillance: Regular evaluation by the multidisciplinary team to determine neurologic status and functional disability.

Pregnancy management: In general there appears to be an increased occurrence of abnormal fetal presentation and maternal postpartum bleeding in women with Charcot-Marie-Tooth disease.

Agents/circumstances to avoid: All drugs or agents known to be hazardous for peripheral neuropathies.

Genetic counseling.

DI-CMTB is inherited in an autosomal dominant manner. Most individuals diagnosed with DI-CMTB have an affected parent. The proportion of cases caused by a heterozygous de novo pathogenic variant is unknown. Each child of an individual with DI-CMTB has a 50% chance of inheriting the pathogenic variant. Prenatal testing for pregnancies at increased risk is possible if the pathogenic variant has been identified in an affected family member. Requests for prenatal testing for conditions which (like DI-CMTB) do not affect intellect and have some treatment available are not common.

Diagnosis

Suggestive Findings

DNM2-related intermediate Charcot-Marie-Tooth neuropathy (DI-CMTB) should be suspected in individuals with the following clinical findings, nerve conduction velocities, and neuropathology:

Clinical manifestations

  • Sensory and motor deficiencies involving the lower legs
    • Sensory loss
    • Depressed tendon reflexes
    • Distal muscle weakness and atrophy
    • Pes cavus foot deformity
  • Asymptomatic neutropenia
  • Early-onset cataracts (noted before age 15 years)

Nerve conduction velocities (NCVs) are "intermediate" (i.e., 25-45 m/s) between a demyelinating and axonal neuropathy using strict electrophysiologic criteria [Davis et al 1978, Nicholson & Myers 2006].

Neuropathology. Sural nerve biopsy has shown diffuse loss of large myelinated fibers, clusters of regenerating myelinated axons, and fibers with focal myelin thickenings [Kennerson et al 2001, Claeys et al 2009].

Establishing the Diagnosis

The diagnosis of DI-CMTB is established in a proband by the identification of a heterozygous pathogenic variant in DNM2.

Molecular testing approaches can include serial single-gene testing, use of a multigene panel, and genomic testing.

Serial single-gene testing can be considered based on the order in which pathogenic variants most commonly occur in individuals with the above suggestive findings:

A multigene panel that includes DNM2 and other genes of interest (see Differential Diagnosis) may also be considered. Note: The genes included and sensitivity of multigene panels vary by laboratory and over time.

For an introduction to multigene panels click here. More detailed information for clinicians ordering genetic tests can be found here.

Genomic testing may be considered if serial single-gene testing (and/or use of a multigene panel) has not confirmed a diagnosis in an individual with features of DI-CMTB. Such testing may include exome sequencing, genome sequencing, and mitochondrial sequencing.

For an introduction to comprehensive genomic testing click here. More detailed information for clinicians ordering genomic testing can be found here.

Table 1.

Molecular Genetic Testing Used in DNM2-Related Intermediate Charcot-Marie-Tooth Neuropathy

Gene 1Test MethodProportion of Probands with a Pathogenic Variant 2 Detectable by This Method
DNM2Sequence analysis 3Nearly 100%
Gene-targeted deletion/duplication analysis 4None reported 5
1.
2.

See Molecular Genetics for information on allelic variants.

3.

Sequence analysis detects variants that are benign, likely benign, of uncertain significance, likely pathogenic, or pathogenic. Pathogenic variants may include small intragenic deletions/insertions and missense, nonsense, and splice site variants; typically, exon or whole-gene deletions/duplications are not detected. For issues to consider in interpretation of sequence analysis results, click here.

4.

Gene-targeted deletion/duplication analysis detects intragenic deletions or duplications. Methods that may be used include: quantitative PCR, long-range PCR, multiplex ligation-dependent probe amplification (MLPA), and gene-targeted microarray designed to detect single-exon deletions or duplications.

5.

No deletions or duplications involving DNM2 as causative of DI-CMTB have been reported.

Clinical Characteristics

Clinical Description

DNM2-related intermediate Charcot-Marie-Tooth neuropathy (DI-CMTB) is a so-called "dominant intermediate form" of CMT neuropathy because it is inherited in an autosomal dominant manner and it is "intermediate" between a demyelinating and axonal neuropathy using strict electrophysiologic criteria for nerve conduction velocities (NCVs). The condition is characterized by a classic, mild to moderately severe Charcot-Marie-Tooth hereditary neuropathy phenotype that often includes pes cavus foot deformity, depressed tendon reflexes, distal muscle weakness and atrophy, and sensory loss.

Age of onset varies greatly among affected individuals and ranges from age two to 50 years. Some persons require AFO braces or other walking aids. Three percent of affected individuals become wheelchair bound; one person in the Claeys et al [2009] study required a wheelchair at age 61 years.

Other findings include asymptomatic neutropenia and early-onset cataracts (often noted in childhood before age 15 years).

Electrophysiologic studies indicate intermediate or axonal motor median nerve conduction velocities (NCV) ranging from 26 m/s to normal values.

Genotype-Phenotype Correlations

Strong genotype-phenotype correlations have not been reported.

The majority of DNM2 pathogenic variants appear to be in the domain encoding homology to pleckstrin [Züchner et al 2005, Fabrizi et al 2007]; however, exceptions have been identified [Claeys et al 2009, Susman et al 2010].

Penetrance

DNM2 pathogenic variants are penetrant over a wide range of ages (age 2-50 years) [Claeys et al 2009, Haberlová et al 2011].

Anticipation

Anticipation is not observed.

Prevalence

DI-CMTB is a rare cause of CMT. Up to 3.4% of CMT (in which CMT1A, 1B, and 1X have already been excluded) is caused by a DNM2 pathogenic variant [Claeys et al 2009].

Differential Diagnosis

Other forms of intermediate CMT:

  • DI-CMTA, linked to the 10q24-q25.1 region
  • DI-CMTC, caused by heterozygous pathogenic variants in YARS (formerly TyrRS)
  • DI-CMTD, caused by heterozygous pathogenic variants in MPZ
  • GNB4-related CMT, also inherited in an autosomal dominant manner

It is usually not possible to differentiate between DI-CMTB, other intermediate forms of CMT, and most CMT2 types based on clinical findings [Nicholson & Myers 2006], unless cataract and/or neutropenia (occasional findings in DI-CMTB) are present.

See CMT Overview, particularly to exclude potentially treatable causes of acquired neuropathy.

Management

Evaluations Following Initial Diagnosis

To establish the extent of disease and needs in an individual diagnosed with DNM2-related intermediate Charcot-Marie-Tooth neuropathy (DI-CMTB), the following evaluations are recommended:

  • Neurologic examination
  • Electrophysiologic studies to establish a baseline for further monitoring of disease progression
  • Complete blood count (CBC) with absolute neutrophil count (ANC) to evaluate for neutropenia
  • Ophthalmologic examination for cataract
  • Consultation with a clinical geneticist and/or genetic counselor

Treatment of Manifestations

Treatment of DI-CMTB is symptomatic and involves evaluation and management by a multidisciplinary team that includes neurologists, orthopedic surgeons, and physical and occupational therapists. Due to the great phenotypic variability, disease treatment should be tailored to the individual's needs.

Treatment may include:

  • Ankle/foot orthoses
  • Orthopedic surgery
  • Forearm crutches or canes; rarely, wheelchairs
  • Treatment of musculoskeletal pain with acetaminophen or nonsteroidal anti-inflammatory agents (NSAIDs)
  • Career and employment counseling

Prevention of Secondary Complications

The most common secondary complications include foot contractures and acquired foot deformities, difficulty walking, and, in severe cases, inability to ambulate. Physical therapies such as stretching and exercise are recommended to prevent these secondary complications.

Surveillance

Surveillance includes regular evaluation by the multidisciplinary team to determine neurologic status and functional disability.

Agents/Circumstances to Avoid

Medications that are toxic or potentially toxic to persons with CMT comprise a spectrum of risk ranging from definite high risk to negligible risk. Click here for an up-to-date list.

Evaluation of Relatives at Risk

See Genetic Counseling for issues related to testing of at-risk relatives for genetic counseling purposes.

Pregnancy Management

Although no systemic studies have been done concerning pregnancy in women with DI-CMTB, there are reports of an increased occurrence of abnormal fetal presentation and maternal postpartum bleeding in women with CMT in general [Hoff et al 2005]. The early miscarriage rate is not increased in women with CMT [Argov & de Visser 2009].

Therapies Under Investigation

Search ClinicalTrials.gov for access to information on clinical studies for a wide range of diseases and conditions. Note: There may not be clinical trials for this disorder.

Genetic Counseling

Genetic counseling is the process of providing individuals and families with information on the nature, inheritance, and implications of genetic disorders to help them make informed medical and personal decisions. The following section deals with genetic risk assessment and the use of family history and genetic testing to clarify genetic status for family members. This section is not meant to address all personal, cultural, or ethical issues that individuals may face or to substitute for consultation with a genetics professional. —ED.

Mode of Inheritance

DNM2-related intermediate Charcot-Marie-Tooth neuropathy (DI-CMTB) is inherited in an autosomal dominant manner.

Risk to Family Members

Parents of a proband

  • Most individuals diagnosed with DI-CMTB have an affected parent.
  • A proband with DI-CMTB may have the disorder as the result of de novo DNM2 mutation. The proportion of cases caused by a de novo pathogenic variant is unknown.
  • If the pathogenic variant found in the proband cannot be detected in leukocyte DNA of either parent, two possible explanations are germline mosaicism in a parent or de novo mutation in the proband. Although no instances of germline mosaicism have been reported, it remains a possibility.
  • Recommendations for the evaluation of parents of a proband with an apparent de novo pathogenic variant include DNM2 molecular genetic testing for the variant identified in the proband. Evaluation of parents may determine that one is affected but has escaped previous diagnosis because of failure by health care professionals to recognize the syndrome and/or a milder phenotypic presentation. Therefore, an apparently negative family history cannot be confirmed until appropriate evaluations have been performed.

Note: (1) Although most individuals diagnosed with DI-CMTB have an affected parent, the family history may appear to be negative because of failure to recognize the disorder in family members, early death of the parent before the onset of symptoms, or late onset of the disease in the affected parent. (2) If the parent is the individual in whom the pathogenic variant first occurred s/he may have somatic mosaicism for the variant and may be mildly/minimally affected.

Sibs of a proband

  • The risk to the sibs of the proband depends on the genetic status of the proband's parents.
  • If a parent of the proband is affected and/or has a pathogenic variant, the risk to the sibs of inheriting the variant is 50%.
  • When the parents are clinically unaffected, the risk to the sibs of a proband appears to be low.
  • The sibs of a proband with clinically unaffected parents are still at increased risk for DI-CMTB because of the possibility of reduced penetrance in a parent.
  • If the pathogenic variant found in the proband cannot be detected in the leukocyte DNA of either parent, the empiric recurrence risk to sibs is approximately 1% because of the theoretic possibility of parental germline mosaicism.

Offspring of a proband. Each child of an individual with DI-CMTB has a 50% chance of inheriting the DNM2 pathogenic variant.

Other family members

  • The risk to other family members depends on the status of the proband's parents.
  • If a parent is affected and/or has a pathogenic variant, his or her family members may be at risk.

Related Genetic Counseling Issues

Considerations in families with an apparent de novo pathogenic variant. When neither parent of a proband with an autosomal dominant condition has clinical evidence of the disorder or the pathogenic variant, it is likely that the proband has a de novo pathogenic variant. However, possible non-medical explanations including alternate paternity or maternity (e.g., with assisted reproduction) or undisclosed adoption could also be explored.

Family planning

  • The optimal time for determination of genetic risk and discussion of the availability of prenatal testing is before pregnancy.
  • It is appropriate to offer genetic counseling (including discussion of potential risks to offspring and reproductive options) to young adults who are affected or at risk of being affected.

DNA banking is the storage of DNA (typically extracted from white blood cells) for possible future use. Because it is likely that testing methodology and our understanding of genes, allelic variants, and diseases will improve in the future, consideration should be given to banking DNA of affected individuals.

Prenatal Testing and Preimplantation Genetic Diagnosis

Once the DNM2 pathogenic variant has been identified in an affected family member, prenatal testing for a pregnancy at increased risk and preimplantation genetic diagnosis for DNM2-related intermediate Charcot-Marie-Tooth neuropathy are possible.

Differences in perspective may exist among medical professionals and within families regarding the use of prenatal testing, particularly if the testing is being considered for the purpose of pregnancy termination rather than early diagnosis. While most centers would consider decisions regarding prenatal testing to be the choice of the parents, discussion of these issues is appropriate.

Resources

GeneReviews staff has selected the following disease-specific and/or umbrella support organizations and/or registries for the benefit of individuals with this disorder and their families. GeneReviews is not responsible for the information provided by other organizations. For information on selection criteria, click here.

  • Association CMT France
    France
    Phone: 820 077 540; 2 47 27 96 41
  • Charcot-Marie-Tooth Association (CMTA)
    PO Box 105
    Glenolden PA 19036
    Phone: 800-606-2682 (toll-free); 610-499-9264
    Fax: 610-499-9267
    Email: info@cmtausa.org
  • European Charcot-Marie-Tooth Consortium
    Department of Molecular Genetics
    University of Antwerp
    Antwerp Antwerpen B-2610
    Belgium
    Fax: 03 2651002
    Email: gisele.smeyers@ua.ac.be
  • Hereditary Neuropathy Foundation, Inc.
    432 Park Avenue South
    4th Floor
    New York NY 10016
    Phone: 855-435-7268 (toll-free); 212-722-8396
    Fax: 917-591-2758
    Email: info@hnf-cure.org
  • My46 Trait Profile
  • National Library of Medicine Genetics Home Reference
  • NCBI Genes and Disease
  • TREAT-NMD
    Institute of Genetic Medicine
    University of Newcastle upon Tyne
    International Centre for Life
    Newcastle upon Tyne NE1 3BZ
    United Kingdom
    Phone: 44 (0)191 241 8617
    Fax: 44 (0)191 241 8770
    Email: info@treat-nmd.eu
  • Association Francaise contre les Myopathies (AFM)
    1 Rue de l'International
    BP59
    Evry cedex 91002
    France
    Phone: +33 01 69 47 28 28
    Email: dmc@afm.genethon.fr
  • European Neuromuscular Centre (ENMC)
    Lt Gen van Heutszlaan 6
    3743 JN Baarn
    Netherlands
    Phone: 31 35 5480481
    Fax: 31 35 5480499
    Email: enmc@enmc.org
  • Muscular Dystrophy Association - USA (MDA)
    222 South Riverside Plaza
    Suite 1500
    Chicago IL 60606
    Phone: 800-572-1717
    Email: mda@mdausa.org
  • Muscular Dystrophy UK
    61A Great Suffolk Street
    London SE1 0BU
    United Kingdom
    Phone: 0800 652 6352 (toll-free); 020 7803 4800
    Email: info@musculardystrophyuk.org
  • RDCRN Patient Contact Registry: Inherited Neuropathies Consortium

Molecular Genetics

Information in the Molecular Genetics and OMIM tables may differ from that elsewhere in the GeneReview: tables may contain more recent information. —ED.

Table A.

DNM2-Related Intermediate Charcot-Marie-Tooth Neuropathy: Genes and Databases

Locus NameGeneChromosome LocusProteinLocus-Specific DatabasesHGMDClinVar
DI-CMTBDNM219p13​.2Dynamin-2DNM2 homepage - Leiden Muscular Dystrophy pages
IPN Mutations, DNM2
DNM2DNM2

Data are compiled from the following standard references: gene from HGNC; chromosome locus from OMIM; protein from UniProt. For a description of databases (Locus Specific, HGMD, ClinVar) to which links are provided, click here.

Table B.

OMIM Entries for DNM2-Related Intermediate Charcot-Marie-Tooth Neuropathy (View All in OMIM)

602378DYNAMIN 2; DNM2
606482CHARCOT-MARIE-TOOTH DISEASE, DOMINANT INTERMEDIATE B; CMTDIB

Gene structure. DNM2 has several isoforms, the longest transcript is isoform 1 (NM_001005360.1), which has 22 exons. See Entrez Gene for a description of isoforms.

Pathogenic variants. Pathogenic missense variants and small deletions in the coding region have been described.

Normal gene product. Isoform 1 encodes the dynamin-2 protein of 870 amino acid residues (NP_001005360.1).

Abnormal gene product. The identification of small deletions suggests that haploinsufficiency is the cause of the disorder.

References

Literature Cited

  • Argov Z, de Visser M. What we do not know about pregnancy in hereditary neuromuscular disorders. Neuromuscul Disord. 2009;19:675–9. [PubMed: 19692244]
  • Bitoun M, Stojkovic T, Prudhon B, Maurage CA, Latour P, Vermersch P, Guicheney P. A novel mutation in the dynamin 2 gene in a Charcot-Marie-Tooth type 2 patient: clinical and pathological findings. Neuromuscul Disord. 2008;18:334–8. [PubMed: 18394888]
  • Bitoun M, Maugenre S, Jeannet PY, Lacene E, Ferrer X, Laforet P, Martin JJ, Laporte J, Lochmuller H, Beggs AH, Fardeau M, Eymard B, Romero NB, Guicheney P. Mutations in Dynamin 2 cause dominant centronuclear myopathy. Nat Genet. 2005;37:1207–9. [PubMed: 16227997]
  • Claeys KG, Züchner S, Kennerson M, Berciano J, Garcia A, Verhoeven K, Storey E, Merory JR, Bienfait HM, Lammens M, Nelis E, Baets J, De Vriendt E, Berneman ZN, De Veuster I, Vance JM, Nicholson G, Timmerman V, De Jonghe P. Phenotypic spectrum of dynamin 2 mutations in Charcot-Marie-Tooth neuropathy. Brain. 2009;132:1741–52. [PMC free article: PMC2724916] [PubMed: 19502294]
  • Davis CJ, Bradley WG, Madrid R. The peroneal muscular atrophy syndrome: clinical, genetic, electrophysiological and nerve biopsy studies. I. Clinical, genetic and electrophysiological findings and classification. J Genet Hum. 1978;26:311–49. [PubMed: 752065]
  • Fabrizi GM, Ferrarini M, Cavallaro T, Cabrini I, Cerini R, Bertolasi L, Rizzuto N. Two novel mutations in dynamin-2 cause axonal Charcot-Marie-Tooth disease. Neurology. 2007;69:291–5. [PubMed: 17636067]
  • Fischer D, Herasse M, Bitoun M, Barragán-Campos HM, Chiras J, Laforêt P, Fardeau M, Eymard B, Guicheney P, Romero NB. Characterization of the muscle involvement in dynamin 2-related centronuclear myopathy. Brain. 2006;129:1463–9. [PubMed: 16585051]
  • Haberlová J, Mazanec R, Ridzoň P, Baránková L, Nürnberg G, Nürnberg P, Sticht H, Huehne K, Seeman P, Rautenstrauss B. Phenotypic variability in a large Czech family with a dynamin 2-associated Charcot-Marie-Tooth neuropathy. J Neurogenet. 2011;25:182–8. [PubMed: 22091729]
  • Hoff JM, Gilhus NE, Daltveit AK. Pregnancies and deliveries in patients with Charcot-Marie-Tooth disease. Neurology. 2005;64:459–62. [PubMed: 15699375]
  • Jungbluth H, Cullup T, Lillis S, Zhou H, Abbs S, Sewry C, Muntoni F. Centronuclear myopathy with cataracts due to a novel dynamin 2 (DNM2) mutation. Neuromuscul Disord. 2010;20:49–52. [PubMed: 19932620]
  • Kennerson ML, Zhu D, Gardner RJ, Storey E, Merory J, Robertson SP, Nicholson GA. Dominant intermediate Charcot-Marie-Tooth neuropathy maps to chromosome 19p12-p13.2. Am J Hum Genet. 2001;69:883–8. [PMC free article: PMC1226074] [PubMed: 11533912]
  • Melberg A, Kretz C, Kalimo H, Wallgren-Pettersson C, Toussaint A, Böhm J, Stålberg E, Laporte J. Adult course in dynamin 2 dominant centronuclear myopathy with neonatal onset. Neuromuscul Disord. 2010;20:53–6. [PubMed: 19932619]
  • Nicholson G, Myers S. Intermediate forms of Charcot-Marie Tooth neuropathy: a review. Neuromolecular Med. 2006;8:123–30. [PubMed: 16775371]
  • Susman RD, Quijano-Roy S, Yang N, Webster R, Clarke NF, Dowling J, Kennerson M, Nicholson G, Biancalana V, Ilkovski B, Flanigan KM, Arbuckle S, Malladi C, Robinson P, Vucic S, Mayer M, Romero NB, Urtizberea JA, García-Bragado F, Guicheney P, Bitoun M, Carlier RY, North KN. Expanding the clinical, pathological and MRI phenotype of DNM2-related centronuclear myopathy. Neuromuscul Disord. 2010;20:229–37. [PubMed: 20227276]
  • Züchner S, Noureddine M, Kennerson M, Verhoeven K, Claeys K, De Jonghe P, Merory J, Oliveira SA, Speer MC, Stenger JE, Walizada G, Zhu D, Pericak-Vance MA, Nicholson G, Timmerman V, Vance JM. Mutations in the pleckstrin homology domain of dynamin 2 cause dominant intermediate Charcot-Marie-Tooth disease. Nat Genet. 2005;37:289–94. [PubMed: 15731758]

Chapter Notes

Revision History

  • 25 June 2015 (me) Comprehensive update posted live
  • 8 July 2010 (me) Review posted live
  • 26 March 2010 (sz) Original submission
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