Conversion disorder
Alternative name: Hysterical neurosis
Conversion
Disorder is a DSM-IV diagnosis which describes neurological symptoms such as
weakness, sensory disturbance and attacks that look like epilepsy but which can
not be attributed to a known neurological disease.
The DSM-IV definition, which is by no means agreed upon by all those working in
the field, is as follows:
One or more
symptoms or deficits are present that affect voluntary motor or sensory function
suggestive of a neurologic or other general medical condition.
Psychological factors are judged, in the clinician's opinion, to be associated
with the symptom or deficit because conflicts or other stressors precede the
initiation or exacerbation of the symptom or deficit. A diagnosis where the
stressor precedes the onset of symptoms by up to 15 years is not unusual.
The symptom or deficit is not intentionally produced or feigned (as in
factitious disorder or malingering).
The symptom or deficit, after appropriate investigation, cannot be explained
fully by a general medical condition, the direct effects of a substance, or as a
culturally sanctioned behavior or experience.
The symptom or deficit causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning or warrants
medical evaluation.
The symptom or deficit is not limited to pain or sexual dysfunction, does not
occur exclusively during the course of somatization disorder, and is not better
accounted for by another mental disorder.
The condition has
a complex history. These symptoms are also described as functional, non-organic,
hysterical, psychogenic, depending on your etiological point of view. In the
International Classification of Diseases they are termed Dissociative. Critics
who refute the concept of dissociative disorders hold that as Frederick Crews
stated "dissociation is the perfect psychoanalytic-style vehicle for creation of
a pseudoscience, since there is no way to disprove its existence and recovered
memories never need be tested by comparing them with conscious memories. After
all, if children dissociate themselves from the experience, one could not expect
them to have any memories of the event. " (Frederick Crews, The Memory Wars:
Freud's Legacy in Dispute)
A more precise label is Functional Neurological Deficit which research has shown
to be a more acceptable term in doctor patient relationships (Stone et al).
Stressing as it does the inabilty of tests to explain the symptom or symptoms.
As neurologists depend upon inconsistency for diagnosis there can be tension
with colleagues in mental health "When I send a patient to a consultant
psychologist I'm told there is nothing wrong with them, that's why I send them
to a psychiatrist he always finds something wrong"- Dr. P. Nichols. Such
disagreement appears to be common.
That there should be a temporal relationship between symptom onset and some
external event of psychological conflict is a question of debate. There has been
a long history of symptoms misdiagnosed as having no underlying physical cause.
In women, the term Female hysteria was used to refer to a wide spectrum of
symptoms ranging from fainting to anxiety. As a term it goes back over 2000
years and was thought to relate to abnormal motions of the uterus. From the 17th
century onwards, Thomas Willis, Robert Whytt and others increasingly realised
the problem was in fact localised to the brain and mind.
In the 19th
century, physicians such as Silas Weir Mitchell in the US and Paul Briquet and
Jean-Martin Charcot in France developed ideas about patients with these
neurological symptoms which would now be classed as neuropsychiatric. Charcot
specialized in treating patients who were suffering from a variety of
unexplained physical symptoms including paralysis, contractures (muscles which
contract and cannot be relaxed) and seizures. Some of these patients
sporadically and compulsively adopted a bizarre posture (christened arc-de-cercle)
in which they arched their body backwards until they were supported only by
their head and their heels.
"Charcot
eventually came to the conclusion that many of his patients were suffering from
a form of hysteria which had been induced by their emotional response to a
traumatic accident in their past such as a fall from a scaffold or a railway
crash. They suffered, in his view, not from the physical effects of the
accident, but from the idea they had formed of it... However many of the most
basic diagnostic techniques which are taken for granted by modern physicians had
still to be discovered. The lumbar puncture, which is the only way in which
Breuer could have tested his momentary hunch that Anna O. was suffering from
meningitis, was not developed until 1891, and was not in general use until the
early part of the twentieth century. X-rays, which would eventually become one
of the most useful of all diagnostic aids, were discovered only in 1895 the
same year in which Studies on Hysteria was published. The electroencephalogram,
which would revolutionize neurology and psychiatry and lead to the final
definition of temporal lobe epilepsy, was not invented until 1929, and was not
in general use until the 1940s. Many other basic techniques of neurological
investigation would not be developed until even later. The computed tomography
scan, for example, which uses X-ray transmission readings to generate an image
of the brain and which can display some lesions, tumors and other signs of
pathology directly, began to be generally used only in the late 1970s. Not only
were these diagnostic techniques unavailable to Breuer, Freud and their
contemporaries, but neurology and psychiatry were relatively young and
under-organized branches of medicine whose stores of knowledge were only just
beginning to be built up." (Webster, Why Freud Was Wrong).
It is also now recognised that many of Charcot's demonstrations of hysteria were
faked (Szasz, the Myth of Mental Illness). As many neurologist's remain ignorant
of Charcot's methodology at the Salpκtriθre in the diagnosis of hysteria he is
often held up as a champion of neuropscyhiatry (Stone et al). It is doubtless
though that as neurology continues to emerge from diagnostic darkness further
techniques are likely to be developed and previously unvisualized abnormalities
and conditions recognized.
The term
"Conversion disorder" is a legacy of Freud and the psychotherapy movement. He
viewed these apparently neurological symptoms as a result of the conversion of
intrapsychic distress in to physical symptoms. It is worth bearing in mind that
much of Freud's work is now viewed with scepticism, and it may be that patients
Freud thought were hysterical may actually have suffered from organic illness,
such as "Anna O." (see Alison Orr-Andrewes, "The case of Anna O: A
Neuropsychiatric perspective" in Journal of the Psychoanalytic Association 1987,
vol 35 p.399).
In the 1960s the
London Psychiatrist Eliot Slater recognized that finding a life event just
before the onset of a symptom was an entirely unreliable way of diagnosing
conversion disorder.
Unfortunately we
have to recognize that trouble, discord, anxiety and frustration are so
prevalent at all stages of life that their mere occurrence near to the time of
onset of an illness does not mean very much. Eliot Slater
He also suggested
that conversion disorder was largely a 'delusion and a snare' since many of the
people said to have it would eventually go on to develop a neurological disease
that in hindsight could explain their original symptoms. This echoed the earlier
sentiments of Steyerthal: "Within a few years the concept of hysteria will
belong to history ... there is no such disease and there never has been. What
Charcot called hysteria is a tissue woven of a thousand threads, a cohort of the
most varied diseases, with nothing in common but the so-called stigmata, which
in fact may accompany any disease." Armin Steyerthal (1908)
Studies since 1970
have shown that misdiagnosis still occurs but at a rate of around 5% which is
the same as for other neurological and pscyhiatric symptoms (Stone et al BMJ
2005). Whether this is a social phenomenon produced by the modus operandi of
health care systems requires further research. Most patients only receive
investigations at the onset of illness and many illnesses, such as MS, are hard
to diagnose initially. Patients also tend to produce functional symptoms in
response to the disbelief and prompting of a neurologist as Slater also
recognized. Inconsistency could thus be seen as merely an expression of
self-consciousness and desperation in the light of distressing symptoms. It is
interesting in this light to note however that 20% of MS patients are
re-classified as having functional symptoms and there is a high co-morbidity of
functional symptoms alongside recognized organic brain disease.
Historically,
conversion disorder was thought to manifest itself in many different ways.
Conversion disorders were thought to be triggered by acute psychosocial stress
that the individual could not process psychologically. This overwhelming
distress was thought to cause the brain to unconsciously disable or impair a
bodily function which would relieve or prevent the patient from experiencing
this stressor again. This is in stark contrast to the modern understanding that
patients remain distressed by their symptoms in the long term (Stone et al JR
Soc Med 2005; 98:547-548) and generally any hypothesized stressor is removed
temporally and symbolically from the onset of symptoms. Therefore, the
psychosocial stress cannot be seen to be "converted' into a physical symptom
that relieve suffering, when in actual fact they increase it. Historically, the
patient, by definition, was considered to be unaware of this process, and often
not concerned with his deficit a feature called la belle indifference.
Research now shows this to be untrue (Stone et al as above).
More recently,
research is attempting to examine the complex nature of these symptoms and the
absurdity of a dualist approach which attempts to suggest that symptoms are
either all organic or all psychiatric. Functional neuroimaging has shown
intriguing findings with respect to the neural correlates of these symptoms
(best example is Vuilleimier et al Brain Vol. 124, No. 6, 1077-1090, June 2001)
Conversion disorder can present with any motor or sensory symptom in the body
including:
Weakness / Paralysis of a limb or the entire body hysterical paralysis or
motor conversion disorders
Impaired hearing or vision
Loss / Disturbance of sensation
Impairment or loss of speech--- hysterical aphonia
Psychogenic non-epileptic seizures
Fixed Dystonia unlike normal dystonia
Tremor, Myoclonus or other movement disorders
Astasia-abasia or Gait Problems
hysterical pregnancy (even though though this is common in other mammals to
ensure enough milk for the group's offspring)
Diagnosis depends
not on the absence of findings of neurological disease but on the finding of
positive evidence of conversion symptoms.
La belle indiffιrence has been described as a characteristic feature of
conversion. It is characterized by the inappropriate and paradoxical absence of
distress despite the presence of an unpleasant symptom. Patients often deny
emotional difficulty. Traditionally associated with conversion disorder, la
belle indiffιrence, histrionic personality, and secondary gain are clinical
features that appear to have no diagnostic significance. Although presence of
these features supports the diagnosis, they have no diagnostic validity because
the diagnosis of conversion disorder ultimately depends upon clinical findings
that clearly demonstrate that the patient's symptomatology is not caused by
organic disease.
One study reported
5 patients with hysterical conversion reactions after injury or infarction to
the left cerebral hemisphere. [3]
Conversion symptoms are remarkably consistent between patients, just as
Parkinson's disease is consistent between patients. There may be positive
evidence of patterns of weakness (for example Hoover's Sign or a non-pyramidal
pattern of weakness) or a typical gait problem (for example a 'dragging
monoplegic gait). For Psychogenic non-epileptic seizures a range of features of
the attacks must be taken in to consideration and the diagnosis may need
confirmation with videotelemetry.
Diagnosis is not
easy and should preferably only be made by a neurologist with experience of the
condition.
Patients with conversion symptoms will typically have multiple other symptoms
which may include fatigue, sleep disturbance, memory and concentration
difficulties, pain (neck, back, muscles), bowel and bladder sensitivity
Prevalence: In the US: True conversion reaction is rare. Predisposing factors,
according to the DSM-IV, include prior physical disorders, close contact to
people with real physical symptoms, and extreme psychosocial stress. In the
United Kingdom however 40% of neurological referrals are deemed to be suffering
from conversion disorder (Stone, Carson & "Wessely School" psychiatrists)
Incidence has been reported to be 15-22 cases per 100,000 people. In patients
with chronic pain, incidence was 0.22%. Conversion reaction may occur more often
in rural settings, where patients may be naive about medical and psychological
issues. In one study, high rates were seen in Appalachian males. The disorder is
observed more commonly in lower socioeconomic groups and may be more common in
military personnel exposed to combat situations.
Cultural factors
may play a significant role. Symptoms that might be considered a conversion
disorder in the US may be a normal expression of anxiety in other cultures. One
study reports that conversion disorder accounts for 1.2-11.5% of psychiatric
consultations for hospitalized medical and surgical patients. Internationally:
At the National Hospital in London, the diagnosis was made in 1% of inpatients.
Iceland's incidence of conversion disorder is reported to be 15 cases per
100,000 persons.
Sex ratio is not
known although it has been estimated that women patients outnumber men by 6:1.
Many authors have related the development of conversion disorder in women with
sexual maladjustment. Other authors disagree, stating that men are as likely to
experience conversion symptoms as women. Men seem to be especially prone if they
have suffered an industrial accident or have served in the military. In a study
at the University of Iowa conducted from 1984-1986, patients diagnosed with
conversion disorder were in large part men, especially those with a history of
military combat.
Studies report that 64% of patients with conversion disorder show evidence of an
organic brain disorder, compared with 5% of control subjects. Some bacterial
pathogens can also mirror conversion symptoms and non-pyramidal weakness as they
alter brain chemistry and function rather than structure (forthcoming
publication). However testing, especially in the United Kingdom, remains
primitive with only dark field microscope studies providing conclusive evidence
of spirochete infection. Progress in the States is much more advanced which
could explain the discrepancy in diagnostic rates. An earlier study revealed
that a medical explanation eventually emerged from presenting chief complaints
in only 7% of patients. Incidence of true neurological disease discovered at a
latter date is extremely rare, largely due to advances in diagnostic testing.
The Extent to Which Age and Life Experiences Influence Incidence
Conversion disorder may present at any age but is rare in children younger than
10 years or in persons older than 35 years. Some studies have reported another
peak for patients aged 50-60 years. In a University of Iowa study of 32 patients
with conversion disorder, however, the mean age was 41 years with a range of
23-58 years. In pediatric patients, incidence of conversion is increased after
physical or sexual abuse. Incidence also increases in those children whose
parents are either seriously ill or have chronic pain.
Often a patients reaction to the diagnosis of conversion disorder is to be
offended that the doctor thinks they are crazy or making their symptoms up. It
is true to say that many doctors still do regard these symptoms as 'not genuine'
and not deserving of attention. However, many doctors do regard them as genuine
but struggle to know how to communicate with patients If patients with
conversion symptoms were malingering there would be a number of problems from
clinical practice to sort out:
Evidence from long term studies showing that symptoms persist at follow up
many years later
Patients with conversion symptoms generally desire tests, malingerers would
not
There is remarkable consistency between patients (who have not met each other)
Treatment may include the following
1. Explanation - This must be clear and coherent. It must emphasise the
genuineness of the condition, that it is common, potentially reversible and does
not mean that the sufferer is a 'psycho'. Taking an aetiologically neutral
stance by describing the symptoms as functional may be helpful but further
studies are required. Ideally the patient should be followed up neurologically
for a while to ensure that the diagnosis has been understood
2. Physiotherapy where appropriate
3. Treatment of comorbid depression or anxiety if present
There is little evidence based treatment of conversion disorder (Ruddy and House
- Cochrane Collaboration). Other treatments such as cognitive behavioural
therapy, hypnosis, psychodynamic psychotherapy need further trials. It should
also be noted that psychoanalytic treatments, on which CBT is based, were
singularly unaffective with Freud and Breuer's patients.
Generally, onset of symptoms is linked to a socially or psychologically
stressful event. The symptom must be clinically significant; ie, it must be
distressing enough to disrupt the patient's social, occupational, or other
important area of functioning. A patient may have a single episode or sporadic
ones; usually, episodes are brief. When hospitalized, patients with conversion
symptoms generally improve within 2 wk; however, 20 to 25% have recurrences
within a year, and in some, symptoms become chronic.
The diagnosis may
be difficult initially because the patient believes the symptoms stem from a
physical disorder. Also, physicians are taught almost exclusively to consider
(and exclude) physical disorders as the cause of physical symptoms. Commonly,
the diagnosis is considered only after extensive physical examinations and
laboratory tests fail to reveal a disorder that can fully account for the
symptom and its effects. Although ruling out a possible underlying physical
disorder is crucial, early consideration of conversion may avoid tests that
increase the costs and risks to the patient and that may unduly delay diagnosis.
The best clue is that conversion symptoms rarely conform fully to known anatomic
and physiologic mechanisms.
Treatment is recommended to help the person understand the underlying
psychological conflict. The integrity of the affected body part or function must
be maintained until the conflict is resolved and the symptoms usually disappear.
For example, paralyzed limbs must be exercised to avoid muscle wasting.
Symptoms usually
last for days to weeks and may resolve spontaneously. Usually the symptom itself
is not life-threatening, but the development of complications as a result of the
symptom can be debilitating. A trusting physician-patient relationship is
essential. After the physician has excluded a physical disorder and reassured
the patient that the symptoms do not indicate a serious underlying disorder, the
patient usually begins to feel better and symptoms fade. When a psychologically
distressing situation has preceded symptom onset, psychotherapy can be
effective. Various treatments have been tried, but none is uniformly effective.
In hypnotherapy, the patient is hypnotized, and potentially etiologic
psychologic issues are identified and explored. Discussion continues after
hypnosis, when the patient is fully alert. Narcoanalysis is similar to hypnosis,
except that the patient is given a sedative to induce a state of semisleep.
Behavior modification therapy, including relaxation training, is effective in
some patients.
Examples of conversion symptoms include blindness, diplopia, paralysis,
seizures, anesthesia, aphonia, amnesia, unresponsiveness, and difficulty
walking. Conversion disorder represents one type of somatoform disorder. The
essential element of all somatoform disorders is the presence of physical
symptoms or signs that cannot be explained by a medical condition. Unlike
factitious disorders and malingering, the symptoms of somatoform disorders are
not intentional or under voluntary control.
It has been postulated that the patient derives primary and secondary gain. With
primary gain, the symptoms allow the patient to express the conflict that has
been suppressed unconsciously. With secondary gain, symptoms allow the patient
to avoid unpleasant situations or garner support from friends, family, and the
medical system that would otherwise be unobtainable. According to sociocultural
theories, the direct expression of emotions is impermissible and somatization
takes its place. In behavioral models, conversion symptoms are viewed as a
learned maladaptive behavior that is reinforced by the environment.
The idea that
conversion disorder does not have an organic basis has become entrenched.
However, some evidence supports the opposite notion. Studies on the natural
history of conversion disorder indicate that many patients subsequently develop
or are found to have preexisting neurological disease. In fact, conversion
disorders may be more frequently observed in patients with a past history of a
central nervous system injury. The simultaneous occurrence of organic brain
disease with conversion symptoms also is observed, most notably in observation
of high rates of organic seizure syndromes associated with psychogenic
nonepileptic seizures. Familial studies have also shown that conversion symptoms
in first-degree female relatives are up to 14 times greater than in the general
population.
In the US: Stefansson et al report that the annual incidence of conversion
reactions is 22 cases per 100,000 persons per year in Monroe County, New York.
However, the reported rates vary widely. In a study of 100 consecutive women
following a normal full-term pregnancy, 33 were noted to have a past history of
conversion symptoms. In a study of 100 randomly selected patients from a
psychiatry clinic, 24 were noted to have unexplained neurological symptoms. It
is reported to be more common in rural populations, in individuals with lower
socioeconomic status, and in individuals with less medical knowledge.
Internationally: Stefansson et al report that the annual incidence is 11 cases
per 100,000 persons per year in Iceland.
Mortality/Morbidity:
Individual conversion symptoms generally are self-limiting and do not lead to
physical changes or disabilities.
Morbidity is often an iatrogenic manifestation of unnecessary diagnostic or
therapeutic interventions.
Patients with chronic conversion symptoms (rarely) may develop atrophy, frozen
joints, and contractures from disuse.
Sex:
The female-to-male ratio is 2-10:1.
Age:
The typical onset is between the second and fourth decades.
The reported range is from children to individuals in their ninth decade of
life.
Patients with conversion disorder may present with hemiparesis, paraparesis,
monoparesis, alteration of consciousness, visual loss, seizurelike activity,
pseudocoma, abnormal gait disturbance, aphonia or dysphonia, lack of
coordination, or a bizarre movement disorder. Patients who are more medically
naοve typically have more implausible presenting symptoms. The presenting
symptoms depend on the cultural milieu, the degree of medical sophistication,
and the underlying psychiatric issue.
Patients with conversion disorder typically deny any emotional problem and
resist a consultation with a psychiatrist. Therefore, responsibility lies with
other medical personnel to perform the initial management prior to conveying the
diagnosis.
Physical: A full physical examination with attention to the mental status
(indifferent affect) and neurological examination should be performed. Certain
principles are used during the neurological examination to distinguish
psychogenic deficits from neurological ones. The pattern of deficits usually
does not conform to known anatomic pathways. For example, patients who present
with monoparesis will not have weakness in a corticospinal tract or neuropathic
or a myopathic distribution. In addition, no changes may be seen in reflexes or
tone that typically would be expected.
The physician
should contrast formal examination from functional observations. Patients who do
not move a limb when asked on examination may be observed to use that limb
inadvertently while dressing or talking. Patients who do not dorsiflex the foot
while seated may walk on the heels when asked to do so. Another example might be
a patient who cannot stand on one leg who may be observed to do so while putting
on pants.
Observations when
the patient is unaware of being examined are helpful. Patients with psychogenic
movements may have no such movements when observed in the waiting room. Multiple
examinations by one or more practitioners may disclose variable results.
However, caution is necessary when applying these rules. No single feature is
absolute. The knowledge pertaining to neuroanatomy and the clinical deficits
that arise from abnormalities is not completely known, thus resulting in
limitations of the neurological examination. In addition, patients can embellish
on organic deficits. Therefore, only a presumptive diagnosis can be made after
the initial evaluation.
Further
complicating the assessment is the knowledge that up to 30% of patients with
conversion disorder develop a physical illness that may account for their
symptoms if followed longitudinally. It also is not uncommon for patients with
conversion disorder to have a comorbid medical or neurological illness. An
example is the patient who exhibits both epileptic seizures and psychogenic
nonepileptic seizures, a clinical situation not uncommon to epilepsy referral
centers.
Other specific
details to help diagnose 3 different conversion symptoms include the following:
-
Psychogenic
hemiparesis
-
Unilateral
weakness or hemiparesis is one manner in which the patient with conversion
disorder may present.
-
Classic
hemiparesis represents a deficit of the corticospinal tract. In an acute
lesion of the corticospinal tract, a patient may demonstrate flaccidity of
the weak limbs, which is associated with decreased reflexes. In more chronic
lesions, the patient may develop spasticity of the affected limbs,
hyperreflexia, and an extensor toe sign (positive Babinski). The patient
with hemiparesis from a corticospinal tract lesion may demonstrate weakness
of the extensor muscles to a greater extent than the flexor muscles and may
show greater weakness distally than proximally.
None of these
findings would likely be seen in the patient with conversion disorder. In
psychogenic hemiparesis, the muscle contractions are poorly sustained and may
weaken abruptly as the patient resists the force exerted by the examiner. This
is felt clinically as a "give-way" or ratchet-like weakness, unlike the fluid
weakness throughout the range of motion usually felt by the examiner in an upper
or lower motor neuron lesion.
The Hoover sign
also may be elicited. When a patient in the recumbent position flexes the thigh
and lifts the leg, the downward movement of the contralateral leg is automatic.
The examiner places a hand beneath the heel and asks the patient to raise the
paretic leg. In feigned weakness, no appreciable downward movement is evident.
In addition, when the patient is asked to raise the normal leg, the downward
movement is appreciated from the "paretic" leg.
Another
helpful tool is examining the sternocleidomastoid muscle. Normal contraction of
this muscle results in the face rotating in the opposite direction. The patient
with psychogenic weakness therefore may display weakness of the contralateral
sternocleidomastoid (ie, weakness in turning the face towards the hemiparetic
side).
Recognizing the patient with psychogenic hemiparesis includes observing the
following:
No changes in reflexes
No changes in tone
Give-way quality of weakness
Extensor and flexor muscles equally weak
Contralateral sternocleidomastoid weakness
Positive Hoover sign
Difference between formal examination and general observations
Psychogenic
nonepileptic seizures
o Distinguishing between a psychogenic nonepileptic seizure, or pseudoseizure,
and an epileptic seizure is challenging. The manifestations of each are diverse,
and the clinical diagnosis rests on historical information from witnesses with
varying observational skills. Simultaneous video electroencephalogram (EEG)
monitoring has significantly improved the accuracy of diagnosis, but this
technique is expensive and not routinely available. Psychogenic seizures may
constitute up to 20% of all patients in an epilepsy referral center. Refer to
the article on Psychogenic Seizures in the eMedicine Neurology section for more
details.
Classic clues that
suggest nonepileptic seizure include the following:
Ineffectiveness of multiple antiepileptic drugs
Induced by stress or emotional upset
Lack of physical injury
Lack of headache or myalgias following convulsions
Lack of incontinence
Biting the tip of the tongue as opposed to the side or the lip
History of sexual or physical abuse
Signs or symptoms suggestive of another conversion
Memory of a generalized ictal event
o Ictal characteristics that suggest nonepileptic seizure include the following:
Gradual onset of ictus
Prolonged duration (>4 min)
Atypical or excessive motor activity such as thrashing, rolling from one side
to the other, pelvic thrusting, or arrhythmic (out-of-phase) jerking such as
alternating side flexion and extension of the arms
Waxing and waning amplitude
Intelligible speech
Bilateral motor activity with preserved consciousness
Clinical features that change from one spell to the next (ie, nonstereotyped)
Lack of postictal confusion
Postictal crying or cursing
Directed violent acts
Eyes closed during the ictus
Resistance to eye opening
Purposeful resistance to passive movements
Psychogenic
movement disorders
o Conversion disorder can imitate the entire spectrum of movement disorders and
include tremor, chorea, myoclonus, dystonia, tics, parkinsonism, and a host of
bizarre gait disturbances. A commonly used term for a type of this last
phenomenon is an astasia-abasia gait pattern, in which the patient will make
wild movements of the trunk and arms during a gait evaluation but does not fall
or err from a stressed gait such as a tandem or toe gait.
Clinical symptoms
or signs that may help distinguish psychogenic movements from organic ones
include the following:
Abrupt onset of symptoms
Character of movements atypical of recognized patterns and have inconsistent
amplitude, frequency, and distribution
Characteristics of movements change over time
Entrainment of the tremor to the rate requested by the examiner
Spontaneous remissions
Movements disappear with distractions
Movements increase with attention
Response to placebo, psychotherapy, or suggestion
Paroxysmal symptoms
Nonobjective weakness or sensory changes also present
Obvious secondary gain (eg, litigation, health insurance claim, military
service)
Causes:
Neuroimaging studies of conversion disorders indicate hypofunction of the
dominant hemisphere and a consequent overactivity in the nondominant side. Other
neuroanatomic findings have been seen with conversion disorder. Marshall et al
reported changes in regional cerebral blood flow (rCBF) in a female patient with
a left leg paralysis and intact sensory modalities for which no anatomic cause
of her weakness could be found. Attempting to move her paralyzed leg did not
show activation of contralateral motor cortex, but rather contralateral
orbit-frontal and anterior cingulated cortex were activated. This implied an
anatomic inhibition of primary motor cortex in one case of hysterical paralysis.
Neuropsychological testing shows evidence of impaired attention and short-term
memory.
Psychodynamic theory postulates that conversion symptoms are the result of
conversion of anxiety regarding an unconscious intrapsychic conflict into
somatic symptoms.
Learning theorists believe that such symptoms develop from conditioning that
occurs during childhood and that these learned behaviors arise again when the
person is subjected to overwhelming stress later in life.
Such symptoms also can be viewed as a form of physical communication of an
emotionally charged idea or feeling when one is unable to verbalize the conflict
because of personal or social taboos.
Other Problems to
be Considered:
The differential diagnosis of conversion disorders is highly dependent on the
manner in which the patient presents. Organic etiologies must be excluded. For
example, the differential for psychogenic hemiparesis includes tumor, stroke,
multiple sclerosis, and many others.
Lab Studies:
Hemiparesis
o MRI of brain with diffusion-weighted imaging
o MRI of cervical region
Pseudoseizure
o MRI of brain
o EEG
o Prolonged video-EEG monitoring
o Provocative EEG with placebo induction
o Echocardiogram
o Holter monitor
o Tilt-table test
o Prolactin level 30 minutes after the event: An elevation above baseline can
occur with partial seizures, generalized seizures, or syncope, but not with
pseudoseizures.
Psychogenic movement disorders
o MRI of brain
o Twenty-fourhour urine copper, serum ceruloplasmin, and slit lamp examination
for evidence of Kayser-Fleisher rings to look for evidence of Wilson disease
o Thyroid-stimulating hormone, thyroid peroxidase antibodies, thyroglobulin
antibodies
o CBC count with smear for acanthocytes
o Erythrocyte sedimentation rate, antinuclear antibody, extractable nuclear
antibody, anticardiolipin antibody, lupus anticoagulant
o HIV antibody, Lyme antibody, anti-streptolysin O (ASO) antibody
o Human chorionic gonadotropin
Procedures:
Hypnosis or amobarbital interview
o To ensure diagnosis
o To disclose underlying psychiatric issues
Brain PET scan - Has demonstrated evidence of left dorsolateral prefrontal
cortex hypofunction
SPECT scan - Has shown decrease in regional blood flow in the thalamus and
basal ganglia contralateral to the deficit
TREATMENT Section 6 of 10
Author Information Introduction Clinical Differentials Workup Treatment
Follow-up Miscellaneous Pictures Bibliography
Current understanding of the phenomenon of conversion disorder implicates some
role of the unconscious in the pathophysiology of this condition. It is
therefore less likely to respond to treatment when the manifestations of the
conversion are confronted directly as a unitary method of therapy. Many patients
who experience a conversion disorder are unable to understand this inner
conflict, which is perhaps occurring on an unconscious level. They may achieve
resolution of the conflict, and their physical symptoms, once they are gently
made aware of this connection. Once the patient is aware of this, the
psychologic currency of the symptom loses value, and the symptom may be allowed
to improve.
Consider hospital admission: The patient may not return for follow-up after
being given a psychiatric diagnosis. A more rapid completion of the diagnostic
workup is possible. In addition, a parallel investigation of physical and
psychologic factors can and should be pursued. One caveat to note is that the
clinical situation may be worsened by providing the patient with the secondary
gain he or she is seeking.
Avoid invasive diagnostic and therapeutic interventions.
Tactful presentation of the diagnosis to the patient includes the following:
o Avoid giving the patient the impression that you feel there is nothing wrong
with them.
o Do not inform the patient of the diagnosis on the first encounter.
o Reassure the patient that the symptoms are very real despite the lack of a
definitive organic diagnosis.
o Provide socially acceptable examples of diseases that often are deemed
stress-related (eg, peptic ulcer disease, hypertension).
o Provide common examples of emotions producing symptoms (eg, queasy stomach
when talking in front of an audience, sweaty palms when asking someone for a
date).
o Provide examples of how the subconscious influences behavior (eg, nail biting,
pacing).
o Provide reassurance that no evidence of an underlying neurological disorder is
present based on the tests that were performed and that the prognosis for
recovery is very good.
o Provide positive reinforcement that the symptoms can improve spontaneously.
o Inform patients that the symptoms are not volitional, and no one believes that
they are faking.
o Provide a graceful way for the patient to improve from the symptoms. (Allow
for the symptom to get better over time, just as an organic entity might
improve.)
No specific pharmacologic therapy is available for conversion disorder;
however, medications for comorbid mood and anxiety disorders should be
considered. Care should be taken to avoid dependence-producing psychotropic
agents.
Physical therapy may be warranted.
Institute patient and family education sensitively in order to not make the
patient feel worse.
Regular follow-up appointments with a neurologist or a psychiatrist should be
provided to limit ER visits, which may lead to contact with multiple healthcare
providers and, in turn, unnecessary diagnostic/invasive tests.
Consultations:
Neurologist: This is the primary evaluation for differentiating conversion
disorders from neurological diseases.
Cardiologist: Consultation is warranted if the patient has episodic
alterations of consciousness.
Physical therapist: Consultation may be warranted.
Psychiatrist: This generally is indicated when the symptoms persist. This can
aid in identification of psychologic stressors symbolically linked to the
symptoms and other risk factors for conversion disorder. The patient must be
informed about the consultation before the psychiatrist does the interview.
Psychiatric treatments that have demonstrated effectiveness include the
following:
Psychodynamic therapy: Patients with borderline intelligence, lack of
motivation or introspection capabilities, important secondary gains, or those
with a tendency for behavioral acting out likely are poor candidates.
Behavioral therapy: The inappropriate behavior no longer is rewarded or may
even be punished. An advantage is that neither normal intelligence nor insight
is necessary for success. A disadvantage is that behavioral therapy relies on
controlling the environmental conditions, which may not be feasible.
Psychologist: Psychosocial interventions that may be helpful include
paradoxical intention therapy and hypnosis.
Family therapist: Interactions and communication within the family are
emphasized rather than only focusing on the individual patient.
FOLLOW-UP Section 7 of 10
Author Information Introduction Clinical Differentials Workup Treatment
Follow-up Miscellaneous Pictures Bibliography
Prognosis:
Spontaneous resolution in most - Approximately 75%
Recurrence of same or different conversion symptoms - Approximately 25% in
15-year follow-up studies
False-positive diagnosis of conversion disorder
o Approximately 25% are diagnosed with neurological disease in 10-year follow-up
that could account for presenting symptoms.
o Multiple sclerosis, neurodegenerative diseases, structural myelopathy,
peripheral neuropathy, and myopathy accounted for the false-positive diagnoses.
Good prognostic factors - Acute onset of symptoms, short duration of symptoms,
healthy premorbid functioning, higher intelligence, absence of coexisting
psychopathology, presence of an identifiable stressor
Poor prognostic symptoms - Pseudoseizure, psychogenic tremor
Patient Education:
Sensitively review the disorder with the patient and the family in such a way
to not make them feel blamed and to not worsen the condition. During such follow
up for review of completed imaging and other studies, continuing to emphasize
the importance of, as well as your concern for the patient's pain or other
symptom is important. The physician may at the same time reassure the patient
that the negative test results are good news for their eventual recovery.
Frequent office visits to ensure the expected resolution of their symptoms may
be helpful.
Medical/Legal Pitfalls:
Delay in diagnosing organic disease due to lack of appropriate evaluation
Unnecessary interventional diagnostic tests resulting in iatrogenic illness
Overly direct or confrontational presentation of the diagnosis, which may
entrench the symptom and lead to prolonged patient disability
American Psychiatric Association: Somatoform disorders. In: Diagnostic and
Statistical Manual of Mental Disorders, Fourth Edition, Text Revision.
Washington, DC: APA Press; 2000.
Boffeli TJ, Guze SB: The simulation of neurologic disease. Psychiatr Clin
North Am 1992 Jun; 15(2): 301-10[Medline].
Bourgeois JA, Chang CH, Hilty DM: Clinical Manifestations and Management of
Conversion Disorders. Curr Treat Options Neurol 2002 Nov; 4(6):
487-497[Medline].
Carter AB: The prognosis of certain hysterical symptoms. Br Med J 1949; 1:
1076-9.
Cloninger CR, Martin RL, Guze SB, Clayton PJ: A prospective follow-up and
family study of somatization in men and women. Am J Psychiatry 1986 Jul; 143(7):
873-8[Medline].
Cohen RJ, Suter C: Hysterical seizures: suggestion as a provocative EEG test.
Ann Neurol 1982 Apr; 11(4): 391-5[Medline].
Devinsky O, Thacker K: Nonepileptic seizures. Neurol Clin 1995 May; 13(2):
299-319[Medline].
Fahn S: Psychogenic movement disorders. In: Movement Disorders. Vol 3. Oxford,
UK: Butterworth-Heinemann; 1994: 359-72.
Gould R, Miller BL, Goldberg MA, Benson DF: The validity of hysterical signs
and symptoms. J Nerv Ment Dis 1986 Oct; 174(10): 593-7[Medline].
Leis AA, Ross MA, Summers AK: Psychogenic seizures: ictal characteristics and
diagnostic pitfalls. Neurology 1992 Jan; 42(1): 95-9[Medline].
Lesser RP: Psychogenic seizures. Neurology 1996 Jun; 46(6): 1499-507[Medline].
Ljungberg L: Hysteria: A clinical, prognostic and genetic study. Acta
Psychiatr Scand Suppl 1957; 112: 1-162.
Marjama J, Troster AI, Koller WC: Psychogenic movement disorders. Neurol Clin
1995 May; 13(2): 283-97[Medline].
Marshall JC, Halligan PW, Fink GR: The functional anatomy of a hysterical
paralysis. Cognition 1997; 64: B1-B8[Medline].
Merskey H: Conversion symptoms revised. Semin Neurol 1990 Sep; 10(3):
221-8[Medline].
Ruddy R, House A: Psychosocial interventions for conversion disorder. Cochrane
Database Syst Rev 2005; CD005331[Medline].
Sar V, Akyuz G, Kundakci T, et al: Childhood trauma, dissociation, and
psychiatric comorbidity in patients with conversion disorder. Am J Psychiatry
2004 Dec; 161(12): 2271-6[Medline].
Sar V, Kundakci T, Kiziltan E: Differentiating dissociative disorders from
other diagnostic groups through somatoform dissociation in Turkey. J Trauma
Dissociation 2000; 1: 67-80.
Schrag A, Lang AE: Psychogenic movement disorders. Curr Opin Neurol 2005 Aug;
18(4): 399-404[Medline].
Shen W, Bowman ES, Markand ON: Presenting the diagnosis of pseudoseizure.
Neurology 1990 May; 40(5): 756-9[Medline].
Spence SA, Crimlisk HL, Cope H: Discrete neurophysiological correlates in
prefrontal cortex during hysterical and feigned disorder of movement. Lancet
2000 Apr 8; 355(9211): 1243-4[Medline].
Stevens H: Is it organic or is it functional. Is it hysteria or malingering?
Psychiatr Clin North Am 1986 Jun; 9(2): 241-54[Medline].
Vuilleumier P, Chicherio C, Assal F: Functional neuroanatomical correlates of
hysterical sensorimotor loss. Brain 2001 Jun; 124(Pt 6): 1077-90[Medline].
