PAIN 



461 



is usually present along with analgesia, a rare patient 

 after such a cordotomy may show only the former 

 without the latter or vice versa, indicating that there 

 are special pathways for pain and others for tempera- 

 ture sensation which are nearly, but not precisely, co- 

 extensive (296, p. 259). Schiff (238) one century ago 

 made the fundamental observation that lesions of the 

 spinal cord in rabbits, sparing only the posterior 

 columns, resulted in animals which would make a 

 number of responses to touch whereas they would ig- 

 nore presumably painful deep stimuli. He recognized 

 the similarity between this state and the clinical con- 

 dition of analgesia without anesthesia to touch, de- 

 scribed in man both by Beau and by Vieusseux [ cited 

 by Schiff (238), p. 253]. 



Such data, though, do not prove that impulses for 

 pain and touch may not use the same fibers in pe- 

 ripheral nerves and there has been no histologic cor- 

 relation between lesions of certain types of peripheral 

 nerve fiber and a disassociated loss of touch or pain. 

 Although such loss may occur in leprosy — the Bacillus 

 leprae typically attacks only the peripheral and not 

 the central nervous system — a focal degeneration of 

 dorsal funiculi has also been seen in this disorder by 

 Wilson (301, fig. 92, p. 753). Hence a purely periph- 

 eral lesion may not be taken for granted here as the 

 explanation of a loss of pain without touch or the 

 reverse. However, conduction by peripheral nerves 

 can become impaired in such fashion that a differ- 

 ential loss of various forms of sensation occurs. Thus 

 Herzen (127) was the first to note that pressure on a 

 human peripheral nerve, the sciatic, caused initially 

 loss of touch sensibility, shortly thereafter that of cold, 

 much later that of warmth and finally of pain. Gold- 

 scheider (102) in the same year likewise observed a 

 differential loss of sensory modalities, although in a 

 different order, when a branch of a peripheral nerve 

 was cocainized. He thought cold was blocked first, 

 then, in sequence, warmth, pain and pressure. Modifi- 

 cations of the first method of compression or asphvxia 

 of the nerve and of the second, pharmacologic block, 

 have since been used extensively in a study of the 

 specificity of nerve fibers for single modalities of 

 sensation. Unequi\ocal proof that one peripheral 

 fiber is devoted to but one type of sensory modality, 

 pain, touch, cold or warmth has not been advanced 

 as yet. The evidence bearing on this and on the ques- 

 tion of special sensory end organs for pain will be pre- 

 sented later. Before studying the nervous system itself 

 we may properly consider the tactics used in arousing 

 its responses. 



STIMULUS, SENSATION AND THEIR MEASUREMENT 



Mechanical Stimuli 



Quantitative assessment of pain involved, of course, 

 measurement both of stimulus and sensation. In the 

 earliest tactics one pricked the surface to be tested 

 with needle points mounted either in fibers which 

 bent at a calibrated force or on a calibrated spring — a 

 method which remains the best for many clinical 

 physiological studies. 



Correlation with Tissue Damage 



The adequate stimulus for pain, whether it is me- 

 chanical, thermal, electrical or chemical, is poten- 

 tially or actually productive of tissue damage. Hence, 

 the immediate zone of reception on which the stim- 

 ulus is acting soon becomes modified in serial determi- 

 nations at the same site. Thus Lewis (171, p. 106) 

 pointed out that, if the skin of the front of the forearm 

 is pricked with a needlejust hard enough to cause pain, 

 most ofthe.se pricks will subsequently show signs of tis- 

 sue damage in the form of little circles of redness. Ther- 

 mal radiation in order to evoke pain requires an en- 

 ergy (expressed in millicalories per second per square 

 centimeter) which is 2000 times that of the threshold 

 for warmth. In fact. Hardy et al. (118, pp. 23, 53), 

 the workei-s responsible for these figures, state that the 

 thermal radiation threshold for ' pricking pain' lies at 

 a skin temperature of roughly 45°C, which is likewise 

 the threshold temperature range for the production of 

 skin damage, according to Moritz & Henriques (192). 

 In agreement with this Benjamin (18) finds the 

 threshold for the production of a cutaneous flare by 

 heat is very clo.se to the pain threshold. 



Heat 



Nevertheless thermal radiation which eliminates 

 simultaneous contact and pressure sensations has 

 formed the basis for much of the modern work on pain 

 thresholds since the description by Hardy et al. (115) 

 of their 'dolorimeter.' This apparatus permits control 

 of the intensity and duration of applied heat and its 

 measurement by a radiometer. With critical, careful 

 use of this instrument so arranged as to provide a 

 radiation time of 3 sec, it is their contention that the 

 pain threshold is constant from person to person and 

 in the same individual from time to time. The three in- 

 vestigators were the initial subjects and they studied 

 themselves nearly every day for almost a year, di- 



