ELECTRICAL EXCITATION OF NERVE 179 



tion, and that in almost the same degree as the opening of the 

 strong current. This effect, however, soon diminishes, and dis- 

 appears completely after a few minutes if the nerve is sufficiently 

 vigorous. With otherwise uniform conditions this characteristic 

 after-effect is the more persistent, in proportion with the previous 

 passage of the strong current, and defective vitality in the nerve. 

 . Any point along the nerve may thus (as in local treatment 

 with potash) be rendered sensible to weak and, under normal 

 conditions, non-effective opening stimuli, by making it for a short 

 time the entrance point of a stronger constant current. And as 

 in the previous case the raised disposition to the opening excita- 

 tion may be neutralised by washing off the toxic substance with 

 an indifferent fluid, so in the excised nerve the continuous process 

 of restitution suffices to neutralise the anodic alterations pro- 

 duced by the current, and to restore the normal insensibility to 

 opening stimuli. 



The break excitation which may be discharged at the anodic 

 points of the nerves after brief closure of a stronger current, by 

 currents of lower intensity, is always expressed, as we have seen, 

 in twitches of the muscle, which correspond throughout with 

 those that appear on treatment with potash salts, or in the 

 immediate proximity of a fresh transverse section. This, apart 

 from the absence of any perceptible interval between the break 

 of the current and the beginning of contraction, is more par- 

 ticularly expressed in the uniformity between the curves of the 

 two twitches, and in the slight effect of intensity and duration of 

 exciting current upon the magnitude of the twitches. 



A further proof of the correspondence between the break 

 twitches discharged after treating a nerve with potassium salts 

 (these again being identical with the " primary opening twitches " 

 of the alcohol effect), and those discharged by strong currents 

 in normal, uninjured nerve, appears in the fact that the latter 

 are discharged simultaneously with " secondary " delayed opening 

 twitches (break twitch II) in the same preparation. Since 

 Eitter's tetanus is equivalent with break twitch II (supra), and 

 since this is sometimes delayed (as pointed out by Wundt), the 

 effect of the opening excitation in such cases either consists in 

 a completely or incompletely separated double twitch, or else 

 break twitch I is introductory to Eitter's tetanus (Figs. 189, 

 192). 



