Freud - Complete Works (64 page)

   It is impossible to pursue an
aetiological investigation based on anamneses if we accept those
anamneses as the patients present them, or are content with what
they are willing to volunteer. If syphilidologists still depended
on the statements of their patients for tracing back an initial
infection of the genitals to sexual intercourse, they would be able
to attribute an imposing number of chancres in allegedly virginal
persons to catching a chill; and gynaecologists would have little
difficulty in confirming the miracle of parthenogenesis among their
unmarried lady clients. I hope that one day the idea will prevail
that neuropathologists, too, in collecting the anamneses of major
neuroses, may proceed upon aetiological prejudices of a similar
kind.

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358

   (2) Löwenfeld says further
that he has repeatedly seen anxiety states appear and disappear
where a change in the subject’s sexual life had certainly not
taken place but where other factors were in play.

   I, too, have made exactly the
same observation, without, however, being misled by it. I myself
have caused anxiety attacks to disappear by means of psychical
treatment, improvement of the patient’s general health, and
so on; but I have naturally not concluded from this that what had
caused the anxiety attack was a lack of treatment. Not that I
should like to foist a conclusion of this sort upon Löwenfeld.
My joking remark is only intended to show that the state of affairs
may easily be complicated enough to render Löwenfeld’s
objection quite invalid. I have not found it difficult to reconcile
the fact brought forward here with my assertion that anxiety
neurosis has a specific aetiology. It will readily be granted that
there are aetiological factors which, in order to exercise their
effect, must operate with a certain intensity (or quantity) and
over a certain period of time - which, that is to say, become
summated
. The effects of alcohol are a standard example of
causation like this through summation. It follows that there must
be a period of time in which the specific aetiology is at work but
in which its effect is not yet manifest. During this time the
subject is not ill as yet, but he is predisposed to a particular
illness - in our case, to anxiety neurosis - and now the addition
of a stock noxa will be able to set the neurosis off, just as would
a further intensification of the operation of the specific noxa.
The situation may also be expressed as follows: it is not enough
for the specific noxa to be present; it must also reach a definite
amount; and, in the process of reaching that limit, a quantity of
specific noxa can be replaced by a quota of stock noxa. If the
latter is removed once more, we find ourselves below a certain
threshold and the clinical symptoms depart once more. The whole
therapy of the neuroses rests upon the fact that the total load
upon the nervous system, to which it has succumbed, can be brought
below this threshold by influencing the aetiological mixture in a
great variety of ways. From these circumstances we can draw no
conclusion as to the existence or non-existence of a specific
aetiology. These considerations are surely indisputable and
assured. But anyone who does not think them sufficient may be
influenced by the following argument. According to the views of
Löwenfeld and very many others, the aetiology of anxiety
states is to be found in heredity. Now heredity is certainly immune
to alteration; thus if anxiety neurosis is curable by treatment, we
should have to conclude according to Löwenfeld’s
argument that its aetiology
cannot
reside in heredity.

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359

   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.’

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360

   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.

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361

   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.

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362

   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.