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Charcot-Marie-Tooth disease, demyelinating, type 1b(CMT1B)

MedGen UID:
124377
Concept ID:
C0270912
Disease or Syndrome
Synonyms: CHARCOT-MARIE-TOOTH DISEASE, AUTOSOMAL DOMINANT, WITH FOCALLY FOLDED MYELIN SHEATHS, TYPE 1B; CHARCOT-MARIE-TOOTH DISEASE, SLOW NERVE CONDUCTION TYPE, LINKED TO DUFFY; Charcot-Marie-Tooth disease, type IB; Charcot-Marie-Tooth Neuropathy Type 1; CHARCOT-MARIE-TOOTH NEUROPATHY, TYPE 1B; CMT1B; Hereditary motor and sensory neuropathy 1B; HEREDITARY MOTOR AND SENSORY NEUROPATHY I; HEREDITARY MOTOR AND SENSORY NEUROPATHY IB; Peroneal muscular atrophy
Modes of inheritance:
Heterogeneous
MedGen UID:
67020
Concept ID:
C0242960
Organism Attribute
Source: HPO
The presence of apparently similar characters for which the genetic evidence indicates that different genes or different genetic mechanisms are involved in different pedigrees. In clinical settings genetic heterogeneity refers to the presence of a variety of genetic defects which cause the same disease, often due to mutations at different loci on the same gene, a finding common to many human diseases including ALZHEIMER DISEASE; CYSTIC FIBROSIS; LIPOPROTEIN LIPASE DEFICIENCY, FAMILIAL; and POLYCYSTIC KIDNEY DISEASES. (Rieger, et al., Glossary of Genetics: Classical and Molecular, 5th ed; Segen, Dictionary of Modern Medicine, 1992)
Autosomal dominant inheritance
MedGen UID:
141047
Concept ID:
C0443147
Intellectual Product
Sources: HPO, OMIM, Orphanet
A mode of inheritance that is observed for traits related to a gene encoded on one of the autosomes (i.e., the human chromosomes 1-22) in which a trait manifests in heterozygotes. In the context of medical genetics, an autosomal dominant disorder is caused when a single copy of the mutant allele is present. Males and females are affected equally, and can both transmit the disorder with a risk of 50% for each child of inheriting the mutant allele.
Autosomal dominant inheritance (HPO, OMIM, Orphanet)
SNOMED CT: Charcot-Marie-Tooth disease, type IB (42986003)
 
Gene (location): MPZ (1q23.3)
OMIM®: 118200
Orphanet: ORPHA101082

Definition

Charcot-Marie-Tooth neuropathy type 1 (CMT1) is a demyelinating peripheral neuropathy characterized by distal muscle weakness and atrophy, sensory loss, and slow nerve conduction velocity. It is usually slowly progressive and often associated with pes cavus foot deformity and bilateral foot drop. Affected individuals usually become symptomatic between age five and 25 years. Fewer than 5% of individuals become wheelchair dependent. Life span is not shortened. [from GTR]

Additional descriptions

From GeneReviews
Charcot-Marie-Tooth neuropathy type 1 (CMT1) is a demyelinating peripheral neuropathy characterized by distal muscle weakness and atrophy, sensory loss, and slow nerve conduction velocity. It is usually slowly progressive and often associated with pes cavus foot deformity and bilateral foot drop. Affected individuals usually become symptomatic between age five and 25 years. Fewer than 5% of individuals become wheelchair dependent. Life span is not shortened.  https://www.ncbi.nlm.nih.gov/books/NBK1205
From OMIM
Charcot-Marie-Tooth disease is a sensorineural peripheral polyneuropathy. Affecting approximately 1 in 2,500 individuals, Charcot-Marie-Tooth disease is the most common inherited disorder of the peripheral nervous system (Skre, 1974). Autosomal dominant, autosomal recessive, and X-linked forms have been recognized. Classification On the basis of electrophysiologic properties and histopathology, CMT has been divided into primary peripheral demyelinating (type 1, or HMSNI) and primary peripheral axonal (type 2, or HMSNII) neuropathies. The demyelinating neuropathies classified as CMT type 1 are characterized by severely reduced motor NCVs (less than 38 m/s) and segmental demyelination and remyelination with onion bulb formations on nerve biopsy. The axonal neuropathies classified as CMT type 2 are characterized by normal or mildly reduced NCVs and chronic axonal degeneration and regeneration on nerve biopsy (see CMT2A1; 118210). Distal hereditary motor neuropathy (dHMN) (see 158590), or spinal CMT, is characterized by exclusive motor involvement and sparing of sensory nerves (Pareyson, 1999). McAlpine (1989) proposed that the forms of CMT with very slow nerve conduction be given the gene symbol CMT1A (118220) and CMT1B, CMT1A being the gene on chromosome 17 and CMT1B being the gene on chromosome 1. CMT2 was the proposed symbol for the autosomal locus responsible for the moderately slow nerve conduction form of the disease (axonal). For a phenotypic description and discussion of genetic heterogeneity of the various subtypes of CMT, see CMTX1 (302800), CMT2A1 (118210), CMT3 (DSS; 145900), CMT4A (214400), and CMTDIB (606482). Genetic Heterogeneity of Autosomal Dominant Demyelinating CMT1 Autosomal dominant demyelinating CMT1 is genetically heterogeneous disorder and can be caused by mutations in different genes (see CMT1A, 118220; CMT1C, 601098; CMT1D, 607678), CMT1E (607734), and CMT1F (607734). See also 608236 for a related phenotype characterized by isolated slowed nerve conduction velocities (NCVs).  http://www.omim.org/entry/118200
From GHR
Charcot-Marie-Tooth disease is a group of progressive disorders that affect the peripheral nerves. Peripheral nerves connect the brain and spinal cord to muscles and to sensory cells that detect sensations such as touch, pain, heat, and sound. Damage to the peripheral nerves can result in loss of sensation and wasting (atrophy) of muscles in the feet, legs, and hands.Charcot-Marie-Tooth disease usually becomes apparent in adolescence or early adulthood, but onset may occur anytime from early childhood through late adulthood. Symptoms of Charcot-Marie-Tooth disease vary in severity, even among members of the same family. Some people never realize they have the disorder, but most have a moderate amount of physical disability. A small percentage of people experience severe weakness or other problems which, in rare cases, can be life-threatening. In most affected individuals, however, Charcot-Marie-Tooth disease does not affect life expectancy.Typically, the earliest symptoms of Charcot-Marie-Tooth disease involve balance difficulties, clumsiness, and muscle weakness in the feet. Affected individuals may have foot abnormalities such as high arches (pes cavus), flat feet (pes planus), or curled toes (hammer toes). They often have difficulty flexing the foot or walking on the heel of the foot. These difficulties may cause a higher than normal step (or gait) and increase the risk of ankle injuries and tripping.As the disease progresses, muscles in the lower legs usually weaken, but leg and foot problems rarely require the use of a wheelchair. Affected individuals may also develop weakness in the hands, causing difficulty with daily activities such as writing, fastening buttons, and turning doorknobs. People with this disorder typically experience a decreased sensitivity to touch, heat, and cold in the feet and lower legs, but occasionally feel aching or burning sensations. In some cases, affected individuals experience gradual hearing loss, deafness, or loss of vision.There are several types of Charcot-Marie-Tooth disease. Type 1 Charcot-Marie-Tooth disease (CMT1) is characterized by abnormalities in myelin, the fatty substance that covers nerve cells, protecting them and helping to conduct nerve impulses. These abnormalities slow the transmission of nerve impulses. Type 2 Charcot-Marie-Tooth disease (CMT2) is characterized by abnormalities in the fiber, or axon, that extends from a nerve cell body and transmits nerve impulses. These abnormalities reduce the strength of the nerve impulse. Type 4 Charcot-Marie-Tooth disease (CMT4) affects either the axon or myelin and is distinguished from the other types by its pattern of inheritance. In intermediate forms of Charcot-Marie-Tooth disease, the nerve impulses are both slowed and reduced in strength, probably due to abnormalities in both axons and myelin. Type X Charcot-Marie-Tooth disease (CMTX) is caused by mutations in a gene on the X chromosome, one of the two sex chromosomes. Within the various types of Charcot-Marie-Tooth disease, subtypes (such as CMT1A, CMT1B, CMT2A, CMT4A, and CMTX1) are distinguished by the specific gene that is altered.Sometimes other, more historical names are used to describe this disorder. For example, Roussy-Levy syndrome is a form of Charcot-Marie-Tooth disease defined by the additional feature of rhythmic shaking (tremors). Dejerine-Sottas syndrome is a term sometimes used to describe a severe, early childhood form of Charcot-Marie-Tooth disease; it is also sometimes called Charcot-Marie-Tooth disease type 3 (CMT3). Depending on the specific gene that is altered, this severe, early onset form of the disorder may also be classified as CMT1 or CMT4. CMTX5 is also known as Rosenberg-Chutorian syndrome. Some researchers believe that this condition is not actually a form of Charcot-Marie-Tooth disease. Instead, they classify it as a separate disorder characterized by peripheral nerve problems, deafness, and vision loss.  https://ghr.nlm.nih.gov/condition/charcot-marie-tooth-disease

Clinical features

Tonic pupil
MedGen UID:
52779
Concept ID:
C0040416
Sign or Symptom
A pupillary abnormality characterized by a poor pupillary light reaction, reduced accommodation, iris sector palsies, an enhanced pupillary response to near effort that results in a prolonged, "tonic" constriction, and slow pupillary redilation. This condition is associated with injury to the postganglionic parasympathetic innervation to the pupil. (From Miller et al., Clinical Neuro-Ophthalmology, 4th ed, pp492-500)
Footdrop
MedGen UID:
88451
Concept ID:
C0085684
Disease or Syndrome
Weakness of the muscles responsible for dorsiflexion of the foot, that is, of the movement of the toes towards the shin. The foot dorsiflexors include the tibialis anterior, the extensor hallucis longus, the extensor digitorum longus, and the peroneus tertius muscles.
Split hand
MedGen UID:
67457
Concept ID:
C0221373
Congenital Abnormality
A condition in which middle parts of the hand (fingers and metacarpals) are missing giving a cleft appearance. The severity is very variable ranging from slightly hypoplastic middle fingers over absent middel fingers as far as oligo- or monodactyl hands.
Pes cavus
MedGen UID:
675590
Concept ID:
C0728829
Congenital Abnormality
The presence of an unusually high plantar arch. Also called high instep, pes cavus refers to a distinctly hollow form of the sole of the foot when it is bearing weight.
Hammertoe
MedGen UID:
209712
Concept ID:
C1136179
Anatomical Abnormality
Hyperextension of the metatarsal-phalangeal joint with hyperflexion of the proximal interphalangeal (PIP) joint.
Ulnar claw
MedGen UID:
871311
Concept ID:
C4025799
Congenital Abnormality
An abnormal hand position characterized by hyperextension of the fourth and fifth fingers at the metacarpophalangeal joints and flexion of the interphalangeal joints of the same fingers such that they are curled towards the palm.
Areflexia
MedGen UID:
115943
Concept ID:
C0234146
Finding
A finding indicating the complete absence of neurological reflexes.
Steppage gait
MedGen UID:
98105
Concept ID:
C0427149
Finding
An abnormal gait pattern that arises from weakness of the pretibial and peroneal muscles due to a lower motor neuron lesion. Affected patients have footdrop and are unable to dorsiflex and evert the foot. The leg is lifted high on walking so that the toes clear the ground, and there may be a slapping noise when the foot strikes the ground again.
Hyporeflexia
MedGen UID:
195967
Concept ID:
C0700078
Sign or Symptom
Reduction of neurologic reflexes such as the knee-jerk reaction.
Peripheral demyelination
MedGen UID:
451074
Concept ID:
C0878575
Pathologic Function
A loss of myelin from the internode regions along myelinated nerve fibers of the peripheral nervous system.
Hypertrophic nerve changes
MedGen UID:
322038
Concept ID:
C1832776
Finding
Myelin outfoldings
MedGen UID:
334341
Concept ID:
C1843168
Finding
The presence of excessive redundant myelin in the peripheral nerve sheath.
Distal sensory impairment
MedGen UID:
335722
Concept ID:
C1847584
Finding
An abnormal reduction in sensation in the distal portions of the extremities.
Onion bulb formation
MedGen UID:
376237
Concept ID:
C1847906
Finding
Repeated episodes of segmental demyelination and remyelination lead to the accumulation of supernumerary Schwann cells around axons, which is referred to as onion bulb formation. This finding affects peripheral nerves.
Decreased number of peripheral myelinated nerve fibers
MedGen UID:
346872
Concept ID:
C1858285
Finding
A loss of myelinated nerve fibers in the peripheral nervous system (in general, this finding can be observed on nerve biopsy).
Decreased motor nerve conduction velocity
MedGen UID:
388130
Concept ID:
C1858729
Finding
A type of decreased nerve conduction velocity that affects the motor neuron.
Footdrop
MedGen UID:
88451
Concept ID:
C0085684
Disease or Syndrome
Weakness of the muscles responsible for dorsiflexion of the foot, that is, of the movement of the toes towards the shin. The foot dorsiflexors include the tibialis anterior, the extensor hallucis longus, the extensor digitorum longus, and the peroneus tertius muscles.
Distal amyotrophy
MedGen UID:
338530
Concept ID:
C1848736
Disease or Syndrome
Muscular atrophy affecting muscles in the distal portions of the extremities.
Cold-induced muscle cramps
MedGen UID:
396193
Concept ID:
C1861675
Finding
Sudden and involuntary contractions of one or more muscles brought on by exposure to cold temperatures.
Distal muscle weakness
MedGen UID:
355271
Concept ID:
C1864696
Finding
Reduced strength of the musculature of the distal extremities.
Split hand
MedGen UID:
67457
Concept ID:
C0221373
Congenital Abnormality
A condition in which middle parts of the hand (fingers and metacarpals) are missing giving a cleft appearance. The severity is very variable ranging from slightly hypoplastic middle fingers over absent middel fingers as far as oligo- or monodactyl hands.
Kyphoscoliosis
MedGen UID:
154361
Concept ID:
C0575158
Anatomical Abnormality
An abnormal curvature of the spine in both a coronal (lateral) and sagittal (back-to-front) plane.
Hammertoe
MedGen UID:
209712
Concept ID:
C1136179
Anatomical Abnormality
Hyperextension of the metatarsal-phalangeal joint with hyperflexion of the proximal interphalangeal (PIP) joint.
Tonic pupil
MedGen UID:
52779
Concept ID:
C0040416
Sign or Symptom
A pupillary abnormality characterized by a poor pupillary light reaction, reduced accommodation, iris sector palsies, an enhanced pupillary response to near effort that results in a prolonged, "tonic" constriction, and slow pupillary redilation. This condition is associated with injury to the postganglionic parasympathetic innervation to the pupil. (From Miller et al., Clinical Neuro-Ophthalmology, 4th ed, pp492-500)

Term Hierarchy

CClinical test,  RResearch test,  OOMIM,  GGeneReviews,  VClinVar  
Follow this link to review classifications for Charcot-Marie-Tooth disease, demyelinating, type 1b in Orphanet.

Professional guidelines

PubMed

Aretz S, Rautenstrauss B, Timmerman V
Eur J Hum Genet 2010 Sep;18(9) Epub 2010 May 26 doi: 10.1038/ejhg.2010.75. PMID: 20512157Free PMC Article

Recent clinical studies

Etiology

Sanmaneechai O, Feely S, Scherer SS, Herrmann DN, Burns J, Muntoni F, Li J, Siskind CE, Day JW, Laura M, Sumner CJ, Lloyd TE, Ramchandren S, Shy RR, Grider T, Bacon C, Finkel RS, Yum SW, Moroni I, Piscosquito G, Pareyson D, Reilly MM, Shy ME; Inherited Neuropathies Consortium - Rare Disease Clinical Research Consortium (INC-RDCRC).
Brain 2015 Nov;138(Pt 11):3180-92. Epub 2015 Aug 25 doi: 10.1093/brain/awv241. PMID: 26310628Free PMC Article
Huang LW, Lin KP, Chang MH, Liao YC, Liao KK, Soong BW, Lee YC
J Chin Med Assoc 2012 May;75(5):197-202. Epub 2012 Apr 29 doi: 10.1016/j.jcma.2012.03.005. PMID: 22632984
Choi BO, Kim SB, Kanwal S, Hyun YS, Park SW, Koo H, Yoo JH, Hyun JW, Park KD, Choi KG, Chung KW
Int J Mol Med 2011 Sep;28(3):389-96. Epub 2011 Apr 18 doi: 10.3892/ijmm.2011.678. PMID: 21503568
Kijima K, Numakura C, Izumino H, Umetsu K, Nezu A, Shiiki T, Ogawa M, Ishizaki Y, Kitamura T, Shozawa Y, Hayasaka K
Hum Genet 2005 Jan;116(1-2):23-7. Epub 2004 Nov 11 doi: 10.1007/s00439-004-1199-2. PMID: 15549395
Kochański A, Kabzińska D, Drac H, Ryniewicz B, Rowińska-Marcińska K, Hausmanowa-Petrusewicz I
Eur J Paediatr Neurol 2004;8(4):221-4. doi: 10.1016/j.ejpn.2004.04.001. PMID: 15261887

Diagnosis

Cortese R, Zoccolella S, Muglia M, Patitucci A, Scarafino A, Paolicelli D, Simone IL
Brain Behav 2016 Dec;6(12):e00580. Epub 2016 Sep 25 doi: 10.1002/brb3.580. PMID: 28032003Free PMC Article
Sanmaneechai O, Feely S, Scherer SS, Herrmann DN, Burns J, Muntoni F, Li J, Siskind CE, Day JW, Laura M, Sumner CJ, Lloyd TE, Ramchandren S, Shy RR, Grider T, Bacon C, Finkel RS, Yum SW, Moroni I, Piscosquito G, Pareyson D, Reilly MM, Shy ME; Inherited Neuropathies Consortium - Rare Disease Clinical Research Consortium (INC-RDCRC).
Brain 2015 Nov;138(Pt 11):3180-92. Epub 2015 Aug 25 doi: 10.1093/brain/awv241. PMID: 26310628Free PMC Article
Huang LW, Lin KP, Chang MH, Liao YC, Liao KK, Soong BW, Lee YC
J Chin Med Assoc 2012 May;75(5):197-202. Epub 2012 Apr 29 doi: 10.1016/j.jcma.2012.03.005. PMID: 22632984
Iida M, Koike H, Ando T, Sugiura M, Yamamoto M, Tanaka F, Sobue G
Neuromuscul Disord 2012 Feb;22(2):166-9. Epub 2011 Sep 21 doi: 10.1016/j.nmd.2011.08.005. PMID: 21940171
Laurà M, Milani M, Morbin M, Moggio M, Ripolone M, Jann S, Scaioli V, Taroni F, Pareyson D
J Neurol Neurosurg Psychiatry 2007 Nov;78(11):1263-6. doi: 10.1136/jnnp.2006.112276. PMID: 17940173Free PMC Article

Therapy

Panosyan FB, Laura M, Rossor AM, Pisciotta C, Piscosquito G, Burns J, Li J, Yum SW, Lewis RA, Day J, Horvath R, Herrmann DN, Shy ME, Pareyson D, Reilly MM, Scherer SS; Inherited Neuropathies Consortium—Rare Diseases Clinical Research Network (INC-RDCRN).
Neurology 2017 Aug 29;89(9):927-935. Epub 2017 Aug 2 doi: 10.1212/WNL.0000000000004296. PMID: 28768847Free PMC Article
Panosyan FB, Tawil R, Herrmann DN
Muscle Nerve 2017 Jun;55(6):922-927. Epub 2017 Feb 12 doi: 10.1002/mus.25453. PMID: 27783406
Ohshita N, Oka S, Tsuji K, Yoshida H, Morita S, Momota Y, Tsutsumi YM
Anesth Prog 2016 Summer;63(2):80-3. doi: 10.2344/15-00010R1.1. PMID: 27269665Free PMC Article
Shen S, Benoy V, Bergman JA, Kalin JH, Frojuello M, Vistoli G, Haeck W, Van Den Bosch L, Kozikowski AP
ACS Chem Neurosci 2016 Feb 17;7(2):240-58. Epub 2015 Dec 7 doi: 10.1021/acschemneuro.5b00286. PMID: 26599234Free PMC Article
Sevilla T, Lupo V, Martínez-Rubio D, Sancho P, Sivera R, Chumillas MJ, García-Romero M, Pascual-Pascual SI, Muelas N, Dopazo J, Vílchez JJ, Palau F, Espinós C
Brain 2016 Jan;139(Pt 1):62-72. Epub 2015 Oct 24 doi: 10.1093/brain/awv311. PMID: 26497905

Prognosis

Fledrich R, Mannil M, Leha A, Ehbrecht C, Solari A, Pelayo-Negro AL, Berciano J, Schlotter-Weigel B, Schnizer TJ, Prukop T, Garcia-Angarita N, Czesnik D, Haberlová J, Mazanec R, Paulus W, Beissbarth T, Walter MC, Triaal C, Hogrel JY, Dubourg O, Schenone A, Baets J, De Jonghe P, Shy ME, Horvath R, Pareyson D, Seeman P, Young P, Sereda MW
J Neurol Neurosurg Psychiatry 2017 Nov;88(11):941-952. Epub 2017 Aug 31 doi: 10.1136/jnnp-2017-315721. PMID: 28860329
Ho AK, Wagstaff JL, Manna PT, Wartosch L, Qamar S, Garman EF, Freund SM, Roberts RC
BMC Biol 2016 Dec 7;14(1):109. doi: 10.1186/s12915-016-0332-8. PMID: 27927196Free PMC Article
Aharoni S, Barwick KE, Straussberg R, Harlalka GV, Nevo Y, Chioza BA, McEntagart MM, Mimouni-Bloch A, Weedon M, Crosby AH
BMC Med Genet 2016 Nov 16;17(1):82. doi: 10.1186/s12881-016-0343-x. PMID: 27852232Free PMC Article
Kochański A, Kabzińska D, Drac H, Ryniewicz B, Rowińska-Marcińska K, Hausmanowa-Petrusewicz I
Eur J Paediatr Neurol 2004;8(4):221-4. doi: 10.1016/j.ejpn.2004.04.001. PMID: 15261887
Eggers SD, Keswani SC, Melli G, Cornblath DR
Muscle Nerve 2004 Jun;29(6):867-9. doi: 10.1002/mus.20034. PMID: 15170620

Clinical prediction guides

Fledrich R, Mannil M, Leha A, Ehbrecht C, Solari A, Pelayo-Negro AL, Berciano J, Schlotter-Weigel B, Schnizer TJ, Prukop T, Garcia-Angarita N, Czesnik D, Haberlová J, Mazanec R, Paulus W, Beissbarth T, Walter MC, Triaal C, Hogrel JY, Dubourg O, Schenone A, Baets J, De Jonghe P, Shy ME, Horvath R, Pareyson D, Seeman P, Young P, Sereda MW
J Neurol Neurosurg Psychiatry 2017 Nov;88(11):941-952. Epub 2017 Aug 31 doi: 10.1136/jnnp-2017-315721. PMID: 28860329
Horga A, Laurà M, Jaunmuktane Z, Jerath NU, Gonzalez MA, Polke JM, Poh R, Blake JC, Liu YT, Wiethoff S, Bettencourt C, Lunn MP, Manji H, Hanna MG, Houlden H, Brandner S, Züchner S, Shy M, Reilly MM
J Neurol Neurosurg Psychiatry 2017 Jul;88(7):575-585. Epub 2017 May 13 doi: 10.1136/jnnp-2016-315077. PMID: 28501821Free PMC Article
Sanmaneechai O, Feely S, Scherer SS, Herrmann DN, Burns J, Muntoni F, Li J, Siskind CE, Day JW, Laura M, Sumner CJ, Lloyd TE, Ramchandren S, Shy RR, Grider T, Bacon C, Finkel RS, Yum SW, Moroni I, Piscosquito G, Pareyson D, Reilly MM, Shy ME; Inherited Neuropathies Consortium - Rare Disease Clinical Research Consortium (INC-RDCRC).
Brain 2015 Nov;138(Pt 11):3180-92. Epub 2015 Aug 25 doi: 10.1093/brain/awv241. PMID: 26310628Free PMC Article
Choi BO, Kim SB, Kanwal S, Hyun YS, Park SW, Koo H, Yoo JH, Hyun JW, Park KD, Choi KG, Chung KW
Int J Mol Med 2011 Sep;28(3):389-96. Epub 2011 Apr 18 doi: 10.3892/ijmm.2011.678. PMID: 21503568
Eggers SD, Keswani SC, Melli G, Cornblath DR
Muscle Nerve 2004 Jun;29(6):867-9. doi: 10.1002/mus.20034. PMID: 15170620

Recent systematic reviews

Roberts-Clarke D, Fornusek C, Fiatarone Singh MA, Burns J, Hackett DA
Int J Rehabil Res 2016 Sep;39(3):189-96. doi: 10.1097/MRR.0000000000000174. PMID: 27177353
Barreto LC, Oliveira FS, Nunes PS, de França Costa IM, Garcez CA, Goes GM, Neves EL, de Souza Siqueira Quintans J, de Souza Araújo AA
Neuroepidemiology 2016;46(3):157-65. Epub 2016 Feb 6 doi: 10.1159/000443706. PMID: 26849231
Gess B, Baets J, De Jonghe P, Reilly MM, Pareyson D, Young P
Cochrane Database Syst Rev 2015 Dec 11;(12):CD011952. doi: 10.1002/14651858.CD011952. PMID: 26662471
Sman AD, Hackett D, Fiatarone Singh M, Fornusek C, Menezes MP, Burns J
J Peripher Nerv Syst 2015 Dec;20(4):347-62. doi: 10.1111/jns.12116. PMID: 26010435
Anens E, Emtner M, Hellström K
Arch Phys Med Rehabil 2015 Feb;96(2):260-8. Epub 2014 Oct 5 doi: 10.1016/j.apmr.2014.09.013. PMID: 25286435

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