The origin of this extensor paralysis has been the subject of much controversy. One party regards the lesion as of central origin, affecting the upper motor neurons or their connections in the spinal cord; the other takes the view that paralysis is mainly of a peripheral type. Tanquerel[12], whose classical work on lead poisoning still contains one of the best descriptions of the disease from the clinical standpoint, describes an associated affection of the peripheral sensory nerves resulting in definite anæsthesia and hyperæsthesia, and there is no doubt that sensory nerve affection, although not very common in lead poisoning, does occur occasionally, and is due to peripheral affection of the nerves. Occasionally generalized peripheral neuritis is to be met with, but even this is much less common than in alcoholism or other toxic forms of peripheral neuritis. In the opinion of most of the observers who regard the neuritis as of peripheral origin, the ultimate interference with the motor nerves is due to an ascending neuritis of the peripheral nerves affecting the spinal ganglia, and Pal and Mannaberg[13] have described polyneuritis; whilst Westphal[14], Dejerine[15], Eichhorst[16], Ramond[17], and others, support particularly the primary lesion of the peripheral nerves as the cause of the disease. Marie and Babinski[18] in 1894 evolved the central theory, and supported it by reference to the apparent bilateral occurrence of the paresis and the analogy with many examples of polymyelitis. Vulpian and Steiglitz[19], examining cords of animals poisoned by lead, described vacuolation of the cells in the anterior cornua of the cord. The original suggestion of the spinal origin of the disease was enunciated by Erb[20], who, without particular reference to either the electrical or histological changes to be found in lead poisoning, based his theory on the similarity of the lesions to polymyelitis. A few cords of persons who have died of lead poisoning do show slight changes in the anterior cornua. One other theory of the nerve affections in plumbism is that advanced first of all by Hitzig[21], and later by Boerwinkel[22] and Eichhorst[23], who regard the initial disease as one related to the circulation, and not necessarily to the nerve lesions themselves. Potain[24], basing his observations on the anatomical distribution of the blood vessels, points out that the flexor muscles, excluding the supinator longus, are drained by the median cephalic vein, whilst the extensors are drained by the interosseous--a peculiarity of considerable importance, as the supinator longus escapes paralysis in the majority of cases of wrist-drop.