Analysis of effects of hypothermia on central nervous system responses.

Abstract

Progressive uniform cooling of the spinal cord and brain was found to produce a phase of hyperresponsiveness between temperatures of 35°C to 25°C. Below this level all recorded reactions were reduced in magnitude. During this phase of hyperresponsiveness the cerebral and cerebellar evoked potentials were increased in amplitude and duration; component waves of the electroencephalogram and electrocorticogram were not increased in frequency but increased in amplitude; all reflexly produced responses were greatly augmented in amplitude and duration; stimuli applied elicited responses from a greater number of elements. Conditioning stimuli which produced no propagated response became effective during the hyperresponsive phase of hypothermia; the following testing stimuli also elicited a greater reflex discharge. The duration but not the amplitude of the action potentials recorded intracellularly from the individual afferent fibers in the dorsal columns, dorsal roots, interneurons and motoneurons were increased during hypothermia. All elements of these potentials were prolonged by cooling the cord. The depressant action which developed as hypothermia progressed eventually abolished the soma-dendritic components of the antidromic and orthodromic single cell potentials but the NM and postsynaptic potentials persisted until lower temperature levels were attained. Fiber action potentials showed a similar diminution at very low temperatures. The longer duration of the signal (the afferent potential), the greater desynchronization of multiple elements involved in transmitting the excitatory process and a possible decrease in accommodation were considered to account for the augmentation in response during the early stages of progressive hypothermia. In hypothermia impulses entering the cord over muscle afferents which normally evoked only a monosynaptic reflex produced a polysynaptic response and a discharge out the spinal sympathetic pathways. There was a loss of specificity of reflex pathways.