966 NUTRITION AND HEAT REGULATION. 



lied upon is the effect of lesions, experimental or pathological, of 

 definite portions of the brain or cord. An important fact, brought 

 out by Ott,* is that injury to the corpus striatum causes a rise in 

 heat production and body temperature. This result has been con- 

 firmed by many other investigators, making use especially of what 

 is known as the '^heat puncture." In this experiment, made upon 

 rabbits, a probe or style is inserted into the brain so as to puncture 

 the corpus striatum. The result in the majority of cases is a rise 

 of temperature together with an increase in heat production which 

 may last for a long time, although the animal shows no paralysis 

 and apparently no other effect from the operation. White and 

 others have described similar disturbances of heat production from 

 lesions of the optic thalamus. Heat centers have been located also 

 in the septum lucidum, in the cortex, the midbrain, pons, and med- 

 ulla. Barbour f has shown that when bj^ a special device the corpus 

 striatum is heated localty to 42° C. or higher there follows a fall in 

 body temperature, while, on the contrary, cooling of the region of 

 the corpus striatum to 33° C. or lower causes a rise in body temper- 

 ature. The impUcation from these experiments is that there exists 

 in the corpus striatum a heat-regulating center whose action is 

 controlled by temperature changes in the brain itself, a rise of 

 brain temperature depressing the activity of the center and leading 

 to a lowering of body temperature, while a fall in brain temperature 

 has the opposite effect. The author finds that similar reactions 

 may be obtained by the local application of various substances, 

 caffein, for example, causing a rise of body temperature, while 

 chloral, antipyrin, quinin, etc., cause a fall. The effect of the 

 action of such a center may be pictured as causing the balance 

 between heat production and heat loss to be set at a different level, 

 higher or lower than the normal, and the same conception may be 

 employed in explaining the rise of temperature in fevers or in heat- 

 stroke. J So-called septic fevers are due probably to the action of 

 some of the cleavage products of protein formed as the result of 

 bacterial growth. We might assume that these toxic products 

 affect directly the heat-regulating center, and through it cause the 

 balance to be set at a higher level, with an increase in both heat 

 production and heat dissipation. Aseptic fevers or reactions can 

 be produced also by conditions that cause the disintegration of 

 tissue elements, hemolysis, for example. The effect in this case 

 also may be due to the action of some of the split products of pro- 



*Ott, "Journal of Nervous and Mental Diseases," 1884, 1887, 1888; also 

 "Fever, Its Thermotaxis and Metabolism," 1914. 



t Barbour, "British Medical Journal," September 13, 1913; also "Journal 

 of Pharmacology and Exp. Therapeutics," 5, 105, 1913. 



{Consult Krehl, "Pathological Physiology." Translation by Beifeld, 

 1916. 



