HYPOTHERMIA AND THE NERVOUS SYSTEM 



CHANDLER McC. BROOKS 



In discussion of Dr. McQueen's paper, I wish to amplify one or two points he 

 touched upon and call attention to a series of phenomena which should be con- 

 sidered by those interested in hypothermia and its effects on the nervous system. 

 I will mention these phenomena and make reference to the literature pertinent 

 thereto. 



The different susceptibilities of nerve fibers to cold block was mentioned. Large 

 diametered A fibers block more readily than do B and C fibers and this is of im- 

 portance in view of the functional roles played by fibers of these different cate- 

 gories. An additional point not mentioned is that afferent fibers as they fan out in 

 the dorsal root are more readily blocked than they are in peripheral nerves. The 

 nerve sheath and the blood supply are such that block of nerves by thermodes or 

 general cooling is harder to achieve than is block of the dorsal (posterior) roots 

 (Brooks and Koizumi, 1956). 



A second point worthy of amplification is this : Cooling below normal body tem- 

 peratures does decrease the excitability of nerves. Thresholds to applied stimuli are 

 raised. However, when nerves cooled to a moderate degree (38°->25° C.) are 

 stimulated the action potentials evoked are enormously increased in amplitude and 

 duration. The action potentials coming in over cooled afferent fibers have a much 

 more potent central action. Cooling initially causes hypoexcitability but also hyper- 

 reactivity of the nervous system. The cord must be cooled below 20° C. to reduce 

 its responsiveness below normal levels (Brooks, Koizumi and Malcolm, 1955). 



Cooling slows speed of conduction in peripheral nerve and spinal pathways. 

 This is due to slow speed of rise of the action potential. The same occurrence 

 explains slowed conduction in the hypothermic heart (see papers by Brooks and 

 Hoffman in this volume). There is also selective block of conduction in the cord 

 and a disproportionate effect on certain pathways (Brooks, Koizumi and Malcolm, 

 1955). Again fiber size and location provide at least partial explanation of this 

 selectivity of action. 



Not only does the higher amplitude and longer duration of the single action 

 potential of a single afferent fiber constitute a greater central stimulus, but the 

 train of impulses coming in over the afferent trunks has a longer duration. Due 

 to the greater depressant action of cold on some fibers conduction is slowed more 

 in these than in others ; thus, afferent volleys are less well synchronized and act 

 more like a tetanus. This gives one explanation of the greater responsiveness of 

 the central nervous system in the cold (Koizumi, Malcolm and Brooks, 1954). 



When one considers that the cooled interneurons are also acting in the same way 

 one can understand another observation and that is that the motoneuron or reflex 

 spike and discharge is increased much more in hypothermia than is the afferent 

 potential (fig. 1, P>rooks, Koizumi and Malcolm, 1955). This provides additional 

 explanation of hyperresponsiveness. 



Another interesting point is that tb.e "purity" of reflexes tends to be lost in hy|)o- 



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