This French thread of refining anxiety reached a final way station in 1901 with Paul Hartenberg’s creation of the diagnosis of timidity, today called social phobia, the last of the anxiety syndromes to spin off before Janet closed the discussion with psychasthenia—and Freud’s “anxiety neurosis” then reunified the anxieties. Hartenberg, who specialized in the walking wounded with their various anxieties and phobias, believed timidity to be a distinctive disorder: “The emotion of timidity seems to be a combination, in varying proportions, of fear and shame.” To emphasize its distinctive nature, Hartenberg did not use the term anxiety. To be sure, “The patient’s emotions … are revealed in palpitations, anguish, a cold sweat.” “And when does this emotion surface? In a unique circumstance, in the presence of a human being.”
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The “crises” of timidity sounded very much like panic, and the background emotional symptoms seemed very much like garden-variety anxiety, but once the carving up of anxiety has begun there is really no stopping it, as we know today, because it is so difficult to prove that a given combination of symptoms is not a disease of its own.
Then the carving up of anxiety stopped. Pierre Janet, a student of Jean-Martin Charcot’s with his own psychological laboratory at the Salpê tri ère Hospital, put a cap on the whole anxiety discussion in 1903 when he announced that there was only one underlying nonpsychotic disorder, and it was psychasthenia. Obsessions, compulsions, and phobias were all psychasthenic in nature, the result of a weakened will, or aboulia, that permitted such disordered behavior to break through. Janet had been trained as a psychologist, but then Charcot encouraged him to study medicine and Janet became a psychiatrist. In his laboratory Janet, 44 years old in 1903, saw a long series of obsessional patients, including a man of 52 whom Legrand had treated 20 years previously. (Legrand had apparently been quite forceful with him and had shoved him around and shaken him up.) The patient had not, however, recovered from his agoraphobia and here he was at the beginning of the new century unable to cross squares and fearing instant death. “When he approaches a square, he shakes himself, he breathes laboriously, he displays his tics, and he repeats this absurd phrase, ‘Maman, ratan, bibi, bitaquo, je vais mourir [I’m going to die].’”
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Summing up, Janet said that although neurasthenia represented physiological insufficiency, in psychasthenia, the insufficiency was psychological, including “phenomena of abulia [lack of will], aprosexia [inability to sustain attention], indifference, and the apathy that we have frequently studied, all as diminutions of the sense of reality. We understand by this term psychasthenia, the totality of psychological functions that play the principal role in the precise adaptation of the individual to a given reality.” And what were those positive qualities that psychasthenia negated? “The will, attentiveness, the belief in that which exists in the present, pleasurable or painful sensations—all in rapport with this reality.”
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We sometimes have the feeling that Janet has been deprived of his fair place in history, marginalized by Freud’s much grander but much more fanciful ideas. In understanding nervous disease, this might have been a point of departure, but the opportunity passed and the world moved on.
The bottom line is that there are forms of anxiety that occur together with other symptoms, such as depression and fatigue, historically recognized as the nervous syndrome. There are forms of anxiety that occur in the guise of panic, in obsessions, compulsions, and phobias. In their severe form, the public would consider them part of the nervous breakdown. Freud, like Janet, asserted that there was but a single anxiety. Yet like the horse galloping out of control, he took this bit in his teeth and ran away with it.
In the 1890s several Central-European clinicians argued that anxiety and anxiety attacks were among the commonest symptoms of neurasthenia.
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This literature has now been forgotten because the attention of historians has been fixed upon one of these investigators (whose main contribution was in quite a different area, hebephrenia), simply because Freud rather ruefully identified him as having been the first to describe anxiety neurosis. This was Ewald Hecker, whom we met doing the spa treatment of nerves and who by 1893 had moved his water-cure institute from a small village on the Rhine River to Wiesbaden. At a meeting of the Southwest German Psychiatric Association in Wiesbaden in November 1893, Hecker argued for the existence of “atypical anxiety conditions” in neurasthenia. In neurasthenia, “anxiety attacks” (Angstanfälle) could occur either sporadically or chronically. Hecker said that for a number of years he had been calling attention in neurasthenia to anxiety equivalents (larvierte Angstzustä nde), such as asthma or dizziness, that are “present in well defined attacks without being accompanied by mental feelings of anxiety.”
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This observation would probably have perished in oblivion—for it was obvious that nervous patients had all kinds of somatic symptoms without necessarily feeling anxious—had Freud not picked it up.
In 1895 Sigmund Freud, a young Viennese neurologist of 39 years, truly did describe an independent anxiety syndrome, which he called “anxiety neurosis,” arguing that it was separate from neurasthenia. Among the characteristics of this new neurosis were general irritability, anxious anticipation of dreaded future events, somatic anxiety attacks such as pounding heart, and the kinds of anxiety-equivalents that Hecker had suggested, among other symptoms. Freud’s account of anxiety neuroses was clinically shrewd, psychologically astute, and kicked neurasthenia over the side. Freud did write, “I am calling this symptom complex [syndrome] ‘anxiety neurosis’ because all of its components may be grouped around the chief symptom of anxiety. I had imagined that my conception of the symptoms of anxiety neurosis was quite original until an interesting lecture by E. Hecker crossed my desk, in which I found my particular interpretation laid out with clarity and completeness.”
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(It is unimportant that Hecker had not done this at all. Yet Freud was showing himself to be a generous colleague in giving Hecker, a water-cure-institute doctor, so much credit.)
Three years later, in an 1898 essay on “Sexuality in the Etiology of the Neuroses,” Freud explained that anxiety and neurasthenic neuroses alike were “actual neuroses,” caused by current sexual events in the patient’s life, while obsessive-compulsive phenomena and hysteria were “psychoneuroses,” caused by sexual events in development. Neurasthenia was caused by excessive masturbation and anxiety neurosis by coitus interruptus, abstinence, or frustrated arousal.
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These were concepts that had an enormous impact, not just on psychiatry but on western society. It took a while for them to be picked up, in these and Freud’s subsequent writings. But by the decade before World War I, anxiety neurosis had become a common diagnosis. In the United States, some of the great names in neurology—it was then the neurologists who did private-practice psychotherapy—seized upon anxiety neurosis. In 1912 Smith Ely Jelliffe, a professor of neurology in the New York Post-Graduate Medical School, reviewing patients recently seen in their outpatient clinic, said, “Some of our cases of menopause psychoneuroses are probably anxiety neuroses. The increase of the libido … accounts in large part for many of these cases. The histories are too direct and to the point to permit dodging the Freudian conceptions of these states notwithstanding one’s reluctance to accept an idea which at first sight seems far fetched.”
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In Zurich, Ludwig Frank, who had a psychiatric private practice and at age 50 was no inexperienced shave-tail, wrote at length in 1913 about “anxiety neuroses and the suppression of the libido.”
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After the war he developed a whole scheme of “thymopathies,” meaning anxiety, inhibition, feelings of inferiority, and other “dysphorias.”
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In Paris, society nerve doctor Paul Hartenberg gave anxiety neurosis (la n évrose d’angoisse) huge play in 1901, bringing anxiety from the wings onto center stage.
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The English have always been cool to psychoanalysis, yet Aubrey Lewis, an Australian who came over from a U.S. post to join the Maudsley Hospital in 1928, held the opinion that whatever interest his colleagues had been able to muster in anxiety was largely due to the influence of Freud. He said in 1971 that “There can be little doubt that the attention paid to anxiety in the last ten years or more has been largely due to the adoption of Freudian concepts and … of Freudian metapsychology.”
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In other words, the impact of Freud’s anxiety neurosis on international psychiatry was immediate and profound. As Freud’s acolyte Wilhelm Stekel said in 1936, just 2 years before he was forced to emigrate from Vienna to London, where he died by suicide in a lonely hotel room, “The picture of neurosis has changed extraordinarily in the course of recent decades. Hysteria has almost disappeared, obsessive-compulsive neuroses and organ neuroses, anxiety conditions, schizophrenia and disturbances of affect have stepped into the foreground.”
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Indeed, the revival of anxiety was part of a larger pivot of diagnosis from hysteria and neurasthenia to disturbances of mood and affect. In doing so, nervous illness too was left behind. Freud himself had almost no interest in fatigue.
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And he considered neurasthenia too uninteresting for words.
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The tradition of identifying anxiety with unconscious Freudian processes lasted long in American psychiatry. In 1971, in an effort to grab the attention of a psychiatric audience still more fixed upon Freud than psychopharmacology, the Hoffmann La Roche company flogged its drug Librium as good for anxiety using the psychoanalytic formulation, “The most characteristic and common feature of neurotic habits is anxiety.”
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The Freudian triumph of anxiety was almost complete.
Were all these new diagnoses pretty much of a muchness, or not? Were serious anxiety and melancholia diseases of their own, or did they merge imperceptibly into all the other diseases? Were illnesses such as melancholia a different order of magnitude from less severe diagnoses of the nervous syndrome, or does it all blend together? The English poet Thomas Grey, then 26 years old, took the two-level approach, though he would not have formulated it in those terms, when contemplating his own symptoms. The two levels existed within him. As he wrote to classmate Richard West in 1742, “Mine, you are to know is a white melancholy … which though it seldom laughs or dances, nor ever amounts to what one calls joy or pleasure, yet is a good easy sort of a state, and ç a ne laisse que de s’amuser [stops me just short of enjoying myself ]. The only fault of it is insipidity [lifeless, dull, flat]; which is apt now and then to give a sort of ennui, which makes one form certain little wishes that signify nothing.” So here Gray is telling West that he feels mildly dysphoric from time to time and even toys with suicide; from other letters it is clear that he is a bit anxious on occasion, but nothing more really; he might have accepted that at moments he was nervous.
Gray continues: “But there is another sort, black indeed, which I have now and then felt … for it believes, nay, is sure of every thing that is unlikely, so it be but frightful [meaning he is delusional]; and, on the other hand, excludes and shuts its eyes to the most possible hopes, and every thing that is pleasurable; from this the Lord deliver us!”
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This black melancholy, in other words, brings paranoia, anhedonia, and hopelessness with it, all symptoms of melancholia. Gray did not experience these different illnesses as a continuum; he did not have them both at the same time; but both dwelt within his breast.
At a meeting of the British Medical Association in 1926, swords clashed less poetically over the same issue. Edward Mapother, the superintendent of the recently opened Maudsley Hospital, England’s premier academic center for the study of psychiatric illness, expressed dubiety about the wisdom of drawing sharp lines. He said it could happen that Freud’s new diagnosis of anxiety neurosis might easily “merge in the same patient, and by a perfectly continuous gradation in a series of patients, into agitated melancholia.”
Robert Dick Gillespie, a brilliant young clinician and scientist at the Cassell Hospital at Penshurst and known as “R.D.,” was in the audience. Gillespie said that melancholia and anxiety neurosis had little overlap. “Who had heard of a melancholic of the manic-depressive type who was well and at ease while he sat in the garden, but was plunged into misery when he returned to the drawing-room? [in other words, manic-depression was a chronic illness not relieved by an afternoon of sun in the garden but anxiety could be dependent on the situation] Dr Gillespie had at the present time a patient with such an anxiety state.”
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Clearly, there were forms of depression, such as Kraepelin’s manic-depressive illness, the depression of which was melancholic, that differed not just in degree but in kind from the anxiety and depression of nervousness. As we watch anxiety liberating itself from melancholia, we keep in mind that some of this new freedom was justified and some was an arbitrary shattering of a real nervous syndrome: Agitated, anxious melancholia was, and is, a real disease.
There are different kinds of paroxystic anxiety, of anxiety attacks, and of panic disorder that sweep over the individual with hurricane-like force. The classic authors tended more to sense this rather than characterizing it neatly, and terms such as “anxious melancholia” and “anxiety psychosis” abound in the literature. Some of this extreme anxiety may be psychotic, involving delusions and hallucinations, and other forms may not. My purpose here is to acquaint readers with a clear historical strain that we have forgotten today and that comes as close to a complete nervous breakdown as anything we encounter in these pages. Readers may judge for themselves whether this is a separate diagnostic entity or not.