Journal article
Dispersion of compound muscle action potential in hereditary neuropathies and chronic inflammatory demyelinating polyneuropathy
Muscle & nerve, Vol.34(4), pp.417-422
2006
DOI: 10.1002/mus.20600
PMID: 16823858
Abstract
Distal compound muscle action potential (DCMAP) dispersion, defined as a DCMAP duration ≥9 ms, and proximal-distal (P-D) CMAP dispersion are considered useful in the electrodiagnosis of chronic inflammatory demyelinating polyneuropathy (CIDP). Distal and P-D CMAP dispersion have not been fully studied in hereditary neuropathies, and it is not known whether these measures distinguish hereditary from acquired demyelination. We compared DCMAP duration and P-D CMAP dispersion in 91 genetically characterized hereditary neuropathies and 33 subjects with CIDP. DCMAP dispersion was more frequent in nerves affected by CIDP (41.5%) than in Charcot–Marie–Tooth disease (CMT)1A (24.4%), CMT1B (7.4%), hereditary neuropathy with liability to pressure palsies (HNPP) (10.5%), or CMTX (9.8%). P-D CMAP dispersion was more frequent in CIDP (27.7% of nerves) than in hereditary neuropathies (16.3%) when applying American Academy of Neurology (AAN) criteria; however, its frequency was similar in CIDP and the hereditary neuropathies using the more restrictive criteria of the American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM). Although dispersion is more common in CIDP than in the hereditary neuropathies, DCMAP and P-D dispersion occur in at least one motor nerve in a significant proportion of hereditary neuropathies, and cannot be used in isolation to distinguish acquired from hereditary demyelination.
Details
- Title: Subtitle
- Dispersion of compound muscle action potential in hereditary neuropathies and chronic inflammatory demyelinating polyneuropathy
- Creators
- Michael STANTON - Department of Neurology, University of Rochester Medical Center, 601 Elmwood Ave., Box 673, Rochester, New York 14642, United StatesValerie PANNONI - Department of Neurology, University of Rochester Medical Center, 601 Elmwood Ave., Box 673, Rochester, New York 14642, United StatesRichard A LEWIS - Department of Neurology, Wayne State University, Detroit, Michigan, United StatesEric L LOGIGIAN - Department of Neurology, University of Rochester Medical Center, 601 Elmwood Ave., Box 673, Rochester, New York 14642, United StatesDemian NAGUIB - Department of Neurology, Wayne State University, Detroit, Michigan, United StatesMichael E SHY - Department of Neurology, Wayne State University, Detroit, Michigan, United StatesJames CLELAND - Department of Neurology, University of Rochester Medical Center, 601 Elmwood Ave., Box 673, Rochester, New York 14642, United StatesDavid N HERRMANN - Department of Neurology, University of Rochester Medical Center, 601 Elmwood Ave., Box 673, Rochester, New York 14642, United States
- Resource Type
- Journal article
- Publication Details
- Muscle & nerve, Vol.34(4), pp.417-422
- Publisher
- Wiley; New York, NY
- DOI
- 10.1002/mus.20600
- PMID
- 16823858
- ISSN
- 0148-639X
- eISSN
- 1097-4598
- Language
- English
- Date published
- 2006
- Academic Unit
- Neurology; Molecular Physiology and Biophysics; Stead Family Department of Pediatrics; Iowa Neuroscience Institute
- Record Identifier
- 9984020767002771
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