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The strengths and weaknesses of DSM IV: How it clarifies, how it blinds psychiatrists to issues in need of investigation

by Simon Sobo, M.D.

Abstract

The strengths and weaknesses of DSM III and IV are explored. It is argued that DSM IV cannot be assessed in a vacuum, by only examining its successes and failures at accomplishing its goals. Accurate descriptions and definitions of syndromes are an important guidepost. This job has generally been done well, especially given the expectation that it will be reevaluated and rewritten often, so that future versions will improve upon shortcomings. Nevertheless, a critique of DSM IV must also address the uses it has been put to, including ways that it can be, and is, being misused.

DSM IVs principles are sound. Scientific investigation is unrivaled as the way to eventually understand clinical phenomena. But, clinical work is not a laboratory. If we were to limit our decisions to scientifically proven information we would be incapacitated, since scientifically valid answers oftentimes do not, as yet, exist. Questions are raised as to whether, when this happens, DSM IV too often is used to create an illusion of understanding, for example, obedience to protocols deemed proper treatment by a polling of “experts”, but not based on scientific discovery. Equally questionable is the use of DSM IV to dictate “evidence based” treatment, which implies unwarranted scientific validity. 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, the trappings of science can be so distracting that science’s core value is overshadowed, absolute clarity about what is known and not known.

Early on, critics charged that DSM IV can lead to tunnel vision1.Crucial information and perspectives that don’t fit into its diagnostic system get ignored. More importantly, in certain clinical contexts, focusing on a diagnosis may not be the best way to help patients deal with their psychopathology. Numerous examples of other ways of conceptualizing patients’ difficulties are presented including medication strategies that are not based on DSM IV, but nevertheless, derive from a sound rationale.

For the layman and many clinicians, making a diagnosis implies the patient has a distinct illness, in the same way as a patient might have a tumor or an infection. But that may not be true of most psychiatric disorders. DSM IV diagnoses are based on operational definitions, rather than pathogenesis or etiology. They are necessarily preliminary, particularly well suited for research purposes. But they are too easily reified and broadened far beyond scientific justification. Moreoever when applying a diagnosis to a given patient the process can be a stretch, given current definitions. Spectrum disorders are a tempting stopgap, creating new diagnostic categories to encompass evolving thinking. But, if this is based on reification it will get us nowhere. Making DSM V more inclusive will not fix the problem, especially if derived from this misunderstanding of what a diagnosis represents in the first place.

The overly frequent need to diagnose patients with multiple diagnosis should raise a red flag. While finding comorbidities is consistent with guidelines, it may also indicate basic deficiencies in our understanding. In physical medicine, more than one diagnosis is not uncommon, but psychiatric patients are so regularly diagnosed with more than one DSM IV disorder that we must consider the possibility that many current diagnoses are failing to broadly enough capture and define psychopathology.

Finally, given its shortcomings, questions are raised as to whether DSM IV and the banner of science (as opposed to the substance) exerts too much control in psychiatric training programs, research, journal content, clinical practice and theory.  Certain problems with DSM IV (and with scientific psychiatry) are inherent. We can only know as much (or as little) as we know. Some of the shortcomings are not intrinsic. Busy clinicians count on the information fed to them by those in universities who have the time to sort out proper treatments. They may not be getting an objective presentation. It is argued that (unfortunately) understanding the culture of psychiatry is as important as the science. The reasons DSM IV came into being are discussed, the assumptions behind its creation. Who are the movers of the ideas that take hold? Are their motivations always driven by scientific curiosity, a passion to get at the truth, or is something else involved? For example, does a flurry of articles on a given topic represent exciting new findings (the usual in science) or stepped up marketing. (See: Big Pharma, Bad Medicine )These topics can generate a lot of heat, ad hominem passions and prejudices, the greatest divergence from scientific discourse imaginable. Nevertheless, if we hope to assess DSM IVs strengths and shortcomings there is no way around this aspect of it. We must step into the ring. This essay will not be the final word in this discussion, but hopefully it will accomplish what good therapy does. Bring the unspoken to the surface so as to clarify key, yet evaded issues, elicit other questions, and move the discussion along.

DSM IV: Some contexts of the arguments

DSM III and later DSM IV, American psychiatry’s current diagnostic system, were widely seen as improvements when they were introduced. The earlier diagnostic manual DSM II, had less specific descriptions and very poor inter rater reliability, completely unacceptable for those demanding scientific exactness. DSM II’s shortcomings had not been addressed previously because psychodynamic psychiatry, the dominant perspective at the time, had a different paradigm. Making a diagnoses based on presenting symptoms was not irrelevant, but for the most part, in the absence of psychosis, symptoms were viewed as manifestations of far more important, more fundamental underlying pathology. It was akin to the way a patient with lupus might be viewed. Kidney abnormalities, skin rashes, arthritis and the like, might present as symptoms, and require attention and care. However, the key to success was addressing the “real” problem (the lupus), not the skin rash.

A short review of the kind of perspectives that psychodynamic psychiatry brings to the table can help us to appreciate the changes represented by DSMs III and its heir, DSM IV. It is also relevant because it allows us to briefly revisit what has, all but, been eliminated from mainstream thinking, the valuable insight that human psychology is built upon inherently conflicting motivations.

We are very often civilized, capable of cooperation and respect for obligations, responsive to the demands of our community. We are able to reason, and strive towards uplifting ideals. Nevertheless, over ninety percent of our genes are shared with rats. Evolution has placed the neocortex, where reason resides, on top of still functioning ancient parts of the brain. It is an addition not a replacement. We have an animal body and animal needs. We kill other animals and eat their flesh. We defecate. We urinate. We need sexual release. There may be an instinct to kill which, under enough stress, exists in everyone. The naked truths of our psyche, Freud argued, particularly our sexuality, but also our secrets and deepest impulses and conflicts, exert a powerful influence on behavior which can take peculiar and distressing forms, interfering with adults’ ability to effortlessly function in day to day reality. We distance ourselves from animals. We bathe, shave, brush our teeth, use tampons, deodorants, toilet paper, and indoor plumbing. We find euphemisms to dress up unpleasant topics. But deep within us is a heart of darkness. Freud claimed we are polymorphous perverse, literally anything goes, including incest. In traditional cultures an attempt is made to ban forbidden images and thoughts. Certain sexual longings must be kept private, or better, forgotten. In secular society many impulses are more out in the open and legitimitized. Either way most find entertainment in movies and novels so that the vices and temptations that secretly reside in the mind can come out for a while. They would not have to be condemned and labeled as vices if the temptation to act on them wasn’t part of our natural equipment.

Psychodynamic psychiatrists maintained that the “real” problems underlying neurotic patients’ difficulties result from this dual nature, from, experiences and conflicts that are so disturbing that they are removed from conscious awareness. The emotions remain but not what was attached to them. Patients experience dread (anxiety), fear that something terrible is about to happen, without knowing what is feared. They feel sadness when there is no apparent reason. They may repeat destructive patterns of behaviors, which they know are irrational, but can’t seem to change.

The goal of treatment was to uncover the source of these half conscious and unconscious toxic motivations so that better solutions were possible. Among purists it was believed that reducing symptoms without finding their psychological underpinnings was destructive, like placing a band-aid over an infected splinter. Or it was like 19th century patent medicines which were once sold door to door. Most of them contained opium to dull or eliminate pain and distress, thereby allowing the patient to ignore gathering signs of illness.

The immediate problem with this perspective was that the treatment advocated by psychodynamic psychiatrists, uncovering and integrating repressed psychic material, took years to accomplish. Only the affluent could afford seeing an analyst the prescribed several times a week. Moreover “analyzability,” also a requirement, character qualities possessed by a minority of patients, meant only the capable need apply for treatment. The number of analysts was kept in such short supply that it was never a viable treatment for the millions of people that could use professional help. Indeed, if psychoanalysis had been as effective as the polio vaccine there might have been riots. Other approaches, some diluted versions of psychoanalysis, some with different content, were substituted. Most shared its emphasis on insight.

Psychodynamic ideas were in the mainstream of psychiatric thought for decades. In its day, it attracted some of psychiatry’s best minds. In many of the finest centers of learning, it was the only theoretical orientation given serious attention. There were criticisms of its scientific credentials, especially by philosophers of science2 and academic psychologists. For the most part, however, even among those who had great respect for scientific methodology, it was widely accepted that the complexities of human behavior that become clarified in therapy, do not loan themselves to exact measurement. Behaviorists could isolate very specific phenomena in their lab using rats, or even test certain qualities in humans, but the knowledge needed to understand psychopathology and treat patients could not be isolated in this way. It was too vast, too complicated. It was hoped that eventually ways could be found to more precisely nail down dynamic theory and observations, but there was no great urgency to do so. While Freud and some of his followers sometimes claimed the prestige of science, the general consensus was that out of necessity, treatment had to remain as much art as science.

More problematic was that successful treatment was hard to define. Perhaps, if therapies based on self understanding had been working spectacularly well, the absence of rigorous scientific thinking might not have been challenged. But, that could not be demonstrated, neither with those undertaking years of psychoanalysis, nor with less intense treatments. Insight can be a powerful tool, regaining a sense of control over what seems like madness, bringing light to the dark corridors of the mind. It is especially empowering for those who place self understanding and honesty on a pedestal. Unfortunately, for others, it often wasn’t, and isn’t, helpful enough. It can be palliative to know why one does something, or has frightening and disruptive emotions and symptoms, but that is no guarantee of change. Abreaction does not occur as reliably as the theory would hold. Inadequate “working through” (the integration of discoveries into the psyche) may explain some of the failures but it also can serve as an excuse for inadequate results. Worse, understanding can be no help at all with severe psychopathology.

There was an even more serious challenge. Over and beyond questions about the effectiveness of insight therapy, the scientific leeway that was allowed psychodynamic thinking created issues that went beyond whether or not Freud’s ideas were valid. It opened the door to pop psychology, which especially took hold in the 1970’s. Without scientific rigor, making sense of psychopathology can easily deteriorate into psychobabble, glib generalizations, prescriptions for behavior which sound nice, but have no connection to the motivation and behavior of actual people. With religion in decline, “healthy” or “unhealthy” behavior and thoughts became the equivalent of a new morality, one presumably based on scientific understanding. Child rearing, marital relations, individual growth and dysfunctions, all fell within the purview of doctors, somehow seen as experts in living. This was not coincidental. Often they tried to denigrate and replace the central role of guilt cultivated by most religions. However, they created mental health ideals of their own, normative values which defined modern virtues or vices. All kinds of competing philosophies, cures, and child rearing attitudes were spawned, which further undermined the legitimacy of psychiatry as a scientific pursuit. Demands for change were inevitable.

DSM III appeared in 1980. It was the defining characteristic of psychiatry’s new culture. Biological and scientific psychiatry had assumed dominance in academia and most of the journals. As part of this, the pendulum in the nature/nurture controversy had swung to the other side. In the new paradigm, the source of anxiety was not fears whose content was cut off from consciousness. The cause of panic attacks was not terror about something unknown. The cause of practically all patients’ psychiatric symptoms was not to be found in the psyche, not in consciousness or unconsciousness, not in psychological conflict, but in the physical brain, in chemicals, neural pathways, and genetics. The NIMH now demanded that those who approached psychiatric problems had to have the same mindset as other physicians. Republican President George Bush and Congress made an official proclamation that the 1990s were to be the “Decade of the Brain.” As it was doing in so many fields of medicine, industry, in this case the pharmaceutical industry, with its vast resources and research capabilities, soon played a pivotal, and then dominant, role in academic clinical psychiatry, in research and training, and the continuing education of physicians. This created a new problem. Conclusions were no longer being evaluated on a level playing field. Billions of dollars were involved in educating physicians and psychiatrists how to think like “experts,” many of them professors from our most prestigious universities who had been hired by pharmaceutical companies to spread their message. 42 Their success has been so complete, that the average psychiatrist, assumes future breakthroughs will come from new medications.

The radical change in paradigm towards the physical brain was partly political, and as such, certain ideas became politically incorrect. Brilliant and not so brilliant insights, arguments, perspectives and discoveries (as noted, much of the previous three quarters of a century of psychiatric thought) essentially disappeared. They were not proven or disproved. They were simply ignored. It wasn’t just Freudian beliefs. There was a broader implicit agenda. If the content of journals serves as a guide, environmental contaminants, inadequate nutrition, physical stress were legitimate enough areas to be studied when exploring the nurture side of the equation. But not issues of the psyche, particularly not issues of problematic development deriving from the relationship between parent and child, an amazing change when we consider how emphasized this area of study had been. Invariably, when differences in parenting were found paired to an illness, the explanation was that the parents were reacting to their child’s brain defect.

The very nature of intellectual communication within psychiatry also changed. Whatever its shortcomings, the older psychiatry required a deep and thorough exploration of the particulars of each patient. In contrast to the emphasis on individual case histories as a key to understanding pathology, qualities unique to an individual case were, for the most part, dismissed as anecdotal, meaning of little scientific interest. There was a huge increase in the emphasis placed on diagnosis, even when there was no scientific basis for this (This will be one of the main areas of focus of this paper). There were also changes in therapeutic approach that accompanied the new zeitgeist. For example, behaviorist experiments using animals in the lab had long been a key focus of scientific psychology in universities. It had also been widely applied in institutional psychiatry, where it had been the mainstay of treatment for the retarded, the insane and the criminal. The new cachet of “scientific psychiatry” made it a respectable treatment for the middle class. Eliminating the yakety-yak of individual psychotherapy, and sticking to proven general techniques of change that worked for anyone, was the goal.

Similarly, cognitive perspectives arguing for the power of calm, logical, positive attitudes, could be applied to anyone regardless of their life story or particular situation. Freud and his followers had emphasized the extraordinary power of the unconscious and the relatively feeble deliberating ego at the mercy of debilitating experiences and unmanageable emotions. The hope was that self knowledge could strengthen the ego. The new perspective was a complete flip-flop. Psychopathology was due to unhealthy attitudes. Wrong thoughts caused the bad emotions, not the other way around. With enough practice, solid, good, rational intentions and thoughts could be taught and bring equanimity, meaning made therapeutically effective. If Henry Higgins devotion to science and detached rationality could transform Eliza Doolittle to speak the Queen’s English, certainly psychopathology could yield to the proper attitudes of an enlightened adult, to better thoughts, regardless of how patients had developed their illness.

Cognitive behavioral and biological psychiatrists argued that the acid test was results. Practice makes perfect. In particular, a combination of cognitive and repetitive behavioral techniques (inculcating proper thinking through “homework”) could be proven to work reasonably well in reducing defined symptoms. Similarly, the argument for the new diagnostic system was valid enough. If psychiatric symptoms are not defined and measured, treatment effectiveness cannot be assessed. For most patients, symptoms brought them to treatment, and the reduction, or elimination of symptoms, is all that matters. The new perspective looked to iron clad statistically significant results as the only form of knowledge meriting serious respect. Empirical validation should guide treatment rather than the speculations of Freudians, Sullivanians, Jungians, and the like. Down with theory and debate. Up with verifiability. What works and what doesn’t is the central question.

It is a compelling argument, but it also can lead to absurdities. Many of the innovators of cognitive treatments saw themselves as rebels against the rigidities of the psychodynamic establishment. They rightly tossed out the psychoanalytic generalization that symptoms eliminated by non analytic techniques will merely reappear in some other form. While this can, and does happen, it is far from invariable. But, they went further than that. The baby was thrown out with the bath water. It is one thing to legitimately argue, for instance, that, in a given case, the kind of quick control of overt symptoms that medication offers is crucial, or, for many cases, it is economically practical. A reasonable argument can be made that in many clinical contexts letting sleeping dogs lie, keeping unconscious material repressed may be a good choice. The belief that with sufficient analysis, the ego will replace the id, or find suitable sublimations may be an overly rosy expectation.

On the other hand, choosing to simply ignore areas which cannot be put to scientific testing, essentially dropping these subjects from training and serious discussion, impoverishes the study of psychopathology so that critical areas are not addressed by students, clinicians, and researchers. The repeated designation of the new kind of care as “expert”, points to an attempt to intimidate, to foster “cascading” in science rather than openness to all data and evidence.

That said, DSM III and IV brought the expected practical benefits to researchers. During the DSM II era those conducting empirical research on the effectiveness of a treatment could exactly define their subjects’ characteristics, so that valid comparisons could be made between their findings and another researcher’s findings, but only if both agreed to monitor exactly the same population. So gathering experts together with a variety of theoretical perspectives, for the purpose of reaching a consensus that correlated diagnosis with precisely defined criteria, was very appealing. Clusters of symptoms now defined the disease. A nosology based on observable signs and symptoms, operational definitions of what they would be investigating, was the way science ordinarily proceeded. While an etiological description of an illness was preferable to an operational definition, since this wasn’t available, agreeing to stick to the same criteria was a decent first step.

DSM IV allows researchers anywhere to gather together a group of patients who meet the described criteria for the disorder, try different treatments, and compare the results. The diagnosis is universal. Thus, a given percentage of patients with social phobia might be helped by placebo, and if a greater number will be helped by paroxetine, or gabapentin, or cognitive behavioral therapy, or whatever the treatment in the research design might be, then these treatments can be designated effective if statistical significance is reached. “Evidence based treatment” appeals to the FDA and, more importantly, seemingly appeals to common sense. Empirical data is usually far more valuable than theories and controversy that cannot be backed up by a test of the facts. In recent years “evidence based medicine” has become a rallying cause. Pressures are exerted for it to become the standard of care.

Leaving aside the above criticism about unreasonably narrowing the focus of research and teaching, there is a more significant problem with this approach. Even within its own terms, it has gone too far. The authors of DSM III and IV were very aware of its shortcomings and warned about them in their introductions. 7 But, as diagnostic psychiatry became the center of most treatment paradigms these warnings have been ignored. Misunderstanding what a diagnosis represents (when etiology and pathophysiology are not known) can lead to conclusions that make no sense whatsoever, when viewed in the light of later understanding of what is actually occurring. For the purpose of illustration let us consider congestive heart failure (CHF) as a model.

An important aspect of CHF treatment is to focus on a manifest symptom such as edema, especially pulmonary edema and pleural effusions. The strain on the heart from excessive fluid demands the use of diuretics (which, of course, do not act on the heart at all but on the kidneys). Unencumbered by fluid in the lungs, shortness of breath and orthopnea will improve. Treatment addresses pathophysiology without taking etiology into account. The actual diseases that brought about the heart failure are once removed from the focus of treatment. Heart failure might be due to muscle damage from an MI or a viral cardiomyopathy. There might be valvular damage from rheumatic fever, or subacute bacterial endocarditis, and so forth through a long list of diseases that can damage the heart. A clinician focusing on the presenting symptoms of CHF is proceeding rationally because regardless of etiology, when the heart doesn’t do its job–when it is not pumping blood powerfully enough–the final common pathway manifested by the accumulated fluid may be of more immediate concern than the underlying cause of the illness. One hundred years ago CHF could be described without an understanding of its many causes, and that description remains therapeutically relevant today, even after we can now better understand underlying causality.

But there is a problem illustrated by CHF as a diagnosis, which is relevant to the way we use DSM IV today. 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 CHF was, for instance, caused, or exacerbated, by atrial fibrillation due to hyperthyroidism. Viewed from the perspective of the heart failure diagnosis, the few patients it might help might 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. Yet, the fact remains that it is precisely the correct treatment for CHF due to 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 to what is possible when a true understanding of etiology can be used to provide rational care.

Analogous to CHF, schizophrenia might be 5 or 7 or 12 different diseases all with the same common final pathway. The heart is basically a pump. Thus, many different illnesses can manifest themselves as the same “disorder” when its pumping action is defective. Similarly, there may be limited numbers of ways that the brain can malfunction when its higher integrative functions are not working properly, or are overpowered by extremely forceful primitive emotional currents. There might be a genetic-caused schizophrenia-like illness with 100% (or 25%) penetrance, a virally based illness, nutritional etiologies (besides known vitamin deficiency induced psychosis.). Some have suggested fetal damage. There might even be (dare I say it) an illness primarily caused by detrimental child rearing. At one time, a syphilitic psychosis resembling schizophrenia used to fill up mental hospitals, so let us not ignore bacterial causality. And what will we learn about prions?

The point is that different diseases sharing common symptoms could easily be lumped together. This might be true of each of the DSM IV disorders. From still another perspective, a person with no symptoms at all might be a closer match to a person with symptoms, than someone with very similar symptoms. For example, we now know that someone with early latent syphilis (two years in to the disease) showing no signs of illness (once again, for arguments sake, before VDRLs were available) should be treated for the disease regardless of symptoms. Someone with optic neuritis (a common manifestation of neurosyphilis) who is not infected by treponema pallidum, would not be helped by penicillin. There is nothing perplexing here. Our understanding of cause and effect allows clear thinking.

Families with schizophrenia running through them have an abundance of schizotypal disorder. 8 Once again, not a surprise; someday in the future we will find certain patients with panic disorder, or obsessive compulsive disorder, or whatever, appropriately grouped, from the standpoint of etiology with some schizophrenics. On the other hand, someone with a biological predisposition, say, towards excessive fearfulness (anxiety), or passivity, might have manifest symptoms that veer towards phobias, avoidant personality, obsessive compulsive disorder, panic disorder, or any one of a number of DSM IV disorders, the differences between them attributable to family or culturally learned defenses, parental models of coping, individual trauma, or individual psychodynamics. For example a person using counter phobic defenses (say sky diving) to “choose” and attempt to master their risks for themselves, will present very differently than a frightened individual passively yielding to that fear, or trying to gain a sense of control through repetitive OCD rituals, or dependent on the protection of others, or idealized love, or through submersion in cults. And medications that treat “anxiety” might be helpful in a large number of disorders that vary greatly from each other in manifest symptoms, but might have in common the fact that the particular symptoms (shaped by other factors) were fundamentally a response to genetically based greater quantities of “fear.”

Are they all the same disease, or as some would have it, are they part of a spectrum? Using the common effectiveness of a given treatment might give hints about etiology, but, not necessarily. Syphilis, pneumococcal pneumonia, and strep throat, are very different diseases, with symptoms that do not resemble each other, but they are all bacterial and are all handled very nicely by penicillin, just as SSRIs are effective for all kinds of different illnesses. To play with the analogy a bit more, strep throat is not really the same disease as rheumatic fever, although the same germ is involved in both diseases. The key point is that current DSM IV disorders are not likely to be equivalent to each other as separate, equal diagnostic entities once we understand the complexity of their underpinnings.

A drug that was a pre-anesthetic calming agent, chlorpromazine, was tried in schizophrenia and found to be hugely successful. Originally, this and other “major tranquilizers” were used not only in schizophrenia, but without a second thought, in panic disorder and other clinical situations where calming agents were helpful. Only later, when tardive dyskinesia presented itself as a problem, did clinicians begin to restrict its use to psychosis. And, within a decade, phenothiazines began to be thought as having unique “antipsychotic” qualities as opposed to tranquilizing efficacy. How interesting it is then, that newer neuroleptics, where tardive dyskinesia is far less of a problem, began to be used (until we began to appreciate their other shortcomings) for panic disorder, obsessive compulsive disorder and bipolar disorder (even when there is no psychosis involved.). Many modern antipsychotics are also being labeled “mood stabilizers” although strong misgivings may be appropriate about that term.9).

The discoverers of Prozac, Drs. Fuller, Molloy and Wong have emphasized how little we truly understand about the brain and Prozac10. However, despite their realism about the science, the remarkable efficacy of SSRIs has had a halo effect on the scientific attitudes underlying DSM IV and ongoing research, so that even practitioners, far away from the laboratory, out in the trenches, where the practice of psychiatry is not governed by a rational understanding of the brain’s effects on the mind, feel they are practicing in a scientific manner. In actual fact, our work often consists of doing our best to play the odds. There is no problem with this. We think in terms of the risk/benefit ratio for a particular patient, and as far as it will take us, use DSM IV categories and evidence based treatment protocols. When necessary, we try various augmentation strategies, but all too often, our chances of success are not always clear from the literature. When treatment is successful, we should not be overly bothered by our lack of understanding about what is “really” going on. Doctors effectively used penicillin for a decade or longer before they figured out that it kills bacteria because of its effects on the bacterial cell wall. And in the last 20 years we have been lucky to be able to discover so many “penicillin” like miracle drugs that are safe and very effective for all kinds of emotional disorders.

On the other hand, while the current understanding of how medications work with the various disorders, may, or may not, be the best guess given what we know, if past experience is a guide, much of it will seem silly when we gain the knowledge we really need. This will be true even of treatments recommended by “expert consensus panels.” Indeed the idea of counting up votes of “experts” is understandable as a guideline for practitioners eager to be guided by the “best” doctors. But it is foolishness if the necessary knowledge simply isn’t there. To use words like “expert” distorts the tentativeness of the information. No one would have to be polled if the phenomena could be explained scientifically. Rational treatment would come from understanding, not faith in authority.

More troublesome, in an age of malpractice suits, pressures are brought on practitioners to follow the lead of the experts. “Standards of care” dictate proper treatment, when the proper treatment is not really known. Similarly, “evidence based medicine” linking diagnosis to treatment, is implied to be the only scientific approach to patient care. It elevates the organization of diagnosis according to operational definitions, which is a tentative approximation of understandable diagnoses, into the only legitimate scientific treatment paradigm. Keeping in mind the earlier discussion of congestive heart failure, given the state or our knowledge, this is not acceptable

It is fair enough to declare that findings using this paradigm can be sanctioned as “evidence based.” In research it is also appropriate to ask that approaches, which might challenge findings, follow through on their hypothesis with empirical data. In clinical settings, however, it isn’t legitimate, to imply that any other way of viewing the material is less scientific than, for example, the leaps of logic that often accompany spectrum disorder speculations, or diagnoses based on response to medication.

Making therapeutic decisions, when hard knowledge is not all we might wish, is a legitimate response to the necessities of practice. Whereas in research it is possible to comply fully with exactly defined criteria for experimental subjects, in the real world patients’ actual symptoms are not always cooperative with these requirements. As clinicians, we must treat patients as they exist. If we limit ourselves only to those who meet strict criteria, we will be treating only a fraction of the patients presenting themselves. Concepts such as spectrum disorders, and NOS (not otherwise specified) diagnoses, are not unreasonable as an attempt to deal with this. They provide a rationale that allows clinicians to use empirical findings derived from the pure version of the disorder, when treating the larger population of actual patients that they see. But, while clinicians should respond to actual patients with the best approximate approach, stretching diagnoses and treatments that are backed by solid evidence, and claiming the prestige of science for expanded usage is of debatable merit. From a common sense perspective, it is perfectly logical to ignore strict criteria in the belief that a patient might have the disease in question even when they don’t match up to criteria for a disorder. However, this perspective needs to be carefully examined. Along with its pragmatic value, it also introduces legitimate questions about what we mean by a DSM IV diagnosis.

Essences, the reification of operational definitions, and the reality of diseases.

In the current paradigm, making a diagnosis first and then treating on that basis is often considered the only way to proceed. But many difficulties have been created by this approach. For example, we all know of children brought to clinician after clinician, each supplying parents with a different diagnosis, or combination of diagnoses, in search of the “real” illness. Sometimes the search for a true “diagnosis” resembles the search for the buried traumatic event that once characterized psychodynamic psychiatry. Aha! There it is, the key to the lock. This patient is really suffering from ADHD or has bipolar disorder or has both, and so forth. If a label can be found, the mysteries of the patient will finally be revealed. Yet, recall that the causes of a particular diagnosis in DSM IV are no better known than they were in DSM II. Somehow, at this point, thinking in terms of disorders in the diagnosis/evidence based pardigm has convinced practitioners that making a diagnosis will best “explain” the problem.

In medicine the search for an accurate diagnosis is crucial. When the mystery of a difficult patient’s symptoms is finally resolved by the discovery of a tumor, a viral or bacterial infection, an autoimmune disease, MS, and so forth, treatment is clarified. An accurate diagnosis points to a rational basis for pursuing further care. But not all diagnoses serve that purpose. Some diagnosis are catch alls, a name to label patients’ symptoms when all tests come back negative. Chronic fatigue syndrome, and fibromyalgia are examples, controversial diagnoses with advocates insisting the illnesses are real, and detractors, not bothering to enter the fray, but privately comfortable in their skepticism. There are less controversial illness like irritable bowel syndrome, which is similarly diagnosed when no other cause for the symptoms has been demonstrated by positive tests. The question is which psychiatric diagnosis are like fibromyalgia, and which are more clearly established like schizophrenia and manic depression (as opposed to bipolar disorder which increasingly is becoming a fibromyalgia kind of diagnosis)

When a clinician claims that a patient is “really” depressed, or has ADHD, or has bipolar disorder, or whatever, even though DSM IV criteria are not met, is that similar to a physician discovering a previously undiscovered illness, astutely uncovering a real hidden disorder, which will now yield to treatment ? Or, are they muddying up the significance of the real disorder by claiming all kinds of patients, “really” have the disorder when they in fact, don’t.

It made sense to broaden the criteria for bipolar disorder so that full episodes of mania are no longer necessary to make the diagnosis. Genetic illnesses can have incomplete penetrance. Infectious diseases can have mild or severe symptoms, as can autoimmune diseases. However, in the case of bipolar disorder, there are numerous vaguely similar symptoms that people without bipolar disorder display that are now getting them diagnosed with the illness. Common examples are people with bad tempers, depressed people who are irritable (the irritability because it is sometimes seen in mania instead of euphoria but it is now all too often being taken as uniquely bipolar) teenagers and drug abusers with mood lability (now being called “mood swings” since the concept of ultradian cycling was speculatively introduced.11) see: Bipolar Disorder in Children and Adolescents: a Caution Other examples are patients whooping it up in their mid 20’s in the big city, whose age related foolishness is interpreted as the impulsivity of hypomanic episodes. While it may be exactly that, it may also be a stage in life, that will be outgrown, with marriage, mortgage, and family.

That there is a grey area in making the diagnosis is perfectly legitimate. The idea of spectrum disorders is also legitimate enough. The problem is the application of the idea. The diagnosis of bipolar disorder in children increased 40 fold between 1994-5 and 2002-3. 12 Are clinicians becoming too facile at labeling patients because of the emphasis on a diagnosis (and evidence based practice) despite the fact that the long term treatment results of this kind of “science” has not been established for patients not fitting criteria? 13,14

Implicit in the decision to stretch the diagnosis to include a patient that doesn’t meet criteria for that disorder is the belief that the disorder exists in the same sense as an infection or tumor or diabetes. It is not just an operational definition. It is real in the same way as say, a child presenting with fever, achiness, vomiting and diarrhea, without complaining of a scratchy throat, may nevertheless be suffering from strep throat. A clinician who claims a child or adult “really” has bipolar disorder, or ADHD despite not meeting its defined criteria, assumes something is going on related to their actually having a specific disease process. Something is wrong with their brain circuitry, or neurotransmitters, or genetics that justifies the diagnosis even if it cannot be demonstrated. And a medicine is going to be effective because it somehow is getting at the fundamental pathological process, The problem is, for the most part, we do not understand how the medications work, so this reasoning is specious.

The problem of reifying diagnoses extends beyond trying to diagnose patients who don’t meet full DSM IV criteria. Some disorders are problematic not only because they are spectrum extensions of a diagnosis, but in pure form, from a common sense perspective might not be considered a disease. For example, it is possible to operationally define the cluster of symptoms that constitutes oppositional defiant disorder. While certainly something is troubling about the behavior, and in theory it may be studied objectively, is classifying this a “disorder” necessarily the best way to conceptualize it?

Merely labeling a syndrome of behavior a disease creates problems. Here is a quote from Educational Horizons Spring 1996: “Once upon a time parents who lacked the courage and/or interest necessary to set limits and impose responsibilities were thought to produce lamed and defiled children. “Spoiled brats” was the common lexicon. Happily, this benighted notion no longer enjoys currency. We now know that a child’s upbringing may really have little to do with “brattiness.” Children behaving like “spoiled brats” are often really suffering from an illness known as oppositional disorder.”

Is this what we meant to do? Have we really solved the problem of oppositional and defiant children by calling it an illness? Going still further, should treatment necessarily be medical? Are physicians really the best at handling these problems? Historically, in addition to parents, taking on children’s misbehavior was the province of moral authorities, clergymen, teachers, and the like. If unsuccessful, it might be a policeman and a judge. When clusters of behaviors are defined as a DSM IV disorder, does that automatically make doctors the experts, or promise the wonders of science even when we have scientifically discovered almost nothing that should make us the “experts?” Do we have the scientific authority to communicate to parents,or teachers that they should back off. It isn’t the child’s fault. They have “an illness.” Does this kind of illness have enough similarity to illnesses like diabetes, cancer, infections, for a medical perspective to be the proper perspective?

The chemical imbalance hypothesis and DSM IV

Unlike oppositional defiant disorder, illnesses such as depression, or the various anxiety disorders seem to fit the analogy to physcial medicine better. While the usefulness of DSM IV is not intrinsically related to the belief that “chemical imbalances” are at the root of most psychiatric difficulties, this has been an implicit assumption of a great many (though by no means all) researchers and practitioners during the DSM III and IV era. In the United States, the chemical imbalance argument has proven to be important in winning legislative support for improved insurance coverage that gives psychiatry parity with other medical conditions. Somehow, if illness can be blamed on chemistry, (or more lately on cellular changes) it becomes real. One other byproduct of the chemical imbalance model is that its simplicity has led to a great deal of comfort, on the part of physicians other than psychiatrists, to dispense psychotropic medications. Believing that they are operating within the logic of cause and effect, they merely have to focus on the improvement of the symptoms of the disorder in question and watch for side effects from the medication. A majority of psychiatrists also work within these parameters. After diagnosing a patient they typically follow up with med checks and that is all.

What are the most glaring difficulties with the chemical imbalance model?

1) Medications such as the Selective Serotonin Reuptake Inhibitors (SSRIs) have found usefulness in so many Axis I and Axis II disorders (e.g. OCD, Depression, Panic Disorder, Eating Disorders, phobias of many varieties, Borderline Personality, PTSD, Body Dysmorphic Disorder, Fibromyalgia, in selected cases Intermittent Explosive Disorder, Pathological Gambling, Kleptomania, not to mention OC Personality, Avoidant Personality, Dependent Personality) that to consider all of these forms of misery part of the same biological spectrum is stretching credulity. Occam’s razor demands a more parsimonious approach.

2) Medications that work in completely different ways are effective for the same disorder. For example, antidepressants such as desipramine and bupoprion have little serotonin effect yet are just as effective agents for depression as SSRIs. To keep the chemical imbalance hypothesis alive speculations have been offered to explain the effectiveness of noradrenergic and dopamine enhancing agents as ultimately influencing serotonin receptors downstream. This is not impossible but it is only a guess. A completely different hypothesis was offered by Petty (1995) who argued that GABAnergic drugs are fundamentally related to mood. 15

In Obsessive Compulsive Disorder (OCD) similar problems emerge. Originally, the fact that serotonin enhancing drugs were uniquely effective led to a belief that there was a causal connection, but as early as 1991 there was confounding evidence. Thirty mg. of dextroamphetamine was found to ameliorate OCD symptoms (Joffe 1991)16 . Moreover, while it is radical to advocate this as treatment, patients have reported that intoxicants such as marijuana, alcohol, and cocaine have given them temporary relief from OCD symptoms. Indeed, oral morphine is reasonably effective (Franz, 2001)17. Once again, it is possible to speculate that there is a downstream effect on serotonin, but if we use this argument we have come full circle in a tautological trap. The original reason for the serotonin-OCD chemical imbalance model was that serotonergic agents were believed to be unique in their effectiveness.

With so called “mood stabilizers” we are faced with similar difficulties in integrating theory with the facts. There is a murkiness in reasoning which can only be explained by the attractiveness of the idea that somehow a chemical imbalance is being corrected, and hence bipolar disorder is being treated on a fundamental, etiological level. However, the etiology is unknown, and the various “mood stabilizers” work through different chemical mechanisms. Thus, valproic acid and gabapentin have been hypothesized to work on GABAdenergic receptors, whereas (for example) the proposed mechanism of action for carbamazepine and lamotrigine is voltage dependent inhibition of Na+ currents. Recent speculations about lithium are that it is affecting G proteins, that it exerts a push/pull effect on the neurotransmitter glutamate. (Dixon And Hokin, 199818 : Lenox et al., 199819 ), or that it alters sodium transport in nerve and muscle cells and effects a shift toward intraneuronal metabolism of catecholamines. (Physician Desk Reference, 199920 ). Even the definition of what constitutes a mood stabilizer is controversial. (Sobo, 199921) . Originally, the idea was that a mood stabilizer had both anti-depressant and anti-manic qualities. When, until Lamictal, anti-depressant effectiveness was not demonstrable for any anti-seizure medicines, Sachs (1996)22 replaced this concept with a new definition, an agent which will “decrease vulnerability to subsequent episodes of mania or depression” and not exacerbate the current episode or maintenance phase of treatment.

So gripping was the appeal of the original mood stabilizer concept, that despite the lack of double blind evidence for the effectiveness of any anti-seizure medication for bipolar depression (this was before Lamictal’s efficacy was demonstrated), and despite the first hand experience of numerous clinicians (who actually saw patients on a consistent basis), they were nevertheless, recommended in the APA’s “expert” consensus protocol as a first line treatment for bipolar depression. Indeed, strangely, as soon as an agent was shown to have anti-manic properties it was invariably labeled as a “mood stabilizer.” Not until 2001 did the APA soften its stand against anti-depressants, finally approximating the practice pattern of the far more experienced, less “expert” clinicians.

3) With all that is unknown about the chemistry of mental illness, using the chemical imbalance model, researchers are not shy about concluding that a given disorder is “really” something else on the basis of the effectiveness of a medication. Thus Donovan, SJ (as reported by Sherman, C) 199823 proposed that a new diagnosis, “Explosive Mood Disorder” be created and replace Conduct Disorder and Oppositional Defiant Disorder, for “children with irritable mood swings” because valproic acid helped his cohort of inner city, out of control, kids. 24Even more extreme, all kinds of problems with impulse control (called compulsions by laymen) such as overeating, gambling, paraphilias, various patterns of alcohol and drug abuse, and so forth have been labeled Obsessive Compulsive spectrum disorders because SSRIs are sometimes effective.24 The reason these “compulsions’ were originally not thought of as related to OCD was that they revolved around giving in to temptation, over indulgence of a forbidden pleasurable activity. They were totally different in character from the extraordinary worrying, and doubting that characterizes OCD obsessive thoughts and compulsive behavior. The fact that SSRIs can be useful in both should change nothing regarding etiology or nosology.

4) The chemical imbalance model is not an important part of the basic (animal) research being done to test new potential anxiolytics and anti-depressant agents. The chemical imbalance model might or might not stimulate a search for agents that effect given neurotransmitters, but while there is some research on genetically predisposed strains of mice and guinea pigs, who may be wired differently, or chemically different, most research is done on ordinary animals that are environmentally stressed and then relieved of this stress by potentially useful chemical agents. For example, the FST (forced swimming test) tests the ability of drugs to postpone hopelessness in animals forced to swim and swim and swim to remain alive. SSRIs do this. So do noradrenergic agents (which interestingly enough, are more likely to cause the rats to try to climb out of their test environment (Detke 1995)25 ). More pointedly, rat pups that are isolated from their mother and litter mates produce “ultrasonic sounds” that are indicative of stress. SSRIs reduce these sounds. (Oliver, 1994)26 For a while there was excitement that substance P antagonists might be useful psychotropic agents because they were shown to reduce “stress induced vocalizations” in guinea pig pups (once again separated from their moms).

A drug successfully screened in this manner will certainly not be presented to patients as a drug that is so good at shutting off distress that it even works to subdue what might be considered the prototypical model of terror, a helpless infant separated from its mother. A patient told he is being given a drug that will kill his reaction to what has been upsetting him will approach that treatment very differently than a patient given a different spin, one told that his medication is treating the chemical imbalance that is causing his specific ailment. Similarly, primary care physicians and psychiatrists will be far more enamored with the thought that an agent has been tested (and even better, FDA approved) for a specific DSM-IV disorder if the mindset is that the effectiveness is due to fixing faulty synapses, rather than that the patient is being drugged out of his suffering. The question is whether following an evidence based treatment protocol for that diagnosis , or an FDA indication for a medication, falsely signals cause and effect, when in fact, diagnosis followed by evidence based treatment means nothing of the sort.

The use of medications within a psychological / clinical context paradigm as opposed to a strictly diagnostic perspective

Herman Van Praag, in his classic paper “Nosological Tunnel Vision In Biological Psychiatry. A Plea For A Functional Psychopathology” ( Van Praag, 1990)1 , warned that exclusively focusing on diagnosis can blind the clinician to other equally useful perspectives in approaching patients’ difficulties. If anything, since his article 17 years ago, this issue has gotten worse, in part because mental health insurance coverage may be limited only to DSM IV defined disorders. Taking a cue from criticism leveled at the DSM II era the rest of a patient’s pathology may be considered analogous to the problems of the “worried well.” This attitude can not be entirely blamed on insurance companies. Many psychiatrists limit their clinical focus exclusively to the treatment of symptoms defined by DSM IV. The rest of the patient’s complaints is considered chaff.

In research, protocols have to be strictly followed, so a cookie cutter perspective limiting the focus of what is to be studied is necessary for objective results. Fifteen minute, once a month med visits, may be all that is needed. However, as will be illustrated, this is unacceptable as a standard for optimal care. It isn’t only frills. A broader view of the patient’s problems may yield more informed use of medication. Clinical context can be just as, or more important, than diagnosis. To illustrate this it will be necessary to resort to the preeminent approach to patient care before DSM III and IV dominated thinking, clinical case histories.

Mr. T. was a thirty-year-old man who was very unhappy in his marriage. He had always pictured a family life with two or three children. His wife, a beautiful woman, whom he had originally been smitten by, had never wanted kids. Mr. T had assumed she would change her mind. But now, six years into the marriage, he had realized that there would be no change of heart. She was to be the project of the marriage, her vulnerabilities, her needs, the vicissitudes of her emotions. It had gotten old. Over the years, he had noticed his impatience with her grow into indifference and then sarcasm. He came for help when he had become depressed. He couldn’t sleep. He couldn’t eat. He couldn’t concentrate at work.

I’ll put the issue in a nutshell. What if the Prozac worked like a charm and completely rid him of his depression? What if Prozac returned bounce to his life and now he found he could, after all, live happily with the status quo? This is, in fact, what happened. As long as he remained on the medication he was fine. But here is the key question. What if 25 years from now, Mr. T. were to wake up and suddenly realize he had wasted his life? He really had wanted children and a family all along. What if he wouldn’t allow a doubling of his Prozac dose at that point? A drug had deceived him, cheating him of what had been meant to be. Would Mr. T. have had major depression if he weren’t biologically predisposed? We don’t know. (Nor do we know with others.) But even if he would not have gotten as depressed without having a biological predisposition, it is wrong to dismiss his marital situation as merely a precipitant. In this case, the depression was an alarm signal. It told the patient that the life he was living would not do.

Ms B. was having an affair with a married man who was on Prozac. Every time he came off his medications he couldn’t stand his marriage for a moment longer and he intended to marry my patient. As soon as he was back on meds his concern switched to his teen-age daughter who needed him to stay. Which was the true judgment? I’ve had patients find the courage to ignore their fear of loneliness and leave an unsuitable marriage with the help of SSRIs, others find the courage on meds to have what proved to be an unwise affair. I’ve seen a medicated patient quit his 9-5 job, use his inheritance and “go for it” as a singer. Was this realistic? I suppose it depended on his talent, connections, luck. He had previously been cautious about his inheritance, recognizing that it was a one-time thing and was his only hope for financial security. Only after he also decided he was going to use this money to develop a solar car did I become concerned. He was not manic or hypomanic, but he was definitely feeling better than he had ever felt. When told he would have to stop the Prozac, so that he could review his choices unmedicated, he stopped therapy and went to a different doctor.

Van Praag argued that instead of correcting imbalances, pharmacological agents may be viewed as inducing particular psychological states which, though not specifically related to diagnosis, are nonetheless the basis for the usefulness of the medication. As an alternative to a chemical imbalance paradigm, a case can be made that SSRIs are efficacious 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 impact 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 impact individuals in ways that are not specific to diagnosis. What is that effect?

The most frequent description of the effects of SSRIs that I have heard from patients are “It doesn’t matter.” or “Don’t sweat the small stuff.” or “What’s the big deal?” It is this “Don’t sweat the small stuff” perspective that I believe is SSRIs unique blessing and curse. 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, then 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. They are the answer to existential angst. Perhaps Sisyphus, if he had only been born in the 90’s, could have left that rock alone and had a nice snooze.

On the other side of the equation, I have a psychiatrist colleague who took Prozac to relax and enjoy his vacation. It worked very well. He told me that he tried it at home when he returned. He quickly stopped it when he found himself thinking, “Who cares?” when his patients described their problems. Pomerantz 28 describes a patient that was getting speeding tickets while on an SSRI and similarly didn’t seem to be bothered.

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, (I once had a patient who described a horrible attack of panic because she feared something was going wrong with her vision. Only later, when she removed her glasses did she realize that her dirty eyeglasses had set her off) 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 (or a lot of) 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. Adolescents often turn to illicit drugs (analogous to adults at cocktail parties), to get rid of their social anxiety. Teenagers are also often extremely up front in social situations, meaning they out and out torture the nerds.

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.” How does that differ from drugging oneself out of problems rather than “learning critical skills during the formative years?” Isn’t discomfort often a stimulant of growth, (the stutterer who becomes the grand public speaker, the short guy who becomes Napoleonic)? I’m not sure it is different, but that discussion will have to await a different article. The fact is however, that SSRIs are used exactly in this way and a myriad of other analogous ways by clinicians to the tune, according to one estimate, of 65 million people in the United States since their introduction. Right now, when they are found effective, the chemical imbalance perspective leads to the conclusion that the patient must have “really” been depressed, or had a subclinical version of an illness or had a spectrum disorder. I am suggesting we can spare ourselves this pseudo logic and address the more important question raised above. Should we or should we not drug people into subjectively improved states when an officially designated “illness” is not at issue?

While diagnostic psychiatry is a useful way to measure treatment success or failure and a helpful way of thinking about how to approach many patients, it is not the only legitimate way to think about a patient’s problems and reason for seeking treatment. As illustrated above, there are other perspectives that may lead to treatment success, characterlogical qualities that may guide our treatment, conflicts causing depression or anxiety, or mood instability, situations that may be highly relevant not only to psychotherapy, but more to the point, to the choice and timing of medications. Like the example of hypothyroidism caused CHF, understanding the clinical particulars behind a given DSM IV diagnosis may give a better result than protocols based on diagnosis alone. Without the science understood, going by diagnosis/treatment statistical results is an extremely crude approach to treatment. It may be useful information, supplying us with the odds of blindly treating a patient on the basis of diagnosis alone, but not when it is passed off as more than it is. When it is making claims that it alone represents true science because it is evidence based, we have moved beyond science to something approaching hucksterism.

It isn’t by the way, only a matter of pharmacology. The same perspective applies when medication is not involved, for example evidence based treatment using cognitive behavioral therapy.

A sixteen years old teenager was evaluated for medication for depression. 29 Early in childhood he had been abandoned by his biological mother and raised by his grandparents. His grandmother/mother had died two years before at the age of 74 after her third stroke. His 79 year-old grandfather had severe emphysema, and judging by his labored breathing in the waiting room, didn’t look like he was too long for this world either. At his prep school the patient kept talking about death. Like others when they are depressed, his dark moods didn’t make him very popular with the other students at school, which made him even more depressed. On the basis of his depression diagnosis, cognitive behavioral therapy was being pursued by his therapist. Attempts were being made to replace his negative thoughts with positive thoughts through homework exercises.

Although I am a non-believer I would have had no problem if he was being comforted by religion, if he was given a positive way to think about death, that his mother was in heaven, and he would one day see her there. But being told to repetitively practice not thinking about death, replacing it with more positive thoughts by doing homework assignments again and again to accomplish this, places psychiatric cure on the level of its behavioristic antecedents, training rats to perform a task through repetitive exercise.

The beauty of science is that it can strip away the attitudinizing, the philosophy and poetry, the accretions of culture, when approaching a subject. “Just the facts, Mam, Just the facts”. Detective Joe Friday, played by Jack Webb on Dragnet, understood how to get the answers to a mystery. Is planning the treatment of a 16 year old boy, upset by the death of his mother, and the impending death of his father, best conceptualized with blinders worn by the doctor, that eliminates every non scientific consideration?

If a boy, about to become an orphan, had asthma, a pulmonologist could properly focus on the asthma alone and leave ministrations of his soul to a priest. It is harder for psychiatrists to take this approach. The cognitive behavioral therapy offered him, while scientifically sound, was alienating him from the reality of his experience. Fine, given his situation and personality he wasn’t going to be the life of the party in high school. He would probably not be invited to a party. But he might be able to learn to love the blues, or read authors who have come to terms with the death of a loved one, or find friends who like to visit sad territory, or be helped by a therapist who wants to visit him in his own experience, who might legitimize his “negative” feelings, bring dignity to his suffering, rather then offer a Henry Higgins conversion to a chipper chap as the healthy way to be. Is a doctor who conceptualized the issues this way no longer practicing legitimate psychiatry because he has left the realm of diagnostic psychiatry and clearly defined symptoms?

Psychological issues that may shape and guide medication strategies or other forms of therapy

Mrs. L. had originally required hospitalization and 40 mg of paroxetine (Paxil)to recover from a postpartum depression. It worked well, but after seven 30 months on the meds, an incident happened which disturbed her. She was visiting her one year old at his daycare center during her lunchtime when one of the workers began screaming at another infant without picking her up. The next day Mrs. L went shopping during her lunch break. Later that week a coworker became tearful during the course of a conversation with Mrs. L. regarding her own child’s daycare center. Only then did Mrs. L. wonder about her decision to go shopping the day after she had witnessed the daycare worker’s inappropriate reaction. She wondered if her paroxetine had made her indifferent, when ordinarily she would have reacted and worried about such a thing.

We decided to taper the dose of medicine to 20 mg. Sure enough, on less medicine there was a dramatic change in her perspective about many things. For the first time I learned about the pressures she had been under at the time of her original hospitalization. Mrs. L. had tried to find time to be the powerhouse worker at her job that had brought her so many promotions in the past, an ideal mother for her newborn infant, and responsive to her husband’s very exacting standards about her housekeeping. Suddenly, without the higher doses of paroxetine, her fury poured out. She described, in detail, episode after episode in which her husband stood to the side and supplied her with a never ending critique of her adequacy as a mother. The higher doses of medication had muted her responsiveness, allowed his criticism to go in one ear and out the other, but now there would have to be change “or else”. Mrs. L. also acknowledged that she had not been doing her job as carefully as in the past and eventually the company would discover her drug induced “what the hell” attitude. At home, she had bounced several checks, something that had never happened before she was on medication.

Therapy now turned to how her life would have to change. She seriously considered stopping her job. She loved being a mother and didn’t want to miss out on her son’s crucial early years. She demanded changes in her husband (with the threat of divorce). Her new assertiveness had rapidly put him on good behavior even before marriage counseling started. A few times, during her sessions, she became tearful about her dilemmas. Although we discussed the possibility of returning to higher doses of medication should the need arise, she was not eager to do this. She felt her tears were about real things and did not consider herself depressed. She did not feel hopeless nor helpless. Her sleep was not as restful. She sometimes tossed and turned. But she was okay. We joked that we might go up on the paroxetine temporarily if, and when, she needed a vacation from her stresses. In fact, throughout I was concerned that her greater emotionality might be a prelude to the return of her original symptoms. But our perspective was quite different than an automatic increase of medicine at the first sign of tears. As it happens she did not need to return to higher doses. She did quite well, eventually deciding to work part time. Three months after making that decision she was the happiest she had been in years.

It is noteworthy that when she was reduced to 10mg (at her urging) there was another improvement (depending on perspective). She again noticed dust on her furniture. She noticed that the pictures on her table had been placed haphazardly. She arranged them more aesthetically. She did not feel driven to take better care by the internalized monster described in obsessives by Shapiro in “Neurotic Styles”31 , by an unending “I should, I should I should.” She took pride in her newly regained “attention to detail.” She also regained a degree of empathy for her husband. There certainly was the danger that she was returning to a dynamic of taking care of everyone and everything, of offending no one, a role that she had assigned herself from early on in childhood. This pattern may have played a part in her original postpartum depression as she tried to juggle her responsibilities and became overwhelmed, consequently generating forbidden anger at her newborn. Certainly, her regained empathy for her husband might be the beginning of permission for him to begin carping again but she thought she “would be able to handle that.”

Mrs. D a computer consultant with a terrible foster home past was successfully treated for depression with an SSRI. She had never felt she was as good as a techie as her 5 male partners. She had a never ending need for reassurance, which was embarrassing to her. Every night on her drive home she tortured herself with the things she felt she had mishandled. On Prozac all of this changed. She acknowledged that she wasn’t as good a techie as her partners, but she wasn’t bad. More importantly, she realized she was indispensable to her team. She was the only one with sufficient social skills to handle their clients. For the first time in her life she was able to ask questions at conferences without feeling like an idiot. No longer hungry for confirmation she was also able to stop a cycle of love affairs, which had led nowhere. On the other hand, her comment coming off meds was noteworthy. “I feel like I’ve been drugged for two years. Now I want to take a look at my checkbook.” She also reported behavior that now, off the meds, seemed bizarre. She had bought a puppy that she kept in an unfinished basement. While medicated she had not cleaned up the poop, reacting with “well whatever.” Off the medicine she was shocked by her behavior

Mr. K., a lawyer for a large corporation, was overwhelmingly depressed at home and work. The apparent cause was a difficult supervisor at his job. Almost daily his supervisor would criticize some aspect of his work and Mr. K. would be immobilized for the rest of the day. Sometimes he would stare at the wall in a daze… “my father always called me a complainer…you don’t have to love your job; you just have to get it done… I’m a loser … all those years in law school and for nothing…” Placed on Prozac Mr. K. was quickly fixed. His supervisor would enter his office, make his usual derogatory remarks and nothing would happen. Mr. K. could again get his work done in fine form. There were other benefits. His overweight wife lost 35 pounds. For the first time in years, Mr. K. put down the TV remote control. They began having good conversations, the kind of talks they used to have when their relationship was fresh and engaging. Everything became new. Mr. K. realized that for years he had been going out on Sundays because he was irritated by the tumult of his children at home. On Prozac, he found himself playing with his children and having a great time. After ten months on the medication we decided to see how he would do without it. Within a few weeks we were back to square one. His supervisor’s remarks were again devastating him and he was a grouch at home. He made a quick recovery once he was placed back on the medication. After 16 months on Prozac Mr. K. found a new job. He loved it. He came off the Prozac. He did just fine.

There were only a few peculiarities that he commented on when he got off the medication. Although overall he had worked far more effectively on Prozac, for the first time in his life he found himself ignoring deadlines. Once or twice, that had caused difficulties. He bought a Mercedes on the medication. He had always wanted a Mercedes, but off of the medication he considered it a budget buster and foolish.

This case is noteworthy not only because his judgment was altered by the meds, but because, at ten months, when we first tried stopping the meds, he would have seemingly illustrated the statistics often replicated in studies, of patients who have a recurrence without their meds, thus providing one more piece of evidence, seeming to confirm the biological basis of his illness. But, at 16 months, with the apparent cause of his depression eliminated (his critical supervisor), he did just fine without an SSRI. This doesn’t diminish the almost miraculous effectiveness of his original meds, or even that Prozac may very well have helped him gain the initiative to find a new job. However, it does highlight the kind of questions that clinicians should ask themselves about the particulars involved in a specific patient’s illness, as opposed to exclusively focusing on the operative factors in a specific diagnosed illness. This perspective is in contrast to the clinical practice guideline issues by the U.S. Department of Health and Human Services which flatly states that where there has been a prior episode(s) of major depression “maintenance of antidepressant medication treatment should be for at least one year” 32 Statistically this assertion may have a basis but surely there are circumstances when this “rule” should not guide us.

The fact that on follow up recurrences are found so frequently in unmedicated, as opposed to medicated, patients does not automatically prove biological origin. Generally speaking, the issues involved in a depression are deeply woven into a patient’s character or the fabric of his life. Miraculous transformations are the stuff of melodrama not reality. One would not expect a change in the original factors that led to depression eight months or nine months into treatment, or even years later unless the patient or his circumstances changed. Hence, depression is going to recur off of meds. But it is not impossible for there to be a dramatic change in circumstances. If a patient has gone into a deep depression because of financial hardship after he/she has been fired from a job, chances are that finding a new terrific job will very effectively keep depression from recurring. Winning the lottery works even better. The same can be said for a person who does not have a neurotic pattern of relationships, who has gone into a depression after being rejected by a spouse or lover. Finding a new mate works wonders whether it is three months or two years after medication was begun.

The other issue that can be gleaned from these clinical vignettes, is the evaluation of proper dosage. If we stick to a strictly DSM IV symptom checklist, the fewer symptoms, the better. Or, the diminution of symptom intensity is an absolute good in terms of the risk/ benefit ratio. While this perspective is often proper, as we saw with Mrs. D, Mr. K and Mrs. L there was a downside to SSRIs as well as an upside. While the dulling of emotions such as anxiety, helplessness, uncertainty, feeling uncomfortable in social situations, feeling dissatisfaction with a spouse’s more obnoxious characteristic, and so forth, this issue would not necessarily qualify as a side effect, unless it reached hypomanic, or a dramatic degree of indifference. ( See Pomerantz 7) But, if the above observations are correct, the qualities we are describing are inherent to this class of drugs. In other words what is good about them is what is bad about them. The evaluation of clinical appropriateness is not always strictly related to diagnosis or symptoms, or the usual side effects. For example when the patient is making critical decisions about their life while on SSRIs is it good or bad to be under the influence? Increasing self esteem, or lowering fears of consequences (such as loneliness or rejection) may be a good thing for someone stuck in a bad marriage or job and afraid to make changes. Indecision can reach total paralysis in severe depression when self esteem is fractured and fears of consequences are gravely multiplied so here symptoms are clearly distorting the ability to act. The same can be said when mania leads to the opposite, reckless impulsivity. But, in the real world, these issues are a question of degree and medication can be a complicating variable.

It isn’t that meds shouldn’t be used, it is that these issues cannot be addressed unless they are conceptualized. Van Praag’s description of tunnel vision resulting from an exclusive focus on nosology is to the point here. Indeed, the combination of once a month 15 minute med checks (which may be all that is necessary when practicing evidence based, symptom vs side effect psychiatry) can lead to practitioners being blind to clinically crucial observations. While I was one of the first to describe SSRI’s “well whatever effect” 33 laymen knew about this phenomenon far earlier than I did. Consider this ad for a tee shirt:

 

The Many Moods of Prozac - tshirt

The Many Moods of Prozac – tee shirt

 

Why did laymen working for the tee shirt company have a better handle on this complication of SSRIs than “experts?” My “discovery” of this characteristic of SSRIs happened because several of my patients described it to me and I began to enquire about it. The important point is that in many of the case histories described above, having this understanding was a crucial part of evaluating the risk/ benefit ratio of medication treatment. Yet, it is almost never part of the literature on this topic. The fact that it is still not described points to how unobservant the psychiatric profession remains, how much 15 minute/ once a month med checks, DSM IV driven “evidence based medicine” and the like, has blinded the profession to obvious findings. Interestingly, internet bulletin boards, while full of misinformation, sometime contains patient self observations that have validity. Many are searching for help in describing the effect SSRIs are having on them. My description of the “well whatever” effect in an unpublished internet article34 led to tens of thousands of readers going to this article on the basis of bulletin board recommendations.

Brainstorming: Further perspectives and unusual uses of drugs resulting from a psychological rather than diagnostic perspective

While SSRIs, and bupropion are believed to be roughly equal in their antidepressant efficacy, bupropion generates an entirely different psychological result due to its effect on dopamine, and to some extent, norepinephrine. It tends to be activating rather than calming. Most clinicians use bupropion in depression when anergia or anhedonia is prominent, and tend to avoid it if anxiety or agitation characterize a depression. It is also one of the few antidepressants that isn’t used with panic disorder because it can give an edgy feeling that can set off panic attacks. Yet, as we saw with the psychological effect of serotonergic medications, there are no hard and fast rules.

When Mr. K., a 50 year old businessman, was transferred to my care, he was already on bupropion for panic disorder. When I took him off it his condition worsened so he was put back on it and he did well. After seeing Mr. K for 8 or 9 months in weekly psychotherapy sessions the reason bupropion seemed to be effective became understandable. His mother, during a bohemian interlude in her 20s, had left Connecticut and went to live in Greenwich Village. There she met and married Mr. Ks father, a ne’r do well charmer and, it turned out, alcoholic. After a few years, when his mother’s trust fund proved inadequate to support the two of them and their 2 sons, she left his father, returned to Connecticut and met and married a responsible to a fault, extremely moral, authoritarian, go by the books, prep school teacher. Mr. Ks father was more than willing to give up parental rights so, along with his brother, he was adopted by his mother’s new husband.

After the blush of their early romance, his parents settled into real life. The atmosphere was tense. His mother had chosen her new husband, because of her attraction to him, but it turned out it wasn’t as simple as physical magnetism. She found his tight ass rule irresistible. And as she had done in an earlier incarnation of her M. O. she was a mighty opponent. Secretly she took laxatives, to keep herself stylishly thin. This time around, she was perfectly presentable to the outside world, but in the privacy of her castle, she almost constantly had gas, which for comfort often had to be released wherever she was in the house. Several times she had to be hospitalized for her mysterious colonic illness. It took 25 years for her laxative abuse to be discovered, long after my patient had left home.

Mr. K’s adopted father was a perfectionist of the worst variety, stern and unforgiving, and when pushed by my patient’s childish half effort, he was capable of furious outbursts. Not all of this was earned by his misbehavior. In reconstructing the probable scenario in therapy, we thought it very possible that both he and his brother were easier targets than their mother. She, after all, was sickly.

Mr K’s adopted father was not all bad. He was capable of play. He coached the prep school’s soccer team. He was extremely stern here too. He could scream at his players’ screw-ups or worse, give them the cold eye. However, he enjoyed soccer and this enjoyment was infectious. Most of those he coached considered him tough, but over all, a good experience. His father’s reaction to non sport derived work was completely different.

As with most people it wasn’t a lot of fun, but here his neurotic patterns let loose the full fury of his frustration. As Marlon Brando put it, and tens of millions working stiffs since and forever after, have put it, when youth had passed them by: He could have been someone, been a champ. He had been off to a good start, before the army and World War II took him away from his career. It never got going again, not like his brother who had had a fantastic career. He told himself that he chose teaching because of his desire to do good, to make a difference for other people. He made sure this wasn’t a cop out, wasn’t simply a flight from the battle field, by dedicating his life to hard labor. He brought the battlefield with him. He heaped on the challenges, took second and third helpings of things he hated to do. He took pride in this stoicism. He felt contempt for the slackers. He felt sorry for himself because of all of the work (as he saw it ) life dumped on him. It made his life gruelingly hard. The work was never done well enough and never done. Mr. K and his brother, as children, were champion slackers. The choice between play and work was not difficult. Both knew to get out of the room when their father was in a foul mood, especially if he had been drinking. Mr. K quickly learned that no matter how hard he worked, his father would be dissatisfied, sometimes exploding over the slightest mistake. In general he perceived how disappointed his adopted father was with him, perhaps in proportion to how disappointed his father was with his own life, his marriage, stymied career, and financial stresses not adequately covered by his salary and Mr. K’s mother’s trust fund.

It was especially tense when it came to school work, whenever Mr. K’s intelligence was challenged. His father seemed to take particular pleasure demonstrating how smart he was and how stupid my patient was, perhaps because he still wanted to prove to Mr. Ks mother that she had made a smart move choosing him and not Mr. Ks biological father. Or perhaps, as noted,it was a way of getting even with his disappointing wife. It is unlikely that Mr. K’s father would have seen things this way ( not unless he was in therapy with me). These theories about his parents’ motivations cannot be proven with scientific certainty. They are a mix of speculation and likelihood. They are offered as an illustration of the kind of thinking that might go on during insight therapy.)

In high school, having been compared to him repeatedly, Mr. K soon resembled his biological father. He goofed off, got high on illicit drugs, faked it when academic challenges called for intellectual effort, essentially bought into his adopted father’s characterization of him as a loser/slacker. Mr K’s behavior was not given a name, to blame it on. Back then ADHD and doctors were not the solution to Mr K’s childhood ways. But, by not making the effort, he lost a lot. He wasn’t able to prove to himself that he had intellectual capacity. In the back of his mind, like most children he wasn’t sure he had much in the brain department ( He had a perfectly normal amount of intelligence) By not trying and not getting good grades , his fear was reinforced that he was as his father saw him. He was dumb, a loser. Possibly, he might fail out of school even if he tried. There were times with his father, where he had given it his all and it wasn’t good enough. So his misbehavior brought relief from this concern. Because of his rule breaking, drug abuse, and failure to do assignments, he was asked to leave the prep school his father taught at. It left an indelible mark on his identity.

In later years, through AA, regular church attendance and conformity to a persona that would have made his now dead adopted father proud, he achieved respectability. There was only one problem. His panic attacks. The first one occurred after a rare visit, when he was 18, to his biological father. His father had actually prospered. After a week together he was driving home in the new car his father gave him, feeling great about himself, great about his car, probably great about the revenge this might exact on his adopted father. It was then that his first panic attack occurred. He was to have several of these throughout his life, whenever he was feeling terrific over his purchase of a new car.

There were other dynamics. It turned out he regularly promised more than he could deliver at work. He did it (in the heat of the moment) to be nice, or because he was too afraid to ask for assistance when he didn’t know how to do something. When there were expectations at work beyond what he believed were his capacities, when it came to being reimbursed for his legitimate business expense, procrastination and more procrastination. He was screwing himself royally with his expense account and was aware and angry about that. As a deadline date approached, the pressure mounted and mounted. There were all kinds of other turds he left here and there, at home as well as work, things left undone, some of them important.

It turned out that his panic was related to a fear that the sh—t was going to hit the fan, a panic that his laziness, incompetence, and dishonesty would be discovered. As a dopamineric agent, the bupropion helped him to get things done, thus alleviating the source of his anxiety and panic. It gave him the confidence to forge ahead, an expectation that he was going to accomplish what he had set out to do and take pleasure doing it. His results weren’t guaranteed to be good when he was influenced in this way by the medication, but it didn’t matter. If we recall, his father was equally perfectionistic when he coached soccer, but because he was having a good time, my patient (and his team mates had a good time.) It put my patient was in a different psychological mode. Like many fathers and sons, whatever tensions might build up during their lifetimes, sports was the one area they could enjoy each other. Mr. K, well into his 40’s, continued to play and coach soccer, capable of great effort and failures, but with a pleasure that forgave all shortcomings. It worked far better at getting work done than a grinding adherence to the work ethos.

Bupropion seemed to put him in that mode, meaning the work he customarily slacked off on became easy, half challenging, sometimes stimulating. This should not be a total surprise. Bupropion is often used in the treatment of depression to augment SSRIs when anhedonia remains. This seems to be a general characteristic of dopaminergic medicines. In the 19th century another dopaminergic agent, cocaine was the most popular miracle drug in the world, regularly used and extolled by the likes of President McKinley, Queen Victoria, Pope Leo Xlll, Thomas Edison, Robert Lewis Stevenson, Ibsen , Anatole France and a host of other renowned members of society. 35 Sigmund Freud wrote the following about it, “You perceive an increase of self-control and possess more vitality and capacity for work.”36 According to the Sears, Roebuck and Co. Consumers’ Guide (1900), their extraordinary Peruvian Wine of Coca “…sustains and refreshes both the body and brain….It may be taken at any time with perfect safety…it has been effectually proven that in the same space of time more than double the amount of work could be undergone when Peruvian Wine of Coca was used, and positively no fatigue experienced.”

Nothing has changed. Here is a headline and blurb from the New York Times 37 regarding the effect of stimulants and amphetamines:

Latest Campus High: Illicit use of Prescription Medication, Experts and Students Say

“Ritalin makes repetitive, boring tasks like cleaning your room seem fun,” said Josh Koenig a 20 year old drama major from NYU.

“Katherinen Plyshevsky, 21, a junior from New Milford, NJ, majoring in marketing at NYU said she used Ritalin obtained from a friend with ADD to get through her midterms. “It was actually fun to do the work,” she said.

What is the difference between tasks that are experienced as drudgery and those that are satisfying? It is a key question because students diagnosed with ADHD, presumably unable to attend to tasks because of a biological deficit, have no problem paying attention when they are having fun. Many can sit for hours with video games that require extraordinary focused attention. Why does their presumed biological attention deficit not operate here? I evaluated a student who told me that his mind completely fogged over when he had to read something for school. Without his medicine he could go over a page a hundred times and absorb nothing. “Really?” I asked, “You aren’t able to read anything?” “Well,” he told me, “there is one exception.” He was totally into mountain biking. Each month his mountain biking magazine arrived and he devoured that without medicine. Also supportive of this argument-unique charismatic teachers, who make educational material fun, can sometimes succeed with these students. Hence the effectiveness of amphetamines and Ritaline.

Besides ADHD diagnosed adolescents, and their friends, who sometimes borrow their meds when they have to do chores that they dread, stimulants (“greenies”), according to David Wells38 , and more recently Mike Schmidt39 have long been part of the professional athletes’ equipment, helping them to step up to the plate with confidence. It changes their state of mind from a passive, reactive, position to a take charge proactive stance. Or as one basketball player put it, “Give me the ball. I can make the shot.” This taking charge, ‘I can do it’ feeling, when approaching tasks, is a key element in most people’s perception of whether they are up to a challenge, and whether it is ‘work’ or pleasurable.

A patient reported to me that one of her employees decided, on her own, that their showroom needed a new paint job. My patient wasn’t sure if this were true, or if she liked the color of paint chosen, but she didn’t object. She came in one day and it was done. Her employee had done a terrific job. If my patient, who was her boss, had asked her to paint the showroom, the reaction would have been, “You have to be kidding. I am not a painter.” It has something to do with the idea, the inspiration coming from her employee. Hence her consequent enthusiasm to make her point.

Observe the new owner of the local diner. He will work ten, twelve, fifteen hours at a clip. He will polish the windows, try to improve the menu, rearrange the napkin holders, move from project to project always with energy to spare. Unless he has a gift for management his teen age employees will be moving along at a snail’s pace, keeping one eye on the clock. They will go home more tired than the boss. Dopaminergic drugs help you feel like the boss. They make you feel in charge. They make you feel like reward will be assured. They make arduous tasks easy.

It was not just Mr. K. I soon learned bupropion seems to often be effective for anxiety whenever it was connected to not getting things done, when, in a person’s psychology, chores hang over them, as both dreaded tasks, and dastardly consequences will ensue if the work isn’t done. When they get the work done the anxiety diminishes. So a drug that at first glance might be expected to make a patient edgy works against anxiety in those with this particular dynamic.

My off the cuff guess is that this dynamic is not particularly common in panic disorder. Mr Ks case was unique. Bupropion could never become an “evidence based” treatment for panic disorder, but like our example of thyroid hormone in CHF it made perfect sense in Mr. Ks case and others with that kind of conflict. It is probably not uncommon in Generalized Anxiety Disorder, but most likely, patients with this relationship to getting work done make up a minority of cases. As noted, dopaminergic drugs makes sense in a large number of children and adolescents with ADHD because there has been a failure to bond and identify with parents’ and teachers’ expectations. Children without ADHD, to a much greater extent, have incorporated into their bond with their parents (and later authority figures) the satisfaction and sense of self initiative when they are asked to do something to please (or not disappoint) them. It is far from perfect but compared to children (or adults) with ADHD, for whom almost any expectations are experienced as drudgery, boredom in the classroom is assured. In that case their behavior is exactly what could be expected from any bored trapped child, daydreams and restless fidgetiness, trying to liven thing up to suit their need to not feel at the mercy of the situation. Doing what they want, including making noise, gives them the feeling that they are in charge of their experience. It may get them in trouble, but they are not vanquished. How much simpler to supply this feeling through stimulants. Thus, instead of stimulating hyperactive qualities, the stimulant becomes calming by making the work pleasurable instead of oppressive. It does not addresses the core problem, the child’s failure to bond with authority figures, or group norms, or transform expected behavior to comply with another’s will, so that they feel like an active participant when obeying. But it is not a bad approximation

The key issue is searching for a connection between symptoms and psychological issues rather than assuming biological causality of a DSM IV diagnosis explains the problem. I have applied this thinking to certain causes of anxiety, and the behavior of children when they are not responding well to tasks, but the same kind of approach offers opportunities in many areas of psychopathology. For example, like patients with obsessive compulsive personality (as well as many with OCD) like Mr. K’s father, often experience their life as continually oppressive, essentially filled with exhausting never ending chores. With every bit of his strength, Sysyphus, had to push his boulder to the top of the hill, then it would roll back to the bottom and he had to begin again. His punishment went on forever. For patients with this curse there is no end to it unless they die and “rest in peace,” or become disabled and receive government checks for their bad backs. Unlike those with ADHD they perform tasks (begrudgingly), or attempt it, or intend to attempt. Their to-do list never gets done.

They cannot deal with the shame associated with goofing up. One way or another, whatever they actually do, the conflict preoccupies and exhausts them. Resentment of those who don’t work as hard as they do is inevitable. Like Mr. K’s father there may be fury at their adolescent children who don’t pitch in, or spouses, or partners in business.

As noted Joffe18 found that amphetamines can help OCD. SSRIs allow obsessive patients to soften their sense of imprisonment from their injunctions. They can let some of them go. In those obsessive patients where I have tried bupropion (I have not yet tried to use stimulants for obsessive symptoms) as expected, it seemed to make work less oppressive, sometimes make it seem, as noted above, easy and “fun.” In two cases, when I used it in this context, some of their anger seemed to diminish (as well as their guilt and feelings of worthlessness for their mysterious unacceptable (often consciously denied) hatred/ anger. Once again I did not make the decision on the basis of diagnosis, but when their resentment over duties, bubbled furiously into the sessions, we went with the bupropion.

Case after case can be cited, where this kind of thinking can be productive, serving as a rich source of hypothesis and hunches that might provide a therapeutic dividend, but we will end with a very unusual use of medication. Once again, it is understandable when the psychological issues are considered. A patient with PTSD for over ten 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. His history revealed that he did not have ADHD. But he reported that on the Adderall his post traumatic stress disorder was the best it had been in over a decade. It took a while to make sense of this but once again the explanation appeared to be found in his history. He and his fiancé had been trainees at a state police academy. His fiancé committed suicide with her gun, blowing her brains out. My patient found her body. He couldn’t clear his mind of the scene. During the day, during his dreams, her brain and skull fragments on the wall remained vivid. To make matters worse, he became a paramedic working on an ambulance which brought him to car crash scenes where horribly damaged bodies were not infrequent. Eventually in therapy 5 years before he came to me, he realized this was not good for him, and for years he had worked on a hospital ward. 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 the Adderall brought back his pre-morbid, 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 salesman who had been a work out 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.

Like the other examples, this is not an endorsement of Adderall for PTSD. It is an endorsement for this kind of thinking in formulating cases where this might be helpful. We are not talking about psychoanalytic understanding being necessary, but it does require training to think psychologically in a productive way. It requires not automatically thinking about diagnosis as the only way to approach treatment. The treatments described here will not prove efficacy to a scientist’s satisfaction. Moreover, some, or all of these formulations may turn out to have been wrong. But it throws down a challenge. My ideas are only a fraction of what might be possible if others were thinking this way. They need encouragement. We all need encouragement. We need psychiatric journals to publish ideas on subjects like these, so that we can discuss and brainstorm, and end the monopoly that DSM IV and scientific psychiatry has imposed on legitimate practice and discussion. Hopefully, some day clinicians will be thinking productively without intimidation from this procrustean bed. One day our patients may be enormously helped by a psychiatry entirely based on science, but we are far, far, away from being there. Not even close. Until we have the knowledge to practice in that way, we are doing a disservice making believe we scientifically know what we do not.

Summary and conclusions

  1. DSM IV is an advance over DSM II when it is used to measure treatment efficacy.
  2. However, as a diagnostic system based on operational definitions rather than etiological understanding, it has inherent weaknesses that have not been properly integrated into the evidence based paradigm. Indeed, the abuse of DSM IV, the claiming of unjustified scientific validity is so widespread that it is fair to ask whether these errors in reasoning are entirely innocent.
  3. DSM IV completely ignores psychodynamic psychiatry and its potential contributions to the understanding of pathology. This is, in part, a product of cultural and political prejudice. Throwing the baby out with the bathwater serves no purpose. The time has long past when scores have to be settled. Political correctness shouldn’t play a role in the content of journals and the training of psychiatrists
  4. Treatments based not on diagnosis and DSM IV specified symptoms, but on a legitimate understanding of psychological factors should not be deemed “unscientific” in a perjorative sense. Nosological psychiatry deserves its honored place, but not if it fosters tunnel vision in approching patients’ situational and psychological dilemnas and treatment strategies based on this information.
  5. Medications can be viewed as having specific psychological effects which may provide guidance about proper usage that is independent of specific DSM IV symptoms and diagnosis. Examples are given about the use of this perspective in guiding the timing, chosen dosage, and sensitivity to side effects that are not ordinarily considered. While a deep psychodynamic understanding of the patient is not necessary to use meds in this way, once a month 15 minute med checks will not give an adequate enough understanding of the patient to pursue this approach. Psychiatric trainees who are not trained in psycholgical issues will be incapable of this kind of medication strategy.
    • Related to the psychological effects of medications, totally radical, but not necessarily nonsenical, approaches to a variety of diagnosis and situations are offered as examples of innovative and effective ways to treat patients. They might not easily loan themselves to protocols which can certify effectiveness for a diagnosis, but they may, nevertheless, be as valid an approach as the promiscuous use of spectrum disorders as a way to conform to DSM IV parameters.
    • Psychiatry should welcome those interested and able to use insight psychotherapy,. While detailed statistics are not available to prove its helpfulness, there is nevertheless little question that self understanding can strengthen patients’ coping ability. Understanding their own motives might also do wonders for psychiatrists’ clarity of vision.
  6. Pharmaceutical companies should be credited with making a major contribution to psychiatric care. However, respect for findings by “experts” would be greatly improved if journals demanded from authors not only a listing of their affiliations with pharmaceutical companies, but the amounts of money they are actually receiving. This would go far to dispel any doubts about objectivity.
  7. A journal dedicated to think pieces such as this essay is greatly needed both for heuristic purposes to stimulate further research and for stepping back to gain perspective about patterns of practice.

Addendum

An additional example of rigidity of thinking related to a preoccupation with diagnosis was the successful use of atypical neuroleptics such as Resperidone and Aripiprrazole for the treatment of Major Depression. 38.39 Neither study distinguished between patients with psychomotor retardation, tiredness, hypersomnolence etc and those with a more agitated presentation. The study simply addressed effectiveness in those with the diagnosis. Thus we don’t know if efficacy was due to a tranquilizing property or an intrinsic antidepressant effect of the meds. I would imagine that further tranquilization would be counterproductive in the lethargic patient. On the other hand, there is clear evidence that those depressed patients who have significant anxiety do far worse when treated with antidepressants alone. 40The fact that these issues were simply not addressed is the key point here. That the FDA is locked into this thinking (it is effective or not for the diagnosis) doesn’t help.

Footnotes

1. Vonpraag, H.(1990) “Nosological tunnel vision in biological psychiatry. A plea for a functional psychopathology” Annals of the New York Academy of Sciences, Vol 600, Issue 1 501-510

2. Nagel, E “Psychoanalysis as a Scientific Theory” Psychoanalysis, Scientific Method and Philosophy, ed Sidney Hook (New York 1960 edition) p 38-55

3. Angell, M. (2000) “Is Academic Medicine for Sale?” New England Journal of Medicine 342: 1516-1518. Also Angell, M. (2004) The Truth About Drug Companies. New York: Random House

4.Kassirer, J P On the Take: How Medicine’s Complicity with Big Business Can Endanger Your Health. xx + 251 pp. Oxford University Press, 2005.

5. Avorn, J Powerful Medicines: The Benefits, Risks, and Costs of Prescription Drugs. . viii + 448 pp. Alfred A. Knopf, 2004

6. Horton, R. (2004) “ The Dawn of McScience” New York Review of Books Vol 51, No. 4 pp7-9

7. See Cautionary Statement in DSM IV. The authors of DSM III and IV were completely aware of this shortcoming. It is the use of DSMs that is at issue here

8. K. S. Kendler, M. McGuire, A. M. Gruenberg, A. O’Hare, M. Spellman and D. Walsh The Roscommon Family Study. III. Schizophrenia-related personality disorders in relatives Arch Gen Psychiatry Vol 50 No. 10 Oct 1993

9. Sobo, S (1999) Mood stabilizers and mood swings: In search of a definition. Psychiatric Times 16 (10):36-42

10. Statement accompanying the Discoverers Award given to Drs. Molloy, Fuller, and Wong, the discoverers of Prozac: “Human science still falls far short of fully understanding how the brain works. It is the most complex organ in the known universe, and though progress has been made in deciphering some of its secrets, much remains to be discovered.”

11. Kramlinger KG, Post RM (1996), Ultra-rapid and ultradian cycling in bipolar affective illness. Br J Psychiatry 168(3):314-323.

12. Mareno,C, et al “National Trends in the Outpatient Diagnosis and Treatment of Bipolar Disorder in Youth” Arch Gen Psychiatry 2007:64 (9): 1032-1039

13. Or more pointedly, in mailings paid for by drug companies, supporters of the new definitions of bipolar disorder in children (presumably to be included in DSM V), many of them from the finest universities, have implied that the diagnosis of bipolar disorder is being missed and causing needless suffering for children and their families, and potentially effecting long term control of the disease. This is a surprising claim considering, there are inadequate longitudinal studies of adult bipolar I patients unequivically establishing that good control helps prevent long term consequences such as increased rapid cycling. Moreover, there are no longitudinal studies that might establish that those who fit the new proposed criteria for childhood bipolar disorder will actually have a life long disease such as adult bipolar. Nor have there been adequate studies demonstrating that the medicines used in adult bipolar are safe and effective for what is being claimed to be childhood bipolar. It is astonishing that this minimum requirement of scientific inquiry is not only being ignored but allowed even a hint of respectability. Before these experts try to intimidate everyone else they should be held to the hot fires of scientific scrutiny. If they want to do research in these area (over the several years it will take to establish their position) that is wonderful, but until then their proclamations should be modest ones, that of inquiring minds with several hypotheses to clarify, not “experts” ridiculing everyone else for “missing” the diagnosis. See Bipolar Disorder in Children and Adolescents: a Caution

In the past year there have also been concerted marketing efforts on the part of pharmaceutical companies in which experts have similarly tried to convince practitioners of the widespread existence of Adult ADHD Once again diagnosis is the main marketing device.

14. Petty F (1995) GABA and mood disorders: a brief review and hypothesis. J Affect Disord, 34(4):275-81

15. Joffe RT, Swinson RP, Levitt AJ Acute psychostimulant challenge in primary obsessive-compulsive disorder J Clin Psychopharmacology 1991; Aug 11(4): 237-241

16. Franz,B (as reported by Sherman, C) (2001) ‘Adjunctive Oral Morphine Effective for Refractory OCD’ Clinical Psychiatry News July 29(7):4

17. Dixon JF, Hokin (1998) LE Lithium acutely inhibits and chronically up-regulates and stabilizes glutamate uptake by presynaptic nerve endings in mouse cerebral cortex. Proc Natl Acad Sci USA. 7;95(14):8363-8

18. Lenox RH, McNamara RK, Papke RL, Manji HK (1998), Neurobiology of lithium: an update. J Clin Psychiatry. 59 (Suppl 6):37-47

19. Physician Desk Reference 59th edition 2005 Thomson 20. Sobo, S Mood Stabilizers and Mood Swings: In Search of a Definition Psychiatric Times October 1999, Vol. XVI, Issue 10

21. Sachs GS (1996) Bipolar mood disorder: Practical strategies for acute and maintenance phase treatment J Clin Psychopharmacol 16(2 suppl 1):32s-47s

22. Donovan, SJ (as reported by Sherman, C) (1998) ‘Explosive Mood Disorder Quelled by Divalproex’ Clinical Psychiatry News Nov, 26(11):29

23. Hollander, E Treatment of obsessive-compulsive spectrum disorders with SSRIs. Br J Psychiatry Suppl. 1998;(35):7-12.

24. Detke MJ, Rickels M, Lucki I (1995) Active behaviors in the rat forced swimming test differentially produced by serotonergic and noradrenergic antidepressants Psychoparmacology (Berl) Sept;121 (1):66-72

25. Oliver B, Molewijk E, van Oorschot R, et al. (1994), New animal models of anxiety. Eur Neuropsycho-pharmacol 4(2):93-102

27. Pomerantz, J Loss of Appropriate Anxiety: An SSRI Overmedication effect? http://pharmacotherapy.medscape.com/SCP/DBT/1999/V11.n10

28. Sobo, S On the Banality of Positive Thinking

Elsewhere I have written that this occurred after 12 months, but after reviewing my notes I discovered it was seven

29. Shapiro, D Neurotic Styles Basic Books 1965

30. Clinical Practice Guideline, Depression in Primary Care: Detection, Diagnosis and Treatment, US Department of Health and Human Services, Agency for Health Care Policy and Research, Washington DC, Quick Reference Guide for Clinicians Number 5, April 1993

31. Sobo, S Psychotherapy Perspectives in Medication Management: The Inadequacy of 15-Minute Med Checks as Standard Psychiatric Practice Psychiatric Times April 1999, Vol. XVI, Issue 4

32. A Reevaluation of the Relationship between Psychiatric Diagnosis and Chemical Imbalances

33.“History and uses of the Coca leaf” http://www2.truman.edu/~marc/webpages/andean2k/cocaine/history.html

34. The Life and Work of Sigmund Freud, Volume I (1856-1900) (New York: Basic Books, 1953), p. 82-83

35. Latest Campus High: Illicit use of Prescription Medication, Experts and Students Say:” NY Times Page B8 3/24/00

36. Wells, D. and Kreski, C. (2003) Perfect I’m Not: Boomer on Beer, Brawls, Backaches, and Baseball. New York: William Morrow

37. Schmidt, M. (2003) Clearing the Bases. New York: HarperCollins

38. Mahmoud et al.( 2007) Risperidone for Treatment-Refractory Major Depressive Disorder: A Randomized Trial Ann Intern Med.; 147: 593-602

39. Berman RM et al. (2007) The efficacy and safety of aripiprazole as adjunctive therapy in major depressive disorder: A multicenter, randomized, double-blind placebo-controlled study. J Clin Psychiatry Jun; 68:843-53

40. Fava M, Rush AJ, Alpert JE, Balasubramani GK, Wisniewski SR, Carmin CN, Biggs MM, Zisook S, Leuchter A, Howland R, Warden D, Trivedi MH. “Difference in treatment outcome in outpatients with anxious versus nonanxious depression: a STAR*D report” Am J Psychiatry. 2008 Mar;165(3):342-51. Epub 2008 Jan 2.

41 Libby, A.M., Heather, D. “Persistent Decline in Depression Treament After FDA Warnings” Arch Gen Psychiatry, 2009 June V 66 (No. 6) 633-9

42. This was a matter of grave concern to the editor of the New England Journal of Medicine, Marcia Angell, who wrote an editorial “Is Academic Medicine for Sale?” See also Big Pharma, Bad Medicine (already cited in the introduction) A later editor of the of the NEJM also raised concerns as well as the editor of the Lancet 3,4,5,6 Their warnings eventually led to Senate hearings and the revelation that leaders in their field were being paid enormous sums of money that they were not reporting to their universities (e.g Joseph Biederman of Harvard an expert on ADHD who received $1.6 million dollars from drug companies that went unreported. Researchers Fail to Reveal Full Drug Pay See also Biederman There was a similar story arising out of a Congressional investigation regarding the chairman of Stamford’s psychiatry department (and president of the American Psychiatric Association) but Stanford was able to show that the money received by this researcher, had been revealed to them. Nevertheless the amounts of money revealed says something about objectivity. Stamford Taking it one step further there have been recent revelations that drug company hired ghost writers who wrote the story the drug company was trying to sell. They then hired world class “experts” to “coauthor the papers.” Medical Papers by Ghostwriters Pushed Therapy.

The fact that doctors can be so easily marketed led drug companies to hire armies of young attractive representatives to pitch their products to doctors at the finest restaurant in town. Reassuring them that they can provide evidence based treatment, the treatment worked out for a given DSM IV diagnosis , can be a very winning message. Doctors need to believe that they are pursuing , the latest standard of care.

But doctors loyalty can be fickle. When antidepressants were suddenly blamed by the media for an increase of suicidal ideation (with the usual media blitz exaggerating the danger of taking them) treatment wasn’t so much changed as the diagnosis being put in charts was altered. If they no longer diagnosed a patient with depression they didn’t have to worry about the alleged suicide danger. After the FDA gave a black box warning of the dangers of antidepressants, the number of people being diagnosed with depression dropped 44% among pediatric patients and 37% for young adults (Libby 2009) 41

Other articles that might be of interest (some already cited)

 

 

Summary of bipolar disorder article and additions since it was written