The inflammatory conditions in the spinal cord of poliomyelitis, which conditions are precisely as striking as those of the paretic cortex, are beyond a question cleared away in the progress of the affection. Reference to the paradigm case (1) will show the type of our argument. There is no manner of doubt that in this paradigm case almost every portion of the nervous system had been sometime swept by spirochetosis and many of its small vessel sheaths stuffed with chronic inflammatory products. As for paretic neurosyphilis itself, a great many of its most striking clinical phenomena, such as loss of memory and disorientation, as well as great degrees of apparent dementia, are found virtually as often in cases with very slight anatomical changes as in cases with marked cortical devastation. The inference is plain, that these phenomena are to a degree functional rather than structural.

In brief, we conclude not only from therapeutic experience but also on a priori grounds that the histological conditions in paretic neurosyphilis are not entirely hopeless, and certainly not more hopeless than conditions in many chronic diseases outside the nervous system. Accordingly, we plead for a temperate optimism as to therapeutic results in general paresis.

A fifth group of neurosyphilitic cases bulking rather largely in textbooks of pathology is the group of the gummata. For a variety of reasons (therapeutic and otherwise) the actual number of gummata of the nervous system available for clinical or even for anatomical study is much smaller than the books might lead one to infer.

The sixth and last of the main groups of neurosyphilitic diseases is that of the juvenile forms, among which we find not only diffuse forms without a special and well-defined course, but also characteristic examples of paretic and tabetic neurosyphilis. The distinction of a juvenile or congenital group of neurosyphilitics is, on theoretical grounds, perhaps hardly defensible. On practical grounds, however, the juvenile neurosyphilitics do form a group having special relations to feeblemindedness, epilepsy and the like.

We must be clearly understood as to the rough, six-unit classification just given. It is practical merely. For comparison we have given in other charts more expanded lists of the diagnostic entities in neurosyphilis among which that of Head and Fearnsides is of special interest, see Chart 2, page [21].

We shall now proceed to a brief analysis of the findings in our chosen series of 137 cases. We shall not reproduce the case headings of these cases, but expand their statements where necessary and tie them together so far as possible into a reasonable and systematic statement of the situation in neurosyphilis. The footnotes will contain references to other cases in which identical points are illustrated as in the leading cases. The leading cases will in all instances be placed first in the footnotes.

The paradigm[[32]] shows meningeal, vascular and parenchymatous lesions and thus illustrates our definition of the term Diffuse which means precisely meningeal, vascular and parenchymatous. The meningeal lesions gave rise to two prominent sets of lesions, first, the marked tabetic lesions of the spinal cord (due to the spinal root neuritis incidental to the spinal meningeal inflammation), secondly, the characteristic asymmetrical and focal atrophy of cranial nerves incidental to a now largely extinct meningeal process at the base of the brain. The vascular lesions are responsible for another important and characteristic factor in the case, namely, the bilateral pyramidal tract sclerosis; the bilateral cysts of softening of the corpora striata are characteristic effects of old syphilitic cerebral thromboses. The parenchymatous disease in our paradigm is everywhere obvious, less so perhaps in the cortex itself than elsewhere, although here also evident in the shape of lesions suggesting an early phase of tissue atrophy.

The paradigm is of interest in demonstrating what in broad lines must be taken as an ascending disease proceeding not only from spinal cord to encephalon but also traceable as proceeding from lower parts of the spinal cord to upper parts thereof and from the lower encephalon to the higher structures of the cerebral cortex itself.

The paradigm insistently calls attention to the advantage of persistent therapy not only in its display of remarkable successive recoveries from permanent looking symptoms but also histologically from the remnants of inflammatory process to be found in an otherwise almost wholly dismantled nervous system with extinct lesions.

Tabetic Neurosyphilis[[33]] (“tabes dorsalis”), of course, often proceeds to death without special complications of syphilitic nature. We have chosen a case, however, to demonstrate a terminal complication with vascular insult. Incidentally the case shows another complication inasmuch as the cause of death was rupture of aortic aneurysm. It is important to bear in mind these complications in tabes dorsalis which go to prove that the spirochetosis of tabetic neurosyphilis is not limited to the region of the spinal roots or to the spinal region in general. Tabetic neurosyphilis is apt to be only a part of a total picture of neurosyphilis just as neurosyphilis itself is only a part of the general syphilitic process.