The Sign of Babinski. A Study of the Evolution of Cortical Dominance in Primates

S AND REVIEWS the important contributions by Sharpey-Schafer and Horsley on the symptoms produced by extirpation of various parts of the cerebral hemispheres. Then came the three memorable papers of Beevor and Horsley on the electrical excitability of the monkey and orang brains, 1887 to 1890. Sherrington and his pupils have since followed with their painstaking studies, mapping out the areas of excitable cortex of the chimpanzee, orang, and gorilla. The present authors have attacked their problem with a thorough comprehension of the progress already made as well as the technical difficulties encountered by previous investigators in the field. An abundance of experimental material and physical facilities combined with utilization of all the modern refinements in neurosurgical technic has enabled them to bring their work to a brilliant conclusion. The pathological extensor plantar reflex, first described by Babinski in 1896, has come to be recognized as evidence of injury of the pyramidal pathway and constitutes one of the most important clinical signs. Suppression of activity of the higher centers of the nervous system gives rise to the sign as shown by the extensor response obtained during sleep and during the phase of apnea in Cheyne-Stokes respiration. Collier, as early as 1899, pointed out that plantar flexion relaxes the skin of the plantar surface so that a sharp object will penetrate less readily than when the skip is taut. The normal flexor reflex appears to have an economic significance in removing the foot from an offending object. The underlying mechanism of the response, and its phylogenetic significance, has never been clearly understood. Experimental removal of various parts of the cerebral hemispheres in lower animals does not give rise to definite alteration in the plantar reflexes. In a study of the factors underlying the evolution of cortical dominance, the problem, with respect to the sign of Babinski, resolves itself into one of the primate foot. The animals employed in this investigation included four well-marked stages of ascendancy in the evolutionary scale-monkey, baboon, gibbon, and chimpanzee. The degree of dominance in any given form was estimated by three important criteria: (1) the rate of recovery of voluntary power following a lesion of the motor area; (2) the extent of the depression of spinal reflexes produced by such a lesion; (3) the occurrence and degree of persistence of pathological reflexes, such as the sign of Babinski and allied phenomena. In all monkeys examined, plantar flexion was the first reflex to reappear during the period of reflex depression following spinal transection. Low thoracic semi-section of the cord gave rise to a well-marked Babinski response on the side of the lesion. Complete removal of one cerebral hemisphere, or removal of the leg area itself from one or both sides, failed to reproduce the Babinski response in any species of monkey examined. Only when the lower lumbar segments are completely free from all forms of higher control is the Babinski reflex seen in the monkey. 419 YALE JOURNAL OF BIOLOGY AND MEDICINE In the baboon, which should be separated on both anatomical and physiological grounds from the long-tailed monkey, localized extirpation of the leg area produced a primitive but nevertheless definite Babinski response characterized by a rapid extension of the outer four toes with fanning. Removal of the second leg area caused an enhancement of the Babinski in the ipsi-lateral limb, probably due to involvement of the uncrossed pyramidal pathway. The course run by the spinal baboon was similar in most respects to that of the spinal monkey. In the gibbon, which is the only primate below man having biped progression, with body held in the erect posture, a strongly positive Babinski response developed, lasting three weeks following the operation. With ablation of the opposite leg area, the pathological plantar reflex reappeared in accentuated form on the ipsi-lateral side, again indicating bilateral representation in the gibbon's cortex. In the chimpanzee, isolated ablation of the leg area was followed within 24 to 48 hours by a consistent and characteristic response in the opposite hind limb. This consisted of two phases, and involved the same muscle groups that are thrown into activity when a positive Babinski sign appears in the human foot, consisting of digital extension and in one animal of lateral deviation or fanning of the toes. The return of voluntary power was much slower and less complete than in either the monkey, baboon or gibbon, indicating that the motor deficit from a cortical injury is increasingly severe as one ascends the evolutionary scale. All those interested in experimental neurosurgery will find in this monograph most valuable data:-the advantages and disadavantages of the barbituric acid anesthetics (Dial-Ciba, sodium amytal and Nembutal); important points in the technic of opening and closing the skull; the ingenious method of mapping the cortex with cellophane; use of the Bovie electrosurgical cutting knife; the importance of ephedrine and metrazol in the postoperative care. The authors close with a word of caution, "The study of the infrahuman primates has taught the important lesson that in experimental neurology it is never safe to generalize from mice or marmosets to man." Possible clinical implications, such as comparison with forms of cerebral diplegia, are wisely discussed in a most interesting but conservative fashion. The very ability to make a sharply circumscribed cerebral defect in a relative of man and the opportunity to analyse its physiological effect immediately constitute an almost irresistible temptation to interpret comparable clinical disorders. But it must always be remembered that even the gorilla, although the closest living relative, is still a far distant cousin of man in the phylogenetic scale. JAMES C. FOX JR. 420