Let’s start with a case from the medical literature. This case of “malingering associated with hysterical ataxia, scissor gait, and aggressive outbursts” was recorded by the late Richard Asher, a physician specializing in psychological medicine (and coiner of the term Münchausen syndrome, among other contributions) (1):

One Sunday, when my daughter was two years old, I promised my wife that, if it was not taken as a precedent, I would myself get her up from her afternoon rest, dress her, and take her for a walk. I performed these duties without difficulty or loss of dignity, until the walk started. Then there was trouble. The child kept falling to the left; she walked with a ridiculous scissor gait, and she frequently fell to the ground. She cried and said she had a pain. She behaved abominably, and I spent a wretched afternoon in Park Square West attempting to coax her into good behaviour. I knew this was sheer devilment, a malignant aggressive demonstration against the father figure; I would not submit.

At last my wife returned and undressed her for her evening bath. There was a sudden cry: “Do you realise you’ve put both her legs through the same hole in her knickers?” I can still remember, after those tortured limbs had been freed from the crippling garments, how that gay, naked figure raced unrestrictedly to the bathroom without a trace of malingering.

Asher’s account raises several points of immediate clinical relevance. Asher notes both the motor phenomena and the poor girl’s nonorganic somatic complaints (“she had a pain”), and emotional and behavioral aberrations—he even has a psychodynamic explanation for them. We will take up the theme of psychiatric disorder in patients with conversion symptoms shortly. Asher makes little distinction between hysteria and malingering—she must have known what she was doing, he implies. We will address this question at the end of the chapter. But prior to both of these issues is a concern central to Asher’s account: when we make the psychiatric diagnosis of conversion disorder, are we missing organic disease? Here is the lesson that Asher took from his experience:

That incident taught me to be cautious about diagnosing malingering or hysteria. These diagnoses must not be made for the sole reason that the clinical picture is not yet hung in the clinical picture gallery of the doctor in charge. It may
be something he hasn’t heard of. There are too many examples of apparent malingering turning out to be cases of organic disease, and jokes about the high mortality of malingering or hysteria are commonplace.

At around the same time as Asher made this point, so did Eliot Slater, writing from the National Hospital, Queen Square, London. Hysteria, he said, is “a disguise for ignorance, and a fertile source of clinical error. It is in fact not only a delusion but a snare (2).” His argument was based on follow-up data (3). Eighty-five patients (of 99 consecutive patients) diagnosed with hysteria were followed up at 7 to 11 years after the diagnosis. Seventy of these were seen for assessment, the remainder rediagnosed from notes or information from relatives. Twelve of the 85 had died, four by suicide. Twenty-two of the remaining 73 (and presumably of the 85) had gone on to receive a diagnosis of organic disease in lieu of hysteria, an alarming 30% (or 26%) of the series. The authors noted that for the most part, this rediagnosis represented a reinterpretation of unchanged medical facts, rather than the result of new information. On these data, one cannot but quaver in announcing a diagnosis of hysteria.

We now know that this concern is exaggerated. To be sure, at times patients with psychiatric symptoms can be disregarded by doctors, their somatic complaints not evaluated with due care. However, when proper evaluations are performed and a diagnosis of conversion disorder made, that diagnosis usually proves to be correct on follow-up; organic disease explanatory of the original symptoms is infrequently found. By way of parallel to Slater’s series, Crimlisk et al. reported the outcome of six years on 73 consecutive patients diagnosed at the National Hospital with “medically unexplained” motor symptoms from 1989 to 1991 (4). Adequate data were available for 64, of whom only three had developed neurologic disorders that “fully or partly explained” their undiagnosed symptoms, in all cases including disordered gait. One was a woman with a learning disability who at follow-up clearly had myotonic dystrophy. A second was a man with whom communication was said to be difficult because English was not his first language, and who proved to have a spinocerebellar degeneration. (Was he interviewed in his native language? The authors do not say.) A final misdiagnosed patient had paroxysmal hemidystonia, a condition not well-recognized at the time of misdiagnosis. In an earlier series from the same institution, Mace and Trimble found that 11 of 73 patients had a neurologic rediagnosis at 10-year follow-up (5). A similar study from Edinburgh was able to ascertain the outcome in 66 of 90 patients with medically unexplained symptoms from a neurology clinic (6). None had acquired a neurologic diagnosis eight months on. In a separate study from the same group, information as to diagnostic outcome was available in 48 of 60 patients with purportedly pseudoneurologic symptoms after a lapse of a mean of 12.5 years (7). In only one had an apparently explanatory diagnosis been made.

All these studies are open to methodological question, for example, as to the representativeness of the patient population at these tertiary care hospitals, or as to how typical the evaluations they underwent might be in ordinary clinical practice. On the other hand, diagnostic tools surely have improved since the time of the cohort studied by Slater more than 4 decades ago. The lesson seems to be that clinicians who take due care in evaluation, especially with regard to adequate communication with patients who may at times be difficult, are justified in a high level of confidence in a diagnosis of conversion disorder. Perfect accuracy, no; importance of keeping an open mind, certainly; but the disorder being a delusion and a snare, hardly.

What of the remaining 51 of the 73 patients in the Slater and Glithero series, those in whom the diagnosis of hysteria was not judged to be in error? Of those, 19 had known organic disease along with a “hysterical overlay,” which was regarded as “temporary” and not influential on the course of the basic disease. Nonetheless, the recognition of this group requires explanation of a mental mechanism productive of the “overlay.” Indeed, Slater fully recognized the existence of hysterical symptoms; “… the dissociative mechanisms of hysteria are known of old, and can lead to symptoms which deserve no other name,” he wrote (8). His allegation was that the presence of the hysterical symptoms and the poor relationship between doctor and patient that resulted from an interaction between the patient’s abnormal personality and the doctor’s impatience to make a diagnosis might lead the doctor to ignore important diagnostic considerations. Further, Slater and Glithero (really Slater, who slipped into the first person singular late in the essay) believed that the personality disorder might itself be due to a fundamental organic brain disease, which “may bring about a general disturbance involving the personality. This personality change may then be a basis for hysterical conversion reactions, or by causing affective lability, hypochondriasis, attention-seeking, self-concern, suggestibility, variability of symptoms, and so forth, lead directly to an unfavorable reaction on the part of the clinician (3).”

The same concern animated his stressing that of the final 32 patients who had no evidence of organic disease on follow-up, in ten a psychiatric diagnosis came to light: Two developed schizophrenia, eight, cyclothymia. The authors speculated that the original diagnosis of hysteria was made during an unrecognized episode of depression.

The concern for missed psychiatric disorder in the Slater and Glithero paper is unfortunate, because subsequent studies clearly demonstrate that other psychiatric disorders are common in patients with conversion disorder. Brown and Ron summarized the literature as suggesting that perhaps three quarters of patients with conversion disorder merit another psychiatric diagnosis (9). A mood disorder is present in 40% to 80%, an anxiety disorder in a similar proportion,
and personality disorder in the majority. These aspects will be taken up in detail in other chapters in this volume. Moreover, the prognosis of conversion disorder itself is poor, if outcome assessment includes psychosocial functioning beyond the presence or resolution of the presenting symptom (10). Having signaled the theme of concurrent psychiatric disorder, I want to focus in this chapter on a particular set of psychiatric symptoms, namely, dissociative symptoms.

A link has been drawn between dissociation and hysteria since the late 19th century, beginning with the work of Janet (11). Dissociation refers to “a disruption in the usually integrated functions of consciousness, memory, identity, or perception of the environment (12).” Perhaps the exact meaning of the term cannot be gleaned from this definition, but fortunately, reliable scales for the ascertainment of dissociative symptoms have been constructed. The most commonly used, the Dissociative Experiences Scale (DES), has factors related to memory symptoms, capacity for absorption in experience, and derealization (Table 14.1).

Applying the DES to an inpatient population of conversion disorder patients, in comparison with a mixed group of psychiatric inpatients, Spitzer and coworkers found that the conversion disorder patients had more dissociative symptoms, despite the lack of a significant difference in a broad range of other symptoms (although there was a consistent trend for the comparison group to have more symptoms in other domains) (15). This finding has not always been replicated, and not all studies have as carefully controlled for the effects of psychopathology in general. However, Nijenhuis et al. argued that the DES does not fully account for the dissociative process in regard to somatic experience (as opposed to perceptions and ideas experienced in the mental realm) (13). They devised a supplementary scale, the Somatoform Dissociation Questionnaire-20 (SDQ-20), and applied this to a group of patients with conversion disorder as well as a number of other psychiatric conditions (Table 14.1). They found that the patients with somatoform disorders had elevated scores on the SDQ-20, in comparison with mood disorder or eating disorder patients, even after covarying out the effect of general psychopathology. In contrast, the DES did not allow this distinction.

The postulated connection between dissociation and conversion disorder has been sufficiently convincing that the International Classification of Diseases (ICD-10) devised an alternative to the Diagnostic and Statistical Manual of Mental Disorders (DSM) categorization of the so-called somatoform disorders. In ICD-10, “dissociative (conversion) disorders” are defined to include pseudoneurologic syndromes, such as pseudoseizures, as well as dissociative fugue or amnesia. This highlights a presumed commonality of underlying mental mechanisms.

Since Janet, and certainly in contemporary psychiatry, dissociative symptoms and dissociation as a mechanism are taken to point to a role for trauma in pathogenesis. In particular, sexual abuse and physical abuse in early life are taken to be key factors in the creation of vulnerability to nonorganic somatic symptoms. Many studies have found an elevated rate of abuse in childhood in patients with pseudoseizures (16) and with other nonorganic somatic symptoms (17). In accord with this conclusion, in the first study of a group of patients with more various sensory and motor conversion symptoms, Roelofs et al. found an association with early abuse (18).