PAIN 



493 



to or part of a focal seizure; A) as a more continuous 

 pain; or c) as a dysesthesia appearing only when the 

 surface of the body was stimulated. Michelsen (189) 

 reviews earlier reports and adds five new cases of 

 his own. Paroxysmal abdominal pain as a form of 

 epilepsy has now been reported in several series of 

 patients. O'Brien & Goldensohn (201) summarize 

 the earlier work and add their own observations 

 which indicate that in at least some of these patients 

 organic cerebral lesions cause attacks of pain pri- 

 marily referred to the abdomen, whereas in other 

 patients the pain is secondary to abnormal gastroin- 

 testinal motility. 



Lesions 



Destruction of appropriate cortex and subcortical 

 white matter may also cause hypalgesia, rarely 

 analgesia. One of the early reports implicating the 

 cerebral cortex with pain perception is Dejerine & 

 Mouzon's (60) account in 191 5 of a war casualty 

 whose small cortical wound produced loss of pain 

 sensibility in the contralateral arm. Kleist (14J, pp. 

 426 to 428) collected 24 patients wounded in World 

 War I in whom a localized parietal lesion brought 

 about disturbances mainly in pain and thermal 

 senses. In eight of these, hypalgesia was the only 

 sensory loss. He noted analgesia changing dining 

 convalescence at times to an abnormally increased 

 appreciation of stimuli, a hyperpathia. He ventured 

 without confirmation post-mortem a precise place- 

 ment of the cortical area for pain and temperature 

 sensations in the posterior bank of the central fis- 

 sure — in Brodmann's narrow fields 3a and 3b. 

 Russell (233) after a study of men wounded in 

 World War H reached essentially identical conclu- 

 sions on all of the above .scores. Davison & Schick 

 (57) have also described two patients with hyper- 

 pathia combined with hypalgesia in whom autopsy 

 revealed only cortical and subcortical lesions, com- 

 pletely sparing the thalamus. 



Foerster (78, p. 146) pointed out that the sub- 

 normality in pain sensation after removal of the post- 

 central gyral representation for a limb soon returns 

 virtually to normal; but subtle changes such as a 

 reduction in the number of pain points or an increase 

 in their threshold persisted for years in seven patients 

 studied by Kroll (147). As early as 1909 Horsley 

 (130) had noted that even after removal of the 

 'whole arm centre' in both precentral and postcen- 

 tral gyri the pain sensation was 'notably diminished' 

 though not abolished. Marshall (184) ably sum- 



marizes the earlier work and adds studies on 12 more 

 war-injured patients examined 5 to 34 years after- 

 ward. In some area contralateral to a shallow cere- 

 bral wound, all experienced slight or no pain when 

 tested both with a heavy pin jab and by injection of 

 0.2 cc of 6 per cent sodium chloride into the muscles 

 in an effort to provoke deep pain. He showed clearly 

 the possibility of protracted focal severe disturbance 

 of appreciation of pain from such lesions. Both he 

 and Russell have commented on the anomalous 

 situation that an extensive cortical injury may leave 

 pain sensibilit\- intact, whereas a small cortical wound 

 in part of the same area in another patient mav pro- 

 duce hypalgesia. 



That a massive area of the cerebral cortex may in 

 some way be associated with irritating sensation was 

 shown by Dusser de Barenne and his collaborators 

 (70) in experiments in lower primates. For example 

 when they applied strychnine locally over a few 

 square millimeters of the cortex anywhere over about 

 the posterior half of the frontal lobe or the anterior 

 three-quarters of the parietal lobe of the chimpan- 

 zee, they set up a diffuse irritation in face, arms or 

 legs, depending on the area of cortex to which the 

 drug was applied. The animal licked or scratched 

 the skin of the zones concerned for about 30 min. 

 more vigorously contralateral than ipsilateral to the 

 side of the placement of the drug. The electrocortico- 

 gram showed "strychnine spikes' within this extensive 

 sensory region, according to Bailey et al. (12). 



The ipsilateral cerebral representation of pain 

 intimated lay these studies is further suggested bv 

 the.se facts. Total hemispherectomy in man does not 

 produce complete contralateral analgesia, but such a 

 degree of cortical removal in the macaque and 

 chimpanzee provokes almost complete degeneration 

 in every thalamic nucleus except those in the medul- 

 lary laminae which do not project to the cerebral 

 cortex (279). This leaves the ipsilateral thalamus and 

 cerebral cortex as the most likely sites mediating 

 pain perception following hemispherectom\-. Some 

 individuals, e.g. Evans' patient reported by Walker 

 (279), show but little disturbance of appreciation of 

 pinprick anywhere except for some delay in response, 

 whereas in two patients of Dandy (52) there was 

 said to be loss of all contralateral cutaneous sensation 

 below the face with a varying but lesser lo.ss in the 

 face. Gardner et al. (88) have recently given a resume 

 of the findings in their own and the earlier reported 

 cases. They found a striking and constant retention 

 of all modalities of sensation in the trigeminal area 

 both in patients whose operation was for infantile 



