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Neurology 2000;55:24-30
© 2000 American Academy of Neurology


Articles

Developmental apraxia arising from neonatal brachial plexus palsy

T. Brown, MD, C. Cupido, MD, H. Scarfone, RT, K. Pape, MD, V. Galea, PhD and A. McComas, MB

From the Department of Medicine, Division of Neurology (Dr. Brown, H. Scarfone, and A. McComas), the Department of Paediatrics (Dr. Cupido), and the School of Rehabilitation Science (Dr. Galea), McMaster University, Hamilton, and Mayatek Incorporated (Dr. Pape), Toronto, Ontario, Canada.

Address correspondence and reprint requests to Alan J. McComas, Division of Neurology (Room 4U1), McMaster University Medical Centre, 1200 Main Street West, Hamilton, Ontario, Canada L8N 3Z5.

OBJECTIVE: To determine whether motor unit activation is impaired in patients with persisting disability arising from neonatal brachial plexus palsy (NBPP).

BACKGROUND: In NBPP patients, the authors previously found more extensive muscle reinnervation than might have been anticipated from the clinical examination.

METHODS: Motor skills were tested in a group of nine boys and seven girls with prior NBPP, who then underwent physiologic investigation of proximal and distal muscles in their affected and unaffected arms. The latter tests comprised measurements of maximal evoked muscle compound action potential (M-wave) amplitude, maximal voluntary torque, twitch torque, and twitch interpolation. A group of 17 children of similar ages served as control subjects.

RESULTS: In the NBPP group, motor skills were diminished and voluntary torque was reduced relative to M-wave amplitude and twitch torque. Moreover, interpolated twitches could be demonstrated in some NBPP patients but not in control subjects.

CONCLUSION: Persisting disability in NBPP patients is due, at least in part, to impaired motor unit activation. The authors suggest that the impairment is a form of developmental apraxia caused by defective motor programming in early infancy.




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