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New article by Edward Shorter: “An Alternative, History-Based, Nosology for Psychiatry”

H-Madness is delighted to present a new piece by Prof. Dr. Edward Shorter, PhD FRSC, the Jason A Hannah Professor of the History of Medicine and Professor of Psychiatry, Faculty of Medicine, University of Toronto. Prof. Dr. Shorter has published widely on the history of psychiatry. His books include the classic A History of Psychiatry: From the Era of the Asylum to the Age of Prozac (Wiley, 1997) and, most recently, How Everyone Became Depressed: The Rise and Fall of the Nervous Breakdown (Oxford,  2013). Here he explores the issue of psychiatric nosology, especially in view of the recent publication of the DSM-V.

An Alternative, History-Based, Nosology for Psychiatry

For their comments on earlier versions, the author would like to thank Tom Bolwig, Bernard Carroll, Max Fink, Gordon Parker, Robert Rubin, Michael Alan Taylor, and Lee Wachtel.

Current efforts to produce a classification of disease have not turned out well.  The fifth edition of the Diagnostic and Statistical Manual of the American Psychiatric Association (DSM-5) was released to general dismay in May 2013.  The current DSM, though vastly influenced by history, pays little attention to it, either in the form of attributing significance to patients’ own histories or in acknowledging the historical diagnostic traditions of psychiatry.

Yet it is possible to take history as our guide in drawing up classifications of diseases.  Here is an analogy: In Traditional Chinese Medicine a sifting process lasting thousands of years has taken place to winnow out effective medications from the ineffective ones lost in the mists of time.  Similarly in psychiatry, a winnowing process of mere tens and hundreds of years has distilled a good deal of the collective wisdom of the profession.  It is, in other words, possible to think about historical diagnoses as having the potential of cutting nature closer to the joints than do current diagnostic systems, drawn up on the basis of whim, fad, and consensus.[1]

There are, in disease classifications, lumpers and splitters. The DSM has taken splitting over the side of the cliff.  Philippe Pinel (1801) was the first lumper. The present effort at classification also is a lumping nosology that tries to discern diseases on the basis of biology and historical integrity. It is not meant to be absolutely inclusive of all psychiatric disorders but to convey some notion of how the main ones should be classified in a way that corresponds better than the present system to natural disease entities. In the absence of definitive biological verifications of many disorders, we have as our guide to “nature” the diagnostic traditions of a century and a half of scientific psychiatry, incubated in Germany and France, and brought today to great blossom in the transatlantic community.

Subsequent versions will need to come to grips with the addictions and the adult dementias.  Personality disorders have not been included.

An Alternative, History-Based, Nosology

 ADULT

I. Acute brief psychosis

II. Neuropsychiatric presentations (eg frontal and temporal dysrhythmia syndromes, Parkinsons, etc.)

III. Chronic psychosis: flat affect with avolition:

(a)—chronic psychosis:  hebephrenia

(b)—chronic psychosis: early progression to personality disintegration

IV. Chronic psychosis: Kraepelin’s disease.  (melancholic syndrome with or without mania; biological markers: DST, cortisol, sleep markers)  This includes such entities as vascular depression.   On a lifetime basis, one should rather think of “para-melancholia,” in which patients are at continuous risk of psychotic complications.

V. Chronic psychosis:  paranoia, meaning well-systematized delusional disorder, without  hallucinations, without disintegration of the personality.

VI. Catatonia.  It may also complicate any of these diseases (biological marker: immediate response to lorazepam)

VII. Non-melancholic, non-psychotic depressive and nervous illnesses

(a) mixed depression-anxiety  (Non-melancholic, non-atypical depression, often accompanied by anxious symptoms)

(b) atypical depression  (Note that this is distinct from the depression of what used to be called “bipolar disorder” and corresponds to the depressive disease described by William Sargant and Donald Klein.)

(c) OCD

(d) phobias

(e) paroxystic anxiety (“panic attacks”) (biological marker: various

panicogens)

VIII. Delirium

IX.  Breakdowns in the mind-body relationship

  X. CHILD

As adult, except for:

—Intellectual disability/learning disabilities

—Autism/catatonia with or without psychosis

—Hyperactivity syndromes (biological marker: abnormal EEG)

—The childhood anxiety disorders, including separation anxiety

Notes

II.  Neuropsychiatric presentations are not in DSM but should be.  There is widespread agreement among clinicians that epilepsy, for example, has its own psychiatric pathology.[2]   One senior American psychopathologist, Michael Alan Taylor, argues that psychiatry has erred seriously in omitting neuropsychiatric indications from the nosology[3], and this should be corrected.  We make an early start here with epilepsy and Parkinsons..

III.  This form of chronic psychosis splits the former “schizophrenia” into chronic psychotic disorders that partially remit, and those that do not.

(NB: positive symptoms may well be present, but they are not essential for the diagnosis of  chronic psychosis.)

“Schizophrenia” has been given here an overdue burial and replaced with several different forms of chronic psychosis that demolish the former firewall between psychosis and affect.  While abolishing the firewall, this nosology does restore the dividing line between “psychosis” and “neurosis,” although the latter term is shunned in favor of “nervous,” or the more modern-sounding but clunkier “non-melancholic, non-atypical depression. “

On the separation of hebephrenia from other forms of chronic psychosis:  hebephrenia does not carry a disastrous prognosis, even though there is no restitutio ad integrum.[4]   Hebephrenia is further distinguished by its onset in adolescence.[5]   In DSM-3 the hebephrenic subtype became the “disorganized type”; it was filled with catatonic symptoms, and was relentlessly progressive, none of which is true of Hecker’s original “hebephrenia.”   The DSM description also perpetuated the myth of the patients being “silly.”  Even though the subtypes have vanished from DSM-5, a disaggregation of “schizophrenia” is long overdue, and this represents a first step.

The term “personality disintegration” is used in the sense of W. Mayer-Gross et al (1954) in preference to the term “dementia.”[6]

IV.  On Kraepelin’s disease, meaning  “melancholic syndrome with or without mania,” this nosology basically restores the unity of Kraepelin’s “manic depressive illness” that he first formulated in the 6th edition of his textbook in 1899, bringing together all the various depressions, of whatever polarity, together with the manias, whether they occurred in the same illness episode or not.  This nosology follows the current of not considering mania and hypomania as separate illnesses[7]; nor are they part of “bipolar disorder,” as the DSM series presents it, because this version of affairs ignores bipolar disorder.

This nosology tackles head-on the issue of the “Kraepelinian dichotomy,” the firewall that Emil Kraepelin constructed between dementia praecox and manic-depressive illness in 1899.[8]  A fundamental issue in the classification of melancholia is whether it belongs under the psychoses or the non-psychoses.  The recent nosological tendency has been to consider psychotic melancholia (psychotic depression) as a rather anomalous subform of  melancholic disease, which, in general, does not involve delusions or hallucinations.[9]  In my view, this issue needs to be re-thought.  The lower boundary of “psychosis” needs to be pushed downward, beneath formal and systematized delusions, to include fixed ideas and highly eccentric notions. It is true that most melancholic patients do not have systematized delusions or hallucinations.  Still, in the words of Tom Bolwig, “They suffer from unjustified feelings of guilt, they don’t accept being ill, and they are unresponsive to all attempts at psychotherapy.  Isn’t that a deficiency in their reality testing, and thus a forme fruste of psychosis?” [10]

On a lifetime basis, psychosis may well be more common in melancholia than has been thought to date (a common assessment is 30 percent – yet the authors Michael Alan Taylor and Max Fink stipulate that an additional number of patients with forme fruste fixed ideas and delusive suspicions should be added on.[11]).  The percent of melancholics who on a lifetime basis may at some point or another be, or have been, psychotic is among the most difficult statistics to nail in the literature, because, as soon as a depressive patient becomes psychotic, the diagnosis is changed to “schizophrenia,” or “schizoaffective disorder.”  It is true that DSM accepts the category “psychotic depression,” but it is quite underused.    (There is also an ascertainment problem.  As one observer pointed out in 1970:  “It is well known that the more we like a patient, the less likely we are to place him on the psychotic end of the psychiatric spectrum.”[12] )

Many European authors considered melancholia basically a psychotic disorder.  As Wilhelm Griesinger noted in the influential second edition of his textbook in 1861, “The core of [the psychic depressive conditions] consists of the pathological prevalence of a distressing, depressive, negative affect.  . . . Corresponding to the mood there then appear false ideas and judgments that have no external basis, true delusions, distressing and painful in content.” [13]   Such authoritative statements continue into the present-day literature as well:  At a conference in 1991 Joseph Zubin  reflected, “Many outstanding diagnosticians first decide whether the patient before them has a psychosis, and then, after that decision is made, go on to determine whether it is schizophrenia or manic-depressive. . . .  Is it possible that what is the basic feature of the illness is psychosis, and that it takes the direction of either manic-depressive psychosis or schizophrenia depending on other factors . . . ?”[14]

In an effort to straddle this as yet unclarified issue of lifetime prevalence of psychosis in melancholic illness, the term “para” has been added to the lifetime version.

On the classification of melancholia, the disorder classically has been said to occur in two versions: (1) anxious, agitated (Angstmelancholie), and (2) stuporous (melancholic stupor).  There is no evidence that these represent separate diseases but are, rather, separate presentations.  There is a body of literature suggesting that psychotic anxiety exists as a separate diagnosis.[15][16]

In the spirit of Kraepelin, mania has been abolished as a separate disease and so there is no “bipolar disorder.”   It makes little sense to classify depressions on the basis of polarity, as the depression of bipolar disorder seems to be melancholic in nature, and identical to the melancholic version of unipolar depression (“major depression”).[17]  DSM-5 now accepts that bipolar and unipolar depression are identical, and calls both “major depression.”

“Major depression,” as well, has not found a place in this nosology on the grounds that it is highly heterogeneous, mixing together melancholic and non-melancholic illness.[18]

On the basis of etiology, there are many “depressions,” such as vascular depression, alcoholic depression, the depression of Parkinson’s, and so forth.  Yet it is unclear that any of these depressions have a distinctive psychopathology not included under either melancholia or non-psychotic nervous disease.  As science elaborates the existence of other distinctive depressions, these should be added to the nosology.   Bernard Carroll has raised a thoughtful objection to letting psychopathology drive the nosology:  “Aren’t you getting it backwards?  Our nosology requires distinctive disorders with distinctive etiologies.  The form of psychopathology is just one plank in the platform, not the main thing.”[19]  One can only respond that this view is indeed correct.  And if we were certain of the distinctive etiologies, we would, of course, let them drive the nosology.  But since we are not quite there yet, driving the nosology with psychopathology is a pis aller.

VII.  The classification of what used to be called “nervous disease” has bedeviled psychiatry for a century and a half, ranging through “nerves,” to “psychoneurosis,” to the current avalanche of micro-diagnoses.  The present nosology tries to lessen reliance on the term “depression,” which has been badly stretched out of shape by overuse.  It has also seemed judicious to revive the classic term “nervous disease,” as has ben recently suggested.[20]  The present version of the nosology seeks a compromise with the use of both terms, depression and nerves.

VII (a) Mixed depression-anxiety has been called “cothymia” by Peter Tyrer.[21]  It was the commonest form of depressive illness (with the exception of the psychoanalytic term “depressive neurosis”) in the decades before the appearance of DSM-3 in 1980, which sundered depression and anxiety.

VII (c-e)  There is no special line in the nosology for adult anxiety, or any of the DSM “anxiety disorders,”  several of which have now been shifted to the nervous category.

On removing OCD from the “anxiety disorders” as classified in DSM-4:  the present nosology argues that OCD be made a “nervous” disease, which simply means a non-psychotic, non-melancholic disorder the proper classification of which will have to await further research.  Patients with OCD do not display the classic somatic symptoms of anxiety, such as racing pulse, dizziness, sweating and tremor, nor the fear and dread of a panic attack.   Rather, the obsessive patient is uneasy and apprehensive about his or her symptoms, while fully recognizing that they are unjustified and unrealistic.

On the omission of PTSD from the nosology:  Traumatic neurosis was first described in the late 19th century, and belongs among the classic “nervous complaints.”  Patients who have experienced severe trauma, in wartime or otherwise, may indeed become symptomatic, but that their symptoms (“the full diagnostic criteria” in DSM terms) first occur after some unspecified duration — which is the essence of “post” — is not at all clear.  The whole diagnosis resulted from a systematic campaign of the Vietnam veterans in the late 1970s, and as a political construct PTSD has little place in a scientific classification of disease.

IX.  Breakdowns in the mind-body relationship:  There needs to be a category for what used to be called “hysteria,” “conversion disorder,” and so forth, symptoms that present in a medical way but are caused by the action of the mind.

Similarly, the personality disorders have been omitted from the nosology as they are considered a holdover from psychoanalysis and may well be abolished in ICD-11.

X.  The classification of childhood disorders poses a special conundrum, because “pure” anxiety without depression is commoner in children than in adults.   Children with “pure” depression more often present as angry.  In the adult section these issues are classified under “mixed depression-anxiety.”

It is now considered possible that hyperactivity has a biological EEG test. [22] This revives Charles Bradley’s original 1938 view of the EEG in hyperactivity.[23]

[1] Shorter E.  “The History of DSM,”  in Making the DSM-5: Concepts and Controversies, ed. Joel Paris and James Phillips.  New York: Springer, 201), 3–19, doi 10.1007/978-1-4614-6504-1_1

[2] Reynolds ED.  Trimble MR.  Epilepsy, psychiatry, and neurology.  Epilepsia, 50 (Suppl 3), 50-55, 2009.

[3] Taylor MA.  Hippocrates cried: the decline of American psychiatry.  New York: Oxford University Press, 2013.

[4] See Ilberg G.  Das Jugendirresein (Hebephrenie und Katatonie).  {Volkmann] Sammlung Klinischerr Vorträge, NF, nr. 67, 1287-1308, 1898. “ganz gut in der Lage, gewohnte Geschäfte zu besorgen.”  (1288)

[5] Taylor MA.  Shorter E. Vaidya NA.  Fink M. The failure of the schizophrenia concept and the argument for its replacement by hebephrenia: applying the medical model for disease recognition.  Acta Psychiatr Scand. 122, 173-183,  2010  doi: 10.1111/j.1600-0447.2010.01589.x.

[6] Mayer-Gross W.  Slater E.  Roth M.  Clinical Psychiatry.  London: Cassell, 1954, 262-264.

[7] Mayer-Gross W.  Slater E.  Roth M.  Clinical Psychiatry.  London: Cassell, 1954, 187f.

[8] Craddock N.  Owen MJ.  The beginning of the end for the Kraepelinian dichotomy.  British Journal of Psychiatry.  186: 364-366, 2005.

[9] Parker G.  Hadzi-Pavlovic D.  Melancholia: a disorder of movement and mood.  New York: Cambridge University Press, 1996.

[10] Bolwig personal communication, 22 July 2013.

[11] Taylor MA.  Fink M.   Melancholia: the diagnosis, pathophysiology, and treatment of depressive illness.  New York: Cambridge University Press, 2006, 16., 55.

[12] Jackson B.  The revised Diagnostic and Statistical Manual of the American Psychiatric Association.  American Journal of Psychiatry.  127: 65-73, 67, 1970.

[13] Griesinger W. Die Pathologie und Therapie der psychischen Krankheiten für Aerzte und Studirende, 2nd ed.  Berlin: Krabbe, 1861,  213.

[14] Zubin J. discussion comment, in Carroll BJ.  Psychopathology and neurobiology of manic-depressive disorders.  In Carroll BJ.  Barrett JE eds.  Psychopathology and the brain.  New York: Raven Press, 1991, 265-285, 283.

[15] Shorter E.  How everyone became depressed: the rise and fall of the nervous breakdown.  New York: Oxford University Press, 2013, 72-75.

[16] Stransky E.  Zur Lehre von der Amentia.  Journal für Psychologie und Neurologie. 6: 37-83, 155-191, 1906, see 163. “hochgradiger Angstparoxysmus.”

[17] Taylor MA.  Vaidya NA.  Descriptive psychopathology: the signs and symptoms of behavioral disorders.  New York: Cambridge University Press, 2009, 383.

[18] Parker G.  Beyond major depression.  Psychological Medicine.  35: 467-474. 2005.

[19] Bernard Carroll personal communication to Edward Shorter, 20 July 2013.

[20] Shorter E.  How everyone became depressed: the rise and fall of the nervous breakdown.  New York: Oxford University Press, 2013.

[21] Tyrer P.  The case for cothymia: mixed anxiety and depression as a single diagnosis.  British Journal of Psychiatry.  179, 191-193, 2001.

[22] Arns M. et al.  EEG phenotypes predict treatment outcome to stimulants in children with ADHD.  J Integrative Neurosci, 7, 421-438, 2008.

[23] Jasper HH.  Solomon P.  Bradley C.  Electroencephalograhic analyses of behavior problem children.  American Journal of Psychiatry, 95, 641-658, 1938.

For a more detailed bibliography of his work, click here.

How Depression Went Mainstream: Interview with Dr. Edward Shorter

George Mason University’s History News Network features a recent article entitled “How Depression Went Mainstream”. In the piece, Robin Lindley interviews renowned psychiatrist and historian of psychiatry Dr. Edward Shorter, who talks about his new book How Everyone Became Depressed: The Rise and Fall of the Nervous Breakdown (Oxford University Press):

Every year, more and more Americans are treated for complaints of depression and often do not derive relief from treatment for their symptoms that may include anxiety, fatigue, poor sleep, and physical problems.

According to acclaimed historian of psychiatry, Dr. Edward Shorter, the diagnosis of depression has increased steadily over the past forty years and, during our lifetimes, “one American in five will receive a diagnosis of depression.” That’s more than sixty million people.

To read the entire article, click here.

Scientific American blog: “Trouble at the Heart of Psychiatry’s Revised Rule Book” (Edward Shorter)

Edward Shorter, Hannah Professor in the History of Medicine and Professor of Psychiatry at the University of Toronto (and recent contributor to our new How I Became a Historian of Psychiatry series), wrote a piece for the Scientific American blog which was published on Wednesday.

The article, entitled “Trouble at the Heart of Psychiatry’s Revised Rule Book“, deals with the DSM and starts thus:

One might liken the latest draft of psychiatry’s new diagnostic manual, the DSM-5, to a bowl of spaghetti. Hanging over the side are the marginal diagnoses of psychiatry, such as attention deficit hyperactivity disorder and autism, important for certain subpopulations but not central to the discipline.

At the center of the spaghetti bowl are the diagnoses at the heart of psychiatry: major depression, schizophrenia, bipolar disorder.

To read the entire article, click here.

How I became a historian of psychiatry: Edward Shorter

For the second installment of the “How I became a historian of psychiatry” series, Edward Shorter, Hannah Professor in the History of Medicine and Professor of Psychiatry at the University of Toronto, author among others of A History of Psychiatry from the Era of the Asylum to the Age of Prozac (1997) and From Paralysis to Fatigue: A History of Psychosomatic Illness in the Modern Era (1992), kindly shares his intellectual biography with the H-Madness community:

This story began in 1967 when, a fresh young history PhD graduate, I came to the University of Toronto.  I had been trained as a social historian and after several projects far away from the history of medicine, in 1975 I wrote a general history of the family, not that it was such a medical contribution – but it called my attention to a number of medical issues in the lives of women historically:  infected abortion, weariness from overwork, and iron-deficiency anemia.  This led to a history of women’s health care (Women’s Bodies) in 1982.  This was full-blast medical history, but researching it made me aware that I knew almost nothing of medicine.  So I went to medical school for two years, taking all the basic medical sciences.

I now felt better equipped to take on a big problem: the history of psychosomatic illness, especially “hysteria,” mainly in women, over the centuries.  Knowing something about medicine was helpful here because of the difficulty in sorting out symptoms that are psychogenic (“hysteria”) from those that are organic-medical, such as endometriosis, often dubbed “hysterical” in the past.  This research resulted in From Paralysis to Fatigue (1992).

I was now thoroughly enmeshed in psychiatry, and went on to write a general history of the discipline, which appeared in 1997 and was read by a number of psychiatrists.  I became friendly with several whose work I greatly admired, and who subsequently influenced the direction of my own studies, in particular David Healy, Max Fink, Bernard Carroll, Tom Ban, Tom Bolwig, and Gordon Parker.  Animated email exchanges with this group produced a sharp research interest on my part in two themes: the history of diagnosis (nosology), and the history of psychiatric medications (psychopharmacology).  This led to a string of publications: A History of Shock Therapy, with David Healy (2007), Before Prozac (2009), and Endocrine Psychiatry; Solving the Riddle of Melancholia (with Max Fink) in 2010.  My latest book, The Rise and Fall of the Nervous Breakdown – And How Everyone Became Depressed, will be published by Oxford early in 2013.  I should say that among contemporary historians of psychiatry there are also several whose work I have learned from, in particular Patrizia Guarnieri and Ian Dowbiggin.  Everyone in our field learned from Roy Porter.

There are two points of more general interest in this cascade of self-esteem: (1) Historians of psychiatry have a real contribution to make to clinical psychiatric diagnosis, subject as it is to the buffeting of fashion and fad; that contribution lies in surveying the enormous historical experience of psychiatry to see which diagnoses seem to correspond most closely to natural disease entities.  (2) Psychiatric historians also have a contribution to make to therapeutics, because many past therapies have been discarded not because they were unsafe or ineffective, but because the patents expired!  Or because (as in the case of electroconvulsive therapy) society turned against them for non-scientific reasons.  Or because, as in the case of the barbiturates, makers of newer drug classes scorned them in advertising as old-fashioned and risky.

Among my current interests are pediatric catatonia and self-injury behavior in autism, and the extent to which they have been relieved in the past with ECT; the early “tranquilizers” and sedatives, discarded as effective treatments largely because of psychiatric urban myths of various kinds; and melancholia as a distinctive illness in its own right with characteristic biological markers.  I find this research tremendously exciting, and hope that historian colleagues will become involved. 

Many thanks, Edward Shorter, for sharing this story!

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