Abstract
Purpose & Background: The spinal muscles are increasingly being linked to spinal complaints. However, little is known regarding the corticospinal control of these muscles. Corticospinal pathways can be activated using transcranial magnetic stimulation (TMS) applied over the motor cortex. This study uses TMS to assess corticospinal input to the paraspinal muscles in the thoracic region.
Methods: Ten individuals (mean [± SD] age 33 ± 10 yrs; mean height 166 ± 10 cm; two left-handed; five male, five female) with no history of neurological disorder were recruited into this study and written informed consent obtained. Subjects lay prone in a relaxed position with the head unsupported. Surface electromyographic (EMG) recording electrodes were positioned bilaterally over the paraspinal muscles adjacent to thoracic spinal processes T1 and T2. TMS was applied using a MagStim 200 stimulator connected to a double cone coil with its cross-over positioned over the vertex so that the maximum induced current flowed in a posterior to anterior direction. The stimulus intensity was adjusted in steps of 5% of the maximum stimulator output (MSO), and ten stimuli were delivered at each strength. Threshold for a motor evoked potential (MEP) in each muscle was determined as the minimum intensity that would evoke MEPs to 50% of stimulus presentations. Latency of MEPs was determined by measuring the time between the stimulus and the start of the first deflection in the MEP. The procedure was repeated for the other pairs of thoracic segments between T3 and T12.
Results: In all subjects, it was possible to evoke MEPs in relaxed paraspinal muscles at all thoracic levels. Mean (±SEM) threshold for evoking a MEP on the left side increased from 47 ± 2.5 %MSO at level T1 to 55 ± 2.5 %MSO at T12 (Pearson correlation, P< 0.05) but remained more constant (P> 0.05) on the right side (T1, 55 ± 3.9 %MSO; T12, 57 ± 3.3 %MSO). Over all levels tested, mean threshold for MEPs was 3.9 ± 0.6 %MSO higher on the right than the left side (Student’s paired t-test, P< 0.05). Mean latency of MEPs on the left increased from 11.9 ± 0.7 ms at level T1 to 15.5 ± 0.6 ms at T12 and on the right from 12.3 ± 0.5 ms at level T1 to 16 ± 0.7 ms at T12 (Pearson correlation, P< 0.05). Throughout the thoracic region, latency of MEPs was 0.8 ± 0.2 ms longer on the right than the left side (Student’s paired t-test, P< 0.05).
Conclusion: The latency of MEPs increased as recordings were made from muscles innervated more caudally. Threshold for MEPs varied between subjects and at different spinal levels but our results indicate that it was higher at more caudal levels, perhaps suggesting weaker corticospinal innervation. Threshold was lower and latency shorter for muscles on the left side raising the interesting possibility that paraspinal muscles have some asymmetry in their corticospinal innervation. This study has provided us with baseline electrophysiological data allowing us to investigate the voluntary control pathways to muscles stabilising the thoracic spinal cord following trauma or disease.
The abstracts were prepared by Dr P Dolan. Correspondence should be addressed to him at the British Orthopaedic Association, Royal College of Surgeons, 35-43 Lincoln’s Inn Fields, London WC2A 3PN.
