Objective: To determine the effects of the voluntary contraction of muscles and magnetic stimulation intensity on the motor evoked potential (MEP) and the silent period (SP).
Method: We studied MEPs and SPs in opponens pollicis muscle in 30 healthy adults (male: 16, female: 14) while varying the amount of the voluntary contraction and the stimulation intensity. We analyzed MEPs and SPs in relation to sex, recording site, opposition power and height.
Results: 1) During the contraction, the latencies of MEP were significantly shorter than during the relaxation. 2) The amplitudes of MEP reached plateau at 30% of maximal voluntary
contraction and increased with increment of stimulation intensity without limitation. The amplitudes of MEP of right hand were bigger than left hand. There were no significant differences according to sex and recording site. 3) The durations of SP were directly proportional to the degrees of voluntary contraction and the stimulation intensity.
Conclusion: Transcranial magnetic stimulation should be performed under the same voluntary contraction and magnetic stimulation intensity. (J Korean Acad Rehab Med 2002; 26: 140-146)
Objective: This study was proposed to evaluate the electrophysiologic changes in central motor conduction and in silent period (SP) after paraspinal transcutaneous electrical stimulation near caudal area of the spinal cord.
Method: Conditioning stimulation was applied to T12 paraspinal area for 20 minutes using interferential current therapy (80∼100 Hz) in 11 healthy subjects. The amplitude and latency of central motor conduction and duration of SP were measured in motor evoked potential (MEPs) by using magnetic stimulator, before and after the conditioning stimulation. These variables were recorded in both tibialis anterior muscle, innervated from stimulated spinal area, and both abductor pollicis brevis, innervated from cervical cord not directly stimulated by electrical stimulation.
Results: After conditioning stimulation, the amplitudes of central motor conduction decreased (p<0.01), and the latencies did not change in both cervical and lumbar muscles in transcranial and spinal MEP studies, and the duration of SP was decreased in same manner (p<0.01).
Conclusion: These results mean that the excitability of anterior horn cells decreases and the supraspinal inhibitory mechanism of the central motor conduction is suppressed by a certain conditioned electrical cutaneous stimulation in entire spinal cord.
Objective: The purpose of this study was to find out whether the duration of the silent period evoked by magnetic transcranial stimulation could be modulated by lorazepam.
Method: Ten healthy volunteers were tested using the transcranial magnetic stimulation. Responses were recorded in the active abductor digiti minimi muscle, and baseline values were compared to the data obtained at 2 and 5 hours after administration of a single oral dose of 2.5 mg lorazepam.
Results: The motor threshold and size of the motor evoked potential remained unchanged after administration of lorazepam. The duration of cortical silent period was prolonged from 169.9⁑33.7 msec at baseline study to 248.1⁑50.4 msec at 2 hours and 248.5⁑47.3 msec at 5 hours after administration of the drug (p<0.01), but the peripheral silent period did not show any significant change.
Conclusion: We have shown that the cortical silent period evoked by magnetic transcranial stimulation can be prolonged by administration of lorazepam. And the lack of effect on the motor threshold and on the size of the motor evoked potential after administration of lorazepam may indicate that these parameters are physiologically distinct from the cortical silent period. Therefore, prolonged cortical silent period may be resulted from the reinforcement of GABA action by lorazepam at the level of the motor cortex.
Conclusion:
Objective: To investigate the influence of high frequency transcutaneous electrical nerve stimulation (TENS) on cutaneous silent period.
Method: Cutaenous silent period was recorded before and after high frequency TENS application in sixteen healthy adults (11 males, 5 females). Onset latency, duration, and minimum stimulation intensity to evoke cutaneous silent period were compared. In 7 male subjects, temporal changes of cutaneous silent period were observed after TENS application.
Results: Minimum stimulation intensity to evoke cutaneous silent period was significantly increased after high frequency TENS application (p<0.05) and yet, onset latency and duration showed no significant change. The increase in minimum stimulation intensity to evoke cutaneous silent period was maintained for 30 minutes after TENS and returned to the baseline level thereafter.
Conclusions: These results suggest that high frequency TENS increase the depolarization threshold of A-δ fiber and this peripheral effect may be one of the pain control mechanisms of TENS.
Objective: To evaluate the usefulness of cutaneous silent period(CSP) in assessing the pain sensory function mediated by the Aδ fiber in diabetic polyneuropathy and to define the proper CSP parameter and method.
Method: We studied 18 diabetic polyneuropathy patients and 20 age-matched healthy subjects. CSPs were recorded in the abductor pollicis brevis muscle and soleus muscle with the surface electrodes and a painful electrical stimulation was given to the mixed nerves(median and tibial nerve) and cutaneous nerve(ulnar and superficial peroneal nerve). Onset latency, end point and duration of CSP were compared between two groups. CSP parameters correlated with the motor and sensory nerve conduction parameters in diabetic polyneuropathy patients.
Results: CSP onset latency and end point were significantly delayed in diabetic polyneuropathy patients for both mixed nerve and cutaneous nerve stimulations. There was no difference in CSP duration between two groups. CSP onset latency was shortend and duration was prolonged in mixed nerve stimulation due to an antidromic collision, which showed a cutaneous nerve stimulation as the propor method. There was no correlation between the CSP parameters and motor and sensory nerve conduction parameters. In 3 cases, the CSPs were unable to the evoked despite the sensory nerve action potential was normally evoked. This suggests that the CSP would give an information about the Aδ fiber function than the large myelinated fiber.
Conclusion: This study indicates that the CSP is a useful supportive electrophysiologic study to assess the Aδ fiber function in diabetic polyneuropathy. The CSP onset latency and cutaneous nerve stimulation are the useful parameter and method for the CSP.