NEUROPATHIC KDKMA 351 



aspliyxial conditions in intlaiiuHl tissues favor acid formation wliichy 

 may cause in the colloids an increased affinity for water. According 

 to Oswald •''''' the pormoability of tlie vi^ssels for proteins becomes spe- 

 cifically altered in inflammation, so that not only the less viscous 

 albumin and pseudoglobulin pass throug'h their walls, but also the more 

 viscous euglobulin and fibrinogen. To this class of edemas belong 

 also the urticarias which follow the ingestion of various toxic sub- 

 stances, many of wliieh can be shown experimentally to be lympha- 

 gogues. A good example is the urticaria which often follows the in- 

 jection of antitoxic or other foreign serums, particularly their re- 

 peated injection ; in experimental animals such a serum may cause 

 death very quickly by acute pulmonary edema. All these poisons 

 probably produce urticarial edema by injury to the capillary walls in 

 the subcutaneous tissues, and possibly changes in the hydrophilie 

 properties of the tissue colloids are also produced by the poisons. In 

 the action of vesicants especially, it may well be questioned if changes 

 in the capillary walls and active hyperemia are not supplemented by 

 local metabolic alterations. The edema which follows the sting of 

 insects, which are known to secrete into the wound such acids as 

 formic, seems to be a particularly' good illustration of the production 

 of edema by the influence of acids on the tissues (Fischer). 



Neuropathic Edema. — Until we understand better than we now 

 do the manner in which nervous impulses modify metabolism, it will 

 be difficult to estimate properly the importance of nervous impulses 

 in the production of edema. That nervous control is a possible factor 

 is well shown by many experiments; for example, simple ligation of 

 the femoral vein in animals does not cause edema, but if the sciatic 

 nerve is cut the vasoconstrictors are paralyzed, and edema may follow 

 (Ranvier).^'- In this case the nervous influence is only indirect 

 through its vasomotor effects. Similarly, stimulation of vasodilator 

 fibers may cause edema. It is furthermore possible that nervous 

 stimulation may lead to excessive metabolic activity, with an ac- 

 cumulation of crystalloidal products and acids sufficient to cause 

 edema when supplemented by active congestion and some resulting 

 pressure upon the lymph-vessels. There are certainly many instances 

 in which edema seems to depend upon nervous disturbance ; for ex- 

 ample, edema in the area of distribution of a neuralgic nei've; sudden 

 joint effusions in tabetic arthropathy ; and especially the typical 

 "angioneurotic" edema. ^-" The only explanation that seems open is 

 the one given above, namely, a combination of local hyperemia and in- 

 creased metabolic activity. Even the urticarias of apparently me- 



37c A. Oswald, Zeit. cxp. Path., 1010 (8), 226. 



3S Similarly, pulmonary edema follows experimental hydremia onlv when the 

 yapfi are cut "(F. Kraus, Zeit. exp. Path.. 1013 ( 14) , 402) . " 



3Sa iletabolism in anfrioneurotic edema is discussed by Miller and Pepper, Arch. 

 Int. Med., 1916 (18), 551. 



