Steiglitz[37], in describing the inflammatory processes produced in animals poisoned by lead, makes special mention of a distinct minute inflammatory change in the grey matter of the brain, with vacuolation occurring in the ganglion cells in the anterior horns of the spinal cord. Prévost and Binet[38], on the other hand, describe an inflammation of the peripheral nerves occurring after administration of lead to rabbits for one month. They produced what they describe as “a lead polyneuritis,” with primary affection of the motor nerves. With the brain, as with other parts of the body, various writers describe widely differing changes. Experimentally, when the doses have been massive and the animals rapidly poisoned, very little has been found, and some regard this as evidence against the central origin of lead paresis. On the other hand, in cases of chronic poisoning (mainly chronic industrial poisoning), where an opportunity of post-mortem examination has been afforded, marked atrophic changes have been discovered both in the brain and spinal cord, in the motor nerves supplying the affected muscles, and throughout the nervous system generally, so much so that anterior polymyelitis of old origin is described, vacuolation and degeneration of the ganglion cells, and various other pathological changes associated with nerve degeneration. On reviewing the literature, it becomes practically certain that in the old and advanced cases of poisoning lesions are invariably found in the central nervous system, while in the less advanced cases the most marked change has been found in the peripheral nerves. In only a very few instances have any observers noted the fact of hæmorrhages occurring in the nervous tissues, and one of the most important observations on this point is the careful description by Mott[39], of a fatal case of lead poisoning in an asylum, in which distinct yielding of the vessel walls with minute hæmorrhages was present in the cerebral cortex. This case is quoted in full on p. 71. In the record of the experiments by one of us (K. W. G.) on p. 95 are described the hæmorrhages occurring in the anterior crural nerves of cats poisoned by lead. These animals showed most distinct loss of power in their hind-limbs, as was evidenced by their inability to jump, and other symptoms homologous to wrist-drop in man. In these animals no nerve degeneration or alteration in the spinal cord was found sufficiently gross to account for the paralysis, whereas the amount of pressure produced by the yielding of the vessel walls on the nerve bundles and the associated exudation was evidently sufficient to cause compression, and thereby loss of function in the nerve in question.