02/19/19

The Death of Melancholia, Part 2

© Jason Salmon | 123rf.com

Dr. Bernard Carroll died of lung cancer on September 10, 2018.  The New York Times heralded him as the “conscience of psychiatry,” but the work that brought him that label happened later in his professional career. At the youthful age of 28, he published a paper, “Resistance to Suppression by Dexmathasone of Plasma 11-O.H.C.S. Levels in Severe Depressive Illness,” that essentially argued there was a “blood test” for severe depression. The dexamethasone suppression test (DST) measures the body’s ability to suppress cortisol, a stress hormone. But it was too late. Melancholia had already died at the hands of Emil Kraepelin.

In a 1968 article in the British Medical Journal, Dr. Carroll announced that when the test was administered to people with the severest species of depression — a paralyzing gloom then called melancholia, or endogenous depression — their bodies were shown to have trouble suppressing the hormone. People with other kinds of mood disorders had normal scores.

He thought it could be a confirmatory test for a diagnosis of depression—not as a way to actually make a diagnosis in the first place. But nothing happened. The DSM was in the midst of an extreme makeover as psychiatry fought for survival (See “The Quest for Psychiatric Dragons” Part 1 and Part 2 for more on this). Its architects weren’t interested in two distinct kinds of depression. Melancholia was lumped into “major depression” with several other mild and moderate disorders. Edward Shorter said:

Barney’s application of the DST to serious depressive illness was a huge step forward in establishing a biological base for serious depression. . . . It identified a biologically homogeneous group of serious depressives that could then be studied with the tools of molecular biology . . . . [But] the DST was pushed aside before anyone had a chance to do this, and one of the few biological tests in psychiatry has since then lain fallow.

Melancholia had successfully separated from the Hippocratic theory of humors by the late nineteenth century, and was gathering credibility as a distinct mood disorder. However,  “Emil Kraepelin … killed off melancholia and prompted its replacement with depression.” In How Everyone Became Depressed, Edward Shorter carefully documented how this took place between the fourth and eighth editions of Kraepelin’s book, Psychiatry: A Textbook for Students and Physicians. By 1913 Kraepelin had convinced himself that what were presented as separate illnesses were instead “a single disease process.”  He said: “It is, as far as I know, entirely impossible to discern any particular boundaries among these individuals clinical pictures, that until now have been separate.”

Shorter said Kraepelin’s influence in renaming melancholia “depression” was enormous. But alone, it was not enough to explain how “everybody became depressed.” Freud and the influence of psychoanalysis upon American psychiatry would also play a crucial role. Ironically, Freud had little interest in depression and only wrote about it within one paper, “Mourning and Melancholia” in 1916. It was one of his disciples, Karl Abraham, who wrote about depression as a neurosis, rather than about melancholia or manic-depression. Abraham thought depressive affect to be as widespread as anxious affect, with both conditions often occurring in the same person. “This was the beginning of neurotic depression as a diagnosis separate from the other big depressive illnesses.”

Otto Fenichel then became a central figure in the acceptance of neurotic depression among psychoanalysts. In his book Outline of Clinical Psychoanalysis, written in 1933, he commented how all varieties of neuroses could develop depression. After moving to Los Angeles in 1938, his revised and expanded edition said: “Neurotic depressions are desperate attempts to force an object to give the vitally necessary [narcissistic] supplies, whereas in the psychotic depressions the actual complete loss has really taken place and regulatory attempts are aimed exclusively at the superego.”

To understand why depression became such a huge diagnosis, we thus have the role of psychoanalysis, the thread that begins with Karl Abraham and passes through the émigré analysts, to make depth psychology such a popular conveyor belt for neurotic depression. It is almost unimaginable to us today that psychoanalysis once represented the very heart and soul of psychiatry.

Meticulously, Shorter then traced the wanderings of neurotic depression through the maze of psychoanalysis and its importance to American psychiatry. Depression had become a significant diagnosis by the time of World War II. “By World War II depression had become the standard term for any accumulation of symptoms involving fatigue, anxiety, and so forth. But this was a depression that was far from melancholia.” Many of the patients who received the diagnosis did not appear depressed. A psychiatrist at the University of Toronto said in 1952: “An outstanding feature of mild depression is that the patient rarely complains of feeling depressed and often does not appear particularly despondent.”

Then in 1974 the American Psychiatric Association chose Robert Spitzer to chair the Task Force to revise the DSM-II. He was a junior figure who at the time had developed an interest in the classification of psychiatric disorders. Shorter said he had little exposure to clinical psychiatry “and did not have that deep intuitive understanding of psychological illness that many senior clinicians acquire.” His strong will and determination to impose his own ideas infuriated other Task Force members and made him difficult to work with. Melvin Sabshin said:

Dr. Spitzer had had an immense degree of effort and dedication to the process of developing a new nomenclature. The problem in that, however, has been that Dr. Spitzer has not necessarily thought through how one goes about educating psychiatrists or other mental health professionals and is so exceedingly sensitive to any negative input (to which he responds as if there were an attack on his knowledge, integrity, etc.) that it is difficult to deal with him.

Shorter said Spitzer saw himself in a political, not a scientific battle in formulating the DSM-III. The goal was to win, not necessarily to establish scientific exactness. Above all he wanted to triumph over the despised psychoanalysts. He was determined to exterminate the diagnosis neurotic depression, which had become a favorite of the analysts. “He negotiated a number of political concessions that made little scientific sense.”

Spitzer had collapsed the two depressions of melancholia and nonmelancholia, in use in psychiatry for over two centuries, into a single depression, called major depression, and ensured that it was the only diagnosis you could get into unless you were seeing a psychoanalyst and could qualify for neurotic depression. Major depression, often simply called “depression,” went on to become the diagnosis of one-tenth of the United States population.

Max Fink, one of the pioneers of biological psychiatry commented on the paradigm shift from manic-depression to major depression: “When it was manic depressive illness, it was a small number of people. When it became major depression . . . 50 percent of the people are depressed. That’s absurd. That means there’s something wrong with the label.”

02/12/19

The Death of Melancholia, Part 1

© Kelly VanDellan | 123rf.com

Being depressed is experiencing five or more of nine diagnostic criteria within a two-week period of time. And despite other mood disorders like bipolar disorder, dysthymic disorder, cyclothymic disorder or depressive disorder NOS, (not otherwise specified), there is not a clear distinction between these kinds of depression. The older conceptualization suggested we had a problem of nerves—that it was an illness of the entire body. But according to Edward Shorter, “The current classification is a jumble of nondisease entities, created by political infighting within psychiatry, by competitive struggles in the pharmaceutical industry, and by the whimsy of the regulators.”

Today, with the ubiquity of the diagnosis of depression, we have the idea that low mood and an inability to experience pleasure are our main problem; we see ourselves as having a mood disorder situated in the brain and in the mind that antidepressants can correct. But this is not science; it is pharmaceutical advertising.

Depression is conceptualized and presented as if it exists on an interval scale, ignoring the possibility it may be two or more disorders overlapping one another. In How Everyone Became Depressed, Edward Shorter persuasively advocated that there are two kinds of depression, “as different as tuberculosis and mumps.” He said it made no sense to lump them together under the general term of “depression.” The first kind of depression was nonmelancholic and nonpsychotic, “heavily admixed with anxiety and fatigue.” It is laced with obsessive thinking and often overcome by somatic complaints. The second kind of depressive disorder was melancholia:

It is an independent and unmistakable disease entity, often not combined with anything, and fearsome in a far different way than nervousness, for it may lead to despair, hopelessness, a complete lack of pleasure in one’s life, and suicide. By the late nineteenth century, the difference between these two depressions lay clear in view and observers often distinguished between them. Subsequently, both swim out of focus; nervous disease is broken up, and what we have emerged with today as “depression” bears little resemblance to these historic ancestors.

According to Shorter melancholia is a disease of the whole body. “The endocrine system is intimately involved, and the blackness of affect reaches into the adrenal gland.” Affect is profoundly flattened. Stupor and dejection can alternate with periods of agitation. Oswald Bumke said in 1908, “The essential characteristic of melancholia is a sadness of mood that is not founded in external circumstances, a strongly depressive affect, from which a gloomy assessment of one’s own situation arises, as well as ideas of having sinned in the past and anxious fears about the future.”

Melancholia appears to be sadness, but is often described by patients as pain. A Florida psychiatrist said, “Most of my patients suffering from major depression have described their malady as the worst pain they have had to beat.” Melancholics often look dejected. They have empty eyes and frozen features. They also have slowed thought and movement—psychomotor retardation. “All movements are conducted slowly, any change of bodily position is avoided; the speech is soft, halting and limited to what is absolutely necessary.”

Melancholics at risk of suicide can be difficult to assess because they complain of everything but their mental pain. Shorter suggested it could be that admitting depression in these circumstances “would cause others to thwart your desire for suicide.” In 1911 The New York Times described a doctor at St. Francis Hospital in Pittsburgh who was suffering from a complete nervous breakdown. After shaving under supervision, he asked a male nurse to accompany him to a bathroom and when there, sent the man on an errand. The man had concealed a razor in his pajamas.  A few minutes later a doctor saw a stream of blood running from under the door. “Dr. Miller was found with his throat cut from ear to ear.”

What emerges from the stories of melancholic patients is how different they are from patients with nervous disease. This is not a continuum of gravity that begins with the mildly nervous and ends with patients curled into a fetal ball, but a discontinuity as two different kinds of illness somehow end up with depression as their name. Melancholia was not neurotic depression.

Shorter said from the seventeenth century medical writers have described melancholia similar to what was said here. This suggests that we are dealing here with a relatively unchanging biological type, according to Shorter. Other psychiatric illnesses seem to be influenced by personal beliefs and social attitudes. However, in medical writing what changes historically is the distinction of melancholic depression from other kinds. “But the basic melancholic prototype has been visible from the beginning.”

Shorter reserves a distinct, biological niche for melancholia and it seems to fit within a modern dispute over the effectiveness of antidepressants with more severe cases of depression. The melding of melancholia into depression brought about confusion with diagnosis and generated the “jumble of nondisease entities,” which we will examine in the second part of this article. I suggest first that we should look back to the origins of the term and how it too has changed its meaning over time.

Melancholia stems from the Greek melan (black, dark) and chole (bile). Medical practitioners once thought the human body had a system of humors—bodily fluids that included black bile, yellow bile, blood and phlegm. An imbalance of the humors was thought to result in sickness of the body and mind. An excess of black bile (thought to be secreted by the kidneys or spleen) meant the person could become unsociable, liable to anger, irritable, brooding and depressed.

Telles-Correia and Gama Marques said in “Melancholia before the twentieth century” that Richard Burton commented in his 1621 book, The Anatomy of Melancholy, on the confused state of melancholia: “The tower of Babel never yielded such confusion of tongues as the chaos of melancholy doth variety of symptoms.” The authors went on to note Hippocrates (460-379 BC) attributed melancholy to the excess of black bile, which was characterized by several symptoms, including fear and sadness. Galen (129-216 AD) followed Hippocrates in his theory of the four humors, but saw melancholics also having what we would call delusions. Aretaeus of Cappadocia (1st century AD) also saw melancholy as having a delusional element. Andreas Laurentius (1560-1609) followed Galen and Hippocrates in seeing it was caused by an excess of black bile and saw melancholics having “a disturbed imagination.”

Richard Burton (1577-1640) began to move away from the humor theory of depression and likened the task of gathering the meanings of melancholia to “capturing [a] many-headed beast.” While people suffering from melancholia present with multiple symptoms, the most frequent are fear and sorrow. He defined melancholy as follows:

Melancholy, the subject of our present discourse, is either in disposition or in habit.  In disposition, is that transitory Melancholy which goes and comes upon every small occasion of sorrow, need, sickness, trouble, fear, grief, passion, or perturbation of the mind, any manner of care, discontent, or thought, which causes anguish, dulness, heaviness and vexation of spirit, any ways opposite to pleasure, mirth, joy, delight, causing forwardness in us, or a dislike. In which equivocal and improper sense, we call him melancholy, that is dull, sad, sour, lumpish, ill-disposed, solitary, any way moved, or displeased. And from these melancholy dispositions no man living is free, no Stoic, none so wise, none so happy, none so patient, so generous, so godly, so divine, that can vindicate himself; so well-composed, but more or less, some time or other, he feels the smart of it. Melancholy in this sense is the character of Mortality… This Melancholy of which we are to treat, is a habit, a serious ailment, a settled humour, as Aurelianus and others call it, not errant, but fixed: and as it was long increasing, so, now being (pleasant or painful) grown to a habit, it will hardly be removed.

Phillipe Pinel (1745-1826) abandoned the humoral theory entirely and favored a more descriptive psychopathology. He narrowed the field of mental disorders into four groups: Melancholia, Mania, Idiocy and Dementia. For Pinel, melancholia had two opposite forms, seemingly describing what we now call bipolar disorder. The first sense was “a heightening of pride and the chimeric idea of possessing infinite richness and power without limits.” And the second form was “the most fearful despondency, a profound dejection or even despair, therefore considering two forms of melancholia: depressive and expansive.”

In the beginning of the twentieth century the term melancholia was replaced by the term depression, largely under the influence of Emil Kraepelin. Today it carries some significance with certain cases of severe depression, but is known as endogenous depression—not a distinct kind of depression. Melancholia (endogenous depression) is characterized by profound sadness, anhedonia, a loss of emotional resonance, insomnia, anorexia, motor retardation, circadian variability in mood, and the presence of delusions and/or hallucinations. In Part 2 we will look at how Emil Kraepelin and Robert Spitzer finally “killed off” melancholia as a separate disease from depression.