50I 



scious sensation, they provide another example of 

 convergence of probable visceral pain and somatic 

 afferent fibers upon a single central neuron. 



Clinical observations have revealed that an added 

 state, that of hyperalgesia or even tenderness upon 

 pressure, may be seen in the area of skin to which 

 pain is erroneously referred. Sinclair el al. (251) have 

 explained this, in their peripheral theory, on the 

 basis of antidromic impulses moving down the cu- 

 taneous branch of the parent axon (after stimulation 

 of the visceral branch) to excite secondarily endings 

 of other overlapping nerve fibers, perhaps via metabo- 

 lites (171, p- 80). Wolff & Hardy (305) after studying 

 referred pain and hyperalgesia in experiments on 

 themselves favor the theory that an increasing central 

 excitatory state presumably in the spinal cord is 

 evoked by an increasing barrage of afferent stimuli. 

 They noted, for example, that placement of the 

 fourth finger in ice water caused pain which spread 

 gradually from the immersed digit to those contiguous 

 to it. They thought the referred pain did not develop 

 quickly enough to he accounted for on the basis of 

 branching primary afferent axons. Moreover pro- 

 cainization of the digital nerves in the painful finger 

 out of the ice water did not stop the pain. It should 

 have done so if antidromically conducted stimuli 

 had produced an irritating metabolite or were other- 

 wise secondarily activating adjoining nerves. 



However, the spread of a central excitatory state 

 would account for the varying findings following pro- 

 cainization of the cutaneous area of referred pain and 

 hyperalgesia. Procaine injection may stop these 

 manifestations (291), perhaps because it diminishes 

 the excitatory state at central cells by \irtue of stop- 

 ping subthreshold impulses from the skin, but a 

 variety of forms of experimental pain will break 

 through and cau.se referred pain within or around 

 the anesthetic zone of .skin when the stimulus becomes 

 more intense. These were the findings of Theobald 

 (262) with respect to referred suprapubic pain caused 

 by faradization of the uterus, and of Jones & Chap- 

 man, cited by White & Sweet (296, p. 74) relative to 

 the cutaneous pain of experimental jejunal disten- 

 tion. In some studies procainization of the cutaneous 

 area of reference did not stop the pain at all; this 

 was the experience of Woollard et al. (309) whose 

 direct stimulation of the phrenic nerve caused shoulder 

 pain, and of McLellan & Goodell, cited by White & 

 Sweet (296, p. 74) who distended ureters causing 

 pain in loin and groin. These results can all be ex- 

 plained by assuming that the central excitatory state 

 from such visceral stimulation was in itself adequate 



to discharge the mechanism pertinent to cutaneous 

 reference. Such increase in the central excitatory level 

 may also arise from an increase in impulses from the 

 cutaneous area. Thus Cohen (47) describes two pa- 

 tients with attacks of cardiac anginal pain never 

 referred to the arm in question until in one instance 

 the inan fractured his elbow and in the other a 

 blistered area developed after a vesicant plaster to the 

 elbow region. Then both patients' anginal attacks 

 included reference to the injured elbow. 



Still another form of erroneous reference of pain 

 may occur after injury to central pathways concerned 

 therewith. Ray & Wolff (222) have studied four 

 patients after anterolateral cordotomy in whom 

 noxious stimuli of high intensity in the analgesic area 

 induced pain of low intensity referred to the same or 

 nearby segments on the opposite normally innervated 

 side. The stimuli included squeezing of muscle, deep 

 pressure against a diseased hip joint and application 

 of heat at 80° to 90°C. The authors pointed out that 

 some of the collaterals of entering primary afferent 

 fibers proceed to synaptic relation in the posterior 

 horns with internuncial neurons whose axons cross 

 in the most dorsal part of the posterior commissure 

 to terminate about cells in the posterior horns of the 

 other side. The foregoing observations suggest that 

 with sufficient background of facilitation and sufficient 

 intensity of stimulation such indirect chains may 

 transmit impulses which eventually excite the intact 

 spinothalamic tract on the other side and are referred 

 to the side opposite that stimulated. Inherent in this 

 explanation is the assumption that with both spino- 

 thalamic pathways functioning before operation, there 

 was some form of interference with the internuncial 

 polysynaptic transmission. That such internuncial 

 relays extend longitudinally in the cord as well is 

 indicated by our observations (296, p. 257) and those 

 of Holbrook & de Gutierrez-Mahoney (128). We all 

 found that some patients after cordotomy may refer 

 pain to a much more rostral segment than that under- 

 going intense stimulation, still either in the analgesic 

 area or above it; the pain experienced was much 

 milder than that produced in normal circumstances 

 by such stimuli. In both types of incorrect reference 

 of the origin of impulses traversing less direct path- 

 ways, the patient interprets them as though they had 

 travelled only the customary direct route. 



We may well close this chapter with a quotation 

 from Foerster & Gagel (80). "Pain has a vital sig- 

 nificance; it is no wonder then that those physical 

 processes associated with the psychic experience of 

 pain have the broadest anatomical basis. The im- 



