THE MECHANISM OF CEREBRAL EVOKED POTENTIALS BY REPETITIVE MAGNETIC STIMULATION OF GASTROCNEMIUS MUSCLE IN DUCHENNE MUSCULAR DYSTROPHY
- Author:
Yuzhou GUAN
1
;
Liying CUI
;
Xiaofu TANG
;
Benhong LI
;
Hua DU
Author Information
1. Peking Union Medical College Hospital CAMS and PUMC
- From:
Chinese Medical Sciences Journal
2001;16(2):115-119
- CountryChina
- Language:Chinese
-
Abstract:
Objective. To study the features and mechanism of the cerebral evoked potentials by repetitive stimulation of calf muscle in Duchenne muscular dystrophy (DMD) patients with obvious muscular dystrophy and psuedohypertrophy. Methods. Cerebral evoked potentials by stimulation of calf muscles and somatosensory evoked potentials (SEPs) by the stimulation of posterior tibial nerves at ankle were measured in 10 patients with DMD and 10 normal controls matched with gender and age. The intensity of the magnetic stimulation was at 30％ of maximal output (2.1 Tesla, MagPro magnetic stimulator, Dantec) and the frequency was 1 Hz. The low intensity of magnetic stimulation was just sufficient to produce a contraction of the muscle belly underneath the coil. Recording electrode was placed at 2 cm posterior to the Cz, reference to Fpz. The latencies of N33, P38, N48 and P55 and amplitude (P38－ N48) were recorded. SEPs were recorded by routine methods. Results. In normal subjects, the amplitudes of cerebral evoked potentials by magnetic stimulation of calf muscle was 40％ lower than that by electrical stimulation of the posterior tibial nerves at ankle. The latency of P38 was 2.9± 2.1 ms longer compared with electrical stimulation of the posterior tibial nerves at ankle. In 6 patients, P38 latency from magnetic stimulation was remarkably prolonged (P<0.01), and in 4 patients, there was no remarkable response. SEPs evoked by electrical stimulation were normal in all of the patients.? Conclusion. DMD is an available model for the study of mechanism of cerebral evoked potentials by magnetic stimulating muscle. We can conclude that the responses from magnetic stimulation were produced by muscle input. The abnormal responses in patients may relate to decreased input of muscle by stimulating dystrophic and psedohypertrophic muscle.
