1. That, for a variable period of time after the injury, the temperature is always subnormal—sometimes so low that it cannot be registered. This is the period of shock.

2. That the patient may die in this state of shock, but that, if he lives, reaction takes place and the temperature rises.

3. That this rise in temperature is, in fatal cases, rapid and progressive. In one case the temperature rose 6° in seven hours, in another 8° in four hours. Death occurs when the temperature is at its highest—anything up to 106°, and even more when registered in the rectum.

4. That the temperature may rise to a moderate height, and there ‘mark time’. This is the ‘crisis’ of the case. A subsequent fall in temperature generally indicates recovery, a further rise usually points to a fatal termination.

5. That the rise of temperature is independent of any special osseous lesion, since similar changes are observed in fractures of the vault and in fractures of the base.

6. That laceration of the brain is present in the majority of cases in which marked temperature changes are observed, but that the changes in temperature are totally independent of any special regional brain-injury.

Richet arrives at the conclusion that two hypotheses present themselves, accounting for temperature changes in general: (1) that there are certain temperature regulators in the encephalon which, when excited, become stimulated in function; (2) that the cortical injury acts in a sort of reflex manner on the regulatory centres situated in the pons or bulb.

Attention was also drawn to the experiments of Lorin and van Benedin, who, after excising the two cerebral hemispheres of a pigeon, showed that the heat regulatory centre was preserved intact, proving that the corpus striatum is not necessarily the head-office for heat-regulation in general.

Till, therefore, more evidence comes to hand with respect to heat-regulation in general, one cannot go beyond the broad statement that, in severe head-injuries, definite temperature changes occur, that the changes are independent of any special lesion of bone or brain, that they are generally associated with some brain-injury, and that they are probably due to the influence exerted by the lesion on the heat-regulating centres in the region of the pons and bulb.

With regard to the value of the temperature, both with respect to prognosis and treatment, a very much more definite statement can be made.