CMT,HSMN,CIDP: Dispersion of compound muscle action potential

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Muscle Nerve. 2006 Jul 5

Dispersion of compound muscle action potential in hereditary

neuropathies and chronic inflammatory demyelinating polyneuropathy.

Stanton M, Pannoni V, RA, Logigian EL, Naguib D, Shy ME,

Cleland J, Herrmann DN.

Department of Neurology, University of Rochester Medical Center, 601

Elmwood Ave., Box 673, Rochester, New York 14642, USA.

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.