Brain and the Conditions of Recovery after Compression. 21 



Experiments 25e and 266 show that a venous congestion of brain 

 (as indicated by its expansion) is not necessarily accompanied by an 

 increase of elasticity. 



The failure to obtain changes in elasticity in every case must, I 

 think, be attributed to the variation in calibre of the various channels 

 of outflow, chiefly, probably, as regards the communications witn the 

 vertebral plexus; the common occurrence of variations in the size of 

 the superior cerebral is patent after a few dissections. 



B. Experiments illustrating the Influence which varying Vascular Con- 

 ditions have in Restoring the Volume of a Brain which has undergone 

 Prolonged or Severe Compression. 



(a.) Influence of a Rise of the General Blood Pressure. After the 

 brain has been compressed as described for six minutes, the elas- 

 ticity, as before mentioned, is considerably reduced, and the brain 

 surface continues depressed for a long period. If now the etherisa- 

 tion be diminished, the blood pressure may be caused to rise 

 gradually, but considerably, without anything more than a com- 

 paratively insignificant rise in the level of the brain surface accom- 

 panying it (see fig. 10, in which the blood pressure rose 35 mm. in 

 the space of 12 minutes). Thus we find a notable difference in 

 the reactions of normal and compressed brains to increase of blood 

 pressure. As is well known, in the uninjured brain the surf act- 

 rises and falls concurrently with variations in the blood pressure. 



(&.) The Influence of Venous Congestion produced by Asphyxia. In 

 cases of prolonged or severe compression the brain surface may 

 nearly always be made rapidly to recover \)y inducing asphyxia 

 In an experiment (fig. 11) the brain had been severely compressed 

 by repeated experiments on the same spot, so that the recoil was 

 small and had become stationary in one minute. A rise of blood 

 pressure of 30 mm., induced by diminishing the degree of etherisa- 

 tion, had no appreciable effect, but total recovery rapidly supervened 

 with the development of asphyxia. This recovery cannot be 

 ascribed to the rise in the general blood pressure induced by the 

 asphyxia (in this case only 10 mm., which contrasts with the 30 mm. 

 produced by diminishing the ether supply). This is also borne oui 

 by the fact that the recovery of the surface may be obtained when 

 there is no rise of the blood pressure, as sometimes occurs during 

 asphyxia, or the expansion may actually progress whilst the blood 

 pressure is in its stage of fall. 



Frequently the surface commences to recover when the asphyxial 

 gasps are at their strongest, but recovery will go on when the respi- 

 rations are small or even when they cease, as they will sometimes, 

 directly the trachea is clamped. 



