Motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (TMS) and transcranial electrical stimulation (TES) of the motor cortex were recorded in separate sessions to assess changes in motor cortex excitability after a fatiguing isometric maximal voluntary contraction (MVC) of the right ankle dorsal flexor muscles. Five healthy male subjects, aged 37.4 +/- 4.2 years (mean +/- SE), were seated in a chair equipped with a load cell to measure dorsiflexion force. TMS or TES was delivered over the scalp vertex before and after a fatiguing MVC, which was maintained until force decreased by 50%. MEPs were recorded by surface electrodes placed over quadriceps, hamstrings, tibialis anterior (TA), and soleus muscles bilaterally. M-waves were elicited from the exercised TA by supramaximal electrical stimulation of the peroneal nerve. H-reflex and MVC recovery after fatiguing, sustained MVC were also studied independently in additional sessions. TMS-induced MEPs were significantly reduced for 20 min following MVC, but only in the exercised TA muscle. Comparing TMS and TES mean MEP amplitudes, we found that, over the first 5 min following the fatiguing MVC, they were decreased by about 55% for each. M-wave responses were unchanged. H-reflex amplitude and MVC force recovered within the 1st min following the fatiguing MVC. When neuromuscular fatigue was induced by tetanic motor point stimulation of the TA, TMS-induced MEP amplitudes remained unchanged. These findings suggest that the observed decrease in MEP amplitude represents a focal reduction of cortical excitability following a fatiguing motor task and may be caused by intracortical and/or subcortical inhibitory mechanisms.

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Vertex transcranial magnetic stimulation (TMS) elicited tibialis anterior motor evoked potentials (MEPs) and silent periods (SPs) that were recorded during and following isometric maximal volitional contraction (MVC). During MVC in 6 healthy subjects, MEP amplitudes in the exercised muscle showed an increasing trend from an initial value of 4539 +/- 809 muV (mean +/- SE) to 550 +/- 908 muV (P < 0.13) while force and EMG decreased (P < 0.01). Also, SP duration increased from 165 +/- 37 ms to 231 +/- 32 ms (P < 0.01). Thus, during a fatiguing MVC both excitatory and inhibitory TMS-induced responses increased. TMS delivered during repeated brief 10% MVC contractions before and after a fatiguing MVC in 5 subjects, showed no change in MEP amplitude but SP duration was prolonged after MVC. This SP prolongation was focal to the exercised muscle. Silent periods recorded after pyramidal tract stimulation were unchanged following the MVC. These results suggest that MEP and SP might have common sources of facilitation during an MVC and that inhibitory mechanisms remain focally augmented following a fatiguing MVC.

Objectives: To describe an electrophysiological method for determining the relation between lumbar cord dorsal roots and cathode of epidural electrode for spinal cord stimulation (SCS). Materials and methods: Data has been collected from 13 subjects who have been under evaluation of eectiveness of SCS for control of spasticity. Induced muscle twitches from both quadriceps (Q), adductors (A), hamstrings (H), tibial anterior muscles (TA) and triceps surae muscles (TS) were simultaneously recorded with surface-electrode polyelectromyography (pEMG) and analyzed for amplitudes, latency times and recruitment order. Results: Stimulation of dorsal lumbar cord structures evoked characteristic EMG events during muscle twitch responses. Their amplitudes varied with stimulus strength. Latency times were rather invariable regardless of stimulus strength. Two distinct recruitment orders were demonstrated depending on whether the stimulating cathode was placed over the upper (=response from quadriceps and/or adductor muscles) or the lower (=response from tibialis anterior and triceps surae) lumbar cord segments. The chances to stimulate upper lumbar cord segments are best around the 12th thoracic vertebra. Conclusions: pEMG recording of muscle twitches enables us to accurately dierentiate between upper and lower lumbar cord segments. Furthermore, our ®ndings regarding amplitude, latency and recruitment order strongly suggest that we stimulate posterior roots not posterior columns of the lumbar spinal cord. Spinal Cord (2000) 38, 394 ± 402