Obsessions and phobias their psychical mechanism and their aetiology 4 страница

For the rest, I might have been spared having to defend myself against these two objections of Löwenfeld’s, if my respected opponent had paid greater attention to my paper itself. In it, both these objections are anticipated and answered. I have only been able to repeat here what I said there; and I have even purposely analysed the same cases over again. Moreover the aetiological formulas on which I have just laid weight are contained in the text of my paper. I will repeat them once more. I maintain that there exists a specific aetiological factor for anxiety neurosis which can be replaced in its operation by stock noxae in a QUANTITATIVE sense, but not in a QUALITATIVE one; I furthermore maintain that this specific factor determines above all the FORM of the neurosis; whether a neurotic illness occurs at all depends on the total load upon the nervous system (in proportion to its capacity to carry the load). As a rule the neuroses are overdetermined; that is to say, several factors operate together in their aetiology.

(3) I need not concern myself so much about refuting Löwenfeld’s next comments, since on the one hand they damage my theory very little and on the other they raise difficulties whose existence I acknowledge. Löwenfeld writes: ‘The Freudian theory is totally insufficient to explain the appearance or non-appearance of anxiety attacks in individual instances. If anxiety-states - i. e. the clinical symptoms of anxiety neurosis - occurred solely through a subcortical storing-up of somatic sexual excitation and an abnormal employment of it, then every person who is afflicted with anxiety-states ought, so long as no changes take place in his sexual life, to have an anxiety attack from time to time,just as an epileptic has his attack of grand and petit mal. But this, as everyday experience shows, is by no means so. The anxiety attacks happen in the great majority of instances only on definite occasions; if the patient avoids these occasions or is able to paralyse their influence by taking some precaution, he remains exempt from anxiety attacks, whether he is consistently given over to coitus interruptus or to abstinence, or whether he enjoys a normal sexual life.’

There is a great deal to be said about this. In the first place, Löwenfeld forces upon my theory an inference which it is not bound to accept. To suppose that in the storing-up of somatic sexual excitation the same thing must be happening as in the accumulation of the stimulus which leads to an epileptic convulsion, is to make a far too detailed hypothesis, and I have given no occasion for it; nor is it the only one that presents itself. I need only assume that the nervous system has the power to master a certain amount of somatic sexual excitation even where the latter is deflected from its aim, and that disturbances only occur when that quantum of excitation receives a sudden increment, and Löwenfeld’s claim would be disposed of. I have not ventured to extend my theory in that direction, chiefly because I did not expect to find any solid points of support along that path. I should merely like to indicate that we ought not to think of the production of sexual tension independently of its distribution; that in normal sexual life this production, when it is stimulated by a sexual object, takes on a substantially different form from what it does in a state of psychical quiescence; and so on.

It must be admitted that the condition of affairs here is in all probability different from what prevails in the tendency to epileptic convulsions, and that it cannot yet be consistently derived from the theory of the accumulation of somatic sexual excitation.

Against Löwenfeld’s further assertion - that anxiety-states only appear under certain conditions and fail to appear when those conditions are avoided, regardless of what the subject’s vita sexualis may be - it must be pointed out that he clearly has in mind here only the anxiety of phobias, as, indeed, is shown by the examples attached to the passage I have quoted. He says nothing at all about the spontaneous anxiety attacks which take the form of vertigo, palpitation, dyspnoea, trembling, sweating, and so on. My theory, on the contrary, seems by no means unequal to explaining the emergence or non-emergence of these attacks of anxiety. For in a whole number of such cases of anxiety neurosis there does in fact appear to be a periodicity in the emergence of the states of anxiety, similar to what has been observed in epilepsy, except that in the latter the mechanism of the periodicity is more transparent. On closer examination we discover the presence, with great regularity, of an excitatory sexual process (that is, a process which is able to generate somatic sexual tension), and which, after the lapse of a definite and often constant interval of time, is followed by the anxiety attack. This role is played, in abstinent women, by menstrual excitation; it is played, too, by nocturnal pollutions, which also recur periodically. Above all, it is played by sexual intercourse itself (harmful from its being incomplete), which carries over its own periodicity to the effects it brings about, viz. to the anxiety attacks. If anxiety attacks occur which break through the usual periodicity, it is generally possible to trace them back to an incidental cause of rare and irregular occurrence - to a single sexual experience, something read or seen, and the like. The interval I have mentioned varies from a few hours to two days; it is the same as that which elapses in other people between the occurrence of the same causes and the onset of the well-known sexual migraine, which has well-established connections with the syndrome of anxiety neurosis.

Besides this, there are plenty of cases in which a single anxiety-state is provoked by the extra addition of a stock factor, by an excitement of some kind or other. The same holds good, therefore, for the aetiology of the individual anxiety attack as for the causation of the whole neurosis. It is not very strange that the anxiety of the phobias should obey different conditions; they have a more complicated structure than purely somatic anxiety attacks. In phobias the anxiety is linked to a definite ideational or perceptual content, and the arousal of this psychical content is the chief condition for the emergence of the anxiety. When this happens, anxiety is ‘generated’, just as for instance sexual tension is generated by the arousal of libidinal ideas. The connection of this process, however, with the theory of anxiety neurosis has not yet been elucidated.

I see no reason why I should try to hide the gaps and weaknesses in my theory. The main thing about the problem of the phobias seems to me to be that when the vita sexualis is normal - then the specific condition, a disturbance of sexual life in the sense of a deflection of the somatic from the psychical, is not fulfilled - phobias do not appear at all. However much else may be obscure about the mechanism of phobias, my theory can only be refuted when I have been shown phobias where sexual life is normal or even where there is a disturbance of it of a non-specific sort.

(4) I now pass on to a remark by my esteemed critic which I cannot leave uncontradicted. In my paper on anxiety neurosis I had written:

‘In some cases of anxiety neurosis no aetiology at all is to be discovered. It is worth noting that in such cases there is seldom any difficulty in establishing evidence of a grave hereditary taint.

‘But where there are grounds for regarding the neurosis as an acquired one, careful enquiry directed to that end reveals that a set of noxae and influences from sexual life...’ Löwenfeld quotes this passage and adds the following gloss: ‘From this it appears that Freud always regards a neurosis as "acquired" whenever incidental causes are to be found for it.’

If this meaning follows naturally from my text, then the latter gives a very distorted expression to my thoughts. Let me point out that in the preceding pages I have shown myself far stricter than Löwenfeld in my evaluation of incidental causes. If I were myself to elucidate the meaning of the passage I wrote I should add, after the subordinate clause ‘But where there are grounds for regarding the neurosis as an acquired one...’, the words ‘because evidence (referred to in the previous sentence) of a hereditary taint is not forthcoming...’ What this means is that I hold the case to be an acquired one, since no heredity is to be discovered in it. In doing so I am behaving like everyone else, perhaps with the slight difference that others may declare the case to be determined by heredity even when there is no heredity, so that they overlook the whole category of acquired neuroses. But this difference runs in my favour. I admit, however, that I am myself to blame for this misunderstanding, on account of the way in which I expressed myself in the first sentence: ‘no aetiology at all is to be discovered’. I shall certainly be taken to task from other directions as well and be told that I have created useless trouble for myself by searching for the specific causes of neuroses. Some will say that the true aetiology of anxiety neurosis, as of neuroses in general, is known: it is heredity. And two real causes cannot exist side by side. I have not, they will say, denied the aetiological role of heredity; but if so, all other aetiologies are merely incidental causes and equal to one an other in value or want of value.

I do not share this view of the role of heredity; and since in my short paper on anxiety neurosis it is precisely to this theme that I have paid least attention, I will now try to make good some of what I have omitted in it and to remove the impression that in writing my paper I had not attended to all the relevant problems. I think we can arrive at a picture of the probably very complicated aetiological situation which prevails in the pathology of the neuroses if we postulate the following concepts:

(a) Precondition, (b) Specific Cause, (c) Concurrent Causes, and, as a term which is not equivalent to the foregoing ones, (d) Precipitating or Releasing Cause.

In order to meet every possibility, let us assume that the aetiological factors we are concerned with are capable of a quantitative change - that is of increase or decrease.

If we accept the idea of an aetiological equation of several terms which must be satisfied if the effect is to take place, then we may characterize as the precipitating or releasing cause the one which makes its appearance last in the equation, so that it immediately precedes the emergence of the effect. It is this chronological factor alone which constitutes the essential nature of a precipitating cause. Any of the other causes, too, can in a particular case play the role of precipitating cause; and this role can change within the same aetiological combination.

The factors which may be described as preconditions are those in whose absence the effect would never come about, but which are incapable of producing the effect by themselves alone, no matter in what amount they may be present. For the specific cause is still lacking.

The specific cause is the one which is never missing in any case in which the effect takes place, and which moreover suffices, if present in the required quantity or intensity, to achieve the effect, provided only that the preconditions are also fulfilled.

As concurrent causes we may regard such factors as are not necessarily present every time, nor able, whatever their amount, to produce the effect by themselves alone, but which operate alongside of the preconditions and the specific cause in satisfying the aetiological equation.

The distinctive character of the concurrent, or auxiliary, causes seems clear; but how do we distinguish between a precondition and a specific cause, since both are indispensable and yet neither suffices alone to act as a cause?

The following considerations seem to allow us to arrive at a decision. Among the ‘necessary causes ' we find several which reappear in the aetiological equations concerned in many other effects and thus exhibit no special relationship to any one particular effect. One of these causes, however, stands out in contrast to the rest from the fact that it is found in no other aetiological equation, or in very few; and this one has a right to be called the specific cause of the effect concerned. Furthermore, preconditions and specific causes are especially distinct from each other in those cases in which the preconditions have the characteristic of being long-standing states that are little susceptible to alteration, while the specific cause is a factor which has recently come into play.

I will try to give an example of this complete aetiological schematic picture:

Effect: Phthisis pulmonum.

Precondition: Disposition, for the most part laid down through heredity, by the organic constitution.

Specific Cause: Bacillus Kochii.

Auxilliary Causes: Anything that diminishes the powers - emotions as well as suppurations or colds.

The schematic picture for the aetiology of anxiety neurosis seems to me to be on the same lines:

Precondition: Heredity.

Specific Cause: A sexual factor, in the sense of a deflection of sexual tension away from the psychical field.

Auxiliary Causes: Any stock noxae - emotion, fright, and also physical exhaustion through illness or over-exertion.

If I consider this aetiological formula for anxiety neurosis in detail, I am able to add the following remarks. Whether a special personal constitution (which need not be produced by heredity) is absolutely necessary for the production of an anxiety neurosis, or whether any normal person can be made to have an anxiety neurosis by some given quantitative increase of the specific factor - this I am not able to decide with certainty; but I incline strongly to the latter view. -Hereditary disposition is the most important precondition for anxiety neurosis; but it is not an indispensable one, since it is absent in a class of borderline cases. -The presence of the specific sexual factor can, in the majority of cases, be demonstrated with certainty. In one series of cases (congenital ones) this factor is not separated from the precondition of heredity, but is fulfilled with the help of it. That is to say, in some patients this peculiarity of the vita sexualis - psychical inadequacy in mastering somatic sexual tension - is innate in the form of a stigma whereas ordinarily it is via that peculiarity that they acquire the neurosis. In another class of borderline cases the specific cause is contained in a contributory one. This is when the psychical inadequacy which I have just mentioned is brought about by exhaustion and such causes. All these cases fall into classes which melt into one another and do not form separate categories. In all of them, moreover, we find that the sexual tension undergoes the same vicissitudes; and for most of them the distinction between precondition, specific and auxiliary cause holds good, in conformity with the solution of the aetiological equation which I have given above.

When I consult my experience on this point, I cannot find that there is any antithetic relation as regards anxiety neurosis between hereditary disposition and the specific sexual factor. On the contrary, the two aetiological factors support and supplement each other. The sexual factor is usually only operative in those who have an innate hereditary taint as well; heredity alone is usually not able to produce an anxiety neurosis, but waits for the occurrence of a sufficient amount of the specific sexual noxa. The discovery of the hereditary element does not, therefore, exempt us from searching for a specific factor. On its discovery, incidentally, all our therapeutic interest as well depends. For what can we do therapeutically about heredity as an aetiological element? It has always been there in the patient and will continue to be there until the end of his life. Taken by itself, it cannot help us to understand the episodic onset of a neurosis or the cessation of a neurosis as a result of treatment. It is nothing but a precondition of the neurosis - an inexpressibly important precondition, it is true, but nevertheless one which has been over-estimated, to the detriment of therapy and theoretical comprehension. To be convinced by the contrasting state of affairs, one has only to think of the cases of nervous diseases that run in families (such as chorea chronica, Thomsen’s disease, and so on), in which heredity unites in itself all the aetiological preconditions.

In conclusion, I should like to repeat the few statements in which I am accustomed, as a first approximation to the truth, to express the mutual relationships between the various aetiological factors:

(1) Whether a neurotic illness occurs at all depends upon a quantitative factor - upon the total load on the nervous system as compared with the latter’s capacity for resistance. Everything which can keep this quantitative factor below a certain threshold-value, or can bring it back to that level, has a therapeutic effect, since by so doing it keeps the aetiological equation unsatisfied.

What is to be understood by the ‘total load’ and by the ‘capacity for resistance’ of the nervous system, could no doubt be more clearly explained on the basis of certain hypotheses regarding the function of the nerves.

(2) What dimensions the neurosis attains depends in the first instance on the amount of the hereditary taint. Heredity acts like a multiplier introduced into an electric circuit, which increases the deviation of the needle many times over.

(3) But what form the neurosis assumes - what direction the deviation takes - is solely determined by the specific aetiological factor arising from sexual life.

Although I am aware of the many still unsolved difficulties of the subject, I hope that, on the whole, my hypothesis of an anxiety neurosis will prove more fruitful for an understanding of the neuroses than Löwenfeld’s attempt to account for the same facts by postulating ‘a combination of neurasthenic and hysterical symptoms in the form of an attack.’

VIENNA, beginning of May 1895.

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