Let's say Mr. Jones, a 75-year-old retired teacher with no personal or family history of depression, comes to you with a classic picture of major depressive disorder. He tells you that his wife of 50 years died two months ago. Since then, he has experienced profound depression, a 15-pound weight loss, early-morning awakening, and inability to concentrate.
Shouldn't “common sense” tell you that Mr. Jones' depression was “triggered” by his wife's death and that it simply represents a “normal” and “proportionate” response to grievous loss? This, at any rate, is the core of a popular and superficially plausible thesis advanced by Professors Jerome Wake-field and Alan Horwitz.
But as Brandeis University biochemist Douglas Theobald, Ph.D., has observed, “common sense” tells us that the Earth is flat, the sun truly rises and sets, and the Earth is not spinning at more than 1,000 miles per hour. Medical science is not founded on “common sense,” but on uncommon investigation: on randomized, controlled studies that try to rule out as many confounding variables as possible.
Psychiatric medicine, too, relies less on common sense than on what the French call sense clinique—that ineffable blend of knowledge, experience, and hard-won wisdom that comes from seeing hundreds of patients over the course of one's career. Your sense clinique is what leads you to respect Mr. Jones' narrative of bereavement, while also contemplating a medical workup to rule out a covert malignancy as another possible trigger for his depression.
Your clinical sense also tells you that myriad other biopsychosocial factors may be causally related to Mr. Jones' depressive symptoms. Making an early calculation that his depression is, or is not, proportionate to any one putative trigger represents clinical naivete and premature closure.
You may discover several months into psychotherapy that Mr. Jones was not grieving the death of his wife so much as castigating himself for an extramarital affair he had 20 years earlier. Similarly, in severely anxious or traumatized patients, facts may emerge that cast serious doubt on what the psychiatrist first assumed was the precipitant of the patient's acute illness.
It is the psychiatrist's job to maintain respectful and open-minded neutrality regarding the cause or causes of a patient's acute disturbance. As Otto Kernberg has pointed out, therapeutic neutrality is not disgruntled indifference to the patient's felt experience; rather, it refers to the therapist's position of “equidistance” from the powerful emotional forces clashing within the patient.
By analogy, diagnostic neutrality means maintaining a position of equidistance from the biological, psychological, social, and spiritual forces impinging on the patient. Diagnostic neutrality is akin to keeping a sailboat steady in the swirl of shifting cross-winds. Such neutrality is especially important early in the clinical encounter.
As more information emerges in the context of evaluation and treatment, the psychiatrist's sense clinique begins to winnow less likely causal factors in the patient's condition. Often, we never discover the ultimate cause, or trigger, of the patient's acute anxiety, depression, or psychosis. But with or without obvious cause, some forms of intense suffering and incapacity represent disease or disorder.
Furthermore, the possibility that bereavement-related major depressive symptoms might remit in a few weeks should not deter us from diagnosing a major depressive disorder, when full criteria for that disorder are met—nor should we be reluctant to provide professional care in such circumstances.
The inherent problem in positing a depressive trigger is that we humans are famous for constructing explanatory narratives, even when the facts of the situation are not clear. Indeed, in her book, Narrative Gravity, linguistics professor Rukmini Nair argues that human beings have a genetic drive to fabricate narratives that serve our emotional needs. Furthermore, Dr. A.M. Ergis and colleagues have demonstrated that memory in depressed patients shows a “recall bias” toward recollection of negatively toned material.
But if the foundational notion of a depressive trigger itself is dubious, then any calculation regarding the “proportionality” of the patient's supposed response is necessarily doubtful. Making such calculations is like trying to measure floor boards while standing atop a scaffold of toothpicks.
This certainly doesn't mean we should dismiss what our patients tell us when they try to explain “why” they are depressed or anxious. It does mean that we must use our sense clinique in weighing such reports as a part of all the available data. Finally, we should base our judgments regarding disordered mood on observations of the patient's degree and duration of suffering and incapacity—not on calculations of“ proportionality” derived from facile causal narratives.▪