Gentlemen!

Progressive paralysis deserved a detailed discussion; but I repeatedly made reference to the aetiology of acute psychoses. My lecture today is a summary, with some expansion of my earlier comments.

Of course, a certain degree of inanition due to such illnesses or other injurious influences is usually no more than a trigger. What is also needed is a pre-existing disposition, before mental illness occurs. This predisposition may be either congenital or acquired. You will long have known the major role that innate predisposition or (according to Griesinger [1]) heredity plays in mentally ill people, and in the so-called functional nervous disorders. Evident degeneration, which can be followed in many families, is based on this. I want to make just one point here, that I still do not find sufficiently emphasized: that a strong hereditary predisposition may be present without its ever leading to acute or a chronic psychosis. However, in all cases where it is present, a doctor must bear in mind the need for his patients to avoid, as far as possible, aforementioned adverse triggers. Nonetheless, hereditary disposition does not in itself enable diagnosis of a mental illness to be made. I should not forget to mention here that I find phthisis to be specified surprisingly often among the forerunners of acute psychoses; yet it is a well-known fact that this does not generally worsen the prognosis of the fundamental hereditary predisposition, this depending, as usual on the clinical form the psychosis takes.

The acquired predisposition to mental illness is based usually on adverse influences that are also expressed as organic changes in the brain. These include Hydrocephalus internus [W], even if this has reached the stage of recovery, as we often see; but we also see it even where no conspicuous alteration of the head has been left behind, but only partial adhesions or diverticular formation within the cerebral ventricles, a finding rightly emphasized by Meynert [2] in particular. Survivors of childhood meningitis, and any head trauma that has definitely been accompanied by concussion, also imply acquired predisposition. I should comment that recovery from meningitis, and also from tuberculars, should be recognized more readily than has been generally accepted. Childhood cramps, for whatever reason, although successfully outlasted, must likewise be regarded as noxious influences predisposing to mental illness. The impact of epileptic seizures, especially if they are clustered, is, in itself, not only a consequence but at the same time, also a cause of gross anatomical changes in the brain that cannot always be totally repaired. Similarly, the relationship between acute psychoses and severe infectious diseases such as typhus or malaria, survived from earlier times, must be taken into account. We assume that during the course of these ailments, anatomical changes can become enduring features in the brain. Finally, I mention as one of the most common precursors of acquired predisposition, certain toxic effects, foremost amongst which is prolonged alcohol abuse.

I have repeatedly drawn attention to the fact that times of normal physical change, such as puberty, menopause, and finally senescence, are particularly likely to predispose to onset of psychoses, based on the great importance that bodily changes have for consciousness. This widespread general predisposition will certainly have an effect, as it does normally and even when acquired disposition already exists through previously mentioned organic changes.

I remind you that we have learned about the chronic and protracted Delirium tremens; but I have occasionally mentioned an even more acute alcoholic psychosis: It is commonly referred to as pathological intoxication [W], and we know that it usually takes the form of a very acute allopsychosis with allopsychic disorientation and dreamlike hallucinations. The content of this altered state seems always to be fantastically threatening, and corresponding to this is an extreme Affective state which accompanies pathological intoxication, which is different from Delirium tremens. This condition lasts no more than a few hours, so that we can regard it as an example of a transient psychosis. It is followed by deep sleep, usually with complete amnesia. I have already mentioned that very similar transient psychoses can occur after a single bout of alcoholic intoxication or even without one, whenever there is a strong predisposition to mental illness.

I dealt with acute hallucinosis in greater detail earlier. However, I may have presented the prognosis of the initial illness in such cases too favourably, because recently I have repeatedly encountered a state of chronic hallucinosis, continuing after acute hallucinosis in alcoholics. On the other hand, it has long been known that the clinical picture of chronic hallucinosis (pp. 102, 103) that I mentioned earlier, whose content is a state of physical persecutory delusions, is often found among alcoholics.

Polyneuritic psychosis, which we have also discussed already, is often mainly alcoholic in origin. This illness, which is usually curable, can, under some circumstances, progress to a clinical picture of visual agnosia and asymbolia. You will recall such a case from my patient presentations [3].

The importance of a circumscribed autopsychosis based on an overvalued idea probably includes the so-called delusional jealousy of drinkers [W]; at least, this is a feature of several pure cases of this type. The overvalued idea on one occasion was based on a husband having been repeatedly rejected in his claims for marital intercourse, by his slightly-older wife, already richly endowed with children. In a second case, the underlying Affective experience could not be definitely proven, but was presumed to be a similar situation, and delusional jealousy was thus actually identified, because the subsequent delusion of reference was directed so specifically to that single issue, that the entire clinical picture could be understood only as a circumscribed autopsychosis based on this overvalued idea. Although these cases are chronic in character, they also belong amongst the acute psychoses on account of their more acute stage of origin.

Much more often, perhaps even most often of all—if you also include abortive cases—are anxiety psychoses in drunks. In my patient presentations you will find a few such cases, amongst them a very instructive case of abortive anxiety psychosis [4].

Alcoholic stupor [W] deserves brief mention. Here, clouding of the sensorium, and somnolence, comparable only to that found in tumour patients, can exist for several weeks or even months, making the clinical picture so similar to that of organic brain diseases that, for my part, I do not doubt that it has an organic basis in hydrocephalus internus [W]. Moreover, the gait disturbance that such patients show as soon as they can leave their beds, can be compared only with that of senile hydrocephalus internus [W]. Correspondingly, the pulse can be fairly slow. General muscle stiffness, with great increase in mechanical excitability of muscles, is common both in these cases and in senile hydrocephalus internus [W]. Papilloedema tends to be absent in both cases, but, as a residue after surviving alcoholic stupor, I have seen atrophy of the optic nerves with significant visual impairment. Generally the disease is curable, sometimes most definitively so, if permanent abstinence can be achieved. In other cases, stupor can turn into a state of deficit to which traits of asymbolia may be added, although to widely varying degrees.