Abstract

The spontaneous electrical activity of human muscle was studied in 197 normals, 67 patients with peripheral nerve involvement and 29 patients with progressive muscular dystrophy. “Noise” was observed in the end-plate zones of normal muscle; after minute displacements of the electrode the noise could be seen to consist of randomly occurring purely negative discharges 0.5–2 msec in duration and up to 100 μV in amplitude. This activity probably represents extracellularly recorded miniature end-plate potentials. Outside the end-plate zones of normal muscle a single site was rarely encountered yielding a spontaneous discharge similar to the fibrillation potentials of denervated muscle. In normal muscle such a discharge may correspond to the propagated disphasic potentials superimposed on the “end-plate noise”. The fibrillation potentials in patients with lower motor neurone disease were found to have longer durations than usually stated (1–5 msec as compared with 0.5–2 msec), a significant proportion of triphasic potentials (30%) and voltages half of which were of the same order (100–300 μV) as those of motor unit potentials. The fibrillations found in 29 of 76 patients with progressive muscular dystrophy had the same average duration, amplitude and shape as in denervated muscles. The fibrillation potentials were initiated in the end-plate zone as evidenced by the initial negative deflection of the potential recorded there and the initial positive deflection outside the end-plate zone. The initiation of the fibrillation potentials cannot be ascribed to mechanical stimulation by the intramuscular needle electrode since fibrillation potentials could also be recorded subcutaneously. With the 50 μ diameter leads of a multi-electrode fibrillation potentials were recorded with peak-to-peak amplitudes as high as 8.5 mV. The decline in amplitude along the multi-lead electrode was the same for fibrillation potentials 1 mV or more in amplitude as for the spike components of motor unit potentials, the voltage falling to less than one-tenth of maximum within 0.45 mm. This suggests that “high voltage” fibrillation potentials represent the spontaneous discharge of a sub-unit. The amplitudes of 100–600 μV fibrillation potentials declined relatively less with distance, suggesting that they were recorded farther away from the generators (about 0.5 mm) than the high voltage potentials. The small amplitude and rapid attenuation of positive sharp waves suggest that they are derived from a single muscle fibre. Cross talk in our multi-lead electrodes was insignificant and cannot explain the discrepancy between our findings and those of other investigators with regard to the voltage decline of spike potentials. The cause of fibrillation potentials is discussed in the light of the present knowledge of the properties of the membrane of denervated muscle fibres.

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