From there, after six days and seven nights, you arrive at Zobeide, the white city, well exposed to the moon, with streets wound about themselves as in a skein. They tell this tale of its foundation: men of various nations had an identical dream. They saw a woman running at night through an unknown city; she was seen from behind, with long hair, and she was naked. They dreamed of pursuing her. As they twisted and turned, each of them lost her. After the dream, they set out in search of that city; they never found it, but they found one another; they decided to build a city like the one in the dream. In laying out the streets, each followed the course of his pursuit; at the spot where they had lost the fugitive’s trail, they arranged spaces and walls differently from the dream, so she would be unable to escape again.

This was the city of Zobeide, where they settled, waiting for that scene to be repeated one night. None of them, asleep or awake, ever saw the woman again. The city’s streets were streets where they went to work every day, with no link any more to the dreamed chase. Which, for that matter, had long been forgotten.

New men arrived from other lands, having had a dream like theirs, and in the city of Zobeide, they recognized something from the streets of the dream, and they changed the positions of arcades and stairways to resemble more closely the path of the pursued woman and so, at the spot where she had vanished, there would remain no avenue of escape.

The first to arrive could not understand what drew these people to Zobeide, this ugly city, this trap.

-Italo Calvino, Invisible Cities (Cities & Desire 5)

Medical explanation has long been a sore spot for psychiatry. The first psychiatrists, known during the asylum period as alienists, were notorious for pushing organic hypotheses about mental illness that even their favored consultants, the neurologists, contemplated with raised eyebrows (Bogousslavksy & Moulin, 2011). Though the alienists’ cerebral-lesion theories are now regarded as little more than Enlightenment-era versions of the bodily ‘humors,’ psychiatric history –now nearly two centuries long– has seen several waves of dogmatic biologism in which varied (and often short-lived) organic hypotheses were held with similar fervor and conviction. Despite the longstanding tradition of interpreting psychological distress in physiological terms–and despite momentous technological advances in neuroscience and molecular genetics, the biological causes of what we now call psychopathology remain just as elusive as they did at the turn of the 20th century, when the French neurologist Charcot complained that hysteria and related conditions “come to us like so many Sphynx [the mythological lion-bird-woman who, in the Greek version, committed suicide after Oedipus answered her riddle], which deny the most penetrating anatomical investigations” (p. 12). It was, indeed, the riddle of biological cause that led the authors of the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5) to put forth –and then abandon– the idea of a new “paradigm shift” in psychiatric diagnosis, a revolutionary change in the very concept of mental disorders that would finally lay out their “underlying etiologies” in presumably stark, biological form (Kupfer, First, & Regier, 2002, p. xix).

In what follows, I’ll provide a cursory overview of the current paradigm-shift dilemma in psychiatry (I encourage interested readers to read the trove of recent commentaries on this issue, most of which can be found in the blogosphere and online psychiatric journals). I’ll put forth the argument that the DSM-5 Task Force never intended to exact a paradigm shift –but that their aspirations were on the plane of magic and revolution nonetheless. Using the focal example of a newly proposed and controversial diagnostic category called Somatic Symptom Disorder (SSD), I will address Task Force’s attempt to solve the problem of Cartesian dualism in psychiatry. Finally, I will conclude with some reflections on the resurrection of hysteria as an official psychiatric disorder.

Paradigm Crises, Paradigm Shifts

When Kuhn (1962/1996) wrote about scientific revolutions, he was describing shifts in worldview so radical and gargantuan that they would be almost unimaginable to scientists working under preceding paradigms. “[A]fter a revolution,” wrote Kuhn, alluding to the popular visual illusion, “scientists are responding to a different world […] What were ducks in the scientist’s world before the revolution are rabbits afterwards” (p. 111).

The shift renders null entire bodies of earlier data, and scientists labor to amass a new body of literature that will work out the kinks in the new paradigm — Kuhn called this the “mopping up” operations of “normal science.” This is the “overwhelming majority” of the work that most scientists do (p. 34), and it involves seeking support for paradigmatic frameworks rather than attempting to dissemble them. But in time, empirical anomalies begin to emerge. These anomalies, which fit within the reigning paradigm only if forced like a piece from a different jigsaw puzzle, are so striking and indubitably problematic that scientists are thrown into a state of crisis. That’s when they start to frantically seek a new paradigm.

This is all antithetical, of course, to what Popper (1963/2009) described as the slow and steady progression of science, where minute scientific advances accumulate through empirical support for this theory here, falsification for that one over there. Paradigm shifts (Kuhn, 1962/1996), in contrast, are Copernican, Newtonian. It is undoubtedly tempting to imagine that psychiatry is on the verge of such a shift (see Frances & Eggers, 1999). Looking at the recent history of psychiatry, the Kuhnian structure does seem to fit, at least in its initial stages: ‘normal science’ aimed at supporting the neo-Kraepelinian diagnostic paradigm; anomalies arose (comorbidity [e.g., Boyd et al., 1984], fuzzy boundaries [e.g., Kendell & Jablensky, 2003], heterogeneity [e.g., Østergaard, Jensen, & Bech, 2011]); we entered into a paradigm crisis; there are controversies, competing camps, the bending of rules. But we’re still at the stage of seeking alternatives; ducks are still ducks, rabbits rabbits. Importantly, Kuhn never said that paradigm shifts were inevitable in any given scientific arena. Quite the contrary: according to Kuhn, when a paradigm crisis hits, revolution is only one of many options. Scientists can also defer progress, declare it the work of future generations with better technologies and tools. They can eventually find a solution through ‘normal science.’ Or they can labor indefinitely under a faltering and untenable paradigm.

In psychiatry, scientific paradigms have become virtually synonymous with diagnostic “paradigms.” We are now more than thirty years into what psychiatric historian Edward Shorter (1997) has termed “the second biological psychiatry,” an era of biomedical technologization that began with the neo-Kraepelinians (APA, 1980; Feighner et al., 1972; Robins & Guze, 1970) and has come to an apex with DSM-5. Contrary to popular belief, DSM-5 did not force or exact the current paradigm crisis in psychiatry, though it perhaps helped to usher it in. The International Classification of Diseases (ICD; WHO, 1993a, 1993b) follows the same conceptual and taxonomic structure, as do numerous local variants (and a steadily growing number of not-so-local variants [Watters, 2010]) across the globe. No diagnostic alternative radical enough to rise to the level of paradigm shift has ever been taken seriously by the psychiatric community, at least not during the last three decades. Moreover, most new models proposed by establishment psychiatrists fall squarely within in the realm of what Thomas Kuhn would have called “normal science.” The National Institute of Mental Health Research Domain Criteria (RDoC; NIMH, 2013) project, aimed at developing “new ways of classifying mental disorders based on dimensions of observable behavior and neurobiological measures,” is one example (para. 1). DSM-5 is another. Given the weight that DSM carries in psychiatric research, any shift in its taxonomic infrastructure, minor or major, would perhaps be more on the level of power-vacuuming than mopping up. But it would not be a shift away from the current techno-biomedical paradigm (see also Cerullo, 2010). The DSM-5 end-goals of establishing biological and laboratory markers for mental illness (Kupfer, First, and Regier, 2002) are clearly laid out in the classic neo-Kraepelinian manifestos (Feighner et al., 1972; Robins and Guze, 1970).

The DSM-5 Task Force eventually concluded that the idea of a paradigm-shift was premature (Kendler et al., 2009). They reluctantly explained that psychiatric science has not yet yielded psychometrically stable biological evidence for inclusion in the diagnostic manual. But it’s not only because the DSM-5 Task Force relinquished the idea of a paradigm shift that they will not achieve one. It’s also because they never really wanted one to begin with. They wanted to perfect the present paradigm, to reassess and re-anatomize those same chimeras the neo-Kraepelinians’ had dreamily dissected into rabbits and ducks–albeit by slightly different means, with slightly sharper blades.

Somatic Shifts

In the transition from -IV to -5, what unites most major revisions to the DSM is the sometimes implicit, sometimes explicit goal of making room for biological theory. This was a tricky enterprise for the Task Force, because the neo-Kraepelinians themselves compromised their biomedical aspirations for an ‘atheoretical,’ descriptive model that would appeal to diverse practitioners and, simultaneously, enhance the scientific hunt for the biological abnormalities that had long held their unshakable trust. But the DSM-5 Task Force was haunted by the fact that the descriptive definitions featured in previous iterations of the manual were “virtually devoid of biology” (Charney et al., 2002, p. 32). So they put biology right back in, through various proposals:

• The redefinition1 of mental disorders as phenomena that reflect “underlying psychobiological dysfunction.” This newly proposed definition, which was featured in an early draft of DSM-5 (see Stein et al., 2010), was withdrawn when critics pointed out the improbability that all mental disorders are manifestations of underlying biological problems.

• Collapsing across the axes. DSM-5 will not include the multiaxial system that, after its introduction with DSM-III, has become so familiar to clinicians that hospital-lingo often uses the axis numbers themselves as synecdochal shorthand to differentiate primary psychiatric (Axis I) from symptoms that relate to personality (Axis II) and general medical conditions (Axis III). By collapsing across axes I through III, DSM-5 discursively effaces the difference between psychiatric and general medical conditions.

• The clinical significance criterion. This criterion, introduced in DSM-IV (APA, 1994) to clarify the threshold between mental disorder and subclinical or “normal” symptoms, holds that the presence of subjective distress or functional impairment are necessary for diagnosing most major mental disorders. Its fate in DSM-5 is up in the air. Indeed, the new manual “could require a significant re-orienting of clinicians – American clinicians, specifically – to a different way of thinking about mental disorders” (Narrow, Kuhl, & Regier, 2009, para. 6). Though this “different way of thinking” has not yet been detailed, if it abandons the concept of subjective distress for biological theory, one can only imagine that diagnostic psychiatry will shift right on the spectrum from clinician-centered to patient-centered.

Somatic Symptom Disorder (SSD)

SSD made its world debut this May, when DSM-5 hit the shelves. According to the manual (APA, 2013), SSD diagnosis will capture “distress that is principally focused on somatic symptoms and their significance” (p. 312), often leading to frequent complaints about pain and what is pejoratively referred to as ‘treatment-seeking behavior.’ It’s a diagnosis that will replace several categories (somatization disorder, hypochondriasis, pain disorder, and undifferentiated somatoform disorder) in what will have been DSM-IV-TR’s (APA, 2000) overarching Somatoform Disorders grouping. On dsm5.org2, the SSD Workgroup’s proposals were described as “major changes [from DSM-IV].” Indeed, even on the surface, SSD is no mere modification of the Somatoform Disorders. As per the website:

The [DSM-5 SSD Work]group considers that the current DSM-IV somatoform diagnoses (Somatization Disorder, Somatoform Disorder NOS, Undifferentiated Somatoform Disorder, Hypochondriasis and the Pain Disorders) are so flawed that complete restructuring of these diagnoses is required. (emphasis added) SSD was born of this “complete restructuring.” The minutiae of the former criteria for the Somatoform Disorders can be found in DSM-IV-TR (APA, 2000), so I won’t reproduce them here. Suffice it to say that SSD varied criteria from its DSM-IV-TR predecessors but excludes the central diagnostic criterion that historically defined them — namely, medically unexplained symptoms. In its place, the SSD Workgroup has proposed the central criterion of “[e]xcessive thoughts, feelings, and behaviors related to these somatic symptoms or associated health concerns”

SSD, the name of which appears nowhere in previous editions of the manual, is viewed as a new diagnostic category by DSM-5 critics and proponents alike. However, the concept is less novel invention than it is anachronism in disguise.

Before looking into the historical roots of SSD, it’s important to address why the disorder category has been one of the most controversial proposals for DSM-5. Indeed, the topic has seen a flurry of recent blogosphere activity and media coverage (e.g., in [Ablow, 2013], Psychology Today [Frances, 2012, 2013a, 2013c; Lane, 2013], and Huffington Post [Kupfer, 2013]). A recent Psychology Today blog on SSD by DSM-IV Task Force chair Allen Frances (2012) received tens of thousands of hits. And the second solicitation of stakeholder comments received more submissions than just about any other diagnostic category in the manual (Brauser, 2011; see also Chapman, 2012, quoted in Frances, 2012, para. 21). Readers who are interested in learning more about SSD and the DSM-5 development process are encouraged to visit Suzy Chapman’s comprehensive and meticulous coverage on her website,

Today, when a cancer, diabetes, Lyme disease, or other chronically ill patient enters a medical office with complaints about persistent pain, they are, more often than not, taken seriously, assessed, and treated. Likewise, when a patient without an identifiable medical condition enters with similar complaints, they are also assessed and often treated for their reported symptoms. But sometimes, after careful medical assessment, when the complaints are persistent enough and the cause equally elusive, they are diagnosed with a DSM- (APA, 2000) or ICD-defined (e.g., WHO, 1993a, 1993b) Somatoform Disorder. Somatoform Disorders are, by definition, signifiers for the presence of symptoms that cannot be explained by an identifiable medical condition.

Psychiatric disorders have always necessitated the exclusion (often known as “rule-out”) of general medical problems that could better account for the symptoms. This practice guides pragmatic decisions, including the determination of where and by whom the patient is treated, what sorts of treatment or medications they receive, and what prognostic possibilities might be communicated to the patient. It is a time-honored differentiation that is meant to ensure proper medical care and prevent doctors from premature and mistaken conclusions that “it’s all in the head.”

What will happen when a cancer, diabetes, Lyme disease, or other chronically ill patient enters a medical office with persistent pain after DSM-5 becomes official? It will depend on the clinician’s subjective judgment as to whether the patient has one of the following diagnostic criteria (APA, 2013, p. 311):

(1) “Disproportionate and persistent thoughts about the seriousness of symptoms”;
(2) “Persistently high level of anxiety re: health or symptoms”; or
(3) “Excessive time and energy devoted to symptoms or health concerns”

If, in the personal opinion of the treatment provider, the patient presents with only one3 of these symptoms, we can only suppose that they will be assessed, as usual — but then sent to a mental health professional or treated by their general medical doctor with psychotropic drugs. There will be no “rule-out” of general medical problems, because SSD –unlike its DSM-III and IV predecessors– can be diagnosed alongside other related medical conditions. Or in the words of the SSD workgroup: “The conceptual framework that we propose will allow a diagnosis of somatic symptom disorder in addition to a general medical condition, whether the latter is a well-recognized organic disease or a functional somatic syndrome such as irritable bowel syndrome or chronic fatigue syndrome” (Dimsdale & Creed, 2009, p. 475).

Of course, the DSM-5 SSD Workgroup does not advocate for curbing of patient complaints by medication alone. They would like multidisciplinary mental health professionals –including and especially those who conduct psychotherapy–to jump on board. In their own words, clinicians might advance strategies for “the identification and modification of dysfunctional and maladaptive beliefs about symptoms and disease, and behavioral techniques to alter illness and sick role behaviors and promote more effective coping” (SSD Workgroup, 2011, p. 5). SSD will thus target illness behaviors that clinicians see as “dysfunctional” and “maladaptive.”4


There is a robust body of biobehavioral, cognitive, and clinical research suggesting that illness behaviors start out as adaptive responses that facilitate recovery and prevent exposure to pathogens and other triggers. Immunocompromise, for example, frequently leads to psychological symptoms that mimic depression and anxiety (e.g., anhedonia, avolition). In the case of a compromised immune system, depressive symptoms are believed to conserve energy and combat inflammation in acute phases. It is only later, in their rarer and chronic form, that they lead to hypothalamic-pituitary-adrenal abnormalities, neuroinflammation, and neurodegeneration (e.g., Maes et al., 2012). Research using animal modeling has led to similar conclusions, with various species displaying behavioral responses to infections that resemble the symptoms of various psychiatric disorders, including depression, anxiety, and anorexia. Indeed, myriad biobehaviorists believe that sick-role behavior is “not a maladaptive response or the effect of debilitation, but rather an organized, evolved behavioral strategy to facilitate the role of fever in combating viral and bacterial infections” (Hart, 2008, p. 123; see also Johnson, 2002).

Like any behavioral strategy, sick-role behavior can get out of hand, and SSD was devised to mark when it does. Yet there is little empirical evidence or operationalized criteria to guide this decision, since the research literature on (mal)adaptive illness behaviors is an empirical quagmire. “Disproportionate and persistent thoughts” to one doctor is “appropriate reality testing” to another. “Excessive time and energy” devoted to health concerns is easily –and often– recast as “doctor-shopping.” The central criterion by which SSD will be diagnosed is a matter of subjective judgment (Frances, 2013b).

The DSM-5 field trials suggested that SSD will apply to 15% of patients with cancer or heart disease, 26% of patients with irritable bowel syndrome or fibromyalgia, and 7% percent of healthy people (Frances, 2013b, 2013c). Frances (2013a) has suggested that the introduction of SSD in DSM-5 may result in “the mislabeling of potentially millions of people with a fake mental disorder that is unsupported by science and flies in the face of common sense” (para. 5). As a result, many now fear that “[t]he DSM-5 [SSD] Work Group is taking a flying leap into the unknown” (Chapman, 2012, quoted in Frances, 2012, para. 9).

DSM-5 sans Descartes

So what is the SSD Workgroup’s rationale for this new category, which seems to rewrite potentially adaptive illness behaviors and complaints about physical pain as psychiatric disorder? According to the Workgroup, their motivation is largely philosophical: the proposal to “[d]e-emphasize medically unexplained symptoms” is an attempt to negate “[…] the implicit mind-body dualism and the unreliability of assessments of ‘medically unexplained symptoms’.” Or, according to an elaborated explanation from the SSD Workgroup’s (2011) validity propositions, “Such terminology [medically unexplained symptoms] enforces a dualism between psychiatric and medical conditions. It bases a diagnosis on a negative—the absence of something, and, as such, runs the risk of misdiagnosis (Kroenke et al, 2007)” (p. 1, emphasis added).

Like its sister discipline psychology, psychiatry owes its existence to this post-Enlightenment philosophical orientation that posited a radical divide between the material world, including soma (body), and the arena of thoughts, ideas, and sensations –i.e., the arena of human consciousness (mind). But psychiatry is often dissatisfied with this reductive dichotomy, and it is not alone in its dissatisfaction; philosophers since Descartes have struggled with the ontological and epistemological dilemmas erected by dualism (e.g., the “uninvolved spectator” and infinite regress). Yet despite frequent complaints, psychiatrists have typically hesitated from chipping away at the Cartesian bedrock of their profession.5 Indeed, as psychiatric historians are prone to lament, mental maladies are ritualistically ceded to neurology when discrete organic causes are discovered (e.g., in the case of general paresis [see Haslam, 2000]), a practice that, it is often argued, belies the popular claim that most mental disorders are epiphenomena with as-yet undiscovered biological etiologies (see Kupfer, First, & Regier, 2002). Sphinxian, as Charcot would have held, for sure: as soon as the riddle is answered, its hybrid bearer has no other choice but to commit suicide –not necessarily because the answer is de facto fatal, but because the riddle was contingent upon (and indistinguishable from) ambiguity, inexplicability.

Put simply, total equivalence to the rest of medicine would leave no reason for psychiatry to remain a distinct subdiscipline. What purpose would psychiatrists serve if their focal pathologies were no different from those of general medical practitioners? The main trouble has been that the archers of psychiatric Cartesianism have led a targeted hunt for etiology (cause). Unique biopsychiatric etiologies would allow for similitude to and participation in the medical world as a distinct subdiscipline. But analogous etiologies would, according to standard practice, necessitate analogous treatment approaches, prognoses, outcomes. As a result, the neo-Kraepelinian imperative to equate psychiatry with general medicine has the structure of a standard implicit double-bind6: maintain fidelity while asserting independence, individuality. Be the same but different. And DSM-5’s SSD is the standard way out of that double-bind: move to the level of the symbolic. So rather than emphasizing the (medically inexplicable) etiology of somatic symptoms, SSD will concede etiology to the anti-Cartesian realm of “multifactorialism” or mind-body monism. But it will maintain the Cartesian split at the level of the symptom itself.

The (In)explicability of Symptoms: When Absence of Evidence Becomes Evidence of Presence

There’s a saying that can often be found lurking around the commentaries on clinical research, “absence of evidence is not evidence of absence.” When the SSD Workgroup lamented that somatoform diagnoses are based on a negative –“the absence of something” (SSD Workgroup, 2011, p. 1)– they were effectively addressing this very problem, and they mounted a quiet revolution in response. DSM-5’s radical solution for the absence of something (medical explication) was to simply assert that it is present. According to the SSD Workgroup, the symptoms of disorders formerly known as somatoform are, in fact, explicable.

At first glance, it may appear that in their move from “medically unexplained” to “excessive,” the DSM-5 Task Force is preserving the notion of medically unexplained on some level. Theoretically, SSD symptoms are not attributable to the disease/pain about which a patient complains. As such, SSD is a signifier for medically inexplicable complaints. But paradoxically, DSM-5 casts these complaints ultimately explicable –by psychiatry. Which is, by virtue of this very claim, equated with general medicine. The implicit syllogism goes something like this:

Major Premise: Some patients make inexplicably excessive medical complaints.
Minor premise: Some excessive medical complaints can be explained by psychiatry.
Conclusion: Psychiatry renders excessive medical complaints explicable (and is thus
indistinguishable from general medicine).

There is a series of “logical” moves here: patients’ complaints are declared medically inexplicable but psychiatrically explicable, and therefore –by a forged equivalence between psychiatry and general medicine– “medically” explicable nonetheless. This type of reasoning is often called the syllogistic fallacy of four terms (a.k.a. equivocation or quaeternio terminorum).

The Medical and the Magical

SSD is the paragon of DSM-5’s attempts to fuse psychiatry with that ultimate horizon towards which it has always strived: general medicine. As a rule, Somatoform Disorders were a vestige of separation between the two fields, because their symptoms mirrored those found in various medical illnesses but, like all other psychiatric diagnoses, required the exclusion of medical etiology. This was conceptually incongruous with the aims of the DSM-5, which sought to “facilitate a better interface between general medical and mental disorder approaches to diagnosis” (Regier, Narrow, Kuhl, & Kupfer, 2009, para. 10). In the words of one SSD Workgroup member, “It is incorrect to equate ‘medically unexplained’ with ‘psychiatric'” (Creed & Gureje, 2012, p. 557). SSD effectively reverses this equation by implicitly equating “psychiatrically explained” with “medical.” But because there is no empirically substantiated psychiatric theory for excessive medical complaints, this reversal is an exercise in rhetoric and quasi-magical thinking. The discursive sleight-of-hand is not necessarily intentional on the part of the DSM-5 SSD Workgroup, but it has pragmatic implications nonetheless.

Traditional medical lingo has markers for the difference between patient experience and physician observations. Illness denotes the subjective experience of disease; symptom refers to patient complaints about the pain/distress that third parties (usually doctors) may or may not recognize through signs. SSD subverts this lingo by transforming the traditional distinction between symptom and sign. The quintessential SSD symptom is an excess of complaints, i.e., an excess of symptoms. But SSD symptoms are not “symptoms” per se, because they are not signifiers for the pain/distress they describe. Indexicality to real disease process will be largely irrelevant. Instead, in the case of SSD, patient complaints will be recast as signifiers for a different sort of problem altogether.

The psychoanalyst Jacques Lacan famously quipped that it is the analyst’s job to convince the paranoiac that his wife is not cheating on him –even if she really is. A similar role will soon be ascribed to clinicians diagnosing SSD. Their task won’t be to assess whether patients do or do not suffer from the physical pain they report, nor will it be to assess whether pain might be expected due to the presence of medical illness. The task will be, put simply, to treat symptoms as signs.

Converting to the Selfsame

This text is about SSD, but it is important to note that the same storyline unfolds in the proposed revisions to SSD’s sister diagnosis, conversion disorder. Historically, in medicine, the term “conversion” has signified the transformation of psychological stressors (or, in psychoanalytic terms, conflicts) into bodily symptoms. The concept appears in DSMs I and II (see Owens & Dein, 2006) and predates the Somatoform Disorders, which, when introduced in 1980 (APA, 2000), included conversion disorder as a (presumably less pervasive) subtype. DSM-IV retained the distinction, as will DSM-5. (In ICD-10 [WHO, 1993a, 1993b], conversion is listed as a dissociative disorder.) However, the SSD Workgroup has added a parenthetical phrase to title of the diagnosis, which will become “conversion disorder (functional neurological symptom disorder),” with rationale that the parenthetical designator is “more frequently used by neurologists who see the majority of these patients.” (Hereafter, I’ll refer to this diagnosis with the shorthand CD-FNSD.) The Workgroup also deleted DSM-IV-TR’s (APA, 2000) Criterion B: “Psychological factors are judged to be associated with the symptom or deficit because the initiation or exacerbation of the symptom or deficit is preceded by conflicts or other stressors” (p. 498), with the rationale that in the majority of cases, “psychological factors cannot be convincingly or reliably demonstrated.” The result is a new disorder category that –by eschewing the psychological factors historically associated with the eponymous diagnosis– rhetorically conflates psychiatric with neurological disorder. And the exclusion of psychological factors from conversion disorder raises the perplexing question: conversion from what to what?

As theoretical concepts, conversion and the somatoform disorders have often been slammed for invoking a reductive Cartesian dichotomy between body and mind. Theoretically, the SSD Workgroup has responded to this critique with the invention of SSD and CD-FNSD. But it is arguable that these two categories do not fare as well in resolving the problem of dualistic reductionism as they do in exacerbating it. By radically divorcing the symptom (complaint) from its referent (content of complaint), SSD and CD-FNSD compartmentalize the symptom into the realm of the “mental” — and, as such, into the very framework of fundamentalist Cartesian dualism that the SSD Workgroup has claimed to negate. Indeed, these diagnoses pose the precise risk of leading doctors to believe that “it’s all in the head” (Frances, 2012, para. 3).

Not listening to the patient is the primary faux-pas that inspired the contemporary patient-centered movement in both general medicine and psychiatry. SSD skirts the faux-pas by allowing clinicians to listen and not listen to the patient at the same time. Clinicians can listen to medical complains, even identify a patient’s organic (or multifactorial) illness, and nevertheless not listen by slapping them with a comorbid diagnosis that has a different kind of meaning altogether. Importantly, once made official, psychiatric diagnoses are applied to real people. They become inscribed in our institutional practices–in hospitals, clinics, and universities– in ways that determine medical/clinical education, treatment decisions, patients’ futures. This process has been called diagnostic reification, the making-concrete of abstract diagnostic concepts by institutionalization and –through the cultural dissemination of psychiatric theory and practice– influence on shared social knowledge. It is also a written analog to what linguists call a speech act, a special type of utterance that changes social conditions by virtue of its being spoken (a common example: “You are hereby sentenced to five years of imprisonment”). When new diagnoses are introduced in the DSM, they are also introduced into human society and public discourse. And they are treated as functionally equivalent to other diagnoses by both doctors and the patients who carry them.

Return to Hysteria

In late-19th and early-20th century France, psychiatrists watched women contort their bodies into U-shaped backbends that resembled the yogis in ūrdhvadhanurāsana (“wheel pose”). During Charcot’s time, these poses were assumed not for the purpose of “well-being,” but unintentionally, compulsively. The arc-de-cercle was, in other words, a symptom. The women were often set on a stage of sorts, before an audience of both medical trainees and seasoned physicians, there to study les maladies du temps. And they, the doctors, took photographs of them. Before ever gracing the pages of the internet and glossy medical-history textbooks, the photographs –as some psychiatric historians have noted– donned the walls of the very rooms in which the women themselves were, like pictures, on display, mise en abyme.

The other name for SSD, the historical one, is hysteria. That retired term was the object of controversy and misunderstanding for two centuries. From the time of ancient Greece up until approximately the 18th century, hysteria (from the Greek ὑστέρα [hustera], or ‘womb’) was thought to result from various disturbances in the female body, often the uterus. Symptoms were a wide panoply of bodily sensations, “excessive” emotions, loss of appetite, insomnia, muscle spasms, and dissociation, among others. In one (in)famous theory, hysteric symptoms were the behavioral consequence of a ‘wandering uterus’ that detached itself and moved throughout the body “like an independent animal” that “moves around of its own accord and is quite erratic” (Aretaeus, quoted in Goldberg, 2003, p. 173). According to this lore, the uterus strayed from foul (internal) bodily stenches and traveled towards pleasant ones, often lingering against the intestines for so long that it would choke the woman (ibid.). That theory –alongside assorted hypotheses about female sexual deprivation and the retention of semen– predominated until the 18th century, when a series of Frenchmen, including Charcot, posited that hysteria was a disease of the brain. The empirically unsubstantiated concept proved controversial, and throughout the mid-20th-century it was often seen as an “all but useless as a diagnosis” because “a third of all women have had such an experience at some time or other” (Morrison, 1978, p. 482). Up until at least the late 1970s, “a physician facing the often thankless challenge of the hysteric patient” was often instructed to “brace himself for some pretty unpleasant feelings of his own” (ibid., pp. 482 & 487).

Kuhn (1962/1996) wrote about the ease with which scientific textbooks are rewritten after a paradigm shift. Researchers, after all, have little time for history. As a formal diagnosis, hysteria was written out of the psychiatric textbooks, but not only (as is commonly held) because it was a gender-biased construct. The neo-Kraepelinians wanted to distance themselves from all things psychoanalytic. In order to do so, they had to negotiate in areas –the personality disorders are a common example– but they managed to transform the manual’s distinctively Freudian flavor. So ὑστέρα –or “Hysterial Neurosis” (APA, 1968)– was one for the wastebasket.

We just took it right back out.

By disavowing the limits of medical explication, DSM-5’s SSD Workgroup effectively shifts not to a new paradigm, but right back to 19th-century France. Then and there, psychiatrists didn’t think hysteria was “medically inexplicable.” Like SSD Workgroup members, the French forefathers believed the ailment to be neurological and genetic, though, like the SSD Workgroup, they had trouble pinning down its precise mechanisms. DSM-5-persuaded clinicians and researchers will take that same epistemological stance. They won’t believe that the symptoms of SSD are de facto inexplicable, nor will they assume that patients with SSD are not sick. It’s just that SSD patients won’t be not sick in the way that the patients describe it. They will sick in a different way, a way they allegedly (in an inverted form of la belle indifferance7) don’t recognize. Sick in a way that, if at all plausible/empirically tenable, would place SSD smack in the center of the psychiatry-neurology chalkcircle.


History will probably confirm that psychiatry fought hard and gallantly to distance itself from its origins in philosophy, especially its parent philosophy, Cartesian dualism. The attempt to individuate still continues, and while psychiatry systematically removes the rhetorical pickets that divide it from general medicine, historical analyses of psychiatric research and practice are often relegated to scholars in the “medical humanities” (e.g., medical history and anthropology), who embody –perhaps even gladly assume– the hybrid identities that once defined psychiatry. Scholars in these disciplines have pointed out that the gaze with which Charcot and colleagues viewed their patients was perhaps no less intense than the gaze that transfixed the so-called hysterics, who got that wide-eyed look on the arc-de-cercle stage, and when memorialized in photographs. In those days, the wide-eyed, eerie, lingering glare of patients was symptomatic, pathological; when medical doctors stared at these patients –gathered in amphitheatres to watch their bodies contort, took photographs– their gaze was clinical. Today, with DSM-5, patients’ attention to pain will be viewed as symptomatic, pathological. And their doctors’ excessive, disproportionate insistence on the medical intelligibility of that sore spot in psychiatric history–medically inexplicable pain–will simply be seen, like it was one century earlier, as le regard médical.

It was over a century ago that Charcot compared hysteria and other mental illnesses to mythological Sphynxes. In the Greek account, Oedipus’s answer to the riddle, “[hu]man,” leads the composite leonine-oscine-human creature to jettison herself from a cliff. One cannot help but wonder why it has taken psychiatric science more than 100 years to reach that the edge of that precipice–and whether or not it ever will take that final step of announcing that the answers to both riddles may be one and the same.

The author would like to thank Frederick Wertz, Suzy Chapman, Donald Kamens, Ben Kamens, and Charles Olbert for their input on this manuscript.

This paper was presented at the Interdisciplinary Graduate Student Symposium in Philosophy & Psychology, Fordham University, March 19, 2013.


1DSM-IV-TR (APA, 2000) defines mental disorder as “a clinically significant behavioral or psychological syndrome or pattern that occurs in an individual and that is associated with present distress (e.g., a painful symptom) or disability (i.e., impairment in one or more important areas of functioning) or with increasingly significant risk of suffering death, pain, disability, or an important loss of freedom (p. xxxi).

2Some quotes from have since been removed.

3In previous drafts of DSM-5, a diagnosis of SSD required two or more symptoms.

4For an excellent, scholarly and meticulous review of the potential impact of these changes on patient populations, see Suzy Chapman’s submission to the DSM-5 Task Force at

5Even the early alienists were shy of approaching conditions that they believed to be born of spontaneous disease processes (as opposed to neurological lesions; see Bogousslavksy & Moulin, 2011).

6Two conflicting, simultaneous messages. In double-bind theory, metaphoric speech is seen as a attempt to wriggle free from the deadlock of two contrasting, literal imperatives (Bateson, Jackson, Haley, & Weakland, 1956).

7La belle indifference, historically associated with conversion/hysteria, refers to patients’ seeming “indifference” to or lack of concern with their symptoms. In SSD, patients are in fact excessively concerned with physical pain, but this excessive concern is putatively a function of indifference to an underlying psychiatric problem.


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About Sarah Kamens

Sarah Kamens is a Ph.D. candidate in clinical psychology at Fordham University and in media & communications at the European Graduate School (EGS). Her work focuses on diagnostic discourse and sociopolitics in the psy disciplines.