

CAUSE OF RIGOR MORTIS. 467 



of a corpse are thus affected, the whole cadaver becomes completely stiff or rigid. 

 The cause of this phenomenon depends upon the spontaneous coagulation of a 

 proteid, viz., the myosin of the muscular fibres (Kilhne). Under certain circum- 

 stances, the coagulation of the other proteids of the muscle may increase the 

 rigidity. During the process of coagulation, an acid is formed, heat is set free 

 (v. Waltker, Fick 223), owing to the passage of the fluid myosin into the solid 

 condition, and also to the simultaneous and subsequently increased density of the 

 tissue. 



Properties of a Muscle in Rigor Mortis. It is shorter, thicker, and somewhat 

 denser (Schmulewitsch) ; stiff, compact, and solid ; turbid and opaque (owing to 

 the coagulation of the myosin) ; incompletely elastic, less extensible, and more 

 easily torn or ruptured ; it is completely inexcitable to stimuli ; the muscular 

 electrical current is abolished, (or there is a slight current in the opposite direction); 

 its reaction is acid, owing to the formation of both forms of lactic acid ( 293), 

 glycero-phosphoric acid (Diakanoiv) ; while it also develops free C0 2 . When 

 an incision is made into a rigid muscle, a fluid, the muscle-serum, appears 

 spontaneously in the wound ( 293). 



The first formed lactic acid converts the salts of the muscle into acid salts ; thus, potassium 

 lactate and acid potassium phosphate are formed from potassium phosphate. The lactic acid, 

 which is formed thereafter, remains free and ununited in the muscle. 



Amount of Glycogen. The newest observations of Bbhm are against the view that, during 

 rigor mortis, a partial or complete transformation of the glycogen into sugar and then into 

 lactic acid takes place. During digestion, a temporary storage of glycogen occurs in the muscles 

 as well as in the liver, so that about as much is found in the muscles as in the liver. There 

 is no diminution of the glycogen when rigidity takes place, provided putrefaction be prevented ; 

 so that the lactic acid of rigid muscles cannot be formed from glycogen, but more probably it 

 is formed from the decomposition of the albuminates (Deviant, B'ohm). 



The amount of acid does not vary, whether the rigidity occurs rapidly or slowly (J. Ranke) ; 

 when acidification begins, the rigidity becomes more marked, owing to the coagulation of the 

 alkali-albuminate of the muscle. Less C0. 2 is formed from a rigid muscle, the more C0 2 it has 

 given off previously, during muscular exertion. A rigid muscle gives off ~N, and absorbs 0. In 

 a cadaveric rigid muscle, fibrin -ferment is present (Al. Schmidt and others). It seems to be a 

 product of protoplasm, and is never absent where this occurs (Rauschenbach). [The myosin- 

 ferment seems not to be identical with the fibrin-ferment (p. 463).] 



[Rigor Mortis and Coagulation of Blood. Thus, there is a marked analogy 

 between the coagulation of the blood and that of muscle. In both cases, a fluid 

 body yields a solid body, fibrin from blood, and myosin from muscle ; the coagula- 

 tion of blood is prevented by neutral salts, and so is the coagulation of myosin ; 

 dilution of the salted plasma produces coagulation in both cases ; and perhaps the 

 coagulation in both is due to the action of a ferment, the one the fibrin-ferment 

 the other the myosin-ferment. There are, however, points of difference, for 

 myosin can be dissolved, reprecipitated, and coagulated several times, while fibrin 

 does not undergo recoagulation ; the formation of myosin from myosinogen, again, 

 is accompanied by the development of an acid, w r hereas that of fibrin from 

 fibrinogen is not ; further, the formation of myosin is not accompanied by the 

 formation of another globulin, whereas that of fibrin from fibrinogen is.] 



Stages of Rigidity. Two stages are recognisable in cadaveric muscles : In 

 the first stage, the muscle is rigid, but still excitable ; in this stage the myosin 

 seems to be in a jelly-like condition. Kestitution, is still possible during this stage. 

 In the second stage, the rigidity is well pronounced, with all the phenomena 

 above mentioned. 



The onset of the rigidity varies in man from ten minutes to seven hours [but as 

 a rule it is complete within four to six hours after death. The muscles of the jaws 

 are first affected, then those of the neck and trunk, afterwards (as a rule) the 

 lower limbs, and finally the upper limbs]. Its duration is equally variable one 

 to six days. After the cadaveric rigidity has disappeared, the muscles, owing to 



