Medical Policy


Subject: Genetic Testing for Inherited Peripheral Neuropathies
Document #: GENE.00033 Publish Date:    10/17/2018
Status: Reviewed Last Review Date:    09/13/2018


This document addresses the use of genetic testing for the identification of genes associated with inherited peripheral neuropathy.

Note:  For additional information regarding related genetic topics, please see the following:

Position Statement

Investigational and Not Medically Necessary:

Genetic testing for inherited peripheral neuropathy is considered investigational and not medically necessary for all indications, including but not limited to:


Charcot-Marie-Tooth (CMT) disease is actually a group of inherited neuropathies characterized classically by distal sensory loss and weakness, abnormal deep tendon reflexes, and skeletal abnormalities.  The majority of inherited polyneuropathies are variants of CMT disease.  The clinical phenotype of CMT is highly variable, ranging from minimal neurological findings to the classic picture with pes cavus and “stork legs” to a severe polyneuropathy with respiratory failure.  More than 40 genes associated with CMT have been described, including autosomal dominant, autosomal recessive, X-linked dominant, and X-linked recessive forms.  CMT type 1 (CMT1) is a demyelinating peripheral neuropathy characterized by progressive peripheral motor and sensory neuropathy, slow nerve conduction velocity, and enlarged nerves.  CMT1 accounts for approximately 50% of all CMT.  There are five genes that are currently associated with CMT1:

  1. peripheral myelin protein 22 (PMP22; CMT1A [common duplication] and CMT1E [point variants]);
  2. myelin protein zero (MPZ; CMT1B);
  3. lipopolysaccharide-induced tumor necrosis factor-alpha factor (LITAF; CMT1C);
  4. early growth response 2 (EGR2; CMT1D); and
  5. neurofilament protein, light polypeptide (NEFL; CMT1F)

CMT1A accounts for 70% to 80% of CMT1, while CMT1B accounts for 5% to 10%; CMT1E and CMT1F each account for less than 5% of cases, and CMT1C and CMT1D each account for less than 2% of identified cases.  Clinical genetic testing for CMT1 is available from several laboratories in the United States.  The most commonly available genetic test is for the common 1.5-megabase duplication of the PMP22 gene associated with CMT1A, which is performed using fluorescence in situ hybridization (FISH) or molecular methods.  Genetic testing is also available from some laboratories for PMP22 point variants (CMT1E) and variants in EGR2, LITAF, MPZ, and NEFL by direct DNA sequencing.

The diagnosis of CMT has historically been based on physical examination to evaluate weakness, atrophy, and sensory loss; nerve conduction velocity (NCV) testing to distinguish specific type of neuropathy; and a detailed family history, along with genetic counseling.  Genetic testing has been proposed as an additional method of diagnosis and as a means to distinguish the various types of neuropathy within the CMT group.  Genetic testing for the presence of CMT- related alleles has also been considered for other clinical situations, such as preconceptional or preimplantation embryonic testing to guide family planning by potentially at-risk individuals.  For example, CMT1A duplication testing can confirm the presence of a familial deletion and could be the first step in the process of identifying asymptomatic family members at risk to pass the duplication on to their children.  Preconceptional and preimplantation embryonic testing, along with genetic counseling, has been proposed to have potential clinical utility in guiding family planning for couples considered to be at risk for carrying and transmitting the genetic defects associated with CMT.

The American Academy of Neurology (AAN), American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM), and the American Academy of Physical Medicine and Rehabilitation (AAPMR) published an evidence-based review addressing the role of laboratory and genetic tests in the evaluation of distal symmetric polyneuropathies.  This review determined that genetic testing is established as “Useful” for the accurate diagnosis and classification of hereditary polyneuropathies in individuals with a cryptogenic polyneuropathy who exhibit a classical hereditary neuropathy phenotype (Level A).  This review also determined that genetic testing “May be considered” in subjects with cryptogenic polyneuropathy who exhibit a hereditary neuropathy phenotype (Level C).  The guideline recommends that initial genetic testing should be guided by the clinical phenotype, inheritance pattern, and electrodiagnostic (EDX) features and should focus on the most common abnormalities which are CMT1A duplication/HNPP deletion, Cx32 (GJB1), and MFN2 mutation screening.  However, the authors also concluded that there is insufficient evidence to determine the usefulness of routine genetic testing in cryptogenic polyneuropathy that does not exhibit a hereditary neuropathy phenotype (Level U) (England, 2009).  The authors of this guideline did not describe how the results of the genetic tests would be used to improve patient-specific clinical outcomes.  The likelihood that genetic testing for the inherited peripheral neuropathies will alter treatment management is low because the diagnosis of an inherited peripheral neuropathy can generally be made clinically, and there is no specifically designated treatment strategy based on the genetic phenotype.  As such, the clinical utility of a genetic confirmation of these disorders has not been demonstrated in the peer-reviewed literature at this time.

One potential area where clinical utility might be found has to do with chemotherapy treatment of individuals with CMT disease with vincristine, since these individuals are particularly susceptible to vincristine neurotoxicity.  However, the additional value of a specific genetic confirmation of a CMT-related gene mutation, when compared to clinical diagnosis, has not yet been demonstrated.  Chemotherapy treatment, particularly with vincristine, in individuals with preexisting neuropathy can quickly exacerbate debilitating symptoms.  Additional research is needed to evaluate the effects of vincristine on individuals with the CMT1A duplication, but no clinical evidence of neuropathy, since vincristine is contraindicated in subjects with clinically evident CMT. 

In 2011, Saporta conducted data analysis at a single center of 787 subjects with a diagnosis of CMT, in an effort to identify the clinical and physiological features of the CMT subtypes to assist with determining an appropriate strategy for genetic testing in CMT.  The results indicated that a genetic subtype was identified in 527 subjects (67%) while 260 subjects (33%) did not have an identifiable genetic mutation.  These subjects were classified based on nerve conduction velocities, physical examination, and family history.  The authors (Saporta, 2011) concluded that:

There is little information available to guide us as to which gene to test…We have developed an algorithm based on clinical phenotypes, neurophysiology, and prevalence that we propose as a guide to help focus genetic testing for various forms of CMT... Despite the clinical similarities among patients with CMT, it is clear that the disorder is genetically heterogeneous.  AD demyelinating (CMT1), AD axonal (CMT2), AR (CMT4), and X-linked (CMTX) forms of CMT exist.  At present, mutations in more than 30 genes have been identified that cause these various forms of inherited neuropathies, and more than 44 distinct loci have been identified.

A review article by Pareyson (2009) commented that:

There are now so many genes associated with CMT that a single laboratory cannot undertake all the investigations…Substantial phenotypic variability occurs even within the same CMT type and substantial overlap exists between CMT1, CMT2, and the intermediate forms and between CMT2 and dHMN (distal hereditary motor neuropathy).  CMT2 can overlap with some of the hereditary sensory neuropathies…The diagnostic approach requires careful assessment of the clinical presentation and mode of inheritance, nerve-conduction studies, and DNA testing.  Current research is focused on assessing the natural history and finding effective treatments.  Disease course is variable because of genotypic and phenotypic heterogeneity.  At present, there is no drug therapy for Charcot–Marie–Tooth disease, and rehabilitation therapy and surgical procedures for skeletal deformities are the only available treatments, although best practice has not been defined.

Currently, treatment for CMT is generally symptomatic, including pain management, exercise, and orthotics or orthopedic surgery for severe foot and ankle problems.  For this reason, confirming a molecular diagnosis of CMT does not affect the course of treatment for this disease.  


The inherited peripheral neuropathies are divided into the hereditary motor and sensory neuropathies, hereditary neuropathy with liability to pressure palsies (HNPP), and other miscellaneous rare types, (for example, hereditary brachial plexopathy, hereditary sensory autonomic neuropathies).  Charcot-Marie-Tooth disease (CMT) is the most common inherited neuromuscular disorder and affects approximately 30 per 100,000 individuals.  A number of subtypes of autosomal dominant CMT have been categorized into two groups, CMT1 (primary peripheral demyelinating neuropathies) and CMT2 (primary peripheral axonal neuropathies).  There are also autosomal recessive (CMT4) and X-linked (CMTX), as well as intermediate forms of autosomal dominant CMT (DI-CMT).  CMT1 is slowly progressive, and clinical findings include distal muscle weakness and atrophy, sensory loss, slow nerve conduction velocity, pes cavus foot deformity, and bilateral foot drop.  Atrophy of muscles in the hands and below the knees and absent tendon reflexes are typical, while proximal muscles are usually normal.  Symptoms can appear at any time from infancy through adulthood, and the lifespan is typically not shortened in individuals with CMT1.  Approximately 70% to 80% of individuals diagnosed with CMT are classified as CMT1.

The majority of individuals with CMT have CMT type 1A (CMT1A), which is an autosomal dominant disorder characterized by 1.5-megabase (Mb) duplication on chromosome 17 at band p11.2, and includes the peripheral myelin protein 22 (PMP22) gene.  PMP22 is required for myelin formation and maintenance.  The duplication is a result of unequal crossing over of homologous chromosomes between repeated sequences called CMT1A-REPs.  It is unknown exactly how duplication results in abnormal myelination, although it is hypothesized that increased PMP22 gene dosage affects intracellular degradation of different membrane components.  There is much phenotype variability both within and between families with CMT.  CMT1A is characterized by early onset and a mild disease course including distal muscle weakness, sensory loss, and absent reflexes.  Slow motor nerve conduction velocities (NCVs) are usually present by 3 to 5 years of age and motor NCVs are usually from 15 to 30 meters per second. Some symptoms associated with CMT1A that typically present in childhood include hypotonia, proximal and distal weakness, scoliosis, calf muscle hypertrophy, and hand deformity.  The average age of onset of clinical symptoms in CMT1A is approximately 12 years of age.  CMT1A is a slowly progressive disease, and few affected individuals will end up wheelchair bound.

Some individuals with CMT are found to carry single nucleotide sequence variants in PMP22 which are categorized into the subgroup CMT1E.  The PMP22 single nucleotide sequence variants found in CMT1E tend to lead to a more severe phenotype than CMT1A, which may include sensorineural deafness and central nervous system symptoms.  HNPP, also called tomaculous neuropathy, involves inadequate production of PMP22 which causes nerves to be more susceptible to trauma or minor compression/entrapment.  The prevalence is estimated at 16 persons per 100,000, although some authors indicate a potential for under diagnosis of HNPP.  An estimated 50% of carriers are asymptomatic and do not display abnormal neurological findings on clinical examination.  HNPP is characterized by repeated focal pressure neuropathies, such as carpal tunnel syndrome and peroneal palsy with foot drop and episodes of numbness, muscular weakness, atrophy, and palsies due to minor compression or trauma to the peripheral nerves.  Approximately 80% of individuals with HNPP have a 1.5-Mb deletion on chromosome 17 at band p11.2, which includes the PMP22 gene and is complementary to the duplication observed in CMT1A.  The remaining 20% of HNPP cases carry single nucleotide sequence variants and small deletions in the PMP22 gene.  About 10-15% of mutation carriers remain clinically asymptomatic which suggests incomplete penetrance.

To date, there are no genotyping tests for the inherited peripheral neuropathies with clearance from the U.S. Food and Drug Administration (FDA).  Genetic testing is offered as a laboratory-developed test.  These tests must meet the general regulatory standards of the Clinical Laboratory Improvement Act (CLIA), and the laboratory offering the service must be licensed by CLIA for high-complexity testing.  At the present time, the FDA does not require any regulatory review of these tests.


Charcot-Marie-Tooth neuropathy (CMT): This condition  refers to a group of inherited demyelinating neuropathies which are associated with decreased motor nerve conduction velocity (less than 38 meters per second).

Deletion/Duplication analysis: Laboratory testing that identifies the absence of a segment of DNA (deletion) and/or the presence of an extra segment of DNA (duplication). 

Fluorescence in situ hybridization (FISH): A laboratory technique that is utilized to detect small deletions or rearrangements in the chromosomes within a given specimen.

Hereditary neuropathy with liability to pressure palsies (HNPP): A neuromuscular disorder associated with deletions of the PMP22 gene.

Molecular genetic testing: Testing that involves the analysis of DNA, either through linkage analysis, sequencing or one of several methods of mutation detection.


The following codes for treatments and procedures applicable to this document are included below for informational purposes. Inclusion or exclusion of a procedure, diagnosis or device code(s) does not constitute or imply member coverage or provider reimbursement policy. Please refer to the member's contract benefits in effect at the time of service to determine coverage or non-coverage of these services as it applies to an individual member.

When services are Investigational and Not Medically Necessary:




PMP22 (peripheral myelin protein 22) (eg, Charcot-Marie-Tooth, hereditary neuropathy with liability to pressure palsies) gene analysis; duplication/deletion analysis


PMP22 (peripheral myelin protein 22) (eg, Charcot-Marie-Tooth, hereditary neuropathy with liability to pressure palsies) gene analysis; full sequence analysis


PMP22 (peripheral myelin protein 22) (eg, Charcot-Marie-Tooth, hereditary neuropathy with liability to pressure palsies) gene analysis; known familial variant


Hereditary peripheral neuropathies (eg, Charcot-Marie-Tooth, spastic paraplegia), genomic sequence analysis panel, must include sequencing of at least 5 peripheral neuropathy-related genes (eg, BSCL2, GJB1, MFN2, MPZ, REEP1, SPAST, SPG11, SPTLC1)



ICD-10 Diagnosis



All diagnoses

When services are also Investigational and Not Medically Necessary:

For the following procedure and diagnosis codes; or when the code(s) describes a procedure indicated in the Position Statement section as investigational and not medically necessary.




Molecular pathology procedure, Level 4 (eg, analysis of single exon by DNA sequence analysis, analysis of >10 amplicons using multiplex PCR in 2 or more independent reactions, mutation scanning or duplication/deletion variants of 2-5 exons)  [when specified as the following]:

  • GJB1 (gap junction protein, beta 1) (eg, Charcot-Marie-Tooth X-linked), full gene sequence


Molecular pathology procedure, Level 5 (eg, analysis of 2-5 exons by DNA sequence analysis, mutation scanning or duplication/deletion variants of 6-10 exons, or characterization of a dynamic mutation disorder/triplet repeat by Southern blot analysis)  [when specified as the following]:

  • EGR2 (early growth response 2) (eg, Charcot-Marie-Tooth), full gene sequence
  • HSPB1 (heat shock 27kDa protein 1) (eg, Charcot-Marie-Tooth disease), full gene sequence
  • LITAF (lipopolysaccharide-induced TNF factor) (eg, Charcot-Marie-Tooth), full gene sequence


Molecular pathology procedure, Level 6 (eg, analysis of 6-10 exons by DNA sequence analysis, mutation scanning or duplication/deletion variants of 11-25 exons, regionally targeted cytogenomic array analysis)  [when specified as the following]:

  • GDAP1 (ganglioside-induced differentiation-associated protein 1) (eg, Charcot-Marie-Tooth disease), full gene sequence
  • MPZ (myelin protein zero) (eg, Charcot-Marie-Tooth), full gene sequence
  • NEFL (neurofilament, light polypeptide) (eg, Charcot-Marie-Tooth), full gene sequence
  • PRX (periaxin) (eg, Charcot-Marie-Tooth disease), full gene sequence
  • RAB7A (RAB7A, member RAS oncogene family) (eg, Charcot-Marie-Tooth disease), full gene sequence


Molecular pathology procedure, Level 7 (eg, analysis of 11-25 exons by DNA sequence analysis, mutation scanning or duplication/deletion variants of 26-50 exons, cytogenomic array analysis for neoplasia)  [when specified as the following]:

  • FIG4 (FIG4 homolog, SAC1 lipid phosphatase domain containing [S. cerevisiae]) (eg, Charcot-Marie-Tooth disease), full gene sequence
  • GARS (glycyl-tRNA synthetase) (eg, Charcot-Marie-Tooth disease), full gene sequence
  • LMNA (lamin A/C) (eg, Emery-Dreifuss muscular dystrophy [EDMD1, 2 and 3] limb-girdle muscular dystrophy [LGMD] type 1B, dilated cardiomyopathy [CMD1A], familial partial lipodystrophy [FPLD2]), full gene sequence
  • MFN2 (mitofusin 2) (eg, Charcot-Marie-Tooth disease), full gene sequence
  • SH3TC2 (SHE domain and tetratricopeptide repeats 2) (eg, Charcot-Marie-Tooth disease), full gene sequence


Nuclear encoded mitochondrial genes (eg, neurologic or myopathic phenotypes), genomic sequence panel, must include analysis of at least 100 genes, including BCS1L, C10orf2, COQ2, COX10, DGUOK, MPV17, OPA1, PDSS2, POLG, POLG2, RRM2B, SCO1, SCO2, SLC25A4, SUCLA2, SUCLG1, TAZ, TK2, and TYMP


Unlisted molecular pathology procedure [all other genes; KIF1B (CMT2A1), MED25 (CMT2B2), TRPV4 (CMTC), HSPB8 (CMT2L), AARS (CMT2N), DYNC1H1 (CMT2O), and LRSAM1 (CMT2P)]



ICD-10 Diagnosis



Hereditary and idiopathic neuropathy


Peer Reviewed Publications:

  1. Antoniadi T, Buxton C, Dennis G, et al. Application of targeted multi-gene panel testing for the diagnosis of inherited peripheral neuropathy provides a high diagnostic yield with unexpected phenotype-genotype variability. BMC Med Genet. 2015; 16:84.
  2. Aretz S, Rautenstrauss B, Timmerman V. Clinical utility gene card for: HMSN/HNPP HMSN types 1, 2, 3, 6 (CMT1,2,4, DSN, CHN, GAN, CCFDN, HNA); HNPP. Eur J Hum Genet. 2010; 18(9).
  3. Bissar-Tadmouri N, Parman Y, Boutrand L, et al. Mutational analysis and genotype/phenotype correlation in Turkish Charcot-Marie-Tooth Type 1 and HNPP patients. Clin Genet. 2000; 58(5):396-402.
  4. Braathen GJ.  Genetic epidemiology of Charcot-Marie-Tooth disease.  Acta Neurol Scand Suppl. 2012; (193):iv-22.
  5. Choi BO, Nakhro K, Park HJ, et al. A cohort study of MFN2 mutations and phenotypic spectrums in Charcot-Marie-Tooth disease 2A patients. Clin Genet. 2015; 87(6):594-598.
  6. Cornett KM, Menezes MP, Bray P, et al. Phenotypic variability of childhood Charcot-Marie-Tooth disease. JAMA Neurol. 2016; 73(6):645-651.
  7. DiVincenzo C, Elzinga CD, Medeiros AC, et al. The allelic spectrum of Charcot-Marie-Tooth disease in over 17,000 individuals with neuropathy. Mol Genet Genomic Med. 2014; 2(6):522-529.
  8. Drew AP, Zhu D, Kidambi A, et al. Improved inherited peripheral neuropathy genetic diagnosis by whole-exome sequencing. Mol Genet Genomic Med. 2015; 3(2):143-154.
  9. Fischer C, Trajanoski S, Papić L, et al.  SNP array-based whole genome homozygosity mapping as the first step to a molecular diagnosis in patients with Charcot-Marie-Tooth disease.  J Neurol. 2012; 259(3):515-523.
  10. Hoyer H, Braathen GJ, Busk OL, et al. Genetic diagnosis of Charcot-Marie-Tooth disease in a population by next-generation sequencing. Biomed Res Int. 2014; 2015:210401.
  11. Hung CC, Lee CN, Lin CY, et al. Identification of deletion and duplication genotypes of the PMP22 gene using PCR-RFLP, competitive multiplex PCR, and multiplex ligation-dependent probe amplification: a comparison. Electrophoresis. 2008; 29(3):618-625.
  12. Karadima G, Koutsis G, Raftopoulou M, et al. Mutational analysis of Greek patients with suspected hereditary neuropathy with liability to pressure palsies (HNPP): a 15-year experience. J Peripher Nerv Syst. 2015; 20(2):79-85.
  13. Laššuthová P, Šafka Brožková D, Krůtová M, et al. Improving diagnosis of inherited peripheral neuropathies through gene panel analysis. Orphanet J Rare Dis. 2016; 11(1):118.
  14. Nam SH, Hong YB, Hyun YS, et al. Identification of genetic causes of inherited peripheral neuropathies by targeted gene panel sequencing. Mol Cells. 2016; 39(5):382-388.
  15. Pareyson D, Marchesi C. Diagnosis, natural history, and management of Charcot-Marie-Tooth disease. Lancet Neurol. 2009; 8(7):654-667.
  16. Rudnik-Schoneborn S, Tolle D, Senderek J, et al. Diagnostic algorithms in Charcot-Marie-Tooth neuropathies: experiences from a German genetic laboratory on the basis of 1206 index patients. Clin Genet. 2016; 89(1):34-43.
  17. Saporta ASD, Sottile SL, Miller LJ, et al. Charcot-marie-tooth disease subtypes and genetic testing strategies.  Ann Neurol. 2011; 69(1):22-33.
  18. Slater H, Bruno D, Ren H, et al. Improved testing for CMT1A and HNPP using multiplex ligation-dependent probe amplification (MLPA) with rapid DNA preparations: comparison with the interphase FISH method. Hum Mutat. 2004; 24(2):164-171.
  19. Stangler Herodez S, Zagradisnik B, Erjavec Skerget A, et al. Molecular diagnosis of PMP22 gene duplications and deletions: comparison of different methods. J Int Med Res. 2009; 37(5):1626-1631.
  20. Taioli F, Cabrini I, Cavallaro T, et al. Inherited demyelinating neuropathies with micromutations of peripheral myelin protein 22 gene. Brain. 2011; 134(Pt 2):608-617.

Government Agency, Medical Society, and Other Authoritative Publications:

  1. American College of Medical Genetics/American Society of Human Genetics (ACMG/ASHG). Technical and clinical assessment of fluorescence in situ hybridization: an ACMG/ASHG position statement. I. Technical considerations. Test and Technology Transfer Committee. 2000; 2(6):356-361. Available at: Accessed on August 16, 2018.
  2. Bird TD.  GeneReviews [website]. Charcot-Marie-Tooth Neuropathy X Type 1. Updated September 1, 2016. Available at: Accessed on August 16, 2018.
  3. Bird TD.  GeneReviews [website].  Hereditary Neuropathy with Liability to Pressure Palsies. Updated September 25, 2014. Available at: Accessed on August 16, 2018.
  4. Dubourg O, Mouton P, Brice A, et al. Guidelines for diagnosis of hereditary neuropathy with liability to pressure palsies. Neuromuscul Disord. 2000; 10(3):206-208.
  5. England JD, Gronseth GS, Franklin G, et al. Practice Parameter: Evaluation of distal symmetric polyneuropathy: Role of laboratory and genetic testing (an evidence-based review). Report of the American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and American Academy of Physical Medicine and Rehabilitation. Neurology. 2009; 72(2):185-192.
  6. Gene Dx, Inc. (Gaithersburg, MD). Charcot-Marie-Tooth Panel Sequence Analysis and Other Testing.   Updated 2017. Available at: Accessed on August 16, 2018.
  7. Holtzman NE, Watson MS, editors. Final Report of the Task Force on Genetic Testing: promoting safe and effective genetic testing in the United States. 1997 Sep. Last reviewed Oct 1, 2012. Available at: Accessed on August 16, 2018.
  8. Pagon RA, Adam MP, Bird TD, et al.  GeneReviews [website].  Additional neuropathies. Available at: Accessed on August 16, 2018.
  9. U.S. Food and Drug Administration (FDA). Center for Devices and Radiological Health. CLIA—Clinical Laboratory Improvement Amendments. Updated March 22, 2018. Available at: Accessed on August 16, 2018.
Websites for Additional Information
  1. National Library of Medicine (NLM). Genetics Home Reference.  Charcot-Marie-Tooth Disease. Reviewed August 2018. Available at: Accessed on August 16, 2018.
  2. National Library of Medicine (NLM). Genetics Home Reference.  Hereditary Neuropathy with Liability to Pressure Palsies.  Reviewed August 2018. Available at: Accessed on August 16, 2018.

Charcot-Marie-Tooth, CMT
Genetic testing, Genotyping
Hereditary Neuropathy with Liability to Pressure Palsies, HNPP
Neuropathy, Inherited Peripheral

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Document History






Medical Policy & Technology Assessment Committee (MPTAC) review. References were updated.



MPTAC review. The document header wording was updated from “Current Effective Date” to “Publish Date.” References were updated. Updated Coding section with 01/01/2018 CPT changes.



MPTAC review. Coding and References sections were updated.



MPTAC review. References were updated. Removed ICD-9 codes from Coding section.



MPTAC review. Updated reference section. Updated Coding section with 01/01/2015 CPT changes.



MPTAC review. Initial document development.