Gentlemen!

We have often met Progressive paralysis in the course of these discussions, and in such different forms that you will have already reached a conclusion as to the importance of this group of illnesses. However, the main theoretical significance of the group is far greater: For, alone among all the psychoses, cases in this group show almost constant anatomical findings, and in addition, as we also know, the constancy of this finding corresponds with constancy of certain symptoms common to almost all cases; while, beyond that, very different localization of the disease process is also to be found, but with corresponding differences in symptomatology. Thus, it gives us an example of a brain disease in which anatomical findings and symptoms correspond with one another. Of course, up to now this principle has applied only to symptoms arising in the projection system, and to the symptom of disintegration, namely dementia. However, by analogy it is permissible to conclude that what applies here, applies also to an equally large diversity of clinical psychiatric pictures, if one were in a position to locate these clinical pictures symptomatologically. Thus, progressive paralysis offers us a way into a general anatomical foundation for the psychoses. You see, gentlemen, that from this point of view, we again need to hold to the view that progressive paralysis represents no more than an aetiological recapitulation of psychoses, which otherwise differ widely from one other.

Paralytic aetiology shows itself to be related most closely to toxic effects, with the sole difference that it is a toxic effect to be seen as arising repeatedly anew within the organism. The progressive deleterious character of the disease can be explained in no other way. This necessary concept can be explained by analogy with the spinal disease Tabes dorsalis [W] and an assumed ‘metasyphilitic toxin’ [Ed], in contrast to the syphilitic aetiology. Despite this, you still cannot avoid accepting bacterial action as the basis for this peculiar behaviour. But I want to comment here that sporadic exceptions to this deleterious progression are to be seen. Over the years, however, amongst thousands of cases of severe paralytic psychosis with a clear syphilitic basis, a few cases have recovered completely, and not relapsed. As you can see from these comments, I perceive paralysis to be the epitome of syphilis-related psychoses, a viewpoint finding increased general recognition, and which appears justified by experiences in our Clinic. It would already be clear to you from my periodic utterances that a certain psychosis cannot be said to have an exclusive [Ed] causal relationship to syphilis. You can never recognize anything more than the preference [Ed] of a particular aetiology for a particular form of illness.

With this restriction, you must consider as specific to paralytic psychosis, the fantastic grandiosity, that is the earlier-mentioned (p. 219) expansive [W] form of autopsychosis [W], seen almost exclusively in the context of syphilis. But I have already alluded (p. 220), though not often, to the occurrence of Kahlbaum’s [1] so-called Progressiva divergens [W], which probably was not syphilitic—and I presented to you the case of an 86-year-old woman with the same fantastic grandiose delusions—which certainly was not. The fantastic grandiosity, like other yet-to-be mentioned, and more distinct psychoses, often forms the first stage of a composite psychosis [2] usually lasting only weeks or months.

The prodromal symptoms [W] of progressive paralysis, usually accompanied by feelings of severe illness, are well known. They consist of headaches, insomnia, and irritable mood, and can precede outbreak of acute psychosis by 1–2 years. However, quite often, headaches are denied. In this prodromal stage, often indistinguishable from severe neurasthenia, you often also hear complaints of forgetfulness and failing ability to perform, although these symptoms cannot be verified objectively. However, early on in some cases, and in this prodromal stage, symptoms derived from the projection system may be prominent. To recapitulate briefly, they usually consist just of a suggestion of facial palsy or tongue deviation; the so-called ‘paralytic speech impediment’ [Ed]; and a tremor of the voice, tongue, and lips. The paralytic speech disorder [W] ranges between two opposites, which we can describe as ‘stumbling over syllables’ [Ed], and blurring of speech—if you prefer to avoid the anatomical terms of cortical and bulbar speech disorder. To assess stumbling over syllables, you can use test words to be repeated, like ‘civilization’ [Ed], ‘army reorganization’ [Ed], ‘extraterritoriality’ [Ed], etc. The voice becomes tremulous, up to the point of aegophony. If these symptoms, which are decisive indicators of palsy, are missing during the prodromal stage, diagnosis may still be possible, as soon as you can detect characteristic spinal symptoms. These spinal symptoms [3] [W] sometimes precede all other paralytic phenomena, and are therefore the most valuable diagnostic tools. Here, they indicate no more than signs of the so-called ‘column disease’ [Ed] of the spinal cord, symptoms derived partly from dorsal columns, partly from lateral columns. From the former, one must expect rigidity of the pupillary reflex. Without doubt, little value can be placed pupillary inequality. I particularly draw your attention to certain characteristic signs of combined columnar disease, although there are two types that are equally valid: Respectively, they are increased passive mobility of the legs with simultaneous increase of tendon reflexes; and reduction of passive mobility, producing prominent rigidity, together with reduction or even a total absence of tendon reflexes. Through prolonged observation, we see one of these patterns being replaced by the other; for example, return of a lost knee jerk! As regards their diagnostic value, it is important to note that in neurasthenia there may be an increase in tendon reflexes, but never a reduction.

As for the immediate precipitant of the illness, undoubtedly strenuous mental activity has often preceded it. However, we would be giving a false impression if we took into account only the ‘quantum’ [Ed] of work; we often see men with unceasing and strenuous mental activity who reach their later years full of vigour. Indeed, I would like to suggest that strenuous mental work is even beneficial to health. What is harmful by itself is to work under emotional pressure. Whoever finds himself forced to work beyond his individual strength, under tight time pressure, taking on responsibilities beyond his capacity, must struggle with excitement, grief, and sorrow which can easily lead to impairment in purely. Undoubtedly all-pervading careerism encourages such damage. From this fact, and similarly from the increased prevalence of syphilitic infection, we can explain the significant predominance of the male sex, particularly amongst educated classes. The age of maximum risk is between 30 and 50 years, especially 35–45.

Alongside expansive autopsychosis we find paralytic mania; in this respect I refer again to my earlier remarks (p. 219). Usually, the picture of mania is coloured by simultaneous presence of fantastic grandiosity. At other times, it is not so pure, in that hypermetamorphosis or hyperkinetic symptoms accompany the mania. Nevertheless, cases of almost pure mania of paralytic aetiology undoubtedly occur [4]; and after running its course, only very rarely is there complete recovery, although there is often very good remission over a prolonged duration. At other times, the mania subsides, but is transformed into a more restrained state of simple fantastic grandiosity.

Affective melancholia may also have a paralytic aetiology, even if it is not usually entirely pure but rather an admixture with either mild delusions of relatedness, or symptoms of anxiety psychosis, or both, these being foreign to pure melancholia. It is widely known that melancholia occurring in the age range 35–45 years raises suspicions of paralysis.

Depressive melancholia of paralytic origin has already been mentioned. Here, too, delusions of relatedness are frequent additions, so that the differential diagnosis of pseudomelancholia comes into question.

Amongst paralytic allopsychoses, I stress the importance of paralytic delirium [W]. In contrast to previously mentioned forms of paralytic psychosis, which occur preferentially in initial stages of the illness, the delirious condition can appear in any phase of the illness, often quite suddenly and unexpectedly. In most cases, it is therefore not difficult to make a correct diagnosis. Incidentally, the clinical picture can be the same in all detail as that of Delirium tremens, as already emphasized (p. 174). However, this is nevertheless rare. Mostly, one is struck by the dominance of the twilight state, and the impossibility of patients being awakened from this state. The most obvious outward feature is clouding of the sensorium, so that one can speak of a paralytic stupor [W]. Delirious features that add a peculiar colour are often no more than adjuncts derived from the projection system through muscle or vocal tremor, and muscle rigidity. Instead of restless movement, akinetic behaviour prevails.

Of other allopsychoses, I must mention one case in which the purest picture of presbyophrenia showed up in its delirious form for several days. Its nature was then clarified as a case of paralysis, when a paralytic attack occurred, with subsequent specific paralytic symptoms derived from the projection systems. Instructive as the case is for relations between concepts, I introduce it only as a rare occurrence. Of the hallucinatory allopsychoses, I remember an equally rare case involving a prostitute, who was in the clinic for 2 years as ‘chronic hallucinosis’ [Ed] to be presented as such every semester. You will remember that, at her last presentation, to my surprise, symptoms derived from the projection system became noticeable, which shed light for us on the paralytic aetiology, a diagnosis which was confirmed during the subsequent course. Moreover, with regard to acute hallucinosis there are cases with paralytic aetiology whose true significance becomes apparent only after the paranoid stage has ended, through striking deficits, loss of retentiveness in memory, and paralytic speech disorders. However, exclusion of alcoholic pseudoparalysis (see later) is often difficult, and can be achieved only through a detailed knowledge of the case history. Here, I want to mention that the belief about the rarity of hallucinations in paralysis, which is still widely held, is quite wrong. In our clinic, we have had many acute paralytic psychoses in which hallucinations were represented as strongly or even more so, than in corresponding cases of different aetiology.

When discussing anxiety psychoses, I have already stressed (p. 149), that they often have a paralytic aetiology. In particular, hypochondriacal anxiety psychosis raises suspicions of paralysis, as indeed does the large class of somatopsychoses which provides some of the most severe cases of paralysis. I already mentioned examples, amongst which bouts of most severe somatopsychic disarray and disorientation occurred, one of which led later to a purely demented form of paralysis (p. 163). However I must also include here an earlier-mentioned case (p. 74) of severe hypochondria that I cited as an example of residual hallucinosis, with a favourable outcome after acute psychosis. Already, in this first illness there was a suspicion of paralysis, since a history of syphilis was known. After 5 years of perfect health, a relapse occurred, this time taking the form of expansive autopsychosis whose deleterious course led to death within a year. A case with the most rapid course deserves mention here. Initially there was a simple intestinal somatopsychosis for some weeks gaining no fantastic significance, and it was treated as a genuine intestinal disorder. However, this was followed by a phase of hypochondriacal symptoms, which were quite fantastic in character: The patient described schemes that were running through his brain, in which an entire factory operation, with all manner of manipulations was going on; and soon it developed into the most severe threatening hypochondriacal delusion. Amongst other things, the patient had been tormented over the last few weeks by a tiger lying on him and tearing away at his liver. The entire course of illness in this 38-year-old man lasted 4 months. It had been preceded 10 years earlier by syphilis and had been treated several times. When total sensory psychosis occurred, as already mentioned (p. 273), acute worsening psychoses occurred, presenting in paralytic form, as a so-called ‘galloping’ [Ed] form of paralysis. Moreover, in such cases, at the very beginning or in the subsequent course, symptoms of threatening hypochondriacal delusions become clear. During cases mentioned, Affective states that are downright fearful made themselves manifest, but sometimes, according to the severity, with content of different coloration; and in other cases, which fortunately are more frequent, just the opposite is seen. The most severe hypochondriacal presentations show themselves with hardly any Affective component, such as having no head, no heart, no lungs, no stomach, or being completely hollow, ‘only a tube’ [W], as one educated patient put it so starkly. This phenomenon stands on its own, in no way dependent on the dementia, which may show up at about the same time. You will find a typical case of this sort in the patient presentations from my Clinic [5]. However, for weeks, in an earlier acute stage of his illness, the same patient presented the picture of most severe somatopsychic disarray, admittedly not as agitation, but only as almost total inaccessibility and helplessness, while only occasionally were there isolated expressions and actions pointing to total loss of bodily orientation.

With regard to motility psychoses of the paralytic variety, I have already often mentioned the hyperkinetic variety. Usually their manic features, fantastic grandiosity, and hypermetamorphosis are mixed together, this clinical picture developing mainly at a later stage of the illness, over several weeks. If worsening sensory psychosis reaches maximum severity, then hyperkinetic symptoms often join in with the paralytic aetiology [6]. A relatively frequent event, I should emphasize here, is the isolated loquacity [W] of paralyzed patients [W], a loquacity linked to flight of ideas, yet without any specific hyperkinetic shading, and also without actual mania. This peculiar isolated loquacity in otherwise apparently circumspect behaviour is limited almost completely to paralytics, the only exceptions known to me being the mildest cases of circular mental illness. Isolated hyperkinetic-parakinetic symptoms such as verbigeration, and stereotyped movements are met with very often in paralytics at later stages. You will remember that I have often used paralytics to demonstrate just such symptoms. Even in their relationship with aphasia and paralysis, these cases are sometimes very instructive. A type of Echolalia [W] may be touched on briefly here. It is occasionally seen in paralytic patients at the same time as severe motor disarray, producing such a rapid ‘reflex’ [Ed] reaction that it is uttered simultaneously, rather than being repeated later. You will find an example of this in patient presentations [7] from my Clinic. Incidentally, elsewhere one usually finds responses in echolalia limited to a one- to two-syllable echo, sometimes in patients who are already quite demented, and in expressionless paralytics. The following conversation would be relatively typical:

Akinetic motility psychosis in progressive paralysis is encountered relatively rarely in pure form, given that widespread muscle rigidity of paralysis originates specifically in the spinal cord. Hints of it are not so rare in later stages. However, in some cases that I know, prominent akinetic motility psychosis appeared as the first acute stage of the paralysis, followed by a second stage of agitated sensory confusion, and then a third stage of paralytic dementia with paralytic seizures. Every so often, you meet clinical pictures exhibiting a peculiar mixture of a paralytic delirium with akinetic motility psychosis. Moreover, akinetic-parakinetic conditions that obtain special coloration through predominance of motor disorientation and disarray should be mentioned [8].

Finally, I do not want to omit mention of certain twilight conditions, with clouding of the sensorium, which occur after paralytic attacks just as they do after epileptic attacks; usually they have certain focal symptoms, for example, combined with signs of sensory aphasia, and they tend to regress after lasting several days.

If we survey the whole picture of progressive paralysis, in so far as it can be regarded as a genuine psychosis, then in most cases, it is virtually the very model of a composite psychosis, passing successively through all different stages. Each stage may be a pure, simple psychosis; yet usually the clinical picture includes strange components, amongst which common falsifications of memory should not be forgotten. One of the more frequent possible combinations is one in which a stage of fantastic grandiosity is followed by one of mania, with allopsychic disorientation, and finally a stage of marked hypochondriac symptoms. However, just as often, a course is observed which is widely regarded as specific: cases of simple psychosis, distinguished from other simple psychoses only because of their rapid transition to dementia, and an admixture of above-mentioned symptoms derived from the projection system. Alternatively, it amounts to a colourful mixture of ever-changing symptoms, and thus to a complex clinical picture related only remotely to each simple psychosis.

The regular outcome in dementia here supports the view—highlighted at this time particularly by C. Westphal [9]—that paralysis almost always allows one to detect early signs of dementia. This is true even for cases developing just as simple psychoses, in which, by the nature of their entire clinical picture, more detailed analysis is often impossible in this regard. Nonetheless, the easiest symptom to establish here is reduced attentiveness, albeit not absolutely attributable to dementia. Even this loses its significance when there is a very severe Affective reaction. On the other hand, there are cases where no trace of deficit or loss of attentiveness can be found, like the examples of paralytic mania already cited. Fantastic grandiosity in such cases does presuppose a definite deficit in judgment, since the reality of things is apparently ignored; however, herein we find a contradiction that is no greater than the known fact (and in my opinion also wrongly evaluated as a symptom of deficit)—the failure that all mentally ill people show, to criticize the veracity of their hallucinations. Incidentally, you can find an example of paralytic mania without [Ed] fantastic grandiosity in my Krankenvorstellungen [10].

Included in the latter course, the most uniform and continuous trajectory is manifest as a curve, rising slowly in its extent, and actually belonging amongst the chronic psychoses. Whenever actual psychoses appear during the course, the illness always shows an acute character, at least temporarily, and Meynert [11] explicitly classed it with the acute psychoses.