CH. XIII.] RIGOR MORTIS 153 



sympathetic nerve in the rabbit, the splanchnic nerve of the dog, and the sciatic 

 nerve in a curarised dog, and have obtained corresponding results. This confirms 

 the work previously published by Eve. Eve excited the cervical sympathetic for 

 twelve hours, and found no loss of excitability at the end of that time. Eve 

 stimulated the nerve below the upper cervical ganglion, and the main object of his 

 work was to ascertain whether any histological evidence of fatigue could be found 

 in the cells of the ganglion. The only change he could find there was a somewhat 

 diffuse staining of the cells by methylene blue, which he attributes to the formation 

 of acid substances in the cells. A blue stain of similar appearance may be induced 

 in the motor cells of the spinal cord, ^fter exhaustion is produced in them by giving 

 strychnine. In such experiments the spinal cord becomes as a rule distinctly acid 

 to litmus paper. Max Verworn has more recently employed strychnine as a means 

 of producing fatigue. He considers that the only specific effect of this alkaloid is 

 increase of reflex activity, and he attributes the subsequent paralysis to vascular 

 conditions and the accumulation of fatigue products, among which he places carbon 

 dioxide in the first rank. Eve, on the contrary, did not find that carbonic acid 

 alone produces the effects. 



We must conclude from such experiments that Dr Waller's theory is unproved, 

 and that while fatigue is demonstrable in nerve-cells, it has never yet been shown 

 to occur in nerve-fibres of either the medullated or non-medullated variety. 



In carrying out these experiments we noticed that though no functional fatigue 

 can be demonstrated, there is noticeable, especially in vaso-motor nerves, a 

 phenomenon which Howell terms stimulation fatigue ; this means that the actual 

 spot of nerve stimulated becomes after a time less excitable, and finally, inexcitable, 

 though it will still transmit impulses, if the excitation is applied above the spot 

 originally stimulated. We think that the use of the term " fatigue " in this con- 

 nection is a mistake ; the prolonged electrical excitation causes injurious polarisa- 

 tion (due to electrolytic changes) of the nerve, which renders it less excitable. This 

 view has been confirmed by Prof. Gotch by means of experiments with the capillary 

 electrometer. This so-called "stimulation fatigue" was not excluded in Miss 

 Sowton's experiments, and will possibly explain her results. The splenic nerves, 

 curiously enough, do not exhibit this phenomenon in any marked degree, and so 

 were peculiarly well adapted to testjthe question of functional fatigue. On a priori 

 grounds we should hardly expect non-medullated nerves to be peculiarly susceptible 

 of real fatigue, when one considers how many of them, like the vaso-constrictors, 

 are in constant action throughout life. 



Rigor Mortis. 



After death, the muscles gradually lose their irritability and pass 

 into a contracted condition. This affects all the muscles of the body, 

 and usually fixes it in the natural posture of equilibrium or rest. 

 The general stiffening thus produced constitutes rigor mortis or post- 

 mortem rigidity. 



The cause of rigor is the coagulation of the muscle-plasma, which 

 is more fully described in the next section. This coagulation results 

 in the formation of myosin, and is gradual in onset. Simultaneously 

 the muscles (a) become shortened and opaque, (b) heat is evolved, (c) 

 they give off carbonic acid, and (d) become acid in reaction ; this is due 

 in part to the formation of sarco-lactic acid, and in part to the forma- 

 tion of acid phosphates. 



After a varying interval, the rigor passes off, and the muscles are 

 once more relaxed. This sometimes occurs too quickly to be caused 

 by putrefaction, and the suggestion that in such cases at any rate 



