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HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY I 



systems of Head and associates. We are still left with 

 the necessityof explaining the above abnormal features 

 of the sensory response. Boring (30, p. 92) agrees 

 with Head to this extent: the abnormal sen.sory in- 

 tensity is achieved by the removal of an inhibition. 

 More recently Landau & Bishop have identified the 

 type of pain which they consider to be tran.'Oiitted 

 over normal 'C fibers with the 'protopathic' forms of 

 sensation of Head et al. (121) and conclude that 

 block of delta-pain fiber responses releases "the per- 

 ception of 'C fiber pain in the otherwise normal 

 subject." 



An alternative explanation has been put forward 

 by Weddell et al. (289) on the basis of their histologic 

 studies of human skin at 39 sites from which the 

 above abnormal qualities of pain were induced. 

 Control studies were made at 20 other sites in cutane- 

 ous scars from which the pain did not have the ab- 

 normal unpleasant quality. In the former group the 

 nerve nets and terminals were isolated from their 

 neighbors instead of interweaving with them as 

 occurs normally, and as was seen in those reinner- 

 vated scars which showed no abnormal quality in 

 the senations aroused from them. Normally, as Bor- 

 ing (30, p. 95) first deduced, "single sensory spots are 

 innervated by more than one nerve fiber and the 

 multiple innervation is projected upon the central 

 nervous system as multiple excitations." Weddell 

 (285) demonstrated this, correlating neurophysio- 

 logic with clinical findings, and Weddell >i al. (289) 

 conclude that the complex pattern of impulses arising 

 from such multiple innervation is essential to the 

 normal quality of pain "of everyday experience," 

 whereas if only a single pain fiber or terminal is ex- 

 cited then the pain is of characteristic unpleasant 

 quality. This conclusion, that reduction in the den- 

 sity of innervation of an area will cause alteration in 

 the quality of pain, has likewise been reached inde- 

 pendently by Livingston (177). In a patient recover- 

 ing from an injury to the median nerve at the wrist 

 there was one area in which pain was of normal t>'pe 

 until one of the main nerve trunks was blocked with 

 procaine, whereupon pinprick became peculiarly 

 unpleasant. This state was exacerbated when two 

 of the three nerves were blocked simultaneously. 

 Weddell et al. (289) have also studied the alterations 

 in pain sensibility in themselves upon compression of 

 the upper limb with a sphygmomanometer cuff. 

 They found the first change to appear was a rela- 

 tively abrupt alteration in the quality of the pain 

 upon a needle prick; when fully de\eloped at ai^out 

 the thirtieth minute of compression the prick caused a 



"singularly unpleasant sensory experience," a slow 

 swelling burning sting lasting for as long as 10 sec. 

 and giving ri.se to a withdrawal reflex difficult to 

 control. There was also an increasing interval be- 

 tween the application of the stimulus and its per- 

 ception. They concluded that these typical features 

 of 'unpleasant pain' were to be correlated with a 

 gradual reduction in the number of fibers conducting 

 impulses as the compression continued. 



Isolation of the pain nets appeared to have no 

 eflfect on the threshold of pain sensibility. In a num- 

 ber of biopsies these workers saw abnormal appear- 

 ances of the nerve endings, ellipsoidal expansions 

 which they called growth cones. The lowest thresholds 

 to pain occurred in their patients in whom such 

 growth cones lay just beneath the basal layer of 

 epidermis. In such cases the mere passing of a camel's 

 hair brush across the area was painful. 



Foerster had earlier (77) .suggested that the peculiar 

 abnormalities of sensation (his hyperpathia) arose 

 from the stimulation of an isolated 'pain point.' 

 The .similarity between this explanation and that of 

 Weddell et al. is only superficial, however, because 

 Foerster contended that as soon as other senory 

 modalities such as touch and pressure were felt the 

 hyperpathia began to recede, a viewpoint which is 

 .simply not substantiated by the observations of 

 others. The sites at which pain has the abnormal 

 quality are not directly correlated with anesthesia to 

 touch. Figure 5 shows the results of an examination 

 in which more spots hypersensitive to pinprick were 

 in fact found outside of the anesthetic zone. Simi- 

 larly Lanier et al. (157) in their study found an area 

 in which, although touch sensibility was perfect, pain 

 sensibility was diminished and unpleasant pain 

 could be elicited from this region. 



Figure 5 also illustrates another observation of 

 Trotter & Davies (270, p. 170), namely that such 

 patterns of 'hyperalgesia,' as they called it, were 

 associated with veins. They say that often the skin 

 over the vein itself was the most sensitixe part of the 

 patch. Although Cobb also thought that "these 

 painful spots were usualh' along the course of a super- 

 ficial vein," the explanation of this is unclear. Trotter 

 & Davies originally regarded the hyperalgesia as a 

 "secondary process due to the presence of some 

 irritating substance produced as the result of the divi- 

 sion and degeneration of the nerve." 



But, in the light of another 17 years of rumination 

 on the subject. Trotter (269) thought that the lack 

 of complete insulation of regenerating nerve fibers 

 would explain the raised threshold to stimuli and the 



