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Does Evidence-Based Medicine Discourage Richer Assessment of Psychopathology and Treatment?

Does Evidence-Based Medicine Discourage Richer Assessment of Psychopathology and Treatment?

The paradigm for modern psychiatry is evidence-based medicine (EBM)—it represents proven treatments for defined diagnoses. But there are major problems with this position, starting with the fact that while they are superior to placebo, evidence-based treatments too often are ineffective. Even with treatment compliance, many patients do not return to their premorbid selves. Their ailment may last for years. A given percentage is not helped at all. Typically, 30% to 50% of depressed patients will not respond, and among nonresponders only 23.5% to 28% are helped by a second medication.1-4 The relatively common failure of evidence-based treatments to achieve remission is not unique to depression. Similar results are found throughout the full spectrum of DSM-IV disorders, which frustrates both doctors and patients.

This is not surprising. The science of psychiatry is still young, its conclusions necessarily preliminary. Psychiatry has not found its penicillin, a drug that will succeed 99% of the time in eliminating strep throat, because it kills the germ causing the illness. DSM-IV diagnoses are operational definitions, the best attempt by committees of experts to group manifestations of psychopathology into “disorders.” This cataloguing is not the same thing as understanding cause and effect. We haven’t yet discovered the etiology of any DSM-IV diagnosis.

It cannot be assumed that doing a better job classifying psychopathology diagnostically is the best way to move forward. Established diagnostic entities are as much wish as reality. The convening of experts to create DSM-5 diagnoses will probably not help researchers find new discoveries. The authors of DSM-III, DSM-III-R, and DSM-IV had it right. They also made committee decisions, but they emphasized that their conclusions were tentative: “. . . there is no assumption that each category of mental disorder is a completely discrete entity with absolute boundaries dividing it from other mental disorders or from no mental disorder . . . [and] boundary cases will be difficult to diagnose in any but a probabilistic fashion.”5

Robert Spitzer, MD, former Chair of the DSM-III Work Group, has rightfully condemned the confidentiality agreements required of DSM-5 committee participants.6 He wants detailed minutes of DSM-5 Task Force deliberations, a no-brainer for those who understand the necessary tentativeness of scientific information, but problematic for those who want to provide an illusion of consensual certainty about diagnostic categories. “EBM” is being touted for its scientific prestige, precisely as the process has forsaken the true spirit of science. Considering how much we still don’t understand, our steps forward should be exploratory, investigative, and not closed off by the chilling effects of authority.

There are those who only respect the exactness of numbers and who believe only statistics can determine what is factual and what is not. This is a given for researchers, but it is not as relevant for clinicians who may need answers for their patients that cannot be organized into questions answered with numbers. Obviously, given the choice between what is understood and proven through scientific method and what is, in essence, opinion or formulation, science should command absolute loyalty. But that doesn’t mean that using a scientific format, or waving its banner, adds validity to those who speak as “scientists.” Its virtues can act as a smokescreen. The language, the prestige, and the trappings of science can be so distracting that science’s core value is overshadowed, absolute clarity about what is known and not known.

What do diagnoses represent?
There is also a more fundamental issue, not answerable to the vote of even the most “expert” committee. For instance, we can operationally define oppositional defiant disorder, binge eating disorder, or all sorts of problematic behaviors. We can classify and subdivide them and epidemiologically count numbers that can be assigned to subcategories—but for what purpose? Does every diagnosis in DSM-IV represent an actual “real” illness, in the sense that polio, cancer, or a strept throat actually exist? Or are we reifying ephemeral qualities? We all know of children who have been diagnosed with one condition after another when behavior does not conform with defined criteria. Parents hope for that moment—“Ah-hah, your child ‘really’ has ADHD [or bipolar disorder or an anxiety disorder]. Now that we know what it is, we can treat it.”

Unfortunately, the search for the “real” diagnosis in psychiatry is often unfruitful therapeutically. The results won’t be the same as when a medical clinician discovers, for instance, a thyroid tumor or diabetes that presented atypically. In that case, elucidating the hard-to-discern illness has a purpose. We are not discovering what is really wrong. Simply finding a label; then another label; and another. (It mostly resembles the kind of diagnostic and treatment chaos that accompanies illnesses such as chronic fatigue syndrome.) I cannot help but add that, too frequently in clinical practice, providing a diagnosis isn’t even driven by the wish to follow a consensus treatment plan (itself a polling of “expert” opinions rather than one that is scientifically based). There may be no doubt the patient has pathology, but the clinician needs to indicate something on the insurance form that justifies medical attention.

Most experts and the FDA (and perhaps insurance companies in the future) argue that EBM should monopolize clinical approaches. But at this stage, the proper question is not should we exclusively use treatments that have proven superior to placebo? It is what is the best way to formulate treatment strategies when now, and in the foreseeable future, science can’t offer answers that we need? Sensible approaches, based on what we know about a particular patient, not limited to statistically validated treatments, are often more fruitful. Out of necessity, reasonable conjectures may play a significant role. Given mediocre treatment results, we need all the help we can get, the art of psychiatry as well as the science.

The core issue: our approach to patients
EBM eschews the anecdotal in the name of generalized conclusions, based on the odds that the patient’s ailments are typical for their group, patients who can be diagnosed with the same illness. This is not a ridiculous consideration, but it can miss important particulars brought by the patient. Knowing a patient well can be the difference between effective and ineffective treatment. It is not unusual for patients to have psychopathology that is central to their condition and treatment, but is ignored by a diagnostic approach that exclusively focuses on symptoms described by DSM-IV. Premorbid defenses, character style, the nature of the patients’ stressors, their story can guide clinicians to a particular treatment including medication. And, it can influence dosage.7 While EBM has a place, especially when low cost is a consideration, cookbook psychiatry cannot lay claim to being optimal treatment. It is especially detrimental if this perspective acts like blinders, obscuring relevant psychopathology more than it clarifies the clinical picture.

Van Praag8 in his “Nosological Tunnel Vision in Biological Psychiatry, A Plea for a Functional Psychopathology” argued that pharmacological agents can be viewed as inducing particular psychological states that, although not specifically related to diagnosis, are nonetheless the basis for their usefulness. I would like to suggest a perspective about how SSRIs affect individuals, and why they are so clinically useful for so many psychiatric conditions. SSRIs can be effective in conditions as disparate as borderline character, depression, obsessive compulsive disorder, anorexia nervosa, panic disorder, social phobias, and so forth because increasing serotonin has a psychological affect that is nonspecific to the disorders in question. Alcohol will produce inebriation in a person with schizophrenia, obsessive compulsive disorder, depression, or someone with no psychiatric diagnosis. Analogously, SSRIs typically affect individuals in ways that are not specific to diagnosis. What is that effect?

The most frequent description that I have heard from my patients is “Don’t sweat the small stuff,” or “What’s the big deal?” It is this calm that I believe is a unique blessing of SSRIs. It means relief from worry, relief from the feeling that something is missing, something needs to be done, something needs to be fixed, “my makeup isn’t right,” “the sky is falling,” “I won’t be able to pay my bills,” “I’m not smart enough,” "I won’t be able to tolerate the loneliness if I leave my lover” (even if he/she is abusive).

SSRIs supply, if not always happiness, a nice contented feeling that all is well and will be well. They can allow parents to be able to play with their children more, fret less over the details, appreciate what is, actually want to do the proverbial modern mantra, stop and smell the roses.

According to this theory it is the “well, whatever” feeling, emotional blunting, that is so useful in the great variety of different syndromes. Thus, for a person with anorexia nervosa to react with “well, whatever” after they have gained a pound or two is to get at the heart of the problem. The same can be said for body dysmorphic disorder, a condition in which a person’s life is completely distorted by imagined or slight body defects (such as thinning hair, a big nose, and the like). In obsessive-compulsive disorder the ability to treat compulsions and obsessional thoughts in this manner is a godsend. Similarly, a depressed person’s preoccupation with the hopelessness of their situation, the gravity of their errors and defects, the inadequacy of their decisions, and so forth will be enormously relieved to regain a less negative perspective.

In panic disorder, a condition characterized by exquisite sensitivity to body sensations, and a catastrophizing of consequences, SSRIs have been found to be effective because the sense of catastrophe leaves. For similar reasons social phobias and bridge phobias and flying phobias often become manageable on SSRIs, as do intermittent explosive disorder which may improve because it is harder to press the patient’s button. Alcoholism, pathological gambling, overeating, and the like may respond if a sense of frustration has significantly contributed to the pathological behavior. (They may worsen these conditions if a heroic disciplined battle is being waged against temptation, which is then weakened by a “well whatever” letting down of the guard.) SSRIs can help perfectionists (“obsessive compulsive personalities”) give themselves a little slack. They can allow borderline personality disorder patients to cool their heels, to not be tortured, like a wounded lover, when the person, upon whom they have passionately centered their survival, is not reciprocally involved with them. And so we can apply this perspective about SSRIs down a long list of DSM-IV defined disorders that have been empirically found to be treatable by a change in brain chemistry.

This perspective also suggests itself as useful in psychological circumstances where a specific DSM-IV diagnosis is not at issue. Thus, for instance, a not uncommon treatment scenario is teenagers who are having a very rough go of it with their classmates, kids who are picked on precisely because of their vulnerability. The popular students are the ones who are cool; that is, they don’t blush easily, are bold with the opposite sex, and so forth. It is not unusual for adolescents to come to therapy because they feel like misfits and to put it bluntly, the use of SSRIs may be very helpful here to magically assist them in having a thicker skin, which is exactly the quality they needed all along to not get picked on and possibly even have the cool to be popular.

Let me describe an unusual use of meds. A patient with PTSD for over 10 years presented on high doses of Adderall that had been given to him for what his family physician diagnosed as adult ADHD. (He had reported difficulty concentrating.) His physician then became uncomfortable administering stimulants and sent him to me. He didn’t have ADHD. But he reported that on the Adderall his PTSD was the best it had been in over a decade. The explanation appeared to be found in his history. He and his fianc had been trainees at a state police academy. His fianc committed suicide, blowing her brains out. My patient found her. He couldn’t clear his mind of the scene. During the day, during his dreams, it remained vivid. Even with SSRIs and benzodiazepines, his PTSD not infrequently took control of his mind. This no longer happened with the addition of Adderall.

My guess was that the Adderall brought back his premorbid, state policeman defensive structure. Instead of experiencing his trauma again and again as a helpless passive victim, the essence of the psychological position occupied by those suffering from PTSD, on the Adderall he had returned to being a take-charge kind of guy. Coincidentally I was also seeing another patient with PTSD. She was a drug rep who had been a workout nut. She spoke in short staccato sentences. Boom boom, bam bam, not a trace of sentimentality in her, not a soft syllable in her repertoire. She had been in a car accident and broken her collarbone, right arm, and one of her legs. She couldn’t work out. She kept re-experiencing her helplessness in the accident. She was on SSRIs which were helpful but not curative. The addition of Adderall worked like a charm.

This is not an endorsement of Adderall for PTSD. It is an endorsement, when formulating a treatment, to think about a patient’s defenses, personality structure, and the like, and how their symptoms may be helped by the psychological consequences of a medication. Diagnosis per se may not be critical in this process. Let me add another example.
A patient presented to me on Wellbutrin for his panic disorder. It is one of the few antidepressants that is not recommended for this condition—it may give an edginess that sets off further attacks. So I took him off it. He got worse. It turned out that he was a procrastinator and his panic attacks were precipitated when something was about to hit the fan, when the passive aggressive mess he invariably made, was on the verge of being discovered.

As a dopaminergic agent, the Wellbutrin was a motivator, an energizer. It helped the patient get things done. I have since discovered that while dopaminergic agents can make anxiety worse, they can have the opposite effect when a patient’s anxiety is specifically driven by the pressure of undone work hanging over their heads. The drug energizes them, helps them to initiate and complete their chores. Thus, with certain generalized anxiety disorder patients, it is an effective treatment.

For what it is worth, let me also mention a seemingly bizarre clinical vignette. I saw a patient with severe obsessive-compulsive disorder (supposedly a serotonin-based illness) whose symptoms completely disappeared when he joined the Jehovah’s Witnesses. He gained a sense of innocence, of safety, of the world and his personal experience making sense, of being directed by a benign and helping force in the universe, a parent watching over him and loving him. He felt it deeply. And that did it. No symptoms. Three months later, when disillusionment began, the symptoms came marching back, some of them as religious compulsive rituals. But still, what is the clinical meaning of his initial cure?

There is one other perspective worth noting for the purpose of illustrating what DSM-IV represents. Let us consider congestive heart failure as a model. It can be described in terms of observable symptoms that respond to specific treatments—evidence-based treatments. But congestive heart failure has many different causes. For argument’s sake, let us say our knowledge base remained at the turn of the 20th century and hypothyroidism was causing the heart failure of a given patient. Thyroid extract would fail miserably when tested in a larger population of patients whose disorder had been defined as congestive heart failure. It might worsen, in particular, the illness of those patients whose congestive heart failure was, for instance, caused, or exacerbated, by atrial fibrillation as a result of hyperthyroidism.

From the perspective of the heart failure diagnosis, the few patients it might help may be described in individual case studies, but would probably be rightly dismissed as anecdotal, if proponents argued that it should be used as a general treatment for congestive heart failure. The fact remains that it is precisely the correct treatment for congestive heart failure as a result of hypothyroidism. My point is obvious. As reasonable as evidence-based treatment protocols for symptom-defined disorders might seem to be in psychiatry, they are, in fact, pathetic compared with what will be possible when a true understanding of etiology can be used to provide rational care.

There are many other examples of treatments that are not evidence based. Clinicians may confirm or not confirm the strategies I have illustrated here. The important issue, however, is the legitimacy of approaching patients in the ways I have described. The journals should be full of similar clinical vignettes and unique perspectives from other authors. The exclusive respectability of scientific psychiatry, based on diagnosis alone, should be ended, until, at least, that perspective has provided us with what only science can provide, proven cause and effect. I don’t believe it is going to come from diagnostic psychiatry and evidence-based treatments, but time will tell.

Collaboration is key
In the meantime, we need to end the tyranny of the paradigm that EBM and diagnostic psychiatry has had on the medical literature and legitimize the many good ideas we can share with each other. It means editors and readers will have to use their judgment about the quality of the presented ideas, rather than exclusively rely on statistical validation. (It might also mean that the FDA allow pharmaceutical salesmen to refer to these articles rather than consider it a crime.) Presumably some of the ideas will work. This beats committees and doctrines and all the certainties of approaches that aren’t getting the job done.

Clinicians need all the help they can get. They can begin by getting to know the particulars of their patients better. Residency training programs might also help this process by teaching greater psychotherapy skills rather than only giving it lip service.

References

References
1. Ruh HG, Huyser J, Swinkels JA, Schene AH. Switching antidepressants after a first selective serotonin reuptake inhibitor in major depressive disorder: a systematic review. J Clin Psychiatry. 2006;67:1836-1855.
2. Nierenberg AA, Keefe BR, Leslie VC, et al. Residual symptoms in depressed patients who respond acutely to fluoxetine. J Clin Psychiatry. 1999;60:221-225.
3. Baghai TC, Moller HJ, Rupprecht R. Recent progress in pharmacological and non-pharmacological treatment options of major depression. Curr Pharm Des. 2006;12: 503-515.
4. Papakostas GI, Fava M, Thase ME. Treatment of SSRI-resistant depression: a Meta-analysis comparing within- versus across-class switches. Biol Psychiatry. 2008;63:699-704.
5. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders DSM-IV. Introduction.
6. Kaplan A. DSM-V Controversies. Psychiatr Times. 2009;26(1):1.
7. Sobo S. The strengths and weaknesses of DSM IV: How it clarifies, how it blinds psychiatrists to issues in need of investigation. http://simonsobo.com/the-strengths-and-weaknesses-of-dsm-iv. Accessed April 3, 2012.
8. Van Praag HM, Asnis GM, Kahn RS, et al. Nosological tunnel vision in biological psychiatry. A plea for a functional psychopathology. A Ann N Y Acad Sci. 1990;600:501-510.
 
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