The presence of paralysis in the muscles and the association of nerve lesions to muscular paralysis led investigators to examine the nervous system, and probably more attention has been paid to the pathology of poisoning in this direction than in any other. Many records of isolated cases are to be found in the literature of the subject, and the examination of the spinal cord has been carried out in many instances; several have been cases of generalized paralysis or dementia, with involvement of the trunk muscles as well as those of the extremities in the paresis.
Many observers who have made histological examinations in such cases have found nuclear changes in the anterior columns of the cord suggesting polymyelitis. A small number only of the total cases of paresis, however, come under this heading. Vulpian[25], Oppenheimer[26], Oeller[27], and others, described degenerative and proliferative changes in the grey matter of the cord. Steiglitz[28] by animal experiments produced inflammatory processes in the anterior grey substance, vacuolations in the ganglion cells, and degeneration in the anterior root ganglia. In the paralyzed muscles the changes of degeneration are found: the muscle nuclei become spindle-shaped, the interstitial tissue undergoes degeneration, the muscle becomes atrophied, takes the stain badly, shows irregular striation, and the muscle bundles become ill-defined and fused.
Scarcely any two observers are agreed as to the exact nerve lesions which are to be found, and so at variance are the various theories based upon the pathological findings that it is by no means uncommon to find two sets of observers quoting the same electrical reactions and histological appearances as proving in the one case peripheral, and in the other the central, origin of the paralysis. On the other hand, in the quite early observations of Hitzig[29] particular attention was called to the bloodvessels and their possible association with the disease. Moreover, as has been already cited, ancient physicians were in the habit of making use of lead as a styptic and hæmostatic because of its peculiar action on the blood.
Probably as a result of improved histological methods of examining the nervous tissue, renewed attention was given to the nerve fibres and nerve cells, with the result that, in the very large number of observations recorded, many different nerve lesions are described as the sequelæ of lead intoxication.
On the other hand, Hitzig’s observations on the associated inflammation of the bloodvessels has received confirmation by several independent workers. Westphal[30] cites a case of chronic lead poisoning resulting in death from encephalopathy, and describes degeneration and œdema of the brain following a process of chronic inflammation in the smallest and minute bloodvessels, and also associated with degeneration of the ganglion cells in the vicinity. Chvostek[31] also publishes a similar case where cerebral degeneration and some œdema had occurred. Kolisko[32], in examining the brain of a girl who had died of encephalopathy, found chronic œdema of the brain and spinal cord, the condition closely resembling that described by Hitzig as chronic cerebral hypertrophy.
Quensel[33], in a man who had died of encephalopathy, found leptomeningitis, atrophy of the cortex with degeneration of the parenchymatous elements of the cells and nerve fibres, degenerative changes in the vessels, nuclear destruction and pigmentation of the cells, and œdema. Nissl[34] described granules, which bear his name, present in the ganglion cells in the cortex, with parenchymatous degeneration. These cases were not associated with paralysis, nor is encephalopathy by any means always complicated with paralysis of muscles.
Berchthold[35] describes a case of typical spastic paraplegia due to lead, and states that the cortical neurons were but little damaged, the weight of the poison having fallen upon the peripheral segments.
Sorgo[36] describes a case of progressive spinal muscular atrophy traced to lead, in which degeneration of the spinal cord was a marked feature.
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].