MUSCULAR RIGIDITY. 553 



digestion a transitory accumulation of large amounts of glycogen takes place in 

 the muscles, as in the liver; so that approximately as much can be found in the 

 former as in the latter. Rigidity causes no diminution of glycogen, provided 

 putrefaction is prevented; < hence, the lactic acid of rigid muscles cannot arise 

 from glycogen, but probably from decomposition of albuminates. Heffter main- 

 tains that lactic acid is not formed at all during postmortem rigidity. 



The amount of acid does not vary, whether the rigidity develops slowly or 

 rapidly. With the onset of acidification, the rigidity becomes more marked, 

 on account of the coagulation of the alkali-albumin in the muscle. The less 

 carbon dioxid there is generated by the rigid muscle the more it had already 

 given off previously during activity. 



Fibrin-ferment is present in muscle in a state of cadaveric rigidity. It is in 

 general a product of protoplasm, and is never wanting where the latter is present. 

 There is thus an analogy between coagulation of blood and muscular rigidity. 



Two stages of rigidity are to be distinguished: In the first stage 

 the muscle is already somewhat stiff, but still excitable; the myosin in 

 this stage acquires a gelatinous consistency. Restitution is still possible 

 from this stage. In the second stage the rigidity is fully developed in 

 all of the characteristics mentioned. 



Rigidity appears in man in from ten minutes to seven hours; the duration is 

 likewise variable, from one to six days. After its disappearance, the muscles 

 again become soft, owing to the onset of further decomposition and an alkaline 

 reaction; the rigidity yields. The onset of rigidity is always preceded by a dis- 

 appearance of nervous activity. Therefore, the muscles of the head and the neck 

 are first affected, and then the others in a descending order. Likewise those 

 muscles that usually degenerate earliest a are the first to become rigid; for example, 

 in the frog the flexors before the extensors. Rigidity disappears earliest also in 

 those muscles that first became rigid. Great muscular activity before death, for 

 example during the convulsions of tetanus, cholera, strychnin-poisoning, or opium- 

 poisoning, causes rapid and intense rigidity. Therefore, the heart becomes 

 strongly rigid and with relative rapidity. White muscles become rigid later than 

 red muscles. Wild animals, hunted to death, may become rigid in a few minutes. 

 Usually the rigidity lasts the longer the later it sets in. Rigidity never occurs 

 in the fetus before the seventh month. Frogs' muscles cooled to o C. become 

 rigid only after from four to seven days. 



Stenson's Experiment. The influence of the amount of blood in the muscles 

 upon the onset of rigidity is especially worthy of notice. Ligation of the muscular 

 arteries in warm-blooded animals causes first increased irritability of the muscular 

 tissue, lasting a few minutes, then rapid diminution in the irritability, followed 

 by the onset of both stages of rigor in succession. If the arteries of the muscles 

 were ligated, Stannius observed that the irritability of the motor nerves disap- 

 peared in the course of an hour, that of the muscular tissue itself in from four 

 to five hours; then rigidity sets in. 



Pathological. Thrombotic occlusion of the muscular vessels will also cause 

 rigidity. Excessively tight bandaging may give rise to true rigidity in man by 

 cutting off the circulation. The muscles become paralyzed and stiff, and later break 

 up into flakes, and the contents of the fibers are subsequently absorbed. The circu- 

 latory disturbances, arising in muscles under the influence of cold, also cause 

 paralyses that are often designated rheumatic. Also in cases of trichinosis the 

 affected muscle-fibers are the seat of rigidity, and the stiffness in the muscles 

 is thus explained. The contractures occurring in cases of cholera should probably 

 be included in the class of muscular contractions resulting from circulatory dis- 

 turbances, the inspissated blood giving rise to stagnation; as should also certain 

 contractions occurring in the presence of atheroma and in the agonal period. 

 The sensory nerves in completely anemic extremities retain their irritability for 

 from five to ten hours. 



If the circulation be restored in the first stage of rigidity, the muscle soon 

 recovers. If, however, the second stage has set in, restitution is impossible. In 

 cold-blooded animals rigidity does not set in for several days after ligature of 

 the vessels. Brown-Sequard, by the injection of fresh blood containing oxygen, 

 succeeded in restoring softness and irritability to a human cadaver in the first 

 stage of rigidity even four hours after death. Heubel obtained the same result 

 with the frog's heart as long as fourteen and one-half hours after death. On pass- 



