• N Alexeeva, J G Broton, and B Calancie.
• The Miami Project to Cure Paralysis, University of Miami School of Medicine, FL 33136, USA.
• Electroencephalogr Clin Neurophysiol. 1998 Aug 1;109(4):297-303.

ObjectivesTo examine the basis for delay in the excitatory effects of transcranial magnetic stimulation (TMS) of motor cortex on motoneuron pools of muscles left partially-paralyzed by traumatic spinal cord injury (SCI).MethodsThe effect of subthreshold transcranial magnetic stimulation (TMS) on just-suprathreshold H-reflex amplitude was examined in subjects (n = 10) with incomplete cervical SCI, and in able-bodied (AB) subjects (n = 20) for comparison. EMG activity was recorded from the soleus and the abductor hallucis muscles, and H-reflex was elicited by stimulation of the tibial nerve behind the knee. Comparison of the peak-to-peak amplitude of the TMS-conditioned H-reflex to that of the H-reflex alone (i.e. unconditioned H-reflex) was made for different conditioning-test intervals with multivariate analysis of variance and (when called for) t testing.ResultsThe absolute latencies of motor responses to suprathreshold TMS delivered during a weak voluntary contraction of the soleus and abductor hallucis were significantly prolonged in the SCI group relative to AB subjects. For the TMS-conditioned H-reflex, the time-course effect of TMS on the H-reflex amplitude in different AB subjects included an early effect (typically facilitation, but occasionally inhibition) seen between -5 and 0 ms, followed by a later period (i.e. >5 ms) of H-reflex facilitation. In contrast, the earliest indication of a TMS effect on H-reflex excitability in SCI subjects was between 5 and 10 ms after TMS. This difference between SCI and AB subjects of approximately 10 ms was similar to the prolongation of TMS-evoked response latencies in the soleus and the abductor hallucis muscles of the SCI subjects.ConclusionsThe results suggest that motor conduction slowing after traumatic SCI most likely occurs across the population of the descending tract axons mediating the TMS-evoked motor responses.

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