Firing behavior of triceps brachii motor units after spinal by umsymums33


									             Firing behavior of triceps brachii motor units after spinal cord injury
                 Christine K. Thomas Mary Tucker, Galina Kozhina, Blair Calancie
 The Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami
                           MILLER School of Medicine, Miami, FL 33136
Triceps brachii muscles are often paralyzed partially after cervical spinal cord injury in humans.
Motor units become paralyzed because inputs from higher center are disrupted, the trauma
induces motoneuron death or both processes occur. Thus, only a few triceps brachii motor units
remain under voluntary control. At the whole muscle level, forces are weak compared to those
generated in the muscles of uninjured people. Our aims were to examine: 1) whether chronic
cervical spinal cord injury changes triceps brachii motor unit firing rates during voluntary
contractions; 2) the prevalence of motor unit firing rate saturation; 3) whether baclofen changes
triceps brachii motor unit firing rates during voluntary contractions. Baclofen is a medication
usually taken to dampen involuntary contractions (spasms) of paralyzed muscles. Baclofen, a
GABAB agonist, largely acts presynatically to block signal conduction at primary afferent
terminals (Price et al. Nature 307: 71-74, 1984). Much higher doses are needed for postsynaptic
effects, which include increases in the amplitude of persistent inward currents in motoneurons
because reductions in calcium currents are less that the increases in sodium currents (Li et al. J
Neurophysiol 92:2694-703, 2004).
        Subjects with chronic (> 1 year) spinal cord injury at C5, C6 or C7 from a motor vehicle
or diving accident, a gunshot or a fall participated in this study. Each person performed a series
of isometric submaximal and maximal voluntary contractions (5 s) of triceps brachii. Records
were made of triceps brachii intramuscular electromyographic activity (EMG) to identify the
firing behavior of different motor units, triceps and biceps brachii surface EMG, and force. Data
were included provided that: 1) there were increases in the triceps surface EMG up to maximal
force. Otherwise force may have been produced by contractions of muscles other than triceps
brachii; 2) the firing behavior of a motor unit could be followed from recruitment to maximal
        Data were obtained from 40 motor units, 1-6 units per muscle. Motor units were recruited
up to near maximal force. At recruitment, motor units fired at low rates (< 20 Hz). Firing rates
increased with force. Most motor units (69 %) continued to increase their firing rate up to
maximal force. Only 31 % of units showed a saturation in motor unit firing rate, and typically at
high forces (≥ 80 % maximal force). There was a broad range of motor units firing rates during
maximal voluntary contractions (12-70 Hz). Within a muscle, the firing behavior of different
motor units varied, both in terms of absolute firing rates and the relative change in firing rate
with force. Approximately half the data came from individuals who take baclofen chronically.
Maximal voluntary motor unit firing rates were higher in individuals using baclofen (mean ± SE:
42 ± 3 Hz) versus not (25 ± 2 Hz), the latter comparable to data from uninjured control subjects.
Higher motor unit firing rates during strong and maximal voluntary contractions with baclofen
were not attributable to differences in coactivation of triceps and biceps brachii, firing rate
saturation, injury level, or sex. Even though baclofen dampens spasms of paralyzed muscles,
more effort may be required to recruit motoneurons voluntarily. However, once motoneurons are
activated, the postsynaptic effects of baclofen may emerge and be reflected in higher motor unit
firing rates. While these higher firing rates will facilitate voluntary contractions, they will also
strengthen muscle spasms. These data suggest that presynaptic control of muscle spasms is
warranted if voluntary strength is to be maintained.
        Funded by USPHS grant NS30226 and The Miami Project to Cure Paralysis.

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