246 PHYSIOLOGY OF INDUCED HYPOTHERMIA 



pattern first in the beta and then in the alpha frequencies occurs. These slower 

 rhythms, when present alone, usually present a synchrony which is both hemi- 

 spheric and inter-hemispheric. The theta rhythms are lost at about the 25° C. level. 

 Very slow delta waves thereafter gradually decline until the end. During the re- 

 warming period this pattern is reversed and reproduced in detail. The frequently 

 observed lag of l°-2° C. is perhaps best explained on the site of temperature re- 

 cording. No significant changes are noted with repeated or prolonged periods of 

 cooling and subsequent electroencephalograms are consistently normal. 



Gaenshirt et al,^" in their study of the cat, described exponential relationships 

 between temperature and frequency, as well as temperature and voltage, for the 

 range of temperatures between 32° and 3S° C. Two l)locking mechanisms for en- 

 zyme systems were incriminated to explain the limits of this relationship. The 

 term structural metabolism was used to denote the estimated 10-20% of normal 

 brain metabolism found at and l^elow the level of quiescence demonstrated with 

 electrical recording. 



Chatfield, Lyman, and Purpura® found the electrocorticogram of the golden 

 hamster during arousal to be quite comparable to that of the rewarmed non- 

 hibernating hamster. They further showed that convulsive activity was not induced 

 in the strychninized cortex of these animals below those temperatures at which 

 spontaneous electrical activity appeared. Evoked cortical potentials from the 

 sciatic nerve were noted with cortical temperatures as low as 9.1° C. and the cortex 

 was further found to be electrically excitable down to a level of 12° C. (although 

 the voltages employed were admittedly enormous ) . They thus demonstrated the 

 functional integrity of the long tracts during cooling, and estal)lished the low re- 

 sistance of the brain stem activating systems to cold. 



Electroencephalographic techniques have further proved of value as an adjunct 

 in the estimation of cerebral damage due to anoxia provoked under hypothermic 

 states. Such techniques have been used extensively by Lougheed ct a/.,-'"' -- Ripstein 

 ct al.,^'^ Jensen and Parkins, -° Scott,"'^ and Gaenshirt ct al}^ These followed the 

 demonstration by Bigelow in 1950- of the survival of dogs held at 20° C. for 15 

 minute periods of circulatory occlusion. Scott^*^ has recently found that, in the 

 human, bilateral compression of cervical vessels at the 30° C. level or below pro- 

 duces no EEG change up to 8 minutes and only occasional delta wave prepon- 

 derance to 12 minutes. Jensen and Parkins -° noted similar protection for periods 

 of 30 minutes in the dog with brain temperatures of 20° C. By comparison, the 

 production of total cerebral ischemia in the normal adult cat at 37° C. results in a 

 flat cortical record in some 15 seconds. Evoked cortical potentials are lost in less 

 than 100 seconds. Gaenshirt, Schneider, ct al^' have recently employed an isolated 

 cat's head preparation to estimate the periods of survival of cortical electrical ac- 

 tivity with anoxia induced through a wide variation of temperatures. These sur- 

 vival times varied inversely as the temperature in an exponential fashion. T\\Qy 

 then measured the periods of recovery of this same electrical activity after one 

 minute of anoxia. These times when ])lotte<l against tem])erature pnxluce an mi- 

 expected curve which is i)aral)olic in form, b'rom 37°- 31 " C". these reco\ery jieriods 

 vary directly with tlie tem])erature as would 1)C anticipated, llelow this level, an 

 inverse relationship is indicatecl. The exi)lanation of this finding is ol)scure — par- 



