Natural History of Psychogenic Movement Disorders

Daniel T. Williams

Blair Ford Stanley

Fahn Marc Williams

ABSTRACT

The term “psychogenic-neuropsychiatric movement disorders” (PNMDs) is advocated here for two reasons. The first reason is for precision of descriptive phenomenology, which will be explored below. The second reason is in the interest of facilitating acceptance of the diagnosis by patients and their families where it applies. This term is less likely than “psychogenic movement disorders” to be perceived as pejorative by these individuals, who often have long labored under the misimpression that the movement disorder symptoms were purely neurologic. Initial clarification of the formidable, and frequently primary, role of psychiatric contributants to these symptoms tends to come as a jarring shock to many such patients. Indeed, if conveyed too confrontationally by the evaluating clinician, this clarification may contribute to the patient’s premature departure and associated refusal of crucial psychiatric intervention.

Psychogenic-neuropsychiatric movement disorders (PNMDs) are abnormal movements that cannot be considered to result directly from traditional “organic” diseases, but which rather derive primarily from psychological and psychiatric causes (1). The presumption inherent in the term “psychogenic movement disorders,” as used over the past 20 years, was that they lacked either definable structural abnormality in the brain, or a definable physiologic abnormality, both of which are demonstrable in “organic” diseases (2,3). Yet we now are coming to appreciate that these distinctions between “organic” and “psychogenic” are arbitrary, representing relative points on a continuum, rather than categoric distinctions. We recognize that the psychomotor retardation that may accompany depression, the bizarre movements and postures of schizophrenia, and the stereotyped movements of autism all represent movement abnormalities characterizing psychiatric disorders where there is strong evidence of a pathologic-neurophysiologic underpinning. In this context, Vuilleumier et al. (4) documented a consistent decrease of regional blood flow in the thalamus and basal ganglia contralateral to the deficit in patients with “psychogenic” sensorimotor loss that were diagnosed as conversion disorders.

It is, therefore, not only to make diagnostic debriefing of patients more palatable, but also because it represents a more sophisticated contemporary understanding of the pathophysiology that the use of the term “psychogenic-neuropsychiatric movement disorders” is preferable. One can reasonably discern a qualitative difference between a relatively transient conversion disorder causing tremor that fully resolves with therapeutic suggestion and the relatively more fixed tremor of a Parkinson disease patient. Yet we know that the Parkinson patient’s tremor can be exacerbated
by emotional stress and that an untreated conversion disorder can become both physically and emotionally chronically incapacitating, such as by generating fixed contractures in extreme cases. This chapter will address the natural history of those neuropsychiatric movement disorders that have traditionally been viewed as “psychogenic,” with a view to exploring relevant diagnostic and treatment considerations, as well as features of developmental course.

The first challenge faced by a clinician dealing with such a patient is to rule out the presence of an underlying “organic” neurologic condition. The second is to see that appropriate psychiatric evaluation and treatment are implemented. Having noted this, it must be added that the pathogenesis of the PNMD conditions discussed remains only partially understood, and the treatment, as in much of psychiatry, is largely empirical.

HISTORICAL CONSIDERATIONS

Most of the presentations at the symposium contributing to this volume that have dealt with the evolution of our understanding of PNMDs have focused on the seminal contributions of Briquet (5), Charcot (6), and Freud (7). It is worth adding that prior to these clinical formulations, the predominant historical perspective on these disorders derived from the variety of religious presumptions that viewed many forms of both physical and emotional illness as derivatives of adverse supernatural influences. As such, the contributions of William James (8) deserve mention in highlighting the role of dissociative phenomena in this domain. The role of dissociative mechanisms continues to be relevant, both regarding our understanding of symptom formation and in elucidating how the potentially powerful role of authoritatively sanctioned suggestion can sometimes be dramatically helpful in symptom alleviation (9), if appropriately applied.

A more contemporary influence of historical relevance is the clarification of the distinction between epileptic and nonepileptic seizures, facilitated greatly by the availability of electroencephalographic technology and its application in epilepsy monitoring units (10). This has provided a clear paradigm for the differentiation of neurologic from neuropsychiatric syndromes that might appear initially indistinguishable, and which may, in fact, coexist within the same patient. The tendency of epileptologists to avoid the pejorative use of such terms as “pseudoseizures” in favor of “nonepileptic seizures” constitutes a useful terminological model for movement disorder clinicians. While epileptologists indeed use the term “psychogenic nonepileptic seizures” in communicating with other clinicians, the tendency in communicating with patients and their families is to use a more neutral term, such as “stress-induced nonepileptic seizures,” a precedent worth considering by movement disorder neurologists.

There was not unanimity of opinion on this issue at the conference that generated this volume, and further evolution of terminology will likely ensue. Most significant clinically in working with a given patient is conveying one’s findings sensitively and supportively so as to facilitate appropriate treatment intervention. This will inevitably involve a shift in linguistic nuance, depending on the intellectual capacity and level of psychological sophistication of a given patient.

EPIDEMIOLOGY

Neuropsychiatric symptoms have been estimated to account for between 1% and 9% of all neurologic diagnoses (11, 12). No specific epidemiologic data exists with regard to the incidence of psychogenic-neuropsychiatric movement disorders in population studies. In specialized movement disorder clinics, which tend to be at tertiary care centers, the rate of PNMDs tends to be around 3% of the total number of movement disorder patients (13,14). It is estimated, based on sampling similar patient populations, that 10% to 15% of patients with PNMDs have an underlying organic movement disorder, as well (1).

NEUROLOGIC DIAGNOSIS

Since most patients with PNMDs present to neurologists before they get to see a psychiatrist, the burden of initial diagnosis generally falls to the neurologist. In this regard, it is best to conceptualize the diagnostic process in these disorders as a two-stage process. The first stage is that of ruling out or circumscribing the role of definable neurologic illness, thus clarifying the necessary presence of a psychiatric disorder as an essential component of understanding some or all of the presenting symptoms. It is generally best for the neurologist to then facilitate the obtaining of a psychiatric evaluation so that a full psychiatric diagnostic assessment can inform treatment planning. It is important to note that delays in correct neurologic diagnosis and associated psychiatric treatment referral are likely to prolong a patient’s pattern of disability (15). Further, some patients with undiagnosed PNMDs are subjected to inappropriate and sometimes aversive testing or potentially dangerous treatment, including unwarranted stereotactic neurosurgery (3).

It should also be re-emphasized that the role of the neurologist is primary in the establishment of the diagnosis of a neuropsychiatric movement disorder. No mental health professional should embark on treatment of such patients without a clear understanding as to the level of confidence
with which the neurologic diagnosis has been either established or ruled out. The role of the mental health professional is to clarify the extent and potential relevance of discernable psychopathology as part of a collaborative assessment. If this appears relevant and a positive rapport has been established with the patient, ideally the psychiatrist will then take the lead in treatment, with appropriate collaborative support from the neurologist. This maintenance of a “team approach” is crucial to enhance acceptance of treatment to which the patient and family are often initially quite resistant.

The issues of movement disorder phenomenology and the differential diagnosis of neurologic versus psychogenic-neuropsychiatric movement disorders have been addressed earlier in this volume as well as elsewhere (1). Since it is our contention that the natural history of PNMDs is generally a byproduct of the patient’s psychopathology and clinical management, rather than a byproduct of the presenting movement disorder phenomenology, we will address this issue with a primary emphasis on considerations of psychiatric referral, psychiatric diagnosis, and psychiatric treatment.

To our knowledge, there is no published prospective data on the natural history of PNMDs. We will review here the modest retrospective literature that is available, with some clinical observations drawn from our experience with these disorders over the past 20 years at the Columbia University Medical Center.

PSYCHIATRIC REFERRAL

As noted above, the issue of facilitating psychiatric referral is crucial with this group of disorders. Despite a close and longstanding collaborative relationship that our movement disorder group has with a psychiatrist experienced in treating patients with neuropsychiatric movement disorders, well over half the patients who are referred for outpatient psychiatric consultation fail to implement this recommendation.

Our initial response to this pattern of noncompliance with psychiatric referral by the neurologist was to preferentially admit all such patients that we could to the inpatient neurology service, once a strong probability of the diagnosis of a neuropsychiatric disorder was ascertained. Under the rubric of a “multidisciplinary diagnostic and treatment approach,” the patient would be seen intensively by the admitting neurologist, the consulting psychiatrist, and a physical therapist. This hospitalization served several functions. It removed the patient from those environmental influences that were frequently contributory to the symptom formation and perpetuation, while it also allowed us to evaluate the patient more thoroughly in a more controlled environment. Further, the introduction of the psychiatrist as a routine member of the evaluation and treatment team made it more difficult for the patient to reject this intervention and allowed for the development of a therapeutic alliance while multiple diagnostic and treatment strategies were ongoing simultaneously, assuring the patient that no organic contributions to symptoms were being overlooked.

Within a few days of admission, with our initial diagnostic impressions usually further clarified, we arranged for a conjoint debriefing session with both the neurologist and psychiatrist present to supportively present to the patient our diagnostic impressions and treatment recommendations. If neurologic workup was negative, this was supportively reviewed, together with the more favorable prognosis for recovery than would be the case with a degenerative neurologic disorder. We observed further that stress of various origins can contribute to physiologic aberrations that generate clear physical symptoms despite the absence of discernable structural lesions on the various diagnostic tests currently available. Commonly encountered clinical examples of how stress can activate the symptoms of hypertension, peptic ulcer disease, and asthma, among others, would often facilitate patient recognition of the plausibility and relevance of this conceptual model. A treatment plan was then outlined, tailored to the needs of the individual patient. Elements of this treatment plan, often including psychotherapy, pharmacotherapy, and physical therapy, would generally be started in the hospital in an effort to achieve as much symptomatic improvement as possible in the available duration of stay, to be continued on an outpatient basis as individually needed. There was always a follow-up appointment with both the neurologist as well as the psychiatrist to assure the patient and family that both spheres were being appropriately monitored in an effort to achieve full symptom resolution.

Over the past 20 years, however, it has become increasingly difficult to admit patients with suspected PNMDs to the inpatient neurology service because of the restrictions of rigid “managed care” guidelines. This is sometimes a shortsighted obstruction of effective treatment for patients who are otherwise resistant to appropriate psychiatric care and consequently suffer prolongation of an otherwise treatable disability. On the other hand, we have been pleasantly surprised by a significant number of positive responders to our revised format of requiring a routine outpatient psychiatric consultation before the full formulation of treatment recommendations by the neurologist, based on the clinically indicated possibility that stress may be contributing significantly to the presenting symptoms. Many of these patients, who were sufficiently insightful, motivated, and emotionally capable of responding to a combined neurologic and psychiatric outpatient treatment program, demonstrated resilience in their capacity to respond to such therapeutic intervention much beyond our initial expectations.

Case Study

Emily, a 30-year-old married attorney, was referred for psychiatric consultation when our senior movement disorder
neurologist doubted, based on office consultation, that Emily’s 10-year history of “myoclonus” was neurologically based. This syndrome had first presented during college, when Emily was academically as well as emotionally stressed and developed an episode of apparent viral encephalitis. This illness further compromised her academic functioning for a while, and left her with residual symptoms of episodic “myoclonic jerks,” particularly at times of stress. Although she graduated both college and law school and married, she continued to be troubled by these persistent symptoms, which were not alleviated by a variety of anticonvulsant and antitremor medications. There was partial benefit from clonazepam, which was used in doses up to 4 mg per day.

Emily had previously participated in supportive-exploratory psychotherapy, albeit irregularly, over many years, without any discernable impact on the myoclonic symptoms. The therapy clarified clear traumatic emotional residua of the divorce of Emily’s parents when she was an adolescent, resulting in Emily being thrust into the role of caretaker for her learning-disabled younger sibling. Emily had considerable residual ambivalence toward both parents, stress associated with her professional obligations as an attorney; and ambivalence regarding the prospect of motherhood. Emily sought consultation at our medical center because of a desire to discontinue medication in the face of her wish to become pregnant.

In psychiatric consultation, prompted by an atypical history for myoclonus and nonphysiologic findings on neurologic and electrophysiologic examination, the above history was reviewed supportively and the plausibility of a neuropsychiatric basis for the myoclonic symptoms was explained, expanding on its initial presentation by the consulting neurologist. There were indications of possible secondary gains associated with added solicitude and support from Emily’s parents, spouse, and her supervisor at work when her myoclonic symptoms were activated by stress. Yet the patient’s maintenance of a relatively high level of functioning, despite her longstanding symptoms, plus her active wish to eliminate medication as she planned her pregnancy, appeared to constitute favorable prognostic and motivational factors. Two additional psychiatric visits were scheduled. In the first, a supportive formulation of the dynamics of conversion disorder was articulated, including the neurophysiologic capacity of dissociative mechanisms to unconsciously transform emotional conflicts into physical symptoms. This was followed by the assessment of the patient’s hypnotizability and the teaching of a self-hypnosis exercise to facilitate emotional-cognitive reorientation geared to facilitating symptom relinquishment. The premise was that, in light of the new incentive of a medicationfree pregnancy, Emily might mobilize the resources to face ongoing conflicts in a more direct and healthy manner with the aid of this new perspective and psychotherapeutically reformulated strategies of adaptation. In the third session, which was a conjoint session with her husband, the overall treatment strategy was further supportively reviewed, with initial observations of symptomatic improvement already evident. A plan for monitoring further symptom attenuation, together with tapering of clonazepam, was outlined. Emily cancelled her next appointment, however, and declined to schedule another.

Follow-up came three years later, when Emily set another appointment with the psychiatrist. She reported having become fully free of myoclonic symptoms in the wake of the prior three office visits, allowing tapering and discontinuation of clonazepam. A subsequent pregnancy was carried successfully to term, with the ensuing birth of a normal infant. Emily continued symptom-free for another one and a half years, when a resurgence of work and family pressures was associated with the recurrence of myoclonic symptoms. She initially returned to the neurologist who had previously maintained her on clonazepam and he chose to restart it. Emily returned to us after a year on clonazepam, which was clearly ineffective in symptom control, when she decided to become pregnant again. A similar course of multimodal psychotherapeutic intervention was commenced, with recommendation for more sustained treatment, in the hope of establishing a more sustained clinical improvement. This was indeed achieved within the course of several weeks. With the re-establishment of a symptom-free state, however, Emily again abruptly discontinued treatment and declined to schedule follow-up visits.

In contrast to Emily’s impressive resilience (albeit resistance to appropriate follow-up treatment), many patients, based on initial outpatient psychiatric consultation, appear clearly unlikely to be responsive to outpatient treatment. Such a clinical assessment may be based on limitations of insight and receptivity to entertaining a neuropsychiatric hypothesis, inadequately supportive or conflicted family situations, and/or severe coexisting psychopathology. In such cases, the detailed report of the initial outpatient psychiatric consultation, coupled with the detailed report of the movement disorder neurologist’s consultation, is frequently sufficient to persuade the relevant insurance carrier of the merits of an elective hospital admission, if the patient is receptive to this recommendation. This recommendation is predicated on the logical clinical and fiduciary premise that it is in the best interest of all concerned, including that of the insurance carrier, to give the patient an opportunity for comprehensive evaluation and treatment in an inpatient setting as an alternative to what otherwise frequently becomes a course of chronic disability, with an associated course of further expensive and unhelpful diagnostic and treatment interventions.

Quite apart from the bureaucratic and administrative constraints that need to be navigated in seeking to establish the most effective possible treatment plan, based on the diagnostic considerations of the individual patient, the attitude and tenor of the referring neurologist is crucial in
influencing the prospects of the patient’s accepting a psychiatric referral. If the psychiatric referral is perceived by the patient as a rejection and devaluation by the neurologist, because the symptoms are “not real” or “all in my mind,” obviously the likelihood of successful referral are poor. Conversely, if the psychiatrist is a valued collaborator in a diagnostic and treatment endeavor which is presented as having a more favorable prognosis than would otherwise pertain, chances for successful referral markedly improve.

PSYCHIATRIC DIAGNOSIS

In our clinical experience, one of the most frequent impediments to the establishment of an accurate psychiatric diagnosis is the reluctance of many mental health professionals to adequately assess psychopathology when they are intimidated by the often dramatically impressive nature of the patient’s obvious physical symptoms, coupled with the patient’s strong conviction that the symptoms are of organic etiology. Faced with this formidable combination, and frequently not being fully informed regarding previous neurologic evaluations, the mental health professional may be reluctant even to consider a psychiatric diagnosis in light of the potentially embarrassing and problematic medical and legal consequences if a “psychiatric label” is mistakenly applied to a patient who actually has an undiagnosed primary neurologic disorder. Many patients consequently present to our group with the contention that they have been given “a clean bill of health” by a previously evaluating mental health practitioner, thereby reinforcing their reluctance to consider further exploration of potentially relevant psychopathology.

The best antidote to this quandary is to have a psychiatrist or psychologist with significant clinical experience in the complexities of the neurology-psychiatry interface who can undertake the process of evaluating potentially relevant psychopathology in such patients. This diminishes the prospects of a premature presumption that documented psychopathology, some of which will inevitably be found in every patient, is necessarily causative of the presenting physical symptoms (16). It should also allow flexibility to consider the possibility that significant psychopathology, when encountered, may be relevant and contributory to presenting neuropsychiatric symptoms. It is crucial to avoid a “rush to judgment,” insofar as an adequate neuropsychiatric evaluation of these complex patients frequently requires several visits and communications between the neurologist and evaluating mental health professional.

Having noted the above, it is advisable that, after completion of the initial neuropsychiatric evaluation, a full multiaxial delineation of relevant psychopathology be organized in accordance with the nomenclature of the most current edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM) of the American Psychiatric Association (17). This substantially facilitates appropriate differential diagnosis and associated treatment recommendations. The three most relevant diagnostic categories for describing the primary psychopathology associated with PNMDs include: somatoform disorders, factitious disorders, and malingering.

Somatoform Disorders

In accordance with current DSM definition, a somatoform disorder is one in which physical symptoms that cannot be explained by a diagnosable medical condition appear, after careful clinical assessment, to derive from psychological factors that are not under the patient’s voluntary control (17). This implies that the symptom formation is not intentionally (consciously) produced by the patient. The two most commonly encountered forms of somatoform disorder, in our experience with patients having neuropsychiatric movement disorders, are conversion disorder and somatization disorder. The latter is also known as hysteria or Briquet syndrome. Other somatoform disorder subtypes that can be encountered as coexisting conditions in these patients include hypochondriasis, pain disorder, body dysmorphic disorder, and undifferentiated somatoform disorder.

In conversion disorder, the patient has one or more symptoms affecting voluntary motor or sensory function that suggest a neurologic or other medical condition. Psychological factors may be discerned to play the primary etiologic role in a variety of ways. There may be a temporal relationship between the onset or worsening of the symptoms and the presence of an environmental influence that activates a psychological conflict or need. Alternatively, the symptom may be observed to liberate the patient from an unwanted activity or encounter. As in all somatoform disorders, the symptom is not intentionally produced or feigned. (This is in contrast to factitious disorder or malingering.) The symptom cannot, after appropriate clinical investigation, be fully explained by a general medical condition, by the direct effects of a substance, or as a culturally sanctioned experience (17).

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