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Brain Advance Access published online on November 10, 2009

Brain, doi:10.1093/brain/awp285
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© The Author (2009). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Effects of baclofen on motor units paralysed by chronic cervical spinal cord injury

Christine K. Thomas1, Charlotte K. Häger-Ross2 and Cliff S. Klein3

1 The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL 33136, USA 2 Department of Community Medicine and Rehabilitation, Umeå University, Sweden 3 Department of Physical Therapy, University of Toronto, Canada

Correspondence to: Christine K. Thomas, The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, 1095 NW 14 Terrace, R48, Miami, FL 33136-2104, USA E-mail: cthomas{at}miami.edu

Baclofen, a gamma-aminobutyric acid receptorB agonist, is used to reduce symptoms of spasticity (hyperreflexia, increases in muscle tone, involuntary muscle activity), but the long-term effects of sustained baclofen use on skeletal muscle properties are unclear. The aim of our study was to evaluate whether baclofen use and paralysis due to cervical spinal cord injury change the contractile properties of human thenar motor units more than paralysis alone. Evoked electromyographic activity and force were recorded in response to intraneural stimulation of single motor axons to thenar motor units. Data from three groups of motor units were compared: 23 paralysed units from spinal cord injured subjects who take baclofen and have done so for a median of 7 years, 25 paralysed units from spinal cord injured subjects who do not take baclofen (median: 10 years) and 45 units from uninjured control subjects. Paralysed motor unit properties were independent of injury duration and level. With paralysis and baclofen, the median motor unit tetanic forces were significantly weaker, twitch half-relaxation times longer and half maximal forces reached at lower frequencies than for units from uninjured subjects. The median values for these same parameters after paralysis alone were comparable to control data. Axon conduction velocities differed across groups and were slowest for paralysed units from subjects who were not taking baclofen and fastest for units from the uninjured. Greater motor unit weakness with long-term baclofen use and paralysis will make the whole muscle weaker and more fatigable. Significantly more paralysed motor units need to be excited during patterned electrical stimulation to produce any given force over time. The short-term benefits of baclofen on spasticity (e.g. management of muscle spasms that may otherwise hinder movement or social interactions) therefore have to be considered in relation to its possible long-term effects on muscle rehabilitation. Restoring the strength and speed of paralysed muscles to pre-injury levels may require more extensive therapy when baclofen is used chronically.

Key Words: baclofen; spinal cord injury; muscle paralysis; muscle weakness; axon conduction velocity; intraneural motor axon stimulation

Abbreviations: EMG, electromyograph; F50, frequency of stimulation that generated half maximal force

Received June 30, 2009. Revised September 8, 2009. Accepted September 26, 2009.


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