Psychiatric uncertainty and the neurobiological buzzword

A few years ago I wrote that uncertainty is inevitable in psychiatry.  We literally don't know the pathogenesis of any psychiatric disorder.  Historically, when the etiology of abnormal behavior became known, the disease was no longer considered psychiatric.  Thus, neurosyphilis and myxedema went to internal medicine; seizures, multiple sclerosis, Parkinson's, and many other formerly psychiatric conditions went to neurology; brain tumors and hemorrhages went to neurosurgery; and so forth.  This leaves psychiatry with the remainder: all the behavioral conditions of unknown etiology.  Looking to the future, my fervent hope that researchers will soon discover causes and definitive cures for schizophrenia, bipolar disorder, and other psychiatric disorders comes with the expectation that these conditions will then leave psychiatry for other specialties.  We will always deal with what is left.  At minimum we psychiatrists should accept this reality about our chosen field.  After all, there appears to be no alternative.  Some of us go beyond this to embrace uncertainty as intellectually attractive.  We like that the field is unsettled, in flux, alive. Yet many of us clutch at illusory certainty.  Decades ago, psychoanalysis purportedly held the keys to unlock the mysteries of the mind.  It later lost favor when many conditions, particularly the most severe, were unaffected by this lengthy, expensive treatment.  Now the buzzword is that psychiatric disorders are "neurobiological."  This is said in a tone that implies we know more than we do, that we understand psychiatric etiology.  It's a bluff.

Patients are told they suffer a "chemical imbalance" in the brain, when none has ever been shown.  Rapid advances in brain imaging and genetics have yielded an avalanche of findings that may well bring us closer to understanding the causes of mental disorders.  But they haven't done so yet — a sad fact obscured by popular and professional rhetoric.  In particular, functional brain imaging (e.g., fMRI) fascinates brain scientists and the public alike.  We can now see, in dramatic three-dimensional colorful computer graphics, how different regions of the living brain "light up," that is, vary in metabolic activity.  Population studies reveal systematic differences in patients with specific psychiatric disorders as compared to normals.  Don't such images prove that psychiatric disorders are neurobiological brain diseases?

Not quite.  Readers of these exciting reports often overlook two crucial facts.  First, these metabolic differences only appear in group studies and cannot be used to diagnose individual patients.  As of this writing there is no lab test or brain scan to diagnose any psychiatric disorder.  Attempting to do so would be like diagnosing malnutrition based on height.  While malnourished people are shorter than the well-nourished on average, there is wide overlap and height is not diagnostic.  Second, etiology — the cause of these differences in brain function — remains unknown.  Differences in brain function (and structure) are not necessarily inborn.  Brain anatomy can change as a result of life experience, and metabolic activity (function) from experimental manipulation of cognitive effort, induced mood, guided imagery, etc.  Just as multiple factors affect a subject's height, multiple biological and psychological factors affect brain findings as well.  Thus, learning that patients with borderline personality show decreased metabolism in the frontal lobes (hypofrontality) is neither surprising nor indicative of a neurobiological etiology.  We already know the frontal lobes inhibit impulsive activity, and we already know borderline personality is characterized by impulsivity.  What else would we expect?

Genetic studies consistently show both heritable and environmental factors at play in psychiatric disorders.  Since the 1960s, psychiatry has called this combination the diathesis-stress model: an inborn predisposition meets an environmental stress, leading to an overt disorder.  The model helped shift the field from "nature versus nurture" to "nature and nurture" — and no research discovery or neurobiological rhetoric so far has shifted it back.  Patients and their doctors still contend with diathesis and stress: recreational drug use tips one patient into psychosis, sudden abandonment tips another into borderline rage.  Indeed, clinicians remain much more able to influence stress than diathesis.  A dispassionate assessment of what we currently know should lead to humble agnosticism about psychiatric etiology.  Genetics, biology, and environment all play a role, but beyond that there isn't much we can say.  This is why all current psychiatric medications treat symptoms and are not curative.

In this light, the popularity and zeal of neurobiological language is startling.   The American Psychiatric Association (APA) subtly changed the wording in its new Diagnostic and Statistical Manual, DSM-5, to imply that all psychiatric conditions are biological in nature.  The National Institute of Mental Health (NIMH) assumes that "Mental disorders are biological disorders...."  The National Alliance on Mental Illness (NAMI) says, "A mental illness is a medical condition...."

A more ground-level version is expressed by editor-in-chief Henry A. Nasrallah, MD in the latest edition of Current Psychiatry.  In an editorial not-so-subtly titled, "Borderline personality disorder is a heritable brain disease," Dr. Nasrallah proclaims BPD a "neurobiological illness" and "a serious, disabling brain disorder, not simply an aberration of personality" — as though these were distinct alternatives rather than two terms for the same thing.  After citing a number of biological findings which fail to prove etiology (e.g., the hypofrontality mentioned above) and which show partial heritability, Dr. Nasrallah concludes that "the neuropsychiatric basis of BPD must guide treatment."

Of course, it already does.  We already treat borderline personality disorder the best we know how, with psychotherapy (shown by functional imaging to modify brain metabolism, by the way) and often with adjunctive medication to treat symptoms.  What more do breathless declarations of brain disease buy us, other than reduced credibility?  It's not as though any of us currently withhold neurobiological treatment as a result of outmoded ideology.  On the contrary, the moment the FDA approves a cure for borderline personality disorder based on an established neurobiological etiology, I will gladly refer my patients to the neurologist, virologist, or genetic counselor who would thereafter treat such patients.

Borderline personality disorder: parasuicide

In my last post, I highlighted diagnostic challenges related to borderline personality disorder (BPD): Sometimes dramatic, self-destructive behavior leads to reflexive, inaccurate use of this label, while other times eagerness to diagnose a medication-responsive illness such as bipolar disorder can lead to overlooking BPD.  Naturally, this barely scratches the surface.  Thousands of books have been written about BPD.  This editorial from the May 2009 issue of the American Journal of Psychiatry provides a concise summary of controversies surrounding the diagnosis.  Even the Wikipedia entry on BPD has extensive useful information.  Today I'll focus on another central feature of BPD that has proven challenging to residents I've supervised (and me): parasuicide. Parasuicide refers to self-harming behavior identified by the patient as suicidal but unlikely to actually result in death.  Sometimes termed a "suicide gesture," typical examples include taking a handful of pills, and cutting one's wrists to draw blood, but not deeply enough to damage veins or arteries.  Often the patient realizes later that suicide was not "really" the aim of the behavior.  (Aim and intent become complex philosophical issues once the idea of a dynamic unconscious comes into play.  Can one intend something without knowing it?  Can intent be discerned by a therapist over the patient's heartfelt disagreement?)  Many patients in therapy eventually describe a very unpleasant, difficult-to-name emotional state that is relieved by these activities — especially painful, self-mutilating actions such as cutting or burning oneself.  There is a sense of tension release.  A communicative aspect is also often apparent, as in showing one's anger or rage to important others, and eliciting an emotional reaction from them in return.

Parasuicide puts families and therapists, especially beginning therapists, in an uncomfortable position.  These actions must be taken seriously, as failure to do so can make the person feel (further) abandoned and even angrier, leading to a spiral of increasingly self-destructive behavior.  "Upping the ante" in this way can even lead to accidental death.  For example, it is not widely appreciated that even modest overdoses of acetaminophen (Tylenol) can cause lethal liver failure.  A seemingly minor overdose can unwittingly prove fatal.  On the other hand, parasuicide looks manipulative.  It is loudly claimed to be suicidal but isn't "serious."  Families and therapists become angry themselves, potentially resulting in isolation, retaliation, and further harm to the patient.  Patients brought to the emergency room after parasuicidal behavior challenge the on-call psychiatrist, often a resident, to walk a tightrope between dismissing the risk too casually, versus overreacting on the principle of "better safe than sorry."  Patients are sometimes hospitalized unnecessarily.  A fascinating theoretical paper on psychiatric risk assessment can be found here.

To its credit, dialectical behavior therapy (DBT) tackles parasuicide head-on, as its top priority.  This is wise not only from the perspective of patient safety, but also as a means to contain the anxiety of treatment providers.  It is very difficult to work collaboratively with a patient who both scares and angers the therapist.  While DBT addresses the problematic behavior itself, the manner in which a patient induces such negative feelings in the therapist is a direct focus of psychodynamic therapies.  Transference-focused psychotherapy (TFT), another empirically validated treatment for BPD, was developed by Dr. Otto Kernberg and colleagues at Cornell, and pays particular attention to the communicative aspect of parasuicidal acts.

Parasuicide may look and feel manipulative to observers, but to the person with BPD it is a desperate attempt to secure relief from painful overwhelming feelings.  It is both highly characteristic of the disorder, and one of its most challenging clinical features.

Borderline personality disorder: diagnosis

Just as I was formulating a few thoughts on borderline personality disorder (BPD), I see the NY Times beat me to it. Jane E. Brody's 6/15/09 "Personal Health" column, "An Emotional Hair Trigger, Often Misread," provides an evocative description of this vexing disorder. Brody's column seems informed largely by her consultant, Dr. Marsha M. Linehan, who devised the best known and best studied treatment for BPD, a combined individual and group therapy called Dialectical Behavior Therapy, or DBT. (Here are some links describing DBT: 1, 2, 3). Dr. Linehan also invited readers' questions about BPD on a related NY Times blog, garnering over 200 comments. She began to answer some of those questions here. In this post I'll offer some of my own views on diagnosing borderline personality disorder, and in the next I'll share some more reflections and thoughts on BPD.

The term "borderline" came from the impression of early clinicians that the disorder originates at the border of neurosis and psychosis: too severe to be the former, not severe enough to be the latter. Over the decades psychiatry has refined its understanding of this syndrome , yet much remains unclear. The May 2009 issue of the American Journal of Psychiatry was devoted in part to BPD. One article by psychiatric diagnostician John Gunderson MD reviews the history of the diagnosis and is well worth reading.

BPD is not as easily diagnosed as people, including many clinicians, think it is. Not all dramatic, irritable, self-destructive, and/or manipulative people have BPD. I currently see two patients in my practice who were referred to me by other well-trained psychiatrists as clearly having BPD. They don't. One is a woman who suffered repeated childhood sexual abuse, leaving her full of mistrust, anxiety, and anger. She hardly discussed her traumatic past with her former psychiatrist of many years, who saw her weekly and maintained her on several antidepressant, tranquilizing, and sedating medications. I confess that I, too, thought she had BPD when we first met: She was overwhelmed by affect and seemed unable to sustain relationships. This has all changed with therapy. Now, about two and a half years later, she takes no psychiatric medications, has several important relationships, and usually can tolerate her own strong emotions. Either I cured her BPD (I don't think so), or she never had it in the first place. My other patient has dramatic affective storms, identity diffusion, frequent limit-testing, "manipulative" suicidal threats, and so forth. But psychotherapy has revealed emotional conflicts, not borderline pathology, at the root of her distress. She too is improving.

I have no doubt that Dr. Linehan's DBT helps a great many patients suffering from BPD. But I can't help but worry about all those who do not really have BPD, and who could be helped in more fundamental ways by a nuanced understanding of their emotional dynamics. It is worth remembering that Dr. Linehan herself does not claim that improvement from DBT is diagnostic of any particular disorder. Who would not benefit by increased mindfulness, improved interpersonal effectiveness, and better emotion regulation and distress tolerance? (These are the four "modules" of DBT.) Perhaps some variant of these modules should be taught to all schoolchildren as a public health measure!

So there are people who "look" like they have BPD, but really have neurotic conflicts. Conversely, I have seen a number of patients who carry a diagnosis of bipolar disorder, usually qualified with terms like "atypical" or "rapid cycling," who really have BPD. The world of psychiatry is divided into those who believe bipolar disorder is under-diagnosed, and those who believe it is over-diagnosed. (The same is true of ADHD and other popular [trendy?] diagnoses.) I happen to believe it is over-diagnosed. Rapid-cycling bipolar is defined as four or more extreme mood states per year. These would be moods that last at least a week or two, usually considerably longer. Dramatic mood swings that occur hour to hour, or day to day, are most likely something else: a personality disorder, an organic brain condition, a drug or alcohol addiction. It's a waste and a risk to take unneeded bipolar medication for years and years, surely worse than undergoing DBT for a mistaken BPD diagnosis. Worst of all, I suppose, is to be given both diagnoses, bipolar and BPD, when neither is correct. I am very wary when patients tell me they have both disorders. While not impossible, it far more likely points to sloppy diagnosis than to a particularly unlucky patient.

The term "borderline" has seeped into public consciousness just enough to make it a powerful putdown, or pseudo-explanation to account for a socially difficult or antagonistic person. Moreover, the DSM-IV does a poor job with personality disorders, perhaps because it aims to be atheoretical, whereas personality assessment relies inherently on a theory of mind. I believe a psychodynamic framework is required to understand BPD, even if effective interventions need not themselves be psychodynamic.

More reflections to follow in the next post.