(In answer to Janet Wilson's question "What happened to neurasthenia?" in the Spring 1998 edition of Emerge)


The answer is somewhat complex but, in short, it fell into disuse.

George Beard, a neurologist, had first described- neurasthenia in 1869 and considered it due to the sufferer's commitments literally over- taxing the nervous system beyond that individual's capacity to do so without adverse consequences. Unlike what was to follow, Beard recommended a regimen of rest, in bed or even hospital if necessary, nourishing food, general TLC from relatives, and consideration from employers.

A good description of the historical development of this syndrome can be found in Sicherman (1977). Wessely (1990) is also worth a look, and a good description of the treatment of the time can be found in Musser and Kelly (1912).

From the sufferer's point of view the situation was reasonably satisfactory, as both diagnosis and treatment were available, and even an explanation; sufferers had exceeded their constitutional limitations. A collection of psychological and physical symptoms were satisfactorily explained, with no real stigma attached to the former.

Unfortunately, a number of factors conspired to change this. Firstly, syndrome began to be seen as over-inclusive; doctors thought there were too many symptoms (and therefore probably multiple conditions) being included under the heading of neurasthenia.

Secondly, of these symptoms a fair number occurred in conditions classifiable as psychological, and in any case no less an authority than Sigmund Freud also considered neurasthenia a neurosis.

Thirdly, during the Great War military personnel were invalided out with similar symptoms but labelled "battle neurosis". Unfortunately, this led to this particular syndrome to be classified as a form of hysteria, thus stigmatising its symptoms.

Fourthly, despite the various outbreaks of the syndrome around the world since then, the laboratory science medicine increasingly relied upon has until recently failed to find any distinctive signs of a biological cause.

As a consequence of all this, although the term neurasthenia was used into the twentieth century, it became a hazy concept which largely fell out of use, having little perceived value as a syndrome after about 1920. But lack of evidence of biological involvement has allowed the term itself to languish in the psychiatric domain.

It would be nice to be able to say that biological findings now being made portend the identification of causes and treatments, but that does not seem to be the case. Findings of all sorts are written up, queried, often not confirmed, and not infrequently ignored. Explanations for CFS/ME are put forward in terms clearly reflecting the specialisations of the authors and sometimes with inadequate regard to symptoms, other findings, or even what sufferers say about their condition. Much of this is par for the course in scientific research, though the last should not be.

It is irritating, of course, that no-one seems to be attempting an overview of findings to see what links can be forged between them both to construct a workable hypothesis and to set aside (but not forget entirely) those which do not seem to fit. It makes the neurasthenic model seem very attractive, especially where treatment is concerned, and it is not surprising that many sufferers turn to unconventional medical and complementary medicine treatments as at least attempting to do something other than just "manage" a condition currently not curable by conventional medicine.

References:
MUSSER, John H. & Kelly, O.A., (eds.) (1912), 'A Handbook of practical Treatment" (Meridian Institute's website at http://pages.prodigy.com/MeridianInstitute/neurasth.htm).

SICHERMAN, Barbara, (1977), "The Uses of a Diagnosis: Doctors, Patients, and Neurasthenia", Journal of the History of Medicine, Vol 33-54.

WESSELY, Simon (1990), "Old Wine and New Bottles - Neurasthenia and ME", Psychological Medicine, vol. 20, pp 35-53.

Reprinted from Emerge, Summer 1998