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"Cutaneous silent period"

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"Cutaneous silent period"

Original Articles
Influence of Transcutaneous Electrical Nerve Stimulation on Cutaneous Silent Period.
Lee, Jongmin , Choi, Jong Chul
J Korean Acad Rehabil Med 2000;24(1):83-87.

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.

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The Usefulness of Cutaneous Silent Period in Diabetic Polyneuropathy.
Lee, Jong Min , Kwon, Yong Wook , Cho, Jong Hoon
J Korean Acad Rehabil Med 1998;22(4):882-888.

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.

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