Electroencephalography and clinical neurophysiology · 1998
Latency of changes in spinal motoneuron excitability evoked by transcranial magnetic brain stimulation in spinal cord injured individuals.
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Alexeeva N, Broton J G, Calancie B
Аннотация
OBJECTIVES: To 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).
METHODS: The 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.
RESULTS: The 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.
CONCLUSIONS: The 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.
METHODS: The 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.
RESULTS: The 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.
CONCLUSIONS: The 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.