In Review

Somatization and Conversion Disorder

Trevor A Hurwitz, MD1

Somatization is the psychological mechanism whereby psychological distress is expressed

in the form of physical symptoms. The psychological distress in somatization is most
commonly caused by a mood disorder that threatens mental stability. Conversion disorder
occurs when the somatic presentation involves any aspect of the central nervous system
over which voluntary control is exercised. Conversion reactions represent fixed ideas about
neurologic malfunction that are consciously enacted, resulting in psychogenic neurologic
deficits. Treatment is complex and lengthy; it includes recovery of neurologic function
aided by narcoanalysis and identification and treatment of the primary psychiatric disorder,
usually a mood disorder.
(Can J Psychiatry 2003;49:172–178)
Information on author affiliations appears at the end of the article.

Highlights
· Somatic symptoms are a psychological defence against mental instability.
· The psychiatric disturbance that drives the somatoform disorders is in most cases a major
affective illness.
· Conversion disorder is a specific form of somatization in which the patient presents with
symptoms and signs that are confined to the voluntary central nervous system.

Key Words: somatization, conversion disorder, narcoanalysis, depression, somatoform

disorder
omatization is the tendency of individuals to experience The spectrum of presentations varies from mild to severe and
S and communicate psychological distress in the form of so-
matic symptoms and to seek medical help for them (1,2). This
may be mostly symptom-based (hypochondriasis) or mostly
sign-based (conversion disorder).
psychological process gives rise to somatoform disorders,
which are typically first seen in nonpsychiatric settings. Their Sickness
core features comprise somatic symptoms and signs that can-
Somatoform disorders are best understood within the context of
not be explained by known disease and that result in social and
sickness, because patients present as physically sick, which ini-
occupational impairment. Table 1 lists the clinical criteria.
tially masks the underlying psychiatric disorder. Sickness com-
Symptoms are typically multiple and vague and may refer to prises 3 components: disease, illness behaviour, and
single or multiple body systems or functions. Presentations predicaments (7,8). Disease is the physical basis of sickness
include cardiopulmonary, gastrointestinal, genitourinary, caused by tissue abnormality or malfunction. Clinically, dis-
musculoskeletal, and neurologic complaints, as well as pain ease manifests by observable signs (what the physician sees),
and fatigue (3,4). The DSM-IV-TR diagnostic categories that such as edema, hemorrhage, or inflammation, and organ and
incorporate the concept of somatization include body system compromise, such as heart failure and paralysis. Illness
dysmorphic disorder, conversion disorder, hypochondriasis, behaviour refers to the subjective experiences and behavioural
somatization disorder, pain disorder, undifferentiated consequences of disease (what the patient complains of).
somatoform disorder, and somatoform disorder not otherwise Illness behaviour presents as symptoms. These may be nonspe-
specified (5). cific symptoms, such as fatigue or nausea. Symptoms may also
be referable to specific systems or physical functions, such as
In clinical practice, somatoform disorders overlap and most shortness of breath or an inability to move; to specific mental
commonly present with multifocal symptoms and signs (6). dysfunctions, such as problems with concentration or sadness;

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 Somatization and Conversion Disorder

Table 1 Clinical criteria for psychogenic somatic the primary gain (10). Primary gain strives to restore
symptoms and signs psychological equilibrium, but at a price. Reality is distorted.
Disease absent
Attention is redirected toward the presenting symptoms, and
· No identifiable organic cause
the real problem and source of mental instability is blocked
· Symptoms and signs do not correlate with known organic
out or only partly experienced and, hence, not addressed (9).
damage patterns Once present, a symptom may be consciously used to achieve
Disease present
optimal interpersonal benefits. This is known as the secondary
· Symptoms and signs do not correlate with the damage pat-
terns of the known disease gain (10). Secondary gain is an ubiquitous interpersonal strat-
· Severity of symptoms and signs is disproportionate to the egy sanctioned by society if the underlying problem is seem-
known disease ingly genuine or if the interpersonal advantages accrue via
· Duration of symptoms and signs is disproportionate to the sophisticated or adaptive behaviour. By contrast, hostility and
known disease
rejection are the usual responses when interpersonal advan-
· Dysfunction induced by symptoms and signs is dispropor-
tionate to the known disease
tages are extracted from seemingly fake problems, such as
sickness without disease, or when interpersonal strategies are
primitive and transparently manipulative and maladaptive.
Such strategies include unsophisticated interpersonal coer-
Table 2 The differential diagnosis of psychogenic
somatic symptoms and signs cion, avoidance of responsibility, avoidance of noxious con-
sequences, undeserved compensation, and financial reward
Somatoform Factitious Malingering
disorder
without labour. Negative physician response to secondary
disorder
gain is unavoidably the result of a value judgement and
Conscious of No No Yes applies regardless of whether behaviours have arisen from
motivation
organic or from psychiatric conditions. In somatoform disor-
Conscious of No Yes Yes
faking
ders, physician hostility is magnified when secondary gain is
felt to derive from signs and symptoms without any under-
lying disease.
or to impaired interpersonal behaviour, such as social with- In somatization, the fundamental disturbance is a psychiatric
drawal or compromised self-reliance. Predicaments are the illness that threatens mental stability. The threat to mental
psychosocial consequences of illness. These are the negative integrity produces anxiety that mobilizes the somatic defences
and positive interpersonal ramifications arising from being (11). These defences are responsible for nonorganic physical
sick. Predicaments include interpersonal dependence; exemp- symptoms or convert psychic pain into physical pain. This ini-
tion from normal domestic and societal obligations such as tial process constitutes the primary psychological gain. Such
work; financial compensation without labour; sanctioning of patients, like anyone else, use the emergent symptoms for
symptom-relieving interventions such as medications, includ- interpersonal advantage to make the most of their predica-
ing the use of narcotic analgesics; granting of special commu- ment. This constitutes the secondary psychological gain.
nity privileges, such as reserved parking, special transport, and
Primary gain occurs unconsciously. As a result, the emergent
first access; and avoidance of noxious consequences by mitiga-
somatic symptoms are experienced as an unwanted and unin-
tion of responsibility, such as being relieved from doing mili-
vited disturbance. Patients believe and feel that they are sick.
tary service or serving jail sentences.
Somatizing patients are not aware of their underlying psychi-
Within the context of sickness, somatoform disorders have the atric disturbance—the motivation that drives the symptoms.
appearance of disease, with the advantages and disadvantages These patients are also not aware that they are deliberating
of illness and predicaments. The conclusion—reached after faking symptoms. However, the specific form of illness that
appropriate investigation—that there is no disease engenders surfaces reflects the patient’s conscious beliefs about how dis-
distrust and hostility on the part of the medical profession. ease should present. Symptoms and signs that derive from
Patients are poorly received and treated, and in this negatively beliefs are known as ideogenic (12). Since they reflect a
charged physician–patient dynamic, the underlying disease of patient’s concept of sickness, rather than organically dis-
psychiatric disorder is often overlooked or ignored. turbed anatomy or physiology, they appear atypical or bizarre
to the examining physician. They either occur in the absence
Pathogenesis of Somatic Symptoms of identifiable disease or the pattern, severity, and duration of
Somatic symptoms are a psychological defence against men- symptoms and signs, as well as the induced dysfunction, do
tal instability. Like all other intrapsychic defences, symptom not match any known disease. Symptom formation in
formation reduces intrapsychic distress (9). This is known as somatization is best studied in conversion disorder, where the

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The Canadian Journal of Psychiatry—In Review

symptoms are externalized as an observable neurologic defi- used (28). The term “functional overlay” is used when pre-
cit. This deficit can be reversed, revealing in the process the existing organically determined symptoms and signs are elab-
operative psychological mechanisms (12). orated and expanded upon by psychogenic mechanisms,
resulting in nonorganic presentations (29).
Malingering and Factitious Disorders
An identical cross-sectional presentation is found in 2 other Conversion Disorder
confounding conditions and is partly responsible for the hos- Conversion disorder is a specific form of somatization in
tile reception given to somatizing patients. In malingering, the which the patient presents with symptoms and signs that are
patient consciously decides to fake illness. The underlying confined to the voluntary central nervous system (5). When
motivation is also conscious and deliberate and is either to conversion symptoms occur in isolation, the primary diagno-
avoid noxious consequences or to gain undeserved benefits sis is conversion disorder. When conversion symptoms occur
(13,14). Patients who malinger know that they are pretending as part of a multisystem somatoform syndrome, the primary
to be ill. Malingered signs and symptoms are ideogenic in that diagnosis is somatization disorder (10). “Conversion” or
they reflect the patient’s conscious understanding of how ill- “conversion reaction” refers to the process whereby
ness should present. As such, the somatic presentation of intrapsychic distress is converted into physical neurologic
malingering is indistinguishable from that of the somatizing symptoms (30). Classically, patients present with psycho-
patient. In factitious disorder, the patient makes a conscious genic seizures or psychogenic motor-sensory deficits. Neuro-
decision to fake an illness. Unlike malingering, however, the logic presentations may, however, involve any aspect of the
underlying motivation has never been understood but is central nervous system over which voluntary control is exer-
caused by an unidentified, unconscious psychological need. cised. Thus, patients may present with a psychogenic demen-
Nonetheless, factitious patients are fully aware that they are tia as well as loss of speech and language or a disturbance of
pretending to be ill, although they cannot clarify either to any of the special senses (30,31).
themselves or to others the purpose, other than to receive med-
The hallmark of a psychogenic neurologic presentation is that
ical attention at any cost, that such a charade serves (14–16)
the disruption in voluntary neurologic function does not fol-
Since the somatic symptoms are ideogenic, they too are indis-
low known neurologic damage patterns (30). This reflects the
tinguishable from those of the somatizing patient or the
fact that the neurologic presentation is ideogenic and derives
patient who is malingering (Table 2).
from patient beliefs about how neurologic symptoms should
present. The emergent symptoms and signs are resilient and
Depression and Symptom Formation in fail to resolve following negative neurodiagnostic investiga-
Somatization and Conversion tions, reassurance, or care-provider rejection and persist
The psychiatric disturbance that drives the somatoform disor- across all settings. Typically, the observed signs—such as
ders is in most cases a major affective illness. Major depres- hemiparesis or blindness—are much worse when they are
sion has been identified in 30% to 60% of patients with being formally evaluated or when circumstances bring the
chronic pain and in 48% to 90% of patients who somatize. deficits to the patient’s attention. However, whether observed
Depressive illness has also been found to be present in 54% to or unobserved, the neurologic dysfunction remains present
88% of patients presenting with conversion symptoms and interferes with the patient’s functioning: the symptoms
(17–23). are fixed because the beliefs are fixed. Somatic symptoms and
There is no agreed-upon explanation about why patients use signs attributable to fixed beliefs provide the grounds for con-
somatic defences. Factors that have been associated with sidering that such beliefs represent somatic delusions (12).
somatization include increasing age, low social class, history
The pathophysiology of conversion symptoms thus begins
of physical illness, family history of physical illness, member-
with a psychiatric illness—most commonly depression—that
ship in cultural groups that discourage emotional expression,
threatens to destabilize mental functioning. The somatic
alexithymia (nonpsychological mindedness), and fear of psy-
defence, the conviction that “I am physically ill,” forms
chiatric stigmatization (24–27).
unconsciously and surfaces as a fixed belief about the pres-
How or why a patient chooses a specific symptom or sign is ence of a specific neurologic malfunction. The patient applies
also unclear. Explanations include a symbolic connection to this belief consciously to govern behaviour, resulting in
an underlying conflict or, alternatively, symptom modelling bizarre, atypical, and nonorganic findings on neurologic
in which patients mimic somatic symptoms that have previ- examination. The role of active inhibition has recently been
ously occurred in themselves or in a family member as a result demonstrated in some, but not all, functional-imaging studies
of organic disease (10). Where the symptom is modelled upon (32–36). In a landmark positron emission tomographic blood
prior organic disease, the term “somatic compliance” has been flow study of chronic and total left-leg psychogenic paralysis,

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 Somatization and Conversion Disorder

attempts by the patient to move the paralyzed leg failed to acti- psychogenic neurologic presentations that involve positive
vate the right primary motor cortex (32). Instead, the right neurologic phenomena such as psychogenic seizures and psy-
orbitofrontal and right anterior cingulate cortex were acti- chogenic movement disorders (37). On neurologic examina-
vated. These activated areas were deemed to be responsible tion, these are also recognizable as psychogenic because they,
for the inhibition of the right premotor and primary too, fail to follow known organic damage patterns.
sensorimotor cortex and the resultant left leg weakness. This
Like other somatoform disorders, conversion disorder can be
active inhibition only became manifest when the patient was
a treacherous condition: in the past, up to 30% of patients
consciously trying to move the paralyzed leg. At rest, there
diagnosed with conversion symptoms were subsequently dis-
was no significant asymmetry of activity in the motor cortices.
covered to have misdiagnosed organic illness (10). In contem-
A similar pattern of simultaneous activation of right frontal
porary medical practice, with the availability of sophisticated
inhibitory areas and inhibition of right somatosensory cortex
neuroimaging techniques such as magnetic resonance imag-
was found in case of left-sided paralysis and paresthesias
ing, missed organic illness may account for 4% to 15% of indi-
studied by single-photon emission computed tomography
viduals initially given a diagnosis of conversion disorder
(SPECT) during electrical stimulation of the left median nerve
(38–43). To avoid this error, all patients must be thoroughly
(33). Following neurologic recovery, the perfusion patterns
medically investigated.
normalized appropriately. In a functional magnetic resonance
imaging study of psychogenic sensory loss, painful and tactile
stimulation deactivated or failed to activate expected primary Management of Conversion Disorder
and secondary somatosensory cortices and associated cortical Patients referred for the treatment of conversion disorder must
and subcortical networks. Simultaneously, and similar to the first be medically cleared for any neurologic condition. All
Marshall and others study (32), the anterior (rostral and such individuals should have undergone appropriate
perigenual) cingulate cortex was activated, but only during neurodiagnostic investigations, including prolonged video-
sensory stimulation that was not subjectively perceived. electroencephalographic monitoring in the event of a seizure
Among other observations, the study findings suggested presentation.
abnormal cognitive or attentional processing during unper- Conversion symptoms, especially when seen acutely, may
ceived stimuli (34). In a SPECT study of acute unilateral psy- resolve spontaneously with explanation and suggestion. In
chogenic motor-sensory loss, bilaterally applied passive some patients, psychogenic sensorimotor deficits may
vibration led to hypoactivation of thalamus, caudate, and respond to treatment in a rehabilitation unit using a behav-
putamen contralateral to the deficit, which resolved with ioural approach with no other psychiatric intervention
neurologic recovery. This study did not show any regions of (44,45). In this group of patients, the primary psychiatric dis-
significant asymmetric cortical activity (35). turbance has seemingly settled. They are left with neurologic
deficits from which they need a face-saving exit. Active reha-
These functional imaging studies provide a growing body of bilitation provides such a vehicle.
data supporting the role of conscious active inhibition in the
Outpatient treatment of patients with conversion symptoms
genesis of psychogenic deficits. Symptom formation that
can be attempted using some of the strategies used in the inpa-
depends upon conscious active inhibition explains why psy-
tient setting. Patients with chronic and entrenched conversion
chogenic neurologic deficits are less severe when patients are
symptoms usually require admission to an inpatient psychiat-
distracted and more severe when patients attend to their prob-
ric unit that has experience with conversion disorders. They
lem (12). The findings on neurologic examination are also
may undergo acute psychiatric decompensation as their
consistent with cortical and subcortical inhibition controlled
neurologic symptoms resolve. This decompensation reflects
and shaped by higher-order brain centres. For example,
the deconstruction of the somatic defence by treatment that
neurologic deficits that are caused by a disturbance originat-
unmasks the underlying psychopathology, usually depres-
ing in the cortex itself should produce a typical damage pat-
sion. The unmasked psychopathology typically emerges over
tern, such as the pyramidal distribution of weakness occurring
weeks, varies from mild to florid, and may include previously
in a patient who presents with paralysis (30). The physical
hidden psychosis (23,46).
findings, however, do not follow these known organic pat-
terns. Instead, physiologically and anatomically naive beliefs Patients with sensorimotor disturbances are told that their
applied consciously and mediated via higher-order brain cen- neurologic deficits result from a loss of conscious control over
tres inhibit downstream cortical and subcortical areas in such the affected function caused by an underlying neurochemical
a way that the nonorganic neurologic pattern results. Last, the disorder, usually, depression. This explanation provides the
role of beliefs in consciously shaping symptoms and signs cognitive framework for treatment. It is accompanied by
provides a coherent and consistent explanation for physiotherapy, which may be all that is needed for neurologic

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The Canadian Journal of Psychiatry—In Review

recovery, provided that the patient’s underlying psychiatric have been identifiable at the onset of their illness (21).
disorder has been identified and accepted and appropriate However, months or years later, when some of these patients
treatment started. In patients with entrenched conversion are finally recognized and accept treatment, their overt, acute,
symptoms, narcoanalysis and narcosuggestion are required to precipitating psychiatric disturbance has become submerged
initiate neurologic recovery. Methylphenidate 5 to 15 mg (a and entwined with their physical symptoms. The retained
1-time dose prior to starting each narcoanalysis) is adminis- physical symptoms now provide a tenaciously held explana-
tered orally. Thirty minutes later, amobarbital is administered tion for their pain, distress, despair, insomnia, lack of energy,
intravenously at a rate of 50 mg/minute until the patient devel- and functional failure.
ops nystagmus and (or) dysarthria (46). The patient is encour-
aged to regain voluntary control through visual imagery and An essential part of treatment is the establishment of a thera-
suggestion. Narcoanalysis is videotaped and reviewed the peutic alliance that allows patients to recover with dignity and
next day with the patient. Videorecorded neurologic recovery, without loss of face. Staff need to be prevented from respond-
no matter how small, cogently confirms that the deficits have a ing to these patients in nontherapeutic ways, such as rejecting
psychological basis. Narcoanalysis is repeated weekly over them or becoming angry because of their “unnecessary” phys-
several weeks, provided that there are additional neurologic ical dependence and nursing needs or suggesting, subtly or
gains with each procedure. At least 2 narcoanalyses should be overtly, that they are attention-seeking, manipulative, and
done, as the first narcoanalysis may not yield any neurologic exaggerating or faking their neurologic difficulties. Patients
gains. Recovery of neurologic function is usually slow and need to be helped to recognize their psychopathology and
takes place over days, weeks, and months; it is rarely abrupt. accept that their symptoms arise from a psychiatric rather than
Any recovered neurologic function is reinforced with physio- a neurologic condition. Patients must also be helped to accept
therapy and appropriate physical aids provided by a physical orthodox psychiatric treatments. At every stage, vigilance
therapist familiar with psychogenic neurologic deficits (47). needs to be maintained for new symptoms. Any emergent
symptom needs to be adequately evaluated and not dismissed
Narcoanalysis is also helpful, but not essential, in uncovering as another conversion reaction.
the underlying primary psychiatric disorder. During the initial
narcoanalysis, which may last up to 2 hours, a formal review Psychogenic seizures require a different approach. Patients are
of the patient’s history and mental status is undertaken. Areas told that they are having spells, not seizures, and that these
covered include a detailed review of the circumstances and spells are caused by a neurochemical, not an electrical, mal-
psychological disturbances present at the onset of the conver- function of the brain. Medical attention is then gradually shifted
sion symptoms; a review of any relevant psychosocial stress- away from the spells. Anticonvulsants should never be abruptly
ors and conflicts; and the identification of psychopathology, abandoned but should be tapered slowly. Provided that the
including any source of symptom modelling and any second- underlying psychiatric illness is addressed by treatment, the
ary gain. spells will resolve over time, which can be weeks or months.
Exploring the patient’s mental status, with or without Helpful psychotherapeutic strategies include cognitive-
narcoanalysis, is an ongoing process throughout treatment; it behavioural and expressive–supportive therapy. An
aims to identify and confirm the underlying primary psychiat- overdetailed history, in which physical symptoms are
ric disorder. This may be immediately recognizable. More reviewed on each and every occasion and in minute detail,
often, the underlying psychiatric disorder emerges over often helps. This task can be demanding for physicians, but it
weeks, but it may surface precipitously. Relevant dynamics reassures patients that their physical symptoms are not being
and psychosocial stressors are also sought and explored. A dismissed or overlooked. A rational cognitive framework for
histrionic personality disorder is not a prerequisite for conver- understanding their symptoms helps patients. This is achieved
sion disorder (10). La belle indifference is not diagnostically by providing a tangible mechanism and nonblaming explana-
helpful, as it may be seen in organic conditions (48). Last, dis- tion to account for their neurologic symptoms (49). Patients
turbed sexuality has no specific connection with conversion are told that current evidence indicates that conversion disor-
symptoms, although historically it has been identified as one der is caused by a neurochemical disorder of the brain, most
of the primary conflicts associated with this condition (10). commonly, depression. This neurochemical disturbance does
In patients whose conversion symptoms have been present for not manifest through typical psychiatric symptoms but,
fewer than 6 months, the underlying psychiatric disorder rather, surfaces via unconscious mechanisms as physical
(most commonly, depression) is often readily discovered symptoms. Typical psychological hurdles to be overcome
(21). With chronic conversion symptoms lasting more than include patients’ reluctance to accept the idea that psychiatric
6 months, the underlying psychiatric disorder is often not eas- disorder can cause the obvious and more acceptable somatic
ily identified. In these patients, the psychopathology may symptoms and their reluctance to accept orthodox psychiatric

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 Somatization and Conversion Disorder

therapies, even though they have usually tried many comple- 68% of patients demonstrated a full neurologic recovery, 12%
mentary therapies. had a variable recovery, and 20% failed to demonstrate any
Family therapy is almost always necessary. Families have recovery (T Hurwitz and B Kosaka, unpublished observations).
often invested heavily in patients’ symptoms and devoted These 20% were felt to have a severe and treatment-resistant
considerable time and resources to helping patients deal with underlying psychiatric disorder. In a subgroup of these
their neurologic disabilities. The family will therefore also treatment-resistant patients, the acute precipitating psychiatric
have to come to terms with the fact that the neurologic disabil- illness has seemingly fully resolved, but the neurologic symp-
ity has been caused by a psychiatric illness. Helping families toms persist, retained as a maladaptive behavioural pattern and
accept this condition as a genuine sickness, but one that is psy- perpetuated by the advantages of the sick role, wherein life as
chiatric rather than neurologic, ensures that they continue to an invalid is preferable to all other options. Slater has described
support patients through the period of recovery and beyond. this group as “invalids of choice” (50).

Pharmacotherapy involves energetic psychotropic medica- Recovery of neurologic function does not, however, end the
tion trials. Narcotic analgesics taken to control the nonorganic patients’ difficulties. In a 6-year follow-up, 36% of patients
pain that may accompany psychogenic neurologic deficits had persistent, active, psychiatric problems; only one-third of
need to be withdrawn. In this setting, they are presumably an patients were working full-time; and 47% were retired on the
attempt to self-treat the dysphoria of the underlying psychiat- grounds of ill-health. At follow-up, the identified psychiatric
ric disorder. disorder was mostly either a continuation or a relapse of the
psychiatric disorder identified at the initial presentation (39).
Patients with conversion disorder commonly demonstrate In another follow-up study of patients with conversion disor-
physiological and psychological medication hypersensitivity der, 34% were suffering an episode of major depression at
characterized by unusual side effects, in part linked to their follow-up. The mean number of years from the index clinical
reluctance to accept that they have a psychiatric disorder. contact to the follow-up interview was 4.2 (42). These studies
They will prematurely abandon medication trials if not given indicate the importance of identifying and treating the under-
adequate reassurance and support. Medications may therefore lying psychiatric disorder.
need to be started at low dosages and gradually titrated
upwards. Here, the goal is to give antidepressants in appropri-
Conclusion
ate dosages and for an adequate duration, similar to the dosing
Conversion disorder is a challenging psychiatric disorder that
regimen of any mood disorder. Standard antidepressant medi-
requires long-term commitment on the psychiatrist’s part and
cations are used and include the selective serotonin reuptake
uses the full spectrum of psychiatric skills. Conversion reac-
inhibitors, tricyclic antidepressants, and novel antidepres-
tions represent a somatic defence against threats to mental sta-
sants such as venlafaxine and bupropion. Neurologic symp-
bility that are most commonly attributable to an underlying
toms that fail to resolve with antidepressants alone should be
mood disorder. Perseverance through the diagnostic and treat-
treated with neuroleptics. Neuroleptics target somatic delu-
ment phases is more often than not rewarded by positive
sions (one hypothesis for the resistance of somatic symptoms
results. Patients require long-term care to manage their mood
in the face of incontrovertible evidence that no organic dis-
disorders and associated psychosocial issues. One important
ease is present). Atypical neuroleptics are preferable because
role of the treating psychiatrist is to ensure that any new physi-
they carry a lower risk of tardive dyskinesia. If this strategy
cal symptom receives appropriate medical investigation from
fails, patients should be offered a course of electroconvulsive
the rest of the medical profession. Physicians are usually baf-
therapy, which may succeed in recovering neurologic func-
fled and annoyed by patients with conversion disorders and
tion and effectively treat the underlying psychiatric disorder
remain too quick to dismiss any new somatic symptom as
(46).
“more of the same,” to the patients’ great detriment.
Prognosis
Few studies describe the prognosis for psychogenic deficits and References
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Résumé : Somatisation et trouble de conversion

La somatisation est le mécanisme psychologique par lequel la détresse psychologique
s’exprime sous forme de symptômes physiques. La détresse psychologique de la
somatisation est le plus souvent causée par un trouble de l’humeur qui menace la stabilité
mentale. Le trouble de conversion survient lorsque la présentation somatique touche un
aspect quelconque du système nerveux central sur lequel s’exerce un contrôle volontaire. Les
réactions de conversion représentent des idées fixes sur la dysfonction neurologique qui sont
consciemment adoptées, ce qui résulte en des déficiences neurologiques psychogènes. Le
traitement est complexe et long; il comprend le rétablissement de la fonction neurologique à
l’aide de la narcoanalyse, de l’identification et du traitement du principal trouble
psychiatrique, habituellement un trouble de l’humeur.

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