499 



But the itching postoperatively seemed 'deeper in' on 

 the side which no longer felt a pin as sharp. No men- 

 tion was made as to whether or not pain from deeper 

 structures was stopped by this operation. There is 

 also the possibility that the itching in this patient 

 was of central origin since he felt it everywhere and 

 had no primary skin disease. Intense itching appears 

 to have been provoked by stimulus to the brain in 

 cats upon intracisternal injections of morphine, 

 physostigmine, pilocarpine or acetylcholine Ci44)> 

 and upon intraventricular injection of diisopropyl- 

 fluorophosphate (DFP) or physostigmine (76). A 

 centrally induced itch probably does not require 

 intact spinothalamic pathways to achieve conscious 

 recognition. 



Investigations of the sense of tickle suffer from the 

 difficulty one has in describing the sensation. For 

 Pritchard (217) and Foerster (78) it is 'itching of the 

 weakest intensity' and corresponding to this concept 

 Rothman (228) describes the after-sensation following 

 light strokes, firm strokes and burning stimuli on the 

 skin as tickle, itch and burning pain, respectively — all 

 mediated by 'C fibers, he says. These speculations 

 lack factual support. Foerster & Gagel (80) and Bick- 

 ford (24), pursuing the subject into the spinal cord, 

 found tickle sensation ab.sent in the analgesic area 

 after cordotomy; but patients of Feet (208), Hyndman 

 & VVolkin (133) and White & Sweet (296, p. 261) 

 said they could still be tickled in such areas. It .scarcely 

 seems worth fussing about. 



PAIN AND INHIBITION 



Head & Sherren (122) first described, and Foerster 

 (77, p. 28) later confirmed, that division of a cu- 

 taneous sensory nerve lowers the threshold to pain in 

 the underlying deep tissues, indicating that the super- 

 ficial system exerts a moderating influence on the 

 threshold and intensity of deep pain. 



Zotterman (315) was one of the first to hypothecate 

 a peripheral inhibiting mechanism on pain within 

 a single nerve. He found only 'C fiber discharge in 

 the after-stimulation period when itching occurs. The 

 relief of itching by rubbing suggested to him an 

 inhibiting action of fast 'A' fibers on the slower 'C 

 fibers. Landau & Bishop (150) have extended this 

 concept to account for at least some of the features of 

 hyperpathia seen in lesions of peripheral nerves. They 

 attribute the sensation upon pinprick after partial 

 asphN'xial compression of nerve to elimination of 

 'delta fiber pain.' The pricking pain then changes, is 



more intense, more persistent and of a different and 

 burning quality — the result they say of release of the 

 central effect of 'C fiber activation normally masked 

 by activity of the delta fibers. We have already dis- 

 cussed objections to the concept that pricking and 

 burning pain are mediated ijy delta and 'C fibers, 

 respectively. However in those explanations of hyper- 

 pathia following central lesions which attribute this 

 state to isolated action of spinoreticulothalamic, 

 spinotectal or other relay routes, there is also implicit 

 the notion that the divided direct spinothalamic 

 pathway normally activated by the same stimulus 

 exerts an inhibiting action on the 'over-response.' 



A number of obser\ations point to an inhibiting 

 interaction between rival stimuli resulting in decrease 

 of pain. Thus Bender (17) found that causalgic pain 

 following peripheral nerve injury was relieved by im- 

 mersion of the opposite normal hand in water, and 

 Graham et al. (108) abolished experimentally-induced 

 itching on the skin of the back by pinprick in the 

 same dermatome on the anterior chest. Hardy et al. 

 (i 17) demonstrated another form of inhibition of one 

 pain by another in the experimental situation of 

 procaine block to a nerve trunk. Stimulation of the 

 trunk proximal to this site then provokes a zone of 

 hyperalgesia. Repeated pinpricks in this area, how- 

 ever, cause its borders to shrink; the investigators 

 suggest that a central inhibition is occurring. 



Further evidence for central inhibitory mechanisms 

 for pain has been adduced by Foerster (77, pp. 77 

 and 78). In two patients with intramedullary cord 

 lesions he made operative incisions into portions of 

 the posterior columns; a severe cutaneous hyperpathia 

 ensued limited to those areas corresponding to the 

 incised pathways. He attributed this to removal of a 

 mechanism inhibiting pain inherent in the normal 

 pathways for touch and proprioception. In view of 

 the extensive incisions into normal dorsal columns 

 without such sequel reported by Browder & Gallagher 

 (35), Pool (215) and White & Sweet (296, p. 407), 

 Foerster's explanation of his results is no longer 

 tenable. His surgery may have exacerbated effects of 

 the original lesion in gray matter or nearby postero- 

 lateral white matter. Regarding the latter possibility, 

 Foerster (77, pp. 79 and 80) has cited the evidence of 

 Fabritius and Brown-Sequard that lesions in the 

 deep posterolateral white matter provoke hyperpathia, 

 i.e. that there is a corticofugal pain inhibiting path- 

 way in this region. 



An extraordinary patient has recently been well 

 studied by Trent (268). Nearly four years after injury 

 to the left temporoparietal cerebrum the man began 



