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Modulation of single motor unit discharges using magnetic stimulation of the motor cortex in incomplete spinal cord injury
  1. H C Smitha,
  2. N J Daveya,
  3. G Savicb,
  4. D W Maskilla,
  5. P H Ellawaya,
  6. M A Jamousb,
  7. H L Frankelb
  1. aDivision of Neuroscience and Psychological Medicine, Imperial College School of Medicine, Charing Cross Hospital, London W6 8RF, UK, bNational Spinal Injuries Centre, Stoke Mandeville Hospital, Aylesbury, Bucks HP21 8AL, UK
  1. Dr Nick J Davey, Department of Sensorimotor Systems, Division of Neuroscience and Psychological Medicine, Imperial College School of Medicine, Charing Cross Hospital, Fulham Palace Road, London W6 8RF, UK email n.davey{at}ic.ac.uk

Abstract

OBJECTIVES Motor evoked potentials (MEPs) and inhibition of voluntary contraction to transcranial magnetic stimulation (TMS) of the motor cortex have longer latencies than normal in patients with incomplete spinal cord injury (iSCI) when assessed using surface EMG. This study now examines the modulation of single motor unit discharges to TMS with the aim of improving resolution of the excitatory and inhibitory responses seen previously in surface EMG recordings.

METHODS A group of five patients with iSCI (motor level C4-C7) was compared with a group of five healthy control subjects. Single motor unit discharges were recorded with concentric needle electrodes from the first dorsal interosseus muscle during weak voluntary contraction (2%–5% maximum). TMS was applied with a 9 cm circular stimulating coil centred over the vertex. Modulation of single motor unit discharges was assessed using peristimulus time histograms (PSTHs).

RESULTS Mean (SEM) threshold (expressed as percentage of maximum stimulator output (%MSO)) for the excitatory peak (excitation) or inhibitory trough (inhibition) in the PSTHs was higher (p<0.05) in the patients (excitation=47.1 (5.9) %MSO; inhibition=44.3 (3.2) %MSO) than in controls (excitation=31.6 (1.2) %MSO; inhibition=27.4 (1.0) %MSO). Mean latencies of excitation and inhibition were longer (p<0.05) in the patients (excitation=35 (1.8) ms; inhibition=47.1 (1.8) ms) than in the controls (excitation=21.1 (1.6) ms; inhibition=27 (0.4) ms). Furthermore, the latency difference (inhibition−excitation) was longer (p<0.05) in the patients (10.4 (2.1) ms) than in the controls (6.2 (0.6) ms).

CONCLUSION Increased thresholds and latencies of excitation and inhibition may reflect degraded corticospinal transmission in the spinal cord. However, the relatively greater increase in the latency of inhibition compared with excitation in the patients with iSCI may reflect a weak or absent early component of cortical inhibition. Such a change in cortical inhibition may relate to the restoration of useful motor function after iSCI.

  • spinal cord injury
  • corticospinal
  • motor unit
  • magnetic stimulation

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