PAIN 



481 



(152) and Cleveland (45) found none on stimulation 

 of the caudal end of this trunk after it had been cut 

 below the superior cervical ganglion. These represent 

 another instance in which studies in man yield results 

 relative to pain opposite to conclusions drawn from 

 work in animals. However, the cats of Davis & 

 Pollock behaved as though in pain upon stimulation 

 of the superior cervical ganglion rather than of the 

 trunk below it and they continued to do .so after: a) 

 all its branches were cut except those to the carotid 

 plexus, b) the posterior roots of the upper 12 spinal 

 nerves were cut and r) the trigeminal posterior root 

 and the upper 1 1 spinal anterior roots were cut. 

 Only when /) was combined with trigeminal posterior 

 rhizotomy were the pain responses stopped. Since 

 Davis & Pollock accepted the evidence of Langley 

 and Ranson that there are no afferent pathways in 

 the cervical sympathetic trunk, they explained their 

 findings on the basis that they were setting up efferent 

 sympathetic impulses. These were presumed to pro- 

 duce a peripheral effect which in turn stimulated the 

 ordinary accepted sensory pathways. 



Helson (126) reported critical sen.sory measure- 

 ments on patients of Frazier who had undergone 

 trigeminal denervation of the second and third divi- 

 sions. He found that such patients reacted violently 

 if a hot cylinder was kept on the face more than a 

 few seconds. But in three patients in whom thoracic 

 sympathectomy had been added to the trigeminal 

 rhizotomy he could sear the skin with a hot cylinder 

 and evoke only a sense of pressure. Hence he agreed 

 with Foerster et al. Cyg) that the cervical sympathetic 

 nerves contain afferent fibers. 



During our own stimulations of the sympathetic 

 nerves in the neck, pain occurred in 9 of to indi- 

 viduals, init it was not elicited from all portions of 

 the trunk or superior cervical ganglion when small 

 bipolar electrodes with points less than i mm apart 

 were used, whereas an effective stimulus (at similar 

 voltage) applied to almost any point on a nerve of 

 the cervical plexus caused pain. The details of the 

 respon.ses are summarized by White & Sweet (296, 

 pp. 84 to 89); we concluded that there must be great 

 variation in the distribution of pain fibers within the 

 cervical sympathetics in man which would account 

 for Frazier's vacillating opinion as to whether or not 

 they were present at all (82). However the appearance 

 of pain upon stimulus to central ends, either of cut 

 peripheral sympathetic branches or of cut gray rami 

 communicantes, made it clear that true afferent 

 fibers do occur in them. Activation of efferent sympa- 

 thetic fibers with subsequent conduction via cranial 



sensory fibers in nervus trigeminus or intermedins 

 could be excluded as the mechanism of pain in such 

 instances and in another patient in whom the fifth, 

 seventh and eighth cranial nerves had been divided. 



That the sensory inflow back to the cord is not 

 confined to the white rami communicantes was fur- 

 ther shown in fi\e other patients in our series in 

 whom stimulus to each member of one or more 

 pairs of rami elicited pain. In several of these each 

 end of each cut ramus was stimulated; pain was 

 elicited only from the end toward the spinal nerve. 

 The pain came immediately upon stimulation, was 

 obtained at about the .same threshold and had the 

 same reference as that from the intact ramus. One 

 is unable to distinguish the white from the gray 

 ramus in anv given pair, but our results indicate 

 that the pain afferents travellino with the sympathetic 

 are not restricted to the portals of entrance to the 

 central nervous system u.sed by the efferent sympa- 

 thetic fibers, i.e. the white rami from C8 to the upper 

 lumbar area. Instead pain afferents may perhaps 

 reach the spinal cord via any of the gray or white 

 rami. 



The presence of many pain fibers in the cardiac 

 and splanchnic branches of the sympathetic trunk 

 has been widely demonstrated by stimulation. Can- 

 non (38) buried electrodes in contact with the vagus 

 or splanchnic nerves in cats. After the wound was 

 healed stimulation of the latter nerves made the 

 animals restless and the presence of pain was in- 

 ferred. Vagal stimulation caused only respiratory 

 effects. White et al. (295) thought they relieved 

 experimental cardiac pain in dogs by resection of the 

 upper four thoracic ganglia and Davis et a!. (54) 

 concluded that the pain of their animals on disten- 

 sion of the gall bladder was stopped by splanchnicec- 

 tomy. Balchum & Weaver (13) reached the same 

 conclusion regarding the pain of gastric distension 

 in the 158 dogs they studied. Leriche & Fontaine 

 (168) provoked pain in the heart and precordial 

 region by stimulation of the lower pole of the stellate 

 ganglion in two patients. In a third patient who had 

 never had angina pectoris, faradization of the stellate 

 ganglion seemed to bring on an intense anginal 

 attack. In at least three other individuals with clinical 

 angina an attack has been elicited during dissection 

 at the stellate ganglion [Jonnesco and Bouchard 

 cited in (168); (167, pp. 375 to 376)]. The effective- 

 ness of upper thoracic sympathectomy in eliminating 

 afferent fibers for pain from the heart is attested by 

 two large series of patients relie\ed thereby of severe 



