(1) Nerve cells. Their changes are: a. In numbers and arrangement: many cells disappear; the different layers are more difficult to distinguish than in the normal state and appear to be confounded; β. In shape: the processes disappear, the angles become blunted, the cell-body tends to reduce itself to a small, granular and pigmented mass; y. In structure: chromatolysis - that is, alteration and destruction of Nissl's corpuscles - which causes the cell to assume a hyaline aspect when the chromatic substance is destroyed, or to present a uniform coloration if stained by the aniline pigments when this substance, reduced to a fine powder, is disseminated through the entire cell. (2) Nerve-fibers: many are destroyed, which fact can be demonstrated by Pal's or Weigert's hæmatoxylin stain. The degeneration affects projection fibers as well as association fibers, but more particularly the superficial tangential fibers of ExnerTuczek. (3) Pia mater and blood vessels: a. The pia mater is thickened, infiltrated by nuclei representing proliferating fixed connective-tissue cells or migrating leucocytes. β. The blood vessels are much more numerous than normally; the walls are thickened, often showing hyaline or fatty degeneration; the perivascular spaces are infiltrated with cells. The appearance of these lesions is similar to those of diffuse cerebral syphilis.1 Among the cells infiltrating the pia-arachnoid and the adventitial coats of the cortical vessels a special variety of cells occurs, known as plasma cells, which are of great importance in pathological diagnosis, since they are absolutely constant in general paresis and are found, according to Nissl, in no other chronic psychosis. These cells are somewhat larger than the ordinary round cells, contain coarse, deeply stained granulations in their nuclei, and a relatively large amount of finely granular protoplasm which, in specimens fixed in alcohol and stained with toluidin blue, takes a deep purple stain. 1 Mahaim. De l'importance des lésions vasculaires, etc. Bullet. de l'Acad. roy. de Méd. de Belgique, July, 1901. (4) Neuroglia. - Proliferation of neuroglia-cells is very frequently seen; when well marked it is especially prominent in the vicinity of the blood-vessels (Mahaim). Scantily distributed here and there may be seen spider-cells of abnormal shape and of gigantic size. Among the most constant neuroglial changes must be mentioned the ependymal granulations already referred to above. These are found under the microscope to consist of irregular hillocks upon the lining of the ventricles, formed by great proliferation of the ependymal glia cells which, instead of consisting of a single layer, as they do normally, are in these hillocks piled up in half a dozen or more irregular layers. (B) Spinal cord. - (1) Nerve cells: degenerative and atrophic lesions identical with those of the cerebral cells. (2) Nerve-fibers. - There are two principal types of lesions the tabetic type and the type of combined sclerosis. (a) Tabetic type. in the posterior columns and is similar to the lesion of tabes; this has led many authors to look upon general påresis and tabes as two different localizations of the same morbid process.1 The degeneration is localized (b) Combined sclerosis. The degeneration involves both the posterior and the lateral columns. Moreover, the process here is more diffuse and affects simultaneously different systems of fibers (tract of Gowers, crossed pyramidal tract). (C) Peripheral nerves. - The lesions of the peripheral nerves consist in the phenomena of neuritis and atrophy, analogous to those encountered in tabes and in alcoholism. . (D) Viscera. - Three classes of lesions may be distinguished in the viscera: (1) Lesions occurring merely as accidental complications: various infections, broncho-pneumonia, tuberculosis. The latter is rare and usually runs a slow course. (2) Lesions which are the direct consequences of the nervous disorders. These have been studied exhaustively by Klippel, who has termed them vasoparalytic lesions. They consist, according to this author, "in a high degree of congestion and capillary engorgement, capillary hemorrhages, and, by consequence, atrophic degeneration of epithelial tissues." 2 (3) Diffuse vascular lesions identical in appearance with those of the cerebral vessels. 1 Nageotte. Tabes et Paralysie générale. Thèse de Paris, 1893. 2 Klippel. Lésions des poumons, du cœur, du foie et des reins dans la paralysie générale. Arch. de méd. expérim. et d'anat. path., July, 1892. - Angiolella. Lésions des petits vaisseaux de quelques organes dans la paralysie générale. Il manicomio, 1895, Nos. 2 and 3. These lesions are met with chiefly in the kidneys, liver, and heart, and are often associated with degenerative lesions, such as fatty or cirrhotic liver, sclerotic kidney, or degenerated myocardium. Etiology. In 1857 Esmarch and Jessen were led by the clinical histories of their cases to conclude that syphilis was the cause of general paresis, but their view gained ground very slowly. In France Charcot always rejected it, and Déjerine wrote in 1886, "Syphilis is very rarely found in the histories of general paretics, and has no influence on the course of the affection; when found it is but a coincidence." Others have held, with Joffroy, that syphilis was a strong factor favoring the occurrence of general paresis but not an essential cause of it. Case histories alone were, naturally, insufficient to establish the essential part played by syphilis in the etiology of general paresis, a history of syphilitic infection being by no means always obtainable; but the case came to be strengthened on anatomical grounds by the similarity between the lesions of general paresis and certain syphilitic lesions. In 1897 Krafft-Ebing presented at the International Congress of Medicine in Moscow further important evidence. A physician, whose name was not mentioned, inoculated with syphilis nine general paretics who had reached the last stage of the disease and in whose history syphilis had not been found; none of these developed a chancre. The advent of the Wassermann reaction with the generally positive finding either in the blood, or in the cerebro-spinal fluid, or in both, led to the general acceptance of the view that in the absence of syphilis there can be no general paresis. But the nature of the disease still seemed obscure; especially perplexing was its resistance to anti-syphilitic treatment in contrast with other syphilitic lesions. The disease was held to be a consequence and not a direct manifestation of syphilis, a "metasyphilitic" (Moebius) or "parasyphilitic" (Fournier) disorder, possibly in the nature of an autointoxication (Kraepelin). Some, however, advanced the view, based on various considerations, that general paresis was but a late and peculiar manifestation of still active syphilis.1 Others, notably Lambert and Dunlap,2 have insisted that a sharp line of demarcation cannot be drawn between general paresis and cerebral syphilis and have brought to attention cases which, in clinical features as well as in post mortem findings, represent transition or combination forms. The nature of the relationship between syphilis and paresis was finally settled by Noguchi and 1 Browning and McKenzie. On the Wassermann Reaction, and especially its Significance in Relation to General Paralysis. Journ. of Mental Science, Vol. LV, 1909. - Plaut and Fischer. Die LuesParalyse-Frage. Allg. Zeitschr. f. Psychiatrie, Vol. LXVI, 1909. Rosanoff and Wiseman. Syphilis and Insanity. Amer. Journ. of Insanity, Jan., 1910. 2 C. I. Lambert. A Summary Review of the Syphilitic and Metasyphilitic Cases in 152 Consecutive Autopsies. N. Y. State Hosp. Bulletin, Aug., 1912. - С. B. Dunlap. Anatomical Borderline between the so-called Syphilitic and Metasyphilitic Disorders. Amer. Journ. of Insanity, 1913. |