Treatment for Patients With a Functional Neurological Disorder (Conversion Disorder): An Integrated Approach
Publication: American Journal of Psychiatry
Which of the following reflects a DSM-5 criterion for conversion disorder (functional neurologic symptom disorder)?
A.
Symptoms of altered voluntary motor, cognitive, or sensory function.
B.
Clinical findings compatible with a recognized neurologic condition.
C.
Symptom onset following an identified stressor.
D.
Evidence of intentional production of neurologic symptoms.
“Ms. A,” a 29-year-old woman, was referred for a second neurologic opinion. Several months earlier, she woke with a pins-and-needles sensation involving both legs from the knees to the toes. The following day, she could not move her legs without help from her fiancé. Several hours later, she developed transient numbness of the left arm. Alarmed by her increasing symptoms, she presented to the emergency department. A brain and cervical MRI with gadolinium contrast showed no abnormalities. The patient was discharged with neurologic follow-up. Results of an electromyogram and nerve conduction study of the upper and lower extremities were normal. Later, because of increasing back and diffuse leg pain, the patient underwent a lumbar MRI, which also showed no abnormalities. She continued to experience lower extremity weakness and paresthesias as well as back and leg pain. No diagnosis was made. The patient had been unable to work since her symptoms began.
Ms. A had a history of posttraumatic stress disorder related to a rape in college. She still endorsed presence of frequent nightmares and flashbacks related to the experience. She denied hypervigilance or avoidance related to her trauma. She denied any history of depression or other anxiety symptoms.
On examination the patient had diffuse lower extremity weakness with variability of effort (the strength of her lower extremities did not consistently show the same response, as would be expected in a physiological motor deficit). Her reflexes were normal and there were no pathological reflexes. Sensation to pinprick was decreased in both legs without a sensory level or a dermatomal pattern (if a patient has a spinal cord abnormality, a sensory level would be an expected finding, or if there were cauda equina involvement, the sensory loss should conform to that of multiple sensory dermatomes). The patient’s vibratory sense was diminished over the thoracic but not the lumbar vertebrae or in her lower extremities (this is inconsistent with a neuroanatomical basis for vibratory sensory loss). She could stand using a walker, but she was slow to initiate movement and tended to collapse at the knees (the gait disorder was inconsistent with her normal motor examination).
A diagnosis of a functional neurological disorder (conversion disorder) was made on the basis of the positive findings of the neurological examination. These included the normal motor, nonphysiological findings of the sensory examination and a gait disorder that was inconsistent with the normal findings of the motor examination.
The care of patients with functional neurological disorders overlaps both the neurology and psychiatry specialties. It is often the case that neither provider thinks that he or she should be the treating clinician, and as a result, this patient group can suffer a substantial gap in care. Here, we illustrate a practical approach toward integration of care to appropriately treat patients with functional neurological disorders.
Definitions
The chapter on somatic symptoms and related disorders in DSM-5 encompasses several psychiatric disorders for which the primary feature is a symptom related to a physical or health-related complaint. The diagnostic criteria for somatic symptom disorder require that the patient have one or more somatic symptoms for at least 6 months. Patients may or may not have a medically diagnosed condition to explain their symptoms, but they should meet psychobehavioral criteria (excessive behaviors, health concerns, or anxiety in the context of the somatic symptoms) (1). In a functional neurological disorder (also called conversion disorder or functional neurological symptom disorder), the cardinal symptom is limited solely to neurological symptoms. Functional neurological symptom disorder is within the DSM-5 chapter on somatic symptom and related disorders but is distinct from somatic symptom disorder. Patients with a functional neurological disorder have symptoms of altered voluntary motor, cognitive, or sensory function that are not compatible with any recognized neurological condition (1). The DSM-5 criteria state that the clinician must establish evidence of preserved physiological function despite the presence of a neurological symptom. For instance, in the case of functional limb weakness, the clinician must demonstrate, through a neurological examination, that the affected limb has preserved strength when tested with specific maneuvers to uncover that finding. In other words, the diagnosis is made on the basis of the positive findings of the examination demonstrating preserved neurological function. DSM no longer requires that there be any temporal relationship between psychological factors and the onset or worsening of the disorder, although the association with psychological stressors remains a specifier. In addition, the criterion that patients are not intentionally producing their symptoms has been abandoned. Disability in functional neurological disorders is like that of structural disease, and neurological outcome at 8 months is poor, with over 50% of patients showing no improvement (2). Neither patients with a somatic symptom disorder nor those with a functional neurological disorder are presumed to fabricate their symptoms volitionally.
Epidemiology
Studies determining the incidence of functional neurological disorders are confounded by how the diagnosis was established and the specific patient population studied. Stefánsson et al. (3), using data from a large psychiatric registry as well as a psychiatric consultation service, found the annual incidence of functional neurological disorders to be 22 per 100,000 in patients from Monroe, New York. In the case of Ms. A in the vignette, the diagnosis of a functional neurological disorder was made by the neurologist. In ambulatory neurology clinics, approximately one-third of new patients have medically unexplained symptoms, the second most common diagnostic category after headache (4). Although “medically unexplained symptoms” is not synonymous with a functional neurological disorder (the former is not a psychiatric diagnosis and only implies unknown etiology, whereas the latter requires that specific diagnostic criteria be met), the evaluation of a patient with a medically unexplained symptom in the context of a neurological complaint should always raise clinical suspicion of, and prompt further evaluation for, a functional neurological disorder.
Studies show that a majority (78%−93%) of patients with functional neurological disorders are women (5, 6). Up to two-thirds of these patients have significant psychiatric disease, with a history of depression and a history of trauma being the most common psychiatric comorbid conditions (7–9). Dissociative symptoms and personality disorders are also prevalent in this patient population (10).
Neurobiology and Psychopathology of Functional Neurological Disorders
The neurobiology of functional neurological disorders is not well understood. However, volumetric studies of the brain, physiological testing, and functional imaging have begun to provide insights.
Structural Abnormalities
Volumetric MRI studies show evidence of differences in both cortical and subcortical brain anatomy in patients with functional neurological disorders. A group studying patients with motor functional neurological disorders with unilateral limb weakness found decreased volumes in the lentiform, thalamic, and caudate nuclei (11). Others looking at patients with motor conversion disorder compared with age-matched comparison subjects found significantly smaller thalamic volumes bilaterally in the patient group (12). A variety of cortical changes have been seen. For instance, patients with motor functional neurological disorders have been found to exhibit increased thickness of the premotor cortex bilaterally, whereas those with psychogenic nonepileptic seizures showed cortical atrophy of the motor and premotor regions in the right hemisphere and bilateral cerebellar atrophy (13, 14). Whether these changes are primary or secondary to changes in neural circuitry is unknown. While the lack of macroscopic brain alterations has traditionally been a core feature of functional neurological disorders, changes in gray matter volume are now well recognized in psychiatric disorders, such as major depression, bipolar disorder, and posttraumatic stress disorder (PTSD) (15, 16), as well as somatic symptom disorder with pain (17). Functional neurological disorder is no exception to these findings.
Physiological Studies
Electromyography in patients with functional neurological disorders with motor symptoms shows a decreased interference pattern. This finding can be seen in patients either with poor effort or with a lesion involving the corticospinal tract. In a set of experiments comparing healthy subjects and individuals with motor manifestations of functional neurological disorders (18), both groups were found to have normal motor evoked potentials. When the groups were then asked to imagine moving the affected limb, the patients with a functional neurological disorder had smaller motor evoked potentials compared with the healthy subjects during motor imagery tasks. This finding suggests that although the structural motor pathways are preserved in motor functional neurological disorders, there is an alteration in the pathways involved in motor planning. Similar studies have been done using evoked potentials in patients with sensory, visual, hearing, and movement disorder manifestations of functional neurological disorders (19–22). These studies show normal function of the primary pathways (motor efferent systems and the sensory afferent pathways) but alterations at the level of premotor and sensory association cortex processing.
Functional Imaging Studies
Neural network dysfunction may underlie the symptomatic manifestation in functional neurological disorders. This is evidenced by multiple studies across different functional neurological symptoms. Functional MRI studies have shown that patients with functional neurological disorders activate their brain differently than do healthy subjects simulating a similar condition. For example, patients with motor functional neurological disorders show hypoactivation of cortical and subcortical motor pathways, and those with visual functional neurological disorders show hypoactivation in either the visual association or primary visual cortex (23). Additional studies point to dysfunction in sensorimotor integration, with hypoactivation of the right temporal parietal region possibly resulting in loss of agency, validating the patient’s experience that functional neurological disorders are involuntary (23, 24). Functional neurological disorders are associated with high rates of trauma (25). Alterations in the mechanisms of emotion regulation and cognitive control in PTSD (where an overactive amygdala is not properly inhibited by medial prefrontal areas) (26–28) may indirectly offer a model of neurobiological dysfunction in functional neurological disorders. Abnormal emotion regulation and cognitive control patterns (possibly facilitated by past trauma history) may secondarily lead to brain activation changes and interfere with motor planning and self-regulation in individuals who are vulnerable to experiencing functional motor manifestations (29, 30).
Psychological Underpinnings
Different psychological theories hypothesize how psychological and cognitive processes give rise to functional neurological symptoms. The classical Freudian theory postulates that intolerable affect is “converted” into somatic symptoms. Theories focusing on dissociative processes, originally postulated by Pierre Janet, frame functional neurological disorder as an “autosuggestive disorder,” with symptoms being like those seen in hypnotic states. Compartmentalization and detachment are specific dissociative mechanisms involved in the origin of the symptom. Finally, a theory on cognitive hierarchy models explains functional neurological disorder as the result of an alteration in the allocation of attentional resources in certain sensory states, leading to activation of dysfunctional sensory and motor networks (26).
Diagnosis and Evaluation
The diagnosis of a functional neurological disorder is based on findings in the neurological examination (or other tests) demonstrating that the symptom is incompatible with a structural neurological illness (31). In the case presented here, for example, Ms. A had diffuse weakness with variability of effort, sometimes giving full strength and at other times able to give only minimal strength, which is not consistent with the pattern seen in structural neurological disease. In addition, Ms. A’s deep tendon reflexes were normal, and pathological reflexes such as those expected in corticospinal disease (the Babinski reflex) were absent. Ms. A’s sensory examination was likewise consistent with a functional problem, with loss of vibratory sense over the thoracic vertebrae but not in the lower extremities. There are many maneuvers neurologists can utilize to establish that the patient’s symptoms are not attributable to structural causes (Table 1) (32, 33). In the case of psychogenic nonepileptic seizures, a subtype of functional neurological disorder, an electrophysiological study that demonstrates normal electrophysiological function at the time of a seizure-like episode (via video EEG monitoring), coupled with signs suggestive of psychogenic nonepileptic seizures, would satisfy the diagnostic criteria (34).
| Sign | Sensitivity, Specificity | Functional Neurological Disorder | Definitions | Comment or Example |
|---|---|---|---|---|
| Motor | ||||
| Variable strength | Sensitivity 63%, specificity 97% (32) | Present | Give-away weakness is inconsistent | Collapsing weakness: as the examiner applies different levels of force, the patient’s resistance varies |
| Hoover’s sign | Sensitivity 94%, specificity 99% (32) | Present | Hoover’s test: the expected response is that the normal limb heel pushes down against the examiner’s hand as the patient tries to raise the weak leg’s hip | Positive Hoover’s sign: if the examiner does not feel the “normal” leg’s heel pushing down as the patient flexes the hip of the “weak” limb, this suggests functional weakness |
| Inconsistent examination | Sensitivity 13%, specificity 98% (32) | Present | The patient can rise from a chair but is unable to lift either leg off the examination table | |
| Co-contraction | Sensitivity 17%, specificity 100% (32) | Present | When both agonist and antagonist muscles are activated | When asked to flex the elbow, both biceps and triceps are activated |
| Hemiparesis in a nonpyramidal pattern | Not validated (32) | Diffuse weakness | Pyramidal weakness: extensors are weaker than flexors in the arm and flexors are weaker than extensors in the leg | |
| Babinski sign | Expert opinion | Absent | ||
| Tremor | ||||
| Entrainment | Sensitivity 91%, specificity 91% (33) | Present | The tremor frequency switches to match the frequency of a voluntary rhythmical movement performed by the unaffected limb | |
| Distraction affecting the tremor | Sensitivity 92%, Specificity 94% (33) | Significant | The tremor changes when the examiner has the patient perform tasks like counting backward | |
| Variability | Sensitivity 22%, specificity 92% (33) | Significant | The amplitude and characteristics of the tremor vary during the examination | |
| Sensory | ||||
| Pattern of numbness | Sensitivity 74%, specificity 100% (32) | Not anatomic | Sensation normalizes at hip or shoulder | |
| Splitting the midline | Sensitivity 20%, specificity 93% (32) | Present | The sensory nerves do not end precisely at the midline | |
| Splitting of vibration | Sensitivity 95%, specificity 14% (32) | Present | The frontalis is a single bone, so vibration sense should be the same bilaterally | |
| Gait | ||||
| Dragging leg | Sensitivity 8.4%, specificity 100% (33) | Present | Patients with pyramidal weakness circumduct their leg | |
| Excessively slow gait | Not validated (33) | Present | Slowness in all aspects of gait | Patients with bradykinesia display the most prominent slowness with gait initiation |
| Inconsistent with known neurological disease | Not validated (33) | Present | Noneconomic, requires more rather than less effort | Knee buckling without a fall requires more strength at knee extensors |
| Consistently falls to or away from examiner | Not validated (33) | Present | Test with the Romberg maneuver | Significant sway, often after a latency |
A literature review (35) showed that the diagnosis of a functional neurological disorder can be made reliably, with a misdiagnosis rate of about 4%. Additional testing should be directed toward excluding other specific diagnostic possibilities and should be limited. Extensive testing gives the impression of diagnostic uncertainty and is both expensive and unproductive. Unnecessary testing may also cause iatrogenic injury and may demonstrate incidental findings that can cause physicians to initiate further testing and procedures that are likely unnecessary (36).
Making the Diagnosis
Patients with functional neurological disorders may present for evaluation to either a neurologist or a psychiatrist. The evaluating clinician’s role is to establish the diagnosis, deliver the news in a way that makes sense to the patient, and engage the patient in treatment. There should be collaboration among treating clinicians to ensure agreement on the diagnosis and treatment plan. While the diagnosis is based on positive findings of the examination, a comprehensive screening of psychiatric risk factors should be conducted early in the process to identify predisposing, precipitating, and perpetuating factors that need to be addressed promptly (37).
Once it is clear that the patient’s symptoms and findings are consistent with a functional neurological disorder, the patient should be informed. Not providing the patient with a clear diagnosis can result in a delay in treatment as well as additional unnecessary consultations, testing, and emergency department visits. The pitfall of not making a clear diagnosis is evidenced in the case described here, as the patient presented for a second opinion without an established diagnosis. Giving a clear diagnosis can itself be therapeutic for some patients, and it diminishes the concern they may have that they are suffering from some obscure neurological illness (38).
The explanation of the diagnosis needs to make sense to the patient. Showing the patient the inconsistencies on examination and explaining how preserved physiological function is ascertained is extremely helpful (39). It is not helpful simply to inform patients which conditions they do not suffer from; rather, it is preferable to focus the discussion on the uncovered diagnosis. Clinicians must carefully explain the term “psychogenic” so the patient does not misinterpret it to imply that he or she is feigning or malingering, which is not correct. Ms. A was told that she had a “functional neurological disorder.” She was shown the inconsistencies on her examination and told that the problem came from an alteration in the integration of motor and sensory function, rather than from permanent damage to her motor and sensory systems. In addition, she was reassured that having a functional neurological disorder is common and treatable and that she has the potential for complete recovery. This information can be reinforced with a clinic letter copied to the patient and other treating clinicians, along with providing the address of a web site where further information can be found (http://www.nonepilepticattacks.info or http://www.neurosymptoms.org) (40). Specific communication strategies to deliver the diagnosis of psychogenic nonepileptic seizures have been described in detail, and some of them have been piloted in clinical settings (41, 42).
After the diagnosis is presented, the next step is to discuss treatment. Given that there is no permanent neurological impairment, there is the capacity for full neurological recovery. Treatment can be described as a form of “brain retraining” in how the brain organizes motor or sensory function and how the brain learns to relate and respond to thoughts and feelings that interfere with motor or sensory function, which can lead to neurological manifestations. If the patient has established health care providers, it is essential to communicate with them to ensure that they understand the new diagnosis.
Both neurologists and psychiatrists may need to follow these patients until they show improvement. Inadequate follow-up of patients with a functional neurological disorder is not best practice for several reasons. First, such patients commonly develop other functional symptoms. Having a preserved connection with the clinician who previously diagnosed their functional neurological disorder can help expedite an evaluation and confirm (or refute) the presence of a new functional symptom. Second, by remaining involved in the patient’s care, the physician is sending a message to the patient that the symptoms are important and real, whereas not recommending follow-up gives a message to the contrary.
Part of the ongoing role of the physician is to promote an integrated treatment approach and to help the patient establish a connection with mental health clinicians or other specialists, such as physical therapists, if indicated. One approach to encourage follow-up with a mental health clinician is to discuss the role of accumulating factors in facilitating and reinforcing the presence of the neurological symptoms, even when the patient does not see a clear connection between those factors and the physical symptom itself. Emphasis should be placed on the brain’s ability to translate the effect of such factors into neurological symptoms.
Ms. A endorsed a good deal of work-related stressors (a possible precipitant) as well as nightmares and flashbacks related to her rape. Trauma is a predisposing factor, and ongoing PTSD symptoms can precipitate and perpetuate functional neurological symptoms. Ms. A was quite amenable to seeing a mental health provider and agreed to see a psychiatrist. However, engaging patients in treatment is often difficult, because they may not acknowledge any link between potential psychological factors and their symptoms and may further perceive that the clinician views their illness as not real. When that is case, reviewing how the diagnosis was made, acknowledging that the disorder is not volitional, and discussing how perpetuating factors contribute to the patient’s disability can be helpful.
Treatment
Psychiatrists, other mental health clinicians, and neurologists need to understand how the diagnosis of functional neurological disorders was made and be comfortable treating this patient group. For instance, one study found that psychiatrists were much less likely than neurologists to believe in the accuracy of video EEG in the diagnosis of psychogenic nonepileptic seizures (43). If the diagnosis is not felt to be accurate, this may lead to more unnecessary referrals, and patients will be unlikely to accept the diagnosis and treatment plan. Initial referral to a mental health professional should help reframe the diagnosis and lead to acceptance of the treatment plan. Identifying vulnerability traits that make patients susceptible to a functional neurological disorder, such as avoidance tendencies, alexithymia, and somatoform tendencies, will create a framework for treatment (37, 44).
Patients with a functional neurological disorder have an increased number of psychiatric conditions, including depressive disorders, anxiety disorders, PTSD, and hypochondriasis (45, 46). The evidence for antidepressant treatment in functional neurological disorders comes from a few uncontrolled studies. No randomized placebo-controlled trials have demonstrated efficacy of any particular antidepressant for this disorder (47, 48). Therefore, choosing which antidepressant or anxiolytic medication is most appropriate, if any, should be based on treatment of the identified psychiatric comorbidities. Clinical judgment should be used as to when it is appropriate to initiate medications to treat comorbid psychiatric conditions.
Psychotherapy should be explained in terms of how it will help the patient’s symptoms. Participation in a treatment process that changes “the way the brain processes information” is essential to minimize the tendency to express distress through physical symptoms and to create new behaviors that break the established, unconscious pattern that leads to those symptoms. A similar argument can be made about participation in physical therapy (PT), where the goal is to change the processing of complex motor programs and to facilitate engagement in more adaptive patterns of movement or gait. A stepwise approach to psychotherapy is recommended. This includes having patients keep a diary of their symptoms and their precipitants to begin to generate a chain analysis as well as giving them strategies to help rescue them from pervasive symptoms.
Physical Therapy
There is evidence that PT is helpful in treating the motor and gait manifestations of functional neurological disorders (49, 50). In a randomized controlled crossover study of 60 patients with a psychogenic gait disorder who were randomly assigned to receive immediate treatment with inpatient PT or treatment after 4 weeks (control group), the benefit of the 3-week inpatient course of PT was substantial, and it was maintained even a year after PT was completed (51). Other studies have validated the efficacy of PT in motor manifestations of functional neurological disorders (52). These studies have led to the development of an expert consensus recommendation supporting the use of PT in the treatment of motor functional neurological disorders (53). PT demonstrates to patients their capacity for normal movement, educates them about their condition, and helps limit maladaptive motor responses. Both the intensity and the educational component of the PT program appear to be important factors for success. If the physical therapist is not familiar with functional neurological disorders, the referring clinician should provide him or her with the consensus guidelines and be available as a resource for ongoing consultation. The patient in our case vignette was referred to PT and given a follow-up appointment with neurology, in addition to seeing a psychiatrist.
Cognitive-Behavioral Therapy
Cognitive-behavioral therapy (CBT) has also been shown to be beneficial in treating functional neurological disorders (54). CBT includes education about functional neurological disorders and the stress response cycle, trains patients in stress management techniques and new behavioral responses, and helps patients identify and change unhelpful thought patterns that reinforce their symptoms. Randomized pilot studies have shown efficacy for CBT in the treatment of psychogenic nonepileptic seizures (55, 56). The use of a self-guided CBT booklet has been shown to reduce symptom burden at 3 and 6 months, and the difference between this treatment benefit and standard medical care was found to be statistically significant (57). CBT treatment workbooks that have been validated in randomized clinical trials can be recommended to help patients (and mental health providers) understand the diagnosis and develop the necessary skills to overcome their symptoms (57, 58). CBT is the preferred treatment modality for patients with episodic symptoms, such as psychogenic nonepileptic seizures.
Other Treatment Modalities
Hypnosis has proven effective in randomized controlled trials in functional neurological disorders (59). A time-controlled trial of immediate and delayed short-term psychodynamic psychotherapy showed benefit in reducing psychogenic movements, both when the treatment was provided immediately after diagnosis and when it was started 3 months later (60). Other uncontrolled interventions studied in functional neurological disorders include a variety of psychotherapies, such as psychodynamic psychotherapy (61–63), prolonged exposure (for those with comorbid PTSD) (64), mindfulness-based psychotherapy (65), inpatient programs (66), psychoeducational interventions (67), and transcranial magnetic stimulation over the motor cortex (68).
When Ms. A returned to clinic 4 months later, she was walking unassisted. She still had complaints of motor and sensory symptoms, but examination produced no nonphysiological findings. She had been treated regularly with an antidepressant for PTSD and PT for her functional neurological disorder. Furthermore, she had begun a transition back to work on a part-time basis.
Conclusions
Most patients with functional neurological disorders will require an integrated multidisciplinary approach to treatment. The diagnosing clinician should communicate with the treating physical therapist and/or mental health clinician, and everyone should agree on the treatment plan. The mental health clinician should keep communication open with the referring provider to clarify any doubts about diagnosis. Other established health care providers should be informed of the functional neurological disorder diagnosis, as patients may present with other physical symptoms of uncertain origin, and there should be agreement on the message among all providers and minimization of unnecessary treatments.
Functional neurological disorders are truly at the intersection of neurology and psychiatry: patients present with neurological symptoms that are a manifestation of a neuropsychiatric disorder. Dualistic thinking is not helpful for these patients, as neurological symptoms and emotional functioning need to be viewed as influencing each other. Integration of care is needed for this patient group.
A. Symptoms of altered voluntary motor, cognitive, or sensory function.
Want more? A CME course is available in the APA Learning Center at education.psychiatry.org
References
1.
American Psychiatric Association: Diagnostic and Statistical Manual of Mental disorders, 5th ed (DSM-5). Washington, DC, American Psychiatric Association, 2013
2.
Stone J, Sharpe M, Rothwell PM, et al: The 12 year prognosis of unilateral functional weakness and sensory disturbance. J Neurol Neurosurg Psychiatry 2003; 74:591–596
3.
Stefánsson JG, Messina JA, Meyerowitz S: Hysterical neurosis, conversion type: clinical and epidemiological considerations. Acta Psychiatr Scand 1976; 53:119–138
4.
Carson AJ, Ringbauer B, Stone J, et al: Do medically unexplained symptoms matter? A prospective cohort study of 300 new referrals to neurology outpatient clinics. J Neurol Neurosurg Psychiatry 2000; 68:207–210
5.
Tomasson K, Kent D, Coryell W: Somatization and conversion disorders: comorbidity and demographics at presentation. Acta Psychiatr Scand 1991; 84:288–293
6.
Deka K, Chaudhury PK, Bora K, et al: A study of clinical correlates and socio-demographic profile in conversion disorder. Indian J Psychiatry 2007; 49:205–207
7.
Carson AJ, Ringbauer B, MacKenzie L, et al: Neurological disease, emotional disorder, and disability: they are related: a study of 300 consecutive new referrals to a neurology outpatient department. J Neurol Neurosurg Psychiatry 2000; 68:202–206
8.
Singh SP, Lee AS: Conversion disorders in Nottingham: alive, but not kicking. J Psychosom Res 1997; 43:425–430
9.
Roelofs K, Keijsers GP, Hoogduin KA, et al: Childhood abuse in patients with conversion disorder. Am J Psychiatry 2002; 159:1908–1913
10.
Sar V, Akyüz G, Kundakçi T, et al: Childhood trauma, dissociation, and psychiatric comorbidity in patients with conversion disorder. Am J Psychiatry 2004; 161:2271–2276
11.
Atmaca M, Aydin A, Tezcan E, et al: Volumetric investigation of brain regions in patients with conversion disorder. Prog Neuropsychopharmacol Biol Psychiatry 2006; 30:708–713
12.
Nicholson TR, Aybek S, Kempton MJ, et al: A structural MRI study of motor conversion disorder: evidence of reduction in thalamic volume. J Neurol Neurosurg Psychiatry 2014; 85:227–229
13.
Aybek S, Nicholson TR, Draganski B, et al: Grey matter changes in motor conversion disorder. J Neurol Neurosurg Psychiatry 2014; 85:236–238
14.
Labate A, Cerasa A, Mula M, et al: Neuroanatomic correlates of psychogenic nonepileptic seizures: a cortical thickness and VBM study. Epilepsia 2012; 53:377–385
15.
Wise T, Radua J, Via E, et al: Common and distinct patterns of grey-matter volume alteration in major depression and bipolar disorder: evidence from voxel-based meta-analysis. Mol Psychiatry 2016; 22:1455–1463
16.
Kühn S, Gallinat J: Gray matter correlates of posttraumatic stress disorder: a quantitative meta-analysis. Biol Psychiatry 2013; 73:70–74
17.
Valet M, Gündel H, Sprenger T, et al: Patients with pain disorder show gray-matter loss in pain-processing structures: a voxel-based morphometric study. Psychosom Med 2009; 71:49–56
18.
Liepert J, Hassa T, Tüscher O, et al: Electrophysiological correlates of motor conversion disorder. Mov Disord 2008; 23:2171–2176
19.
Lorenz J, Kunze K, Bromm B: Differentiation of conversive sensory loss and malingering by P300 in a modified oddball task. Neuroreport 1998; 9:187–191
20.
Yoneda T, Fukuda K, Nishimura M, et al: A case of functional (psychogenic) monocular hemianopia analyzed by measurement of hemifield visual evoked potentials. Case Rep Ophthalmol 2013; 4:283–286
21.
Fukuda M, Hata A, Niwa S, et al: Event-related potential correlates of functional hearing loss: reduced P3 amplitude with preserved N1 and N2 components in a unilateral case. Psychiatry Clin Neurosci 1996; 50:85–87
22.
Terada K, Ikeda A, Van Ness PC, et al: Presence of Bereitschaftspotential preceding psychogenic myoclonus: clinical application of jerk-locked back averaging. J Neurol Neurosurg Psychiatry 1995; 58:745–747
23.
Aybek S, Vuilleumier P: Imaging studies of functional neurologic disorders. Handb Clin Neurol 2016; 139:73–84
24.
Voon V, Cavanna AE, Coburn K, et al: Functional neuroanatomy and neurophysiology of functional neurological disorders (conversion disorder). J Neuropsychiatry Clin Neurosci 2016; 28:168–190
25.
Roelofs K, Pasman J: Stress, childhood trauma, and cognitive functions in functional neurologic disorders. Handb Clin Neurol 2016; 139:139–155
26.
van Harmelen AL, van Tol MJ, Demenescu LR, et al: Enhanced amygdala reactivity to emotional faces in adults reporting childhood emotional maltreatment. Soc Cogn Affect Neurosci 2013; 8:362–369
27.
Grant MM, Cannistraci C, Hollon SD, et al: Childhood trauma history differentiates amygdala response to sad faces within MDD. J Psychiatr Res 2011; 45:886–895
28.
Hayes JP, Vanelzakker MB, Shin LM: Emotion and cognition interactions in PTSD: a review of neurocognitive and neuroimaging studies. Front Integr Nuerosci 2012; 6:89
29.
Aybek S, Nicholson TR, O’Daly O, et al: Emotion-motion interactions in conversion disorder: an fMRI study. PLoS One 2015; 10:e0123273
30.
Aybek S, Nicholson TR, Zelaya F, et al: Neural correlates of recall of life events in conversion disorder. JAMA Psychiatry 2014; 71:52–60
31.
Stone J, Carson A, Sharpe M: Functional symptoms and signs in neurology: assessment and diagnosis. J Neurol Neurosurg Psychiatry 2005; 76:i2–i12
32.
Daum C, Hubschmid M, Aybek S: The value of “positive” clinical signs for weakness, sensory, and gait disorders in conversion disorder: a systematic and narrative review. J Neurol Neurosurg Psychiatry 2014; 85:180–190
33.
van der Stouwe AM, Elting JW, van der Hoeven JH, et al: How typical are “typical” tremor characteristics? Sensitivity and specificity of five tremor phenomena. Parkinsonism Relat Disord 2016; 30:23–28
34.
LaFrance WC Jr, Baker GA, Duncan R, et al: Minimum requirements for the diagnosis of psychogenic nonepileptic seizures: a staged approach: a report from the International League Against Epilepsy Nonepileptic Seizures Task Force. Epilepsia 2013; 54:2005–2018
35.
Stone J, Smyth R, Carson A, et al: Systematic review of misdiagnosis of conversion symptoms and “hysteria”. BMJ 2005; 331:989
36.
Orme NM, Fletcher JG, Siddiki HA, et al: Incidental findings in imaging research: evaluating incidence, benefit, and burden. Arch Intern Med 2010; 170:1525–1532
37.
Baslet G, Seshadri A, Bermeo-Ovalle A, et al: Psychogenic non-epileptic seizures: an updated primer. Psychosomatics 2016; 57:1–17
38.
Stone J: Functional neurological disorders: the neurological assessment as treatment. Neurophysiol Clin 2014; 44:363–373
39.
Stone J, Edwards M: Trick or treat? Showing patients with functional (psychogenic) motor symptoms their physical signs. Neurology 2012; 79:282–284
40.
Carson A, Lehn A, Ludwig L, et al: Explaining functional disorders in the neurology clinic: a photo story. Pract Neurol 2016; 16:56–61
41.
LaFrance WC Jr, Reuber M, Goldstein LH: Management of psychogenic nonepileptic seizures. Epilepsia 2013; 54(suppl 1):53–67
42.
Hall-Patch L, Brown R, House A, et al: Acceptability and effectiveness of a strategy for the communication of the diagnosis of psychogenic nonepileptic seizures. Epilepsia 2010; 51:70–78
43.
Harden CL, Burgut FT, Kanner AM: The diagnostic significance of video-EEG monitoring findings on pseudoseizure patients differs between neurologists and psychiatrists. Epilepsia 2003; 44:453–456
44.
Beghi M, Negrini PB, Perin C, et al: Psychogenic non-epileptic seizures: so-called psychiatric comorbidity and underlying defense mechanisms. Neuropsychiatr Dis Treat 2015; 11:2519–2527
45.
Hoge CW, Terhakopian A, Castro CA, et al: Association of posttraumatic stress disorder with somatic symptoms, health care visits, and absenteeism among Iraq war veterans. Am J Psychiatry 2007; 164:150–153
46.
Waller E, Scheidt CE: Somatoform disorders as disorders of affect regulation: a study comparing the TAS-20 with non-self-report measures of alexithymia. J Psychosom Res 2004; 57:239–247
47.
Voon V, Lang AE: Antidepressant treatment outcomes of psychogenic movement disorder. J Clin Psychiatry 2005; 66:1529–1534
48.
Kleinstäuber M, Witthöft M, Steffanowski A, et al: Pharmacological interventions for somatoform disorders. Cochrane Database Syst Rev 2014; 11:CD010628
49.
Kaur J, Garnawat D, Ghimiray D, et al: Conversion disorder and physical therapy. Delphi Psychiatry Journal 2012; 15:394–397
50.
Ness D: Physical therapy management for conversion disorder: case series. J Neurol Phys Ther 2007; 31:30–39
51.
Jordbru AA, Smedstad LM, Klungsøyr O, et al: Psychogenic gait disorder: a randomized controlled trial of physical rehabilitation with one-year follow-up. J Rehabil Med 2014; 46:181–187
52.
Nielsen G, Ricciardi L, Demartini B, et al: Outcomes of a 5-day physiotherapy programme for functional (psychogenic) motor disorders. J Neurol 2015; 262:674–681
53.
Nielsen G, Stone J, Matthews A, et al: Physiotherapy for functional motor disorders: a consensus recommendation. J Neurol Neurosurg Psychiatry 2015; 86:1113–1119
54.
Sharpe M, Walker J, Williams C, et al: Guided self-help for functional (psychogenic) symptoms: a randomized controlled efficacy trial. Neurology 2011; 77:564–572
55.
LaFrance WC Jr, Baird GL, Barry JJ, et al: Multicenter pilot treatment trial for psychogenic nonepileptic seizures: a randomized clinical trial. JAMA Psychiatry 2014; 71:997–1005
56.
Goldstein LH, Chalder T, Chigwedere C, et al: Cognitive-behavioral therapy for psychogenic nonepileptic seizures: a pilot RCT. Neurology 2010; 74:1986–1994
57.
Williams C, Carson A, Smith S, et al: Overcoming Functional Neurological Symptoms: A Five Areas Approach. London, Hodder Arnold, 2011
58.
Reiter JM, Andrews D, Reiter C, et al: Taking Control of Your Seizures: Workbook. New York, Oxford University Press, 2015
59.
Moene FC, Spinhoven P, Hoogduin KA, et al: A randomised controlled clinical trial on the additional effect of hypnosis in a comprehensive treatment programme for in-patients with conversion disorder of the motor type. Psychother Psychosom 2002; 71:66–76
60.
Kompoliti K, Wilson B, Stebbins G, et al: Immediate vs delayed treatment of psychogenic movement disorders with short term psychodynamic psychotherapy: randomized clinical trial. Parkinsonism Relat Disord 2014; 20:60–63
61.
Hinson VK, Weinstein S, Bernard B, et al: Single-blind clinical trial of psychotherapy for treatment of psychogenic movement disorders. Parkinsonism Relat Disord 2006; 12:177–180
62.
Mayor R, Howlett S, Grünewald R, et al: Long-term outcome of brief augmented psychodynamic interpersonal therapy for psychogenic nonepileptic seizures: seizure control and health care utilization. Epilepsia 2010; 51:1169–1176
63.
Barry JJ, Wittenberg D, Bullock KD, et al: Group therapy for patients with psychogenic nonepileptic seizures: a pilot study. Epilepsy Behav 2008; 13:624–629
64.
Myers L, Vaidya-Mathur U, Lancman M: Prolonged exposure therapy for the treatment of patients diagnosed with psychogenic non-epileptic seizures (PNES) and post-traumatic stress disorder (PTSD). Epilepsy Behav 2017; 66:86–92
65.
Baslet G, Dworetzky B, Perez DL, et al: Treatment of psychogenic nonepileptic seizures: updated review and findings from a mindfulness-based intervention case series. Clin EEG Neurosci 2015; 46:54–64
66.
Kuyk J, Siffels MC, Bakvis P, et al: Psychological treatment of patients with psychogenic non-epileptic seizures: an outcome study. Seizure 2008; 17:595–603
67.
Zaroff CM, Myers L, Barr WB, et al: Group psychoeducation as treatment for psychological nonepileptic seizures. Epilepsy Behav 2004; 5:587–592
68.
Chastan N, Parain D: Psychogenic paralysis and recovery after motor cortex transcranial magnetic stimulation. Mov Disord 2010; 25:1501–1504
Information & Authors
Information
Published In
History
Received: 21 April 2017
Revision received: 3 July 2017
Accepted: 24 July 2017
Published online: 1 April 2018
Published in print: April 01, 2018
Keywords
Authors
Funding Information
The authors report no financial relationships with commercial interests.
Metrics & Citations
Metrics
Citations
Export Citations
If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Simply select your manager software from the list below and click Download.
For more information or tips please see 'Downloading to a citation manager' in the Help menu.
View Options
View options
PDF/EPUB
View PDF/EPUBLogin options
Already a subscriber? Access your subscription through your login credentials or your institution for full access to this article.
Personal login Institutional Login Open Athens loginNot a subscriber?
PsychiatryOnline subscription options offer access to the DSM-5-TR® library, books, journals, CME, and patient resources. This all-in-one virtual library provides psychiatrists and mental health professionals with key resources for diagnosis, treatment, research, and professional development.
Need more help? PsychiatryOnline Customer Service may be reached by emailing [email protected] or by calling 800-368-5777 (in the U.S.) or 703-907-7322 (outside the U.S.).