In response to scientific and clinical criticism of the Diagnostic and Statistical Manual, the National Institute of Mental Health has developed a different kind of classification system for use in research, one that takes into account the rapidly accumulating findings from genetics, neuroimaging, molecular biology and neuropsychology. The system, the Research Domain Criteria, seeks to integrate data from patterns of gene expression, epigenetics, protein and signaling data, and brain circuits and physiology into higher-order systems of cognition, motivation, and social behavior. These new criteria, with their emphasis on mechanisms and dimensions, reflect the important reality that the symptoms of mania and depression overlap with other psychiatric syndromes and that they exist on a spectrum of behavioral and cognitive functioning that includes physiological variation in mood, activity, motivation, impulsiveness, and disruptions in circadian rhythm.
Diagnostic and research classification, together with our basic understanding of psychiatric genetics, structural changes in the brains of patients with mood disorders, and how the brain functions during mania and depression, is advancing rapidly. They are the future of clinical practice and an important part of our understanding of the brain. They hold profound implications for treating and understanding not only mania and depression but temperament, thinking, imagination, and many of the most important things that make us human.
NOMENCLATURE
“Manic-depressive illness,” the diagnostic term used during Robert Lowell’s lifetime, has been largely supplanted by “bipolar disorder,” which is the standard term now used in research and clinical practice. The change in nomenclature is a result of attempts by clinicians and scientists to distinguish between those patients who have a history of both mania and depression from those who have a history of depression only. The distinction is an important one in scientific research and it carries significant implications for treatment. There are, however, good reasons not to abandon entirely the term “manic-depressive illness.” Recurrent depressive illness, historically included as part of the diagnosis of manic-depressive illness, is in most important ways—family history, course of illness, symptomatic presentation of depression, and response to treatment—more similar to bipolar illness than it is to nonrecurrent major depression. It is premature, until we have better science, to make fixed distinctions between bipolar disorder—a term applied only when there is a history of mild to severe mania—and recurrent depression, where there is no history of mania. In addition, “bipolar disorder” perpetuates the misconception that mood disorders cycle neatly between opposite mental and physical states. Nothing could be further from the truth. Mania and depression combine to form unstable clinical states that are a mixture of manic and depressive mood, behavior, and thinking.
There is a belief that the term “bipolar disorder” is more acceptable—less “stigmatizing”—than “manic-depressive illness.” For many people this is true. For others, including myself, it is not. “Bipolar disorder” seems misleading, rather trivializing, and far removed from the clinical reality of depression and mania by those who experience them. The diagnostic language that is used is an individual preference, of course; clinicians and their patients will choose which they prefer for their individual reasons. Yet language has consequences. The pharmaceutical companies, for example, have good cause to use “bipolar disorder” rather than “manic-depressive illness.” It is a more benign-sounding term and, as such, can be helpful in marketing medications to physicians and to a broader range of patients. If diagnostic criteria expand and the diagnostic label is more socially and psychologically acceptable, more people will meet criteria for the illness and more doctors will be inclined to prescribe for them.
This dilution and broadening of diagnostic language can be a good thing if it means that more people who truly need treatment are receiving it, that more research is being funded, and that the general public is better educated and less judgmental about mental illness. But the risks of misrepresentation and trivialization are real. It should be possible to realize that mania and depression are painful and damaging illnesses that need to be treated but also to understand them as broader concepts: to understand them as the important part of human history that they are, and to appreciate mania and depression as illnesses disproportionately associated with great accomplishment in the arts, sciences, and other fields of human endeavor. Replacing ancient, graphic language with euphemistic diagnostic labels risks minimizing the suffering and complexity of an often deadly illness. Losing the historical and social perspective on manic-depressive illness, its contributions as well as its awfulness, is also to risk minimizing the social and ethical implications of our increasing capacity to manipulate the human genome. This is a significant risk. It is not enough to describe and diagnose mania and depression accurately, and it will not be enough to understand them at their basic molecular level. It is necessary to understand moods and their aberrations in the context of individual lives and imaginations; the role they have in shaping societies; and the meaning they assume in the human condition.
APPENDIX 3
Medical History of Robert Lowell
Robert Lowell died suddenly at about 6:00 p.m. on September 12, 1977, at the age of sixty. There was no autopsy and the death certificate was signed by a doctor at Roosevelt Hospital in New York; at that time and place there was no requirement to identify the cause other than to affirm that death was due to natural causes. In light of the rest of Lowell’s medical history it is likely that sudden death was from ventricular fibrillation, the final consequence of severe chronic heart-muscle injury. In common parlance he suffered sudden death in the context of chronic cardiac failure. His heart failure was probably the result of widespread coronary artery disease, but one should also consider the possibility that he suffered heart damage from alcohol, or even from his treatment with lithium.
In February, seven months before Lowell died, he had been admitted to Massachusetts General Hospital (MGH) with severe lung congestion resulting from his heart disease. The history he gave is characteristic, and the notes from the time leave no room for speculation about what was happening. For two months he had experienced progressive breathlessness, and his respiratory difficulty was aggravated at night. He was unable to tolerate lying flatter than at an angle of seventy-five degrees and would be woken at night by acute shortness of breath, so-called paroxysmal nocturnal dyspnea. This is unlike breathlessness that might be related to pulmonary complications of his smoking, and he described it in a letter to his wife, Caroline Blackwood: “I sleep sitting up,—good for breathing, bad for sleep.”
According to Dr. Timothy Guiney, his attending physician, and Dr. Jerome Groopman, the resident in Phillips House Coronary Care Unit, there was no previous history of pain in the chest. But in his poem “Phillips House Revisited,” a seemingly autobiographical account of the hospital admission, Lowell alludes to “this irreverent absence of pain, / less than the ordinary that daily irks.” This might refer to a past experience of angina, and it has to be noted that Dr. Brass, his doctor in London, had indeed seen him for pain in the chest. Dr. Brass was generally inclined to optimism and attributed Lowell’s thoracic pain, felt as it was in the back and the side, to arthritis of the spine. With hindsight, one cannot be so sure; a cardiologist reading the poem, while recognizing it is a poetic and not a literal account, will be tempted to recognize the story of daily chest pains giving way to breathlessness when coronary heart disease progresses from angina to heart failure. There are other indications that Lowell had heart disease even before 1977: not only the abnormal electrocardiogram (ECG), but the comment in 1974 that he was on digitalis; in September 1975 that his ability to walk and exercise was impaired; and from Dr. Curtis Prout, his physician in Boston, that he undoubtedly had a heart attack of some kind around Christmas 1975.
Other previous medical history included treatment in 1968–69 for hypothyroidism. There was thyroid swelling, and his condition eventually seems to have improved (thyro
id hormone was discontinued in March 1969), so one imagines he had thyroiditis. He had an unexplained episode of loss of consciousness in 1974, which seems to have been a simple faint.
The diagnostic studies performed during the admission to MGH were: a chest X-ray, which confirmed lung congestion and cardiac enlargement; electrocardiogram; and a nuclear heart scan. The nuclear scan confirmed the expectation that the left ventricle’s contractile function was drastically reduced and is reported as showing that this weakness was distributed unevenly in the heart muscle, as would be expected if it was the result of multiple previous heart attacks, each injuring a separate region of the ventricular muscle. The electrocardiogram is extremely abnormal and fits with the suspicion of multiple previous areas of injury. It shows Q waves in the inferior and anterior distributions, consistent with but not necessarily diagnostic of past coronary attacks. The tracing is more pathological than ones that had been described in previous checkups in London and Cambridge, Massachusetts.
At the time he was admitted, his only medication was lithium, with a blood level of 1.1–1.2 mEq/L (Lowell evidently reported to the attending physician that it earlier had been measured at 1.7 mEq/L, a toxic level). His lithium had been reduced or stopped in late 1975, and at some point subsequently the drug had been restarted. He was on no medicines for heart disease and he made a rapid and gratifying response to standard measures, namely digitalis (digoxin) and the diuretic furosemide (Lasix). He was discharged from MGH taking 0.25 mg of digoxin daily, 40 mg of furosemide twice a day, and 300 mg of lithium carbonate three times a day. There are no notes extant concerning his follow-up, but he was seen in the summer by his physician in Boston and given to understand that he was doing well. We do not know if he had blood testing for electrolytes, or digitalis or lithium levels. During the summer in Castine he worked hard writing, and according to Elizabeth Hardwick he was ostensibly in fairly good health, though still somewhat short of breath. This clinical course, of doing quite well with respect to circulatory function, yet still falling victim to a sudden arrhythmia, is not unusual. It fits well with what has been learned in the last thirty years, that for many patients with severe heart muscle dysfunction, particularly those in whom the cause is coronary heart disease (patients with so-called ischemic cardiomyopathy), death comes abruptly, from cardiac arrhythmia, rather than necessarily from continued worsening of the heart’s pump strength. It is why today many patients with this diagnosis are given implantable defibrillators.
Even for the times, Lowell was a very heavy smoker, two packs every day for most of his adult life. The deep lining and premature aging of his face betray the extent of his habit, not to mention the presence of cigarettes and overflowing ashtrays in photographs and contemporary descriptions of the poet. Even after the MGH admission with cardiac failure he continued to smoke, claiming that his doctors allowed that it was too late to stop. There was a family history of coronary heart disease, but one that is not unusually strong. His father died from a heart attack at the age of sixty-three, his mother from a stroke when she was sixty-five, and both had high blood pressure. He had moderately high cholesterol (in the 1970s doctors had begun to pay serious attention to blood lipids), but, beyond cigarettes, the other significant contributor to his vascular disease was the high blood pressure that ran in his family.
In 1949, when he was thirty-two, Lowell’s blood pressure was recorded as 138/90, borderline high, and when he was forty it was recorded as 150/110. In 1967, when at fifty he began treatment with lithium, he was already on medication for blood pressure, probably the methyldopa that he alludes to by name in 1971 and continued to be on through at least 1975, in which year Dr. Brass in London recorded a pressure of 150/100. Considering that a fair number of these medical observations were made at times of psychiatric hospital admissions for mania and that his blood pressure may have been higher then than at times when he was less excited or stressed, one accepts that he had significant hypertension, but not really exceptional.
The other likely potential cause or contributor to his heart muscle weakness is the effect of alcohol. When Lowell was excited or manic he drank very heavily, and even during the calm periods of his life he participated at the high end of the heavy social drinking normal for his era and literary set. The existence of alcohol cardiomyopathy is well accepted by cardiologists, but there is no test to confirm this diagnosis other than to see whether heart function improves after the patient quits drinking. There is no set amount of alcohol required to cause the condition; some people drink prodigious amounts without sustaining heart damage, whereas others develop heart toxicity after years of steadily drinking far less. The arguments against alcohol as the cause of his heart disease and death are that the really heavy drinking was episodic, that the ECG is more suggestive of coronary heart disease than of a diffuse injury, and that the nuclear scan in February reportedly showed discrete patches of heart muscle injury, as would be caused by coronary occlusions, rather than the diffuse pattern of damage caused by a toxin. We cannot know whether alcohol or coronary disease was the main or only culprit in causing Lowell’s heart muscle weakness, and indeed Dr. Guiney at MGH was as ready to blame the former as to invoke coronary artery disease, primarily, I believe, because of the purported absence of a history of cardiac pain.
There have been reports that lithium is toxic to the heart, and some cardiologists believe strongly that the drug, even in therapeutic doses, may cause heart damage after years of use. The evidence for this in the medical literature is thin. Lithium treatment affects the appearance of the ECG, as would be expected given that the lithium ion is so similar chemically to the potassium and sodium ions that participate in the electrical activity of the heartbeat. Lithium treatment may also lead to minor forms of cardiac arrhythmia, but there has never been evidence of a consistent effect on the mechanical function of cardiac muscle. The literature contains a scattering of case reports, fewer than ten, of patients taking lithium who had heart failure, and in none of these was lithium the only possible medication or toxin that might have accounted for the illness. On balance, lithium seems vastly less likely than coronary heart disease or alcohol to have contributed to Lowell’s heart failure and death.
Patients with manic depression have significantly shorter life expectancy than normal. Even when, despite the odds, sufferers do not succumb to suicide, or die from overdose, accident, or violence—more or less direct consequences of their condition—they are still likely to have diminished access to care; may, on account of their mental instability, find themselves ineligible for complex or demanding treatments; may adhere poorly to medical regimens; and may not be people who naturally follow healthy lifestyles. They suffer from fractured sleep, fatigue, and frequent overexcitement. The physiologic overstimulation that accompanies mania can be acutely lethal and surely takes its own toll in the long term. Lowell’s early death at sixty seems to offer some insight into these factors at work, yet with so little available to treat blood pressure effectively, and in a society that readily accepted the volume of his cigarette and alcohol habits, we can be grateful that he could live well and remain so productive even to the end.
Thomas A. Traill, FRCP
Professor of Medicine
The Johns Hopkins University
School of Medicine
Acknowledgments
I am indebted to Harriet Winslow Lowell for her permission to obtain and review her father’s psychiatric and medical records, for our many interesting discussions about her father and his work, and for allowing me to look at his unpublished writings and family photographs. It has been a great pleasure to get to know Ms. Lowell, who put no conditions on what I wrote. Her husband, Neal Earhart, was generous with his time and his memories of his mother-in-law, Elizabeth Hardwick.
Robert Lowell’s stepdaughters, Evgenia Citkowitz and Ivana Lowell, were kind enough to discuss their memories of their stepfather and to answer additional questions as they came up. Several of Lowell’s friends, colleagues, and
former students talked with me at length about their relationships with him and about his work. I am particularly grateful to Grey Gowrie, Jonathan Raban, Helen Vendler, Kathleen Spivack, Richard Tillinghast, John Julius Norwich, Jonathan Miller, James Atlas, Christopher Ricks, Dana Gioia, Steven Gould Axelrod, Douglas Dunn, Wendy Lesser, Rose Styron, Polly Kraft, and Cornelia Foss. I am indebted to the poet Saskia Hamilton, editor of The Letters of Robert Lowell and co-editor of Words in Air: The Complete Correspondence Between Elizabeth Bishop and Robert Lowell. Her scholarship is formidable and she has been singularly encouraging and helpful to me in writing this book. Professor Frank Bidart, the poet and editor of Robert Lowell’s Collected Poems, read an early version of my manuscript, as did Lowell’s publisher at Farrar, Straus and Giroux, Jonathan Galassi. Both were very supportive of what I had written, and I am deeply appreciative.
I am particularly indebted to two of Robert Lowell’s psychiatrists, both of whom offered rich insight into his illness and treatment: Erik Linnolt, M.D., who was Lowell’s psychiatrist during his three hospitalizations at the Institute of Living in Connecticut during the 1960s, and Dr. Marian Woolston-Catlin, M.D., who treated him at the Massachusetts Mental Health Center during the late 1950s, a critical time for his poetry, as well as for his manic-depressive illness.
It was not easy to find Lowell’s psychiatric and medical records, some of which were eighty years old, as hospitals are rarely required to preserve their records for more than ten years. I was helped by the staff and administrators in many of the hospitals that treated Robert Lowell: Jack Barchas, M.D., Chairman of Psychiatry at Weill Cornell Medical College in New York, and Pamela Thrower-Webb, also at Weill Cornell; Elizabeth Simpson, M.D. at Massachusetts Mental Health Center in Boston; Harold Schwartz, M.D., Psychiatrist in-Chief of the Institute of Living in Hartford, Connecticut, and Joanna Fogg-Waberski, M.D., also at the Institute of Living; Shelly Greenfield, M.D., Chief Academic Officer at McLean Hospital in Belmont, Massachusetts, an affiliate of Harvard Medical School, and Terry Alan Bragg, Archivist of the McLean Hospital; Jeffrey Lieberman, M.D., Chair of the Department of Psychiatry, Columbia University Medical Center; John Belknap, Chief Compliance Officer of Massachusetts General Hospital, and Jerrold Rosenbaum, M.D., Chief of Psychiatry at Massachusetts General Hospital.
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