The indications are at the present time that the psychiatry of the future will not deal with a consideration of general paralysis and cerebral syphilis, as such, but will differentiate preferably between parenchymatous and interstitial, or mesoblastic, syphilitic processes of the nervous system. The retention of the designation general paresis is little, if anything, more than a concession to the claims of tradition. Cerebral syphilis may be said in a general way at this time to include all syphilitic involvements of the brain other than general paresis, which must be accorded the precedence due to priority of recognition if nothing else. In the light of our present knowledge we may speak in rather definite terms in considering cerebral syphilis from the standpoint of pathology. On an anatomical basis it is usually divided into three forms,—the meningitic, the endarteritic and the gummatous types. It is, of course, not to be understood that these represent separate and distinct processes. Combined forms are nearly always to be expected and the different types practically always coexist more or less.
The onset of the disease may be expected anywhere from one to ten or even fifteen years from the date of the initial lesion. The early appearance of cerebral symptoms would indicate brain syphilis as a general rule rather than general paresis. Oppenheim[182] in his second edition says that cerebral syphilis often develops within a year after infection, a majority of the cases being noted within two years. He finds it a very rare occurrence after ten years. "Because," as Barker[183] puts it, "of the lawlessness of the occurrence of syphilitic lesions in the central nervous system, all clinical classifications of these cases are based only on the predominance of certain associations of lesions." Certainly the pathology of the disease is quite varied in its manifestations.
The meningeal form is the one most often encountered. This may appear on the convexity or on the base of the brain and is spoken of as being either localized or diffuse in character. It may or may not be associated with gummatous formations or cortical vascular involvement. The essential process is a leptomeningitis. The pia is thickened, opaque and adherent to the cortex. The microscope shows the presence of inflammatory elements consisting largely of lymphocytes and plasma cells which may be confined entirely to the meninges or may extend downward to the superficial cortical layers directly or by extension along the adventitial sheaths of the vessels. An examination of the cortex, however, shows a limitation of this invasion to the immediate neighborhood of the meninges. The cortical involvement, in other words, is entirely secondary and is not the important part of the pathological picture that it always is in general paresis. The meningeal condition is practically the same in the two diseases but more likely to be localized in syphilitic processes. Dunlap[184] calls attention to the important fact that in a group of cases occurring many years after infection he found involvements of the deeper cortical layers strongly suggesting general paresis pathologically and impossible of differentiation clinically. In these cases, even in the deep cortical vessel walls, occasional lymphoid and plasma cells were found, as well as typical syphilitic endarteritis in some instances. There is frequently, in addition to the simple meningeal involvement at the base, a widespread gummatous infiltration of the pia-arachnoid or in some instances numerous miliary granulomas. This is especially common in the region of the chiasm and may involve the origin of various cranial nerves, obviously in such cases determining the symptomatology to be expected. The optic and oculomotor nerves particularly are affected. The large vessels at the base are often involved either by syphilitic inflammatory processes or by direct invasion of their walls by gummas. An extensive specific meningo-encephalitis may lead either to foci or extensive areas of actual softening.