Gentlemen!

To gain a firm standpoint, it was most opportune for us to see initially the two clinical pictures, of hyperkinetic and akinetic motility psychosis, conceived as narrowly as possible; and from these it would seem possible to penetrate the area in which we find by far the majority of cases defined specifically by motor symptoms, yet which in one way or another are more complicated than cases already considered.

Primarily we have to consider here the differences in course, and in the combinations between the opposing states of hyperkinesia and akinesia. We find such combinations represented by two main types. The first [Ed] type consists of a picture in which, either from its onset, or at some time during the course of a hyperkinetic motility psychosis—within hours or a few days at most—an akinetic motility psychosis occurs. In such cases, it is evident that, as the disease process becomes augmented, deficit symptoms appear in place of symptoms of activation. Likewise, in the clinical picture of agitated confusion, one can sometimes see such an increase from hyperkinetic to akinetic symptoms. In two cases of this kind, the acute onset of confused mania was made up of a 1- and a 2-day akinetic-parakinetic stage. The second [Ed] type of combination consists in mutual separation of the opposed states of hyperkinesia and akinesia, with each single phase producing pictures of hyperkinetic or akinetic motility psychosis, as described above. The main difference from the first type lies therefore in the more protracted continuous course of each phase. You see, gentlemen, that it is a parallel with the familiar circular psychosis, which in pure cases shows just such an alternation between mania and melancholia. In fact, just as in circular psychoses, frequent changes from akinetic to hyperkinetic phases may occur, even if not with the regularity of circular psychoses. These cases seem to stand out by their poor prognosis.

Much more frequently, however, the combination results in only a single cycle of this sort, in which case I avoid the term ‘circular’ [W] and speak of the special form of cyclic motility psychosis [W]. I have seen cases of this sort almost exclusively in young girls and women, and their aetiology seems to be predominantly menstrual and post-natal. The hyperkinetic stage always occurs first; and a distinct stage of exhaustion stupor is often inserted between it and the akinetic stage, or after the latter; the final outcome is either recovery, death or profound dementia. Mixed in with the hyperkinetic stage is often a stage of mania, whilst in the akinetic state, a state of melancholia is often added; in other words, at one time intrapsychic hyperfunction, at another, loss [Ed] of intrapsychic function. At the same time, patients are usually completely disorientated; and motor disarray is always very prominent. In these cases, one could speak of the substitution of one clinical picture for the other. More often, however, here also the akinetic symptom is always an expression of increased intensity. In such cases, of cyclic motility psychosis onset of the akinetic phase may appear earlier in some subdomains of motility than in others. In particular, it is observed that motor loquacity has already passed into mutism, while the motor impulse lasts a few days more, before it passes on in similar fashion to immobility. In unfavourable cases, the hyperkinetic stage often has an anxious hypochondriacal content, with corresponding phonemes [1].

Gentlemen! Experiences in the clinic do not allow us to define any exclusively parakinetic form of motility psychoses. Where altered forms of movement dominate for a long time, or throughout an entire illness (as you saw in one case [2]), it transpires that phases of akinesia and hyperkinesia can be differentiated, so that the parakinesia, even when striking, does not exist independently. The concept of parakinesia is evidently only an abstraction, just as we might analyze paraesthesia arising in peripheral nerves in part as hyperaesthesia, in part as paraesthesia, without losing any essential part of the symptomatology.

Gentlemen! As we have seen above, it is in the nature of akinetic symptoms, that it is often totally impossible to decide how far they are intermingled with other identification disorders, and at other times this is possible only after the akinetic stage is over. So we must then take into account the possibility that the above clinical picture of akinetic motility psychosis, derived entirely empirically, is too broad, and still contains cases in which the motor symptom complex is merely grafted onto another syndrome, which is just as significant, and encompasses it. How justified this concept is, we see in some cases of ‘complete motility psychosis’ [Ed]. These reveal at the outset, apart from the ever-changing motor symptoms, images of ‘fantastic menacing delirium’ [Ed] with severe disorientation in all three areas of consciousness, and which always seem to have an unfavourable outcome. Very similarly, the fantastic menacing delirium in the paranoid stage of an akinetic motility psychosis is sometimes the only expression of disorientation, that was previously concealed by the akinetic stage. These cases also have a largely unfavourable prognosis. At other times, the fantastic menacing delirium occurring within well-retained allopsychic orientation is to be seen in the same paranoid stage, combined only with hypochondriacal sensations, mainly intestinal in nature. These cases also follow a predominantly unfavourable course, so that we are to some extent justified in regarding the fantastic menacing delirium in motility psychoses as a generally unfavourable prognostic feature.

Gentlemen! To understand other more complicated cases of motility psychoses, it may help to discuss together all those symptoms based on disorders of identification within the psychomotor pathway Zm, as we always did hitherto in analogous cases. However, it has been proved necessary, above all, to clarify how intrapsychic akinesia is to be differentiated from psychomotor akinesia. A digression into intrapsychic akinesia [W] therefore cannot be avoided.

Gentlemen! Affective melancholia presented us with an example where symptoms derived from a hypothetical scheme, and these alone, make up a clinical picture which, in reality, is met very often. The situation is not so simple for that state of illness—a more severe grade of intrapsychic functional disorder—namely a deficiency of psychically induced movements, which is a striking form of akinesia in objective terms. The independent significance of such a condition, which provisionally, I would like to call depressive melancholia [W], has become more and more questionable over the years. To begin with, I want briefly to present the hallmarks of this condition, as derived from our schema. Patients of this type, of their own volition, stop speaking or doing anything; they therefore present symptoms of mutism and akinesia for initiative movements. Expressive movements are correspondingly fewer, the face less animated, while reactive movements are also involved, but less severely so. Insofar as reactive movements are [Ed] affected, this depends on the patient’s intrapsychic capacity, certainly not on changes in activation of muscle groups. With complete failure of processes of association, the Affective response that is linked to subjective feelings of inadequacy likewise ceases, and in place of that overvalued idea, a lack [Ed] of thought prevails, perhaps even, at times, complete standstill of thinking. An anxious Affective state might be possible once we remember that failure of processes of association represent, in a certain sense, a threat to the body. On the other hand, specific motor symptoms such as flexibility, pseudo-flexibility, muscular rigidity and negativity are missing.

Patients fitting this picture are not rare. Affective melancholia may occasionally show some similarities, and I believe that in the past, I have observed transitions of one condition into the others, in which the picture of depressive melancholia corresponded to more severe grades of the illness, cases which always showed a much longer course than the vast majority of cases of Affective melancholia. In particular, a characteristic of these cases, it seems to me, is strangely intact reactivity in speech, a clearly difficult way of giving an answer, with just a soft flat voice, or with much effort—just when I have turned away from the patients. The same hesitancy, the same complication and retardation, apparently involving overcoming some sort of inhibition can, in such cases, also extend to all other reactive movements. I now think it likely that these transitions from Affective to depressive melancholia do sometimes actually occur, and so I can no longer maintain that depressive melancholia is significant as an independent illness. More detailed examination of such cases during the last few years has always revealed to me additional symptoms which are there to be found, but only when you know what you are looking for. Without having arrived at a conclusive judgment of this, I want briefly to share my experiences.

First [Ed], I have collected a series of statements, in part from the patients themselves, in part from their relatives, according to which a specific condition continued for hours, or occasionally days, at the time of onset of motility psychoses, corresponding most closely to what I have just described—the cessation of any kind of ideation. Sometimes a definite body position was maintained which, in itself was in no way abnormal or constrained. Information given later by patients indicated a complete stand-still of thoughts, as occurs normally in the state of the so-called bewilderment, but then only momentarily. A female patient of this kind was found in such a state on her admission, persistently immovable, her clothes pulled up, and in a foot bath ordered for her. The motor character of this disorder only became clear later on, because she had had mutism already for a long time and could not protrude her tongue, while all other reactive movements were carried out promptly. A second [Ed] series of cases consists not only of short-lasting conditions, such as those just described, but correspond to a separate clinical picture of longer duration, always lasting over a year, for which the name pseudomelancholia [W] might be appropriate. This ‘pseudomelancholia’ [Ed] usually forms the first stage of a compound psychosis, which in general has an unfavourable prognosis, although the possibility as an exception, of a favourable outcome always exists. This clinical picture has been spoken of before (p. 103). Cases in this class usually present with some signs of Affective melancholia, so that they might be identified as borderline cases between this and the above clinical picture, constructed on the basis of theory. However, sooner or later in their course, they produce further signs, in that delusions of relatedness join in, this being entirely foreign to melancholia. Cessation of melancholia—which may last for a year or more—then usually gives way to a further, worsening stage of persecutory delusion, and soon also of grandiosity.

The third [Ed] case, is the most important, which, on its own would justify establishing a separate clinical entity of depressive melancholia. I have often seen cases of illness, which by any criterion, present primarily with a pure type of intrapsychic akinesia, but which, later on, sometimes after 6 months, turn out to be cases of progressive paralysis. Paralytic symptoms, particularly ones arising from the projection pathways, first emerge here when supposed depressive melancholia is starting to improve and a favourable turn of events is anticipated. Far more often, however, we meet cases of depressive melancholia in which hallmarks of paralysis are there right from the outset, either through participation of the projection system, or by actual deficits. When combined with a mild degree of somnolence, a special subgroup among such cases seems to be defined, which, to judge by results of specific therapy, should be grouped among the luetic brain diseases. Of Heubner’s cases [3], a few might belong here.

Gentlemen! As you see, in these cases, as in pseudomelancholia, we are dealing with a definite phase—usually the initial one—of a compound psychosis (see later). In the case of a combination of severe loss of intrapsychic function and hypochondriacal symptoms, it is different, and allows one to interpret the first of these, and the resulting akinesia representing as merely the sequel, induced psychologically, of a severe feeling of physical illness. These cases, which are in large part curable, present the same combination of symptoms throughout the entire illness, and thus form a uniform, albeit mixed, clinical picture. In contrast to hypochondriacal melancholia, mentioned earlier (p. 162), this is driven throughout by disorders of psychosensory identification of the patient’s own body, except that, by its very nature, this exercises special influence over motility. The Affective reaction is psychosensory, and thus consists of hypochondriacal feelings of misery and attendant anxiety. At times of remission, or with a favourable response to a medication such as opium, you may hear from patients that they feel too ill to think, or speak or to do anything. In brief, the akinetic reaction is therefore psychologically motivated and not reflexly induced as in the previously mentioned (p. 132) cases. Aberrant sensations can have various locations, usually intestinal.