•248 



ri: V i; K. 



\vrotif,'lit by iimlaria, many of which may occur out of all proportion to tlie febrile 

 paroxysm or uvea without the librile rtMcliou, arc not necessarily the result of an 

 iutitience exerted upon tlie nervous system — whether they ure or ure not so pro- 

 duced is foreiijn to the present iiKjuiry. 



Further, of all diseases su|ipost'd to be due to the presence of a poison in the 

 blood, none is more clearly and certainly so than is septicaemia. It has already 

 been demonstrated that the fever of septicaemia, or at least the elevation of tempera- 

 ture of septica-miu in dogs, is largely due to retention of heat: such retention of heat 

 call only l>e prodiued through tlie intervention of the nervous system, no conceivable 

 influence upon the general protoplasm being able to cause the superficial capillary 

 contraction to which this retention must be in a measure due. The fever must 

 therefore in septicaemia be neurotic in origin. From all the facts and reiisons which 

 have been given, the following proposition seems to be the logical conclusion : 

 Jiritatirr /ever, if it ij-i»t, is jiroiliical by an cwlioii iijxm tin- wnou« Ki/nkm. Fvcir 

 occurrinj in caitctt nf hltMid-jxiifKininy ix oftcn^ ami jirnlm/ili/ alirdijH^ (he result of a 

 direct or indirect action of the poison njton the central Hcrvoue system, and hincc u 

 a neurosis. 



Before elaborating further the mechanism of ftvcr i)rodiKtion, two problems are 

 naturally suggestetl for solution by our knowledge of the relation of tlie nervous 

 system to the bodily temperature: — 



First. AN'iiat is the relation of the general vaso-motor system to the febrile state? 



Second. What is the relation of the so-called inhibitory heat centre to the febrile 

 state ? 



The only experimental evidence wliicli 1 have, throwing light upon the solution 

 of the first of these questions, is found in the ettect of section of the cord upon heat 

 ])roduction and dissipation in fibrile animals. The record of these experiments 

 may be found in E j- in r intents 112 and 113. 



In tlu" second of tliese, the rectal temperature of the animal, the hour preceding 

 the section, varied from 104''.1 F. to 104 .!S, and the hourly production of heat at 

 the last taking was I15.:i:3n units, the dissipation being the same. In the hour 

 and 2'i minutes immediately following the section, the bodily temperature fell 

 10 ^.(j, whilst the dissipation of heat rose to 14(>.9.>42 units, and the production 

 of heat fell to lo.9277 units. In KxpcTiment 112 the bodily temperature in the 2 

 hours preceding the section of the cord was from 104 .1 to 104 .3, the heat dissi- 

 pation and production respectively 8(5. 1(525 units and 8S ()()2 ; after section of the 

 cord the bodily temperature fell 10°.6 in 103 minutes, and the heat dissipation 

 rose to 115.778 units, whilst the heat production fell to 25.148 units. These two 

 experiments show that in fever as in health, section of the cord is followed by an 

 increase of heat dissipatiim and a decrease of heat production. It will also be 

 further noted that the eft'ect as compared with that in the normal animal is greatly 

 exaggerated. There are various ways of accounting for this exaggeration. A 

 plausible method of exjdaining the enormous dimiiiMtiou of heat production is in 

 Riipposiii^j that in fever there is paresis of the so-call(>d inhibitory centre. ^^ hen 

 the normid cord is cut, the paralysis of the heat inhibitory nerve in some measure 



