Abstract

Earlier concepts on the central action of procaine appear to have been limited to such untoward effects as restlessness, tremor and convulsion. Clinical experiences during the past decade, however, have revealed the usefulness of procaine as an analgesic when administered intravenously in a nontoxic dose. Bigelow and Harrison (1) evidenced this effect experimentally by the measurement of cutaneous pain threshold in human subjects. As Goodman (8) and Keats et al. (15) pointed out, such an action cannot be attributed, to the local action on sensory nerves, since the concentration of procaine in the peripheral tissue should be far below the minimal concentration necessary for nerve block. This naturally leads to the concept that the central nervous system should be responsible for the procaine analgesia.

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