Our Closing Argument in Defense of Psychiatric Diagnosis

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This article is a response to the article “Will Denial Make DSM’s Validity Problem Go Away? A Reply to Pies and Ruffalo” by Jani Kajanoja, MD, PhD, and Jussi Valtonen, PhD.

“A map is not the territory it represents, but if correct, it has a similar structure to the territory, which accounts for its usefulness.”-Alfred Korzybski¹

We appreciate the latest rejoinder from Jani Kajanoja, MD, PhD, and Jussi Valtonen, PhD, (Drs K & V) in this ongoing exchange.² Let us all agree that there are serious problems with the DSM categories and the entire categorical approach to diagnosis; that many of the DSM conditions have low or marginal inter-rater reliability (kappa)—including major depressive disorder—and that the vast majority do not have specific biological validators.³ There is nothing new or startling in these observations, which were never the focus of our initial rejoinder⁴; namely, our objection to K & V’s broad-brush claim that psychiatric diagnoses are little more than a repackaging of the patient’s presenting signs and symptoms, with no explanatory value and no causal relationship to these presenting features.⁵

We also acknowledge that “disease,” “disorder,” “illness,” etc are complex and contested terms that remain areas of controversy in the philosophy of psychiatry literature, and that there are compelling arguments in favor of noncategorical/alternative diagnostic systems in psychiatry.⁶ There is also controversy surrounding the complex concepts of “causality,” “natural kinds, “diagnostic kinds,” “practical kinds,” and other essentially metaphysical issues, which are best dealt with in journals specializing in the philosophy of science and psychiatry.^7,8 However, we will draw upon psychologist Peter Zachar, PhD’s concept of “practical kinds” as they relate to psychiatric categories.^9,10

Notwithstanding these complexities, we have argued that several of the most serious diagnoses in psychiatry—such as bipolar disorder, schizophrenia, obsessive-compulsive disorder (OCD), and anorexia nervosa—have considerable explanatory value and validity. Furthermore, conceptualizing them as causes of the patient’s signs and symptoms can be substantively informative—even though we do not yet know the precise causes of these illnesses. For example, it is clinically useful and informative to say that a patient is experiencing fatigue and impaired concentration because they are depressed—and not because of, say, a viral infection. We find nothing in K & V’s latest rejoinder that seriously impugns this assertion. [see footnote].

Historically, Kraepelin considered schizophrenia (dementia praecox) and bipolar disorder (manic-depressive illness) to be disease processes (Krankheitsprozessen), as contrasted with clinical pictures (Zustandsbilden).^3,11 Kraepelin almost certainly regarded these disease processes as causes of their associated signs and symptoms—eg, he believed that “…dementia praecox causes a breaking-down of the self…”¹²

And while our goal was never to sing the praises of the DSM-5 or its latest revision, we have repeatedly pointed out that the correct use of this manual requires much more than simply matching the patient’s signs and symptoms to those of a DSM category; rather, the manual explicitly requires that the coded diagnosis must be supported by a biopsychosocial case formulation of the patient’s presenting problem. This critical point is conspicuously unacknowledged in both of K & V’s rejoinders.

With that prologue, we now point out some specific areas of disagreement with Drs K & V:

• Contrary to K & V’s claim, there is plainly no logical contradiction in saying that a psychiatric diagnosis can be both descriptive and at least partially explanatory, just in so far as it “points to” an underlying condition.
• K & V state that “It is highly unlikely that current DSM categories pick out natural kinds that exist in the world independently of our categorizations and cause the listed symptoms.” To back up a bit: to say that a kind is natural is to say “that it corresponds to a grouping that reflects the structure of the natural world rather than the interests and actions of human beings…”¹³ Natural kinds may also be understood as independently existing “essences” or “…bounded categories that have necessary and sufficient internal conditions for their diagnosis.”⁹ In the material world, the chemical element gold is one example of a “natural kind,” which has affinities with the medieval concept of a substance.
• We have never argued that the DSM categories pick out “natural kinds” or that psychiatric diagnosis in general does so. In fact, Zachar explicitly notes that “the DSM does not assume natural kinds.”⁹ Thus, when K & V exhort us to “openly acknowledge that no causal essences have been discovered in psychiatry…” they are merely urging us to embrace what we already believe, and which the DSM-5 already reflects.
• In contrast, Zachar has argued that psychiatric categories identify practical kinds, which are“stable patterns that can be identified with varying levels of reliability and validity.”⁹ This is an anti-essentialist model that accords with our own concept of psychiatric categories, and with that of the DSM-5. Practical kinds do not exist in the same way natural kinds like sodium or granite or electrons exist, but neither are they are fictional entities like unicorns or chimeras.
• In our view, practical kinds like schizophrenia and bipolar disorder point to actual psychophysical states of affairs with causal properties, which have probably existed throughout most of human history. For example, Avicenna (c. 980 – 1037 CE) described melancholia and mixed mood episodes more than a millennia ago.14And had there never been classification schemes or classifiers, there would still have been humans who experienced suffering and incapacity owing to the constellation of command auditory hallucinations, paranoid delusions, thought process disorder and the other features we have come to call schizophrenia. A person alone on a desert island experiencing these symptoms may indeed need a classifier to declare this condition to be schizophrenia—but no classifier is needed for the psychophysical condition itself to exist and to cause debilitating symptoms. That is, the actual experience of psychiatric illness exists, independent of our ability to identify it, and irrespective of our wishes, desires, or preferences.
• Contrary to K & V’s claim (“Pies and Ruffalo’s assumption of “actual clinical conditions” that cause psychiatric symptoms is just that: an assumption”), we make no such assumption. Rather, our claim regarding clinical conditions is a heuristic and testable hypothesis. It is heuristic in that it promotes a search for the underlying physiological, environmental, and psychosocial causes of the patient’s psychiatric presenting problems. It is empirically testable by determining whether a putative clinical condition corresponds to external validators, such as course of illness, genetic and familial risk factors, biomarkers, family history, and response to treatment.³ As Kendler has put it, “Our disorders become more real as they fit better and better into our emerging empirical knowledge of the causes and consequences of psychiatric illness… a true disorder is one that over time grows more and more valid, [and] explains things about the world…” He calls this a soft realist position.¹⁵
• Drs K & V write, “Pies and Ruffalo evoke unseen entities that are not identical to diagnostic criteria but happen to magically correspond to them…” This comment strikes us as warmed-over positivism—not unlike Thomas Szasz’s long-discredited claim that the presence of a disease requires a demonstration of an anatomical lesion or abnormal physiology.¹⁶ If being unseen signified that a putative medical condition was somehow not real, we would have to throw many neurological conditions into the diagnostic rubbish bin. For example, nobody has ever seen a migraine headache, nor is there any lab test, biomarker, or imaging study that can reliably diagnose this condition, whose pathophysiology is still not fully understood. The diagnosis is made on purely clinical grounds, through essentially the same process psychiatrists use to diagnose schizophrenia, bipolar disorder, OCD, etc.¹⁷ The same goes for the equally invisible persistent idiopathic facial pain (PIFP), which—despite its poorly understood causes—is nevertheless considered an actual disorder with an underlying (albeit enigmatic) pathophysiology.¹⁸ By the way, according to a neurologist colleague of ours, nobody in neurology ever hears the charge that the diagnosis of migraine is tautological or reflects “circular logic”¹⁹—and nobody argues that the patient has been labeled with migraine, rather than diagnosed.
• Drs K & V are rightly concerned about the validity of psychiatric categories, but do not seem to appreciate that validity encompasses more than biological (or etiological) validity.²⁰ As the late Bernard J. Carroll, MD, PhD, famously observed, “Laboratory measures are the servants of clinical science, not the other way around.”²¹ Furthermore, specific biological abnormalities are neither necessary nor sufficient for the ascription of disease.¹⁶ Nevertheless, recent reviews of both schizophrenia and bipolar disorder leave no doubt that numerous neurobiological factors are involved in the genesis and expression of these illnesses.^22,23
• Predictive validity is a measure of how well a diagnostic category allows us to make accurate predictions of course of illness; stability of the illness over time; episode recurrence, degree of impairment, morbidity and mortality, and response to treatment. To be sure, not all DSM categories have high predictive validity, but many do. For example, DSM-III-R and ICD-10 diagnoses of schizophrenia have high predictive validity for long-term (13-year) outcome, and both prove to be relatively stable diagnoses.²⁴ Similarly, the diagnosis of DSM-III-R schizophrenia in childhood and adolescence has good predictive validity.²⁵ Similarly, using mainly DSM-IV criteria, one study found that early onset bipolar disorder persists over time through adolescence, with diagnostic continuity of early onset bipolar disorder from adolescence into early adulthood.²⁶ Borderline personality disorder, too—long known for its “stable instability”²⁷—has demonstrated high predictive validity and coherence as a clinical syndrome.²⁸
• Ironically, when Drs K & V write that, “Psychiatrists have long known that the illnesses of patients they see in the clinic cannot be broken down into discrete groups”,, they are merely affirming what the DSM-5 clearly acknowledges (page 8): “Although some mental disorders may have well-defined boundaries, scientific evidence now places many, if not most, disorders on a spectrum, with closely related disorders that have shared symptoms, shared genetic and environmental risk factors, and possibly shared neural substates…”²⁹ This assertion is not flawed science. On the contrary, as Kenneth F. Schaffner, MD, PhD, has noted, “The notion that the entities that are fundamental in a scientific area need to be discrete and separable is an idea that works well in some sciences such as physics and chemistry. But these types of entities are rarely found in biology…”³⁰ Indeed, as Silvano Arieti, MD, noted decades ago, “All differences in nature are basically quantitative differences, but it is the difference in quantity that produces the qualitative difference.”³¹
• Harold Pincus, MD’s tongue-in-cheek comment on the DSM-III process (“A bunch of guys sitting around a table”), cited by K & V, needs to be placed in the larger context of medical nosology. In truth, all diagnostic criteria in all fields of medicine are devised by fallible individuals coming together and rendering judgment as to what is or is not a disease, and what signs and symptoms constitute the diagnostic criteria for a particular category. Psychiatry is hardly alone in this complex endeavor, for which the science is often unclear. For example, a recent expert American Medical Association panel charged with deciding if obesity is a disease concluded that there was no “single, clear, authoritative and widely accepted definition of disease.”³² That is, the identification of all medical disease—not just psychiatric disease—rests on a subjective determination about what constitutes abnormality.

Figure. Evolution of Disease Entity

• Drs K & V use the hypothetical (and improbable) example of “major loneliness syndrome” to cast doubt on the reality and legitimacy of the DSM categories. But this crude caricature bears little resemblance to how psychiatric nosology actually works. New disorders do not spring up out of nowhere, at the whim of a “bunch of guys sitting around a table.” For the most part, they begin as a response to demonstrable suffering and incapacity of some type, such as that of returning Vietnam veterans. Initially, this was termed “combat fatigue” or “post-Vietnam syndrome.” But as these individuals were studied in the decades that followed, a constellation of recurring signs and symptoms began to coalesce, such as emotional numbing; nightmares; intrusive thoughts; “flashbacks”, etc. This led to the construct of posttraumatic stress disorder (PTSD), officially recognized by the DSM-III in 1980. An abundance of external validators has since emerged, such as pretrauma psychopathology; familial risk factors; and genetic predisposition.³³ There is also substantial evidence of the cross-cultural validity of PTSD.³⁴ This chronology typifies the long, steady, iterative process by which a clinical syndrome evolves into a disorder or disease, as shown in the diagram (Figure).³⁵ Similarly, S.N. Ghaemi, MD, adopting Kraepelin’s distinction, refers to the progressive evolution from a “clinical picture” to a “disease process.”³
• Finally, we do not accept K & V’s broad-brush claim that merely framing the patient’s condition “as an illness” is necessarily (or even usually) “disempowering,” that it “engenders pessimism,” or “…renders the human being and their social and societal context irrelevant.” Yes, some patients do have quite negative reactions to receiving a psychiatric diagnosis, but others find that diagnosis

“…can help them have a better understanding of themselves…and their symptoms. It can provide validation, and knowledge that some symptoms may relate to their diagnosis and not them as a person…[diagnosis] may provide reassurance that the individual’s situation is not unique, mysterious or inexplicable… [and] can reduce stigma by explicitly acknowledging the presence of illness.”³⁶

Indeed, over the course of more than 25 years, one of us (RP) witnessed many instances in which a patient newly-diagnosed with bipolar 1 disorder expressed great relief at finally having received an explanation for years of severe mood swings—and many found their lives vastly improved with lithium treatment.³⁷

Concluding Thoughts

We have acknowledged the drawbacks of categorical diagnostic systems, such as the DSM and ICD. We also acknowledge the controversies surrounding the ontological status—the “is-ness”—of psychiatric disorders and the complex nature of “causality.” But to deny the reality of serious psychiatric illness—or to trivialize it as mere “psychological distress”—is to do a great disservice to those who entrust us with their care. It seems to us equally unhelpful to deny that psychiatric disorders cause the symptoms identified in their diagnostic criteria—which merely point to, and do not fully capture or define, the underlying psychophysical condition.

Indeed, as the Table shows,^38-44 the ordinary language of mental health care attributes causality to many of our diagnostic categories. We believe the burden of proof rests with Drs K & V to show why—collectively and individually—all these sources are misguided in their use of the term, “cause”. To recall Wittgenstein’s maxim: “Ordinary language is alright.”⁴⁵ And in our view, there is much to be said for common usage and common sense!

Table. Psychiatric Disorders Cause Symptoms

We have enjoyed these exchanges and are happy to give the last word to our Finnish colleagues, should they wish it.

Acknowledgments: The authors wish to thank Drs Kenneth Schaffner and Peter Zachar for their comments on some aspects of this debate. However, the views presented here are solely those of the authors, unless otherwise noted.

Footnote: When we say, for example, that schizophrenia "causes" auditory hallucinations and paranoid delusions, we are not positing a mechanical kind of causality, akin to how billiard ball A collides with billiard ball B, causing it to move into the side pocket. (Of course, the philosopher David Hume famously noted that we do not actually "see" causality in this scenario—only the temporal sequence of events). Rather, we are hypothesizing (not “assuming”) that a recognizable and characteristic psychophysiological state—the product of innumerable antecedent biological, psychological, and social factors—is responsible for the patient's signs and symptoms. That is, we hypothesize that the term "schizophrenia" (as a practical kind) points to a characteristic pathological condition of the human mind that is responsible for the symptoms we call "schizophrenic." One type of causal reasoning expresses this idea as a counterfactual statement; ie, "If Smith did not have schizophrenia (or a related condition), he would not be experiencing auditory hallucinations and paranoid delusions." We may justifiably posit this type of causation without necessarily knowing the pathophysiology of schizophrenia.

Dr Pies is Professor Emeritus of Psychiatry and Lecturer on Bioethics and Humanities, SUNY Upstate Medical University; Clinical Professor of Psychiatry Emeritus, Tufts University School of Medicine; and Editor in Chief Emeritus of Psychiatric Times (2007-2010). Dr Pies is the author of several books. A collection of his works can be found on Amazon. Dr Ruffalo is an assistant professor of psychiatry at the University of Central Florida College of Medicine in Orlando and adjunct instructor of psychiatry at Tufts University School of Medicine in Boston, Massachusetts.

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For Further Reading

Maj M. Why the clinical utility of diagnostic categories in psychiatry is intrinsically limited and how we can use new approaches to complement them. World Psychiatry. 2018;17(2):121-122.