EXPERIMENTAL EVIDENCE ON THE NATURE OF CUTANEOUS HYPERALGESIA

Abstract

Hyperalgesia is a state of increased intensity of pain sensation induced by either noxious or ordinarily non-noxious stimulation, and occurring in both superficial and deep tissues. The cutaneous hyperalgesia associated with injury or noxious stimulation of the skin and visceral structures has been studied in approx. 500 expts. on 23 subjects. Primary hyperalgesia occurs at the site of tissue damage, whereas secondary hyperalgesia associated with an injury occurs in undamaged tissues. Experimentally induced secondary hyperalgesia is characterized by normal pain threshold to thermal and mechanical stimulation; intensification and prolongation of pain relative to control areas from painful stimulation; 2- to 10-min. delay in initial development following an injury, and disappearance within 48 hrs.; secondary hyperalgesia occurring in undamaged tissues the innervation of which is in the same or adjacent segments to that of the site of the injury; association with either deep or superficial injury or sustained noxious stimulation, and in general, the more intense the injury, the more intense is the secondary hyperalgesia; sustained heat stimulation near but below the pain threshold induces secondary hyperalgesia; interruption of the neural pathways from the site of injury by procaine block eliminates associated secondary hyperalgesia; transient elimination by hypoalgesia induced by cooling; development in spite of occluded blood and lymph flow; and it is not appreciably affected by central acting analgesics. Spatial summation of pain and facilitation can be demonstrated within its borders; and pricking with a pin within its borders temporarily abolishes it. It is suggested that a central excitatory state in a network of internun-cial neurons is responsible for secondary hyperalgesia occurring in undamaged tissues.