Infectious Disorders
Cryptococcal meningitis
May. 01, 2026
Worddefinition
At vero eos et accusamus et iusto odio dignissimos ducimus qui blanditiis praesentium voluptatum deleniti atque corrupti quos dolores et quas.
Functional neurologic disorder and related disorders …
- Updated 06.20.2025
- Released 04.18.2001
- Expires For CME 06.20.2028
Functional neurologic disorder and related disorders
Introduction
Overview
This article reviews functional neurologic disorder, factitious disorder imposed on self (previously called Munchausen syndrome), factitious disorder imposed on another (previously called Munchausen syndrome by proxy), and Ganser syndrome. These behavioral disorders are similar in their (1) resemblance to more familiar neurologic disorders, (2) lack of established objective biomarkers from conventional medical work-up (eg, structural lesions on brain imaging studies), and (3) aggravation of symptoms or those reported by a caregiver because of the patient’s or caregiver’s attention to the symptoms. However, the features and causes of these disorders differ significantly from one another. This article also reviews several widespread manifestations of functional neurologic disorder, including Havana syndrome (now called “anomalous health incidents”), mass psychogenic illness that is disseminated by social media, and post-vaccination functional neurologic disorder, in particular following COVID disease vaccination. For functional neurologic disorder, new biomarkers are being intensively investigated and are reviewed here.
Key points
• Functional neurologic disorder is commonly encountered in general neurologic practices and, hence, knowing its manifestations and treatment is crucial for clinical care. | |
• The disturbance is involuntary, and yet at the same time, it can be intermittently improved by the patient, depending on the patient’s reduced attention to the deficits. | |
• Although it can be improved intermittently by the patient, the disturbance is generally disabling unless expert professional care intervenes. | |
• There is no consistent association between functional neurologic disorder and either posttraumatic emotional stress, psychiatric disease, or sexual abuse. | |
• The terms Munchausen syndrome and its related disorder, Munchausen by proxy, are gradually being replaced in the research literature with the terms factitious disorder imposed on self and factitious disorder imposed on another, respectively. | |
• Anomalous healthy incidents, purported to represent acute brain injury resulting from exposure to either electromagnetic microwave or subsonic waves from weapons directed at diplomatic employees, have been found not to have a specific neuropathology. This raises the question of whether traumatic brain injury is responsible. Functional neurologic disorder is the more plausible explanation. |
Historical note and terminology
"Hysteria" was the original term in Western medicine for fluctuating and disabling neurologic disorder in alert sufferers, which was attributed from classical times to a "wandering uterus" because of its predominance in women (296). Offray de La Mettrie, for example, published in 1738 an account of episodic catalepsy (waxy immobility of the limbs) in a woman that he attributed to hysteria arising from amenorrhea (283). Eighteenth-century treatments for hysteria were radical and untested, including bloodletting, beatings, diet, fresh air, and writing (178).
Broca’s 1861 seminal and replicated discovery that aphasia follows from a focal lesion in the brain, as found on autopsy, more often in the left cerebral hemisphere, inspired subsequent neuroscientists to trace other neurobehavioral disorders to specific brain regions (see the MedLink article, “Non-progressive aphasia”). Broca’s contemporary neuroscientist Briquet related functional neurologic disorder of both women and men also to cerebral disease, but in contrast to aphasia, these disorders did not leave visible lesions at autopsy (64). Nonetheless, Briquet relocalized functional neurologic disorder from the uterus to the brain. Reynolds published in 1869 a prescient overview of functional movement or sensory disorders that appeared to be based on an ideological fixation and were amenable to compassionate behavioral retraining (209). In 1888, Blocq comprehensively described a case series of the acute inability to stand and walk despite full motor control of the legs while the patients were supine, which he termed “astasia-abasia,” a term that continues today (191). Although he doubted that the disturbance had a purely psychological etiology, his pathophysiologic hypothesis—that marked emotional distress can aggravate cerebral inhibition over spinal walking mechanisms—is remarkably similar to current pathophysiologic hypotheses for functional disturbances. Late in his career, in the 1880s, Charcot opined that functional disorders emanated from focal disturbances of the nervous system, but which did not affect a specific part of the body. Therefore, Charcot hypothesized that functional neurologic disorder did not seem to result from a structural central nervous system lesion. Instead, he postulated that functional neurologic disorder may emerge from an anatomically “dynamic” lesion, for which extant neurologic examination techniques could not identify (105).
In the late 19th century, Freud (who, as a neurologist, attended Charcot’s clinical rounds and observed his demonstrations of hysteria in his patients) hypothesized that an unconscious and involuntary cognitive process called “conversion” caused functional neurologic disorder (43; 96). In this model, emotionally conflicting memories of young life abuse or other upsetting personal experiences are involuntarily repressed and “converted” to severe somatic involuntary disturbances years later. Although no experimental evidence for this process was adduced for this nonfalsifiable model, this concept became firmly established and continues today in contemporary medical care (54). Commonly, functional neurologic disorder is called “conversion disorder,” including in present-day medical diagnostic classifications for clinical billing.
Interest in functional neurologic disorder increased with World War I, when European soldiers returned from combat with a variety of fluctuating neurologic deficits without demonstrable physical traumatic brain injury (129; 160). This post-combat disorder was considered to be neurologic, though its etiology was unclear. However, the neurologic interest in the causes, physiologic basis, and treatment of functional disorder became overshadowed by the successful outcomes of psychoanalysis developed by Freud (64). Over the 20th century, the lack of rigorous empirical evidence for unconscious repression eventually led to a resurgence of research interest in the neurophysiological basis of functional disorder in the 1960s, which continues today.
A wide variety of synonyms for these disorders are used, which hampers understanding. Alternate terms for functional neurologic disorder include hysteria, conversion disorder, medically unexplained disorder, shell shock, combat neurosis, psychogenic neurologic disorder, and pseudoseizure. Edwards and Bhatia recommended the term “functional neurologic disorder” on the grounds that patients find this less objectionable than rival terms (255; 76), which emphasizes the potential reversibility of the disorder (208; 249). The term, however, says little, only that it indicates it “functions” as a neurologic disorder, but without referring specifically to its mechanism. From the perspectives of the patients, their illness is “dysfunctional,” not “functional” (128). In response, Mark proposed the alternate term “attentionally-modifiable disorder,” to emphasize that self-attention is key for the symptoms of functional neurologic disorder (166).
PubMed shows an increasing use of the term “functional neurologic disorder” or the alternate terms “functional neurological disorder” and “functional neurological symptom disorder” since 2005. The term “anomalous health incidents” was more recently introduced in the medical literature after multiple government employees for the US State Department abruptly developed multiple sensory disturbances while they were posted in foreign locations. The term refers to “the abrupt onset of disruptive symptoms, including dizziness, pain, visual problems, and cognitive dysfunction,” according to the United States Government, and replaces the term “Havana syndrome” (95; 55; 204).
"Somatization disorder" or "Briquet syndrome" is a variant of functional disorder in which diverse bodily complaints (eg, fatigue, insomnia, irritable bowel) occur without resembling specific neurologic disorders and without objective physiologic evidence (138; 249). "Malingering" is the fully aware simulation of a medical disorder (frequently neurologic) for personal gain, particularly for money, material goods, or improved access to specific privileges (eg, transfer from jail). "Factitious disorder" is the willful simulation of a medical disorder without clear financial or opportunistic gain (21). Instead, sufferers have a need for a greater sense of control or attention. "Factitious disorder imposed on self” is a form of factitious disorder (often with diverse complaints) in which the patient undergoes frequent clinic or hospital evaluation, sometimes resulting in invasive, even injurious, testing or treatment. The term was originally coined as “Munchausen syndrome” by Asher (10), who thought that the wide meanderings of afflicted patients from clinic to clinic and their elaborate health histories resembled the fantastic travels regaled by a fictitious character depicted by Raspe in 1785, Baron Munchausen (196). In contrast, “factitious disorder imposed on another” refers to a caregiver's bearing false evidence of medical illness in another individual who is incompetent to represent himself (a child in most cases) (177). The term was originally termed “Munchausen syndrome by proxy,” and was changed to the present term to draw attention to the psychopathology of the perpetrator (04). Ganser syndrome involves the inconsistent answering of questions concerning the patient’s fund of knowledge (either general facts or autobiographical information), where the answers are closely related to the correct answers (99).
Clinical manifestations
Presentation and course
Functional neurologic disorder is a form of automatic-voluntary dissociation (addressed in a separate article in MedLink Neurology). “Functional neurologic disorder” (alternately termed “functional neurological disorder” or “functional neurological symptom disorder”) is the general term for the intermittent neurologic symptoms that disable everyday life activities and are aggravated by the patient’s attention to them or by emotional upset. Affected persons may have one or more such symptoms. The symptoms may also progress in their quality or severity, or spontaneously recede. Functional neurologic disorder can affect nearly any widely recognized neurologic function (eg, voluntary limb or facial movement, vision, memory). Unlike many more familiar neurologic disorders, functional neurologic disorder is not consistently associated with objective biomarkers on standard instrumented assessments (eg, structural damage evident on brain MRI). In addition, more familiar neurologic disorders are considered either to be unaffected or not improved by attention. This latter tenet, however, has not been rigorously or critically examined, and numerous examples of contradictory evidence occur in Parkinson disease (see below), dystonia, and stroke (166). An emerging interest is in the placebo or nocebo responses to treatments of Parkinson disease and other common neurologic disorders (225; 91; 290). In addition, persons with either Parkinson disease or stroke overestimate the daily frequency of their motor deficits (200; 280). These characteristics should prompt reconsideration of the consistency of classical symptoms in more familiar neurologic disorders in relation to self-directed attention.
Common features of functional neurologic disorder include the patients’ limited awareness that their attention to their symptoms can aggravate their severity, a lack of a sense of self-agency, limited awareness of intact neurologic control for the specific symptom, and perceived great effort when attempting to control their symptoms (80; 265). Patients usually view their disorders as stressful and disabling. In contrast, la belle indifference, or the lack of concern for the neurologic symptom, does not occur in most patients with functional disorder and is not a specific finding (252).
Often, functional neurologic disorder is preceded by an abrupt physical event in the preceding few months, most often physical injury, infection, or traditional acute neurologic illnesses (eg, facial neuritis, migraine, brachial neuritis) (199). Therefore, physical triggers may be key to the onset of many instances of functional neurologic disorder. However, functional symptoms can also develop in progressively neurodegenerative disorders without a preceding physical injury, particularly in Parkinson disease (289). This raises the possibility that functional neurologic disorder may be a nonspecific characteristic of progressive neurologic disorder.
Case reports of functional movement disorder have followed vaccination for the COVID-19 illness (48; 79; 86). The author of this article himself has treated two adults with functional movement disorder after the COVID vaccination and two others following the mumps vaccination. This also followed accidental inhalation of toxic fumes in a different patient. Consequently, the common factor may be minor soft tissue injury, rather than the chemical content of the invasive agent. A significant concern is that as these reports become widespread, skepticism about vaccination against the COVID-19 illness may increase. It is consequently essential for general practitioners to become alert to the possibility of post-vaccination functional neurologic disorder and refer for appropriate management immediately. This author, however, has advised against repeat vaccination when there is a pattern of recurrent functional neurologic disorder after the treatment.
Espay and colleagues categorize the diverse manifestations of functional neurologic disorder according to either the part of the body involved or behavioral characteristics (80). These major categories are reviewed below.
Functional movement disorder affects predominantly one or more limbs when the patient is not walking, or the face or oral cavity. Functional paresis has a reported incidence of four in 100,000 (254). In contrast, functional parkinsonism (tremor, generalized weakness, rigidity) is considered less common (150). Among functional dyskinesias, action tremor is most common, followed by resting tremor, dystonia, bradykinesia, and myoclonus (120). Functional palatal tremor has occasionally been observed. However, as noted above, functional movement disorder may co-occur with traditional neurologic disorders. Parkinson disease, as diagnosed by Hoehn and Yahr diagnostic criteria, or abnormal 123I-ioflupane SPECT scanning (dopamine transporter or DaTscan evaluation) consistent with Parkinson disease, was preceded by functional movement disorder in 26% of patients (289). Therefore, functional movement disorder may be an inherent part of Parkinson disease in the same way that rapid eye movement sleep behavior disorder may also be inherent. Moreover, functional movement disorder may follow deep-brain stimulator implantation for refractory parkinsonism (42).
The classical involuntary motor symptoms of Parkinson disease can improve with environmental modifications and therapeutic suggestions, and they can be aggravated by attention to symptoms. Thus, Parkinson disease has characteristics of functional movement disorder. Freezing of gait, common in Parkinson disease, can also be aggravated by attention to walking and improved by distraction to high-contrast visual stimuli (189); gait speed can be increased by marching to an auditory metronome (266); rest tremor, rigidity, and bradykinesia can be reduced by placebo medication (106; 16); and various adverse effects can also follow placebo treatment in drug studies (the nocebo effect), including aggravated dyskinesias (241). The latter may result from patients’ having been informed of potential adverse effects, as required by the ethics of human drug research, despite their having received biologically inert medication.
Functional movement disorder can be present with nonhyperkinetic disorders, including functional limb paresis that resembles poststroke changes and functional dystonia, which can involve sustained muscular contraction. In orthostatic surgery practices, the “clenched fist” or the “psycho-flexed fist” can occur. In contrast to many hyperkinetic functional movement disorders, the functionally maintained flexion can develop gradually. In many instances, functional flexed limbs can lead to soft tissue changes over lengthy periods, including reversible maceration, atrophy, contracture, swelling, and joint dislocation (231; 97; 87; 239; 295; 270). These disorders can reveal their functional character by symptom improvement with testing the passive range of motion during general anesthesia and following counseling.
A special subcategory of functional movement disorder is the task-specific disruption of either hand or mouth control in individuals who require precise motor control for these parts of their bodies for their professions. This disorder develops gradually following years of prolonged, extreme practice and is aggravated by strong concentration and anxiety. For golfers, this disturbance is known as the “yips” (175). For gymnasts, it has been called the “twisties” (103). “Runner’s dystonia” has often been recognized, and limb dystonia can also appear in other sports (eg, tennis, table tennis, pétanque, billiards, baseball, or ice skating) (159). For deer hunters, “buck fever” can occur when aiming a rifle toward wildlife, which can include temporarily impaired vision and hearing as well as loss of motor control, and can occur in novices (44). Musicians can endure “performance dystonia” (214). Less famous individuals may suffer from “writer’s cramp” (227). One notable instance was unilateral athetosis specific to using a spoon for self-feeding in a 30-year-old woman, which lasted for at least three years (235). Other than mild writer’s cramp, the woman had no other complaints and no abnormality in using other handheld implements. The literature on performance-specific dystonia does not attribute such disturbances to functional movement disorder, but the rationale for differentiating between these two types of disturbances has not been specified.
Functional movement disorder also occurs in the common experience of involuntary limb and eyelid tremor during acute anxiety (109) without other symptoms. The research literature does not classify this as functional neurologic disorder, despite its occurrence being triggered by emotion. Tremor can be provoked by anticipation of personal harm (271).
Axial functional neurologic disorder affects the body’s core. This most often appears as a gait disorder. A common subtype is astasia-abasia (from the Greek for inability to stand and walk). Astasia-abasia involves very unstable and marked lower extremity incoordination during walking, but with normal leg control in other contexts, for example, when asking the patient to walk backwards or move in bed. This category also includes abnormal posture, such as functional camptocormia (ie, variable marked forward flexion of the trunk) (232).
A variant of axial functional neurologic disorder is tonic immobility. The behavior was first coined as “reflexive immobility” by Crozier in 1923 and retitled as “tonic immobility” (121) on the common observation in diverse animal species of the body’s reversible freezing of movement when it is unexpectedly handled or threatened (65). The presumed adaptive value of this instinctive behavior is the simulation of death (thanatosis), which may discourage potential predators. In 1979, biologists recognized that tonic immobility could occur in humans following rape (259). The behavior has been noted to involve not only bodily immobility but also mutism (100). In one study, the vast majority of rape victims indicated that they had suffered from tonic immobility (183). Moreover, tonic immobility can be followed by involuntary tremor (68). Thus, the term “immobility” does not seem accurate.
A related disorder is “resignation syndrome” (216). This involves the gradual restriction of voluntary activity to the point of stupor and needing feeding support. This illness has been observed only since 2005, primarily in Sweden and primarily in individuals who are refugees from war-torn countries, and for whom social support by the accommodating country has been withdrawn. Because this disorder is not noted to recur or to be reversed, it does not qualify as functional neurologic disorder, but to be considered in the assessment of individuals who have acquired immobility.
Oculomotor functional disorder is most often observed as convergence spasm (132). In this disorder, the patient looks medially with one eye (ie, cross-eyed), even when attempting to look at a distant object. The functional aspect of this disorder can be revealed by normal eye movements during optokinetic stimulation. Other oculomotor disorders include functional nystagmus, oscillopsia, and blepharospasm.
Functional sensory disorder can affect nearly any of the traditional special senses (eg, vision, touch). Some of the more common presentations include functional visual field deficits, including tunnel vision (the visual field deficit on perimetry that changes in relation to the distance of the object that is being viewed) (80). A classic presentation is splitting the dermatome when applying a vibrating tuning fork to the forehead’s midline. Seldom discussed in this regard is Morgellons syndrome, also termed delusional parasitosis, in which patients complain of the sensation of crawling arthropods on or under their skin, and even the assertion that alien fibers are protruding through their skin, despite normal tissue demonstrated on professional examination (145). In contrast to these preceding disorders, diagnosing functional auditory disorder, in contrast with other auditory disorders, has not been well developed (14). However, functional perception of tones without a clear source has been recognized in incidents of mass psychogenic illness and is described below (17).
To a greater extent than functional auditory disorder, functional disequilibrium disorder has been recognized. The disorder termed persistent postural perceptual dizziness, or PPPD, has been recognized (80). This involves fluctuating dizziness that is aggravated by looking at complex or moving visual patterns and often follows inner ear disease (72). A similar disorder is mal de debarquement syndrome (French for “sickness from exiting a boat”), a persisting perception of rhythmic bobbing of the body, without actual movement, which can follow travel by boat or train (215). This may result from excessive stimulation of the ordinary vestibulo-ocular reflex that occurs normally during sea travel.
Functional cognitive disorder involves the patient’s complaint of intermittent cognitive impairment (most often memory loss), yet with generally normal performance on standard cognitive assessments. However, some cognitive test abnormalities are consistently found, including slowed cognitive processing speed and working memory (265). In addition, patients with functional amnesia have a “reversed temporal gradient,” ie, with better recall of recent rather than remote events, which is opposite to the progressive memory loss that typifies neurodegenerative diseases such as Alzheimer disease (112). A striking variety of functional cognitive disorder is fugue, which involves inconsistent disruption of autobiographical knowledge, along with wandering from home for extended periods, unaccountably. In some instances, patients temporarily fail to recognize family members, nor recall their own identities.
Ganser syndrome is a special form of functional cognitive disorder (163), except that such patients do not complain of the disorder. The disorder involves the tetrad of recurrent incorrect answers to questions that are semantically closely related to the correct response, despite intact speech comprehension (eg, 1 + 1 = “4; ” how many legs does a duck have? = “8”), impaired arousal, somatic sensory disorders, and hallucinations (99). The first sign--incorrect answers (vorbeigehen [“passing by”] in Ganser’s terminology)--gives the appearance of dementia or psychosis and has been frequently used to diagnose Ganser syndrome even in the absence of the other original features. The four features may variably coexist from patient to patient (229), which raises the question of whether Ganser syndrome describes a genuine symptom complex. When inappropriate answers to questions appear prominently in illness without all of the other diagnostic features, clinicians either loosely diagnose “Ganser syndrome” (201) or more properly report “Ganser symptom” (180). Consistent with functional neurologic disorder, Ganser syndrome may abruptly resolve with psychotherapy (66). However, in other instances, the symptoms may persist for months despite therapy (180) or the absence of obvious gain (67), which challenges the impression that the confabulatory answers strictly result from an intention to simulate neurologic illness. Furthermore, Ganser syndrome is frequently associated with brain injury, as well as being a feature of schizophrenia (83). Moreover, Ganser syndrome is described across cultures; thus, it is not a culture-bound phenomenon (245).
The occurrence of inaccurate responses to questions of facts or events in one’s life in Ganser syndrome, particularly semantically closely related to the correct answer, is similar to many other disorders. Deep dyslexia (less often termed deep alexia in the research literature) involves semantic errors when reading single words aloud (24). For example, when shown the word “attorney,” the patient may say instead “lawyer.” Further detail is provided in the MedLink article on “Alexia.” Semantic paraphasias are characteristic of Wernicke or fluent aphasia following stroke, in which words are produced in conversation that are semantically related to the target word, such as saying “north” instead of “south” (45). Further discussion is provided in the MedLink article, “Non-progressive aphasia.” Similar disturbance occurs in the semantic dementia variant of primary progressive aphasia (141). Categorical errors can also occur in action selection during formal apraxia testing in brain disease. Ideational apraxia involves a conceptual disturbance in tool selection, where an incorrect object is used as either a tool or the target object of action, despite the movement itself being appropriate for a particular goal. For example, a child diagnosed with Ganser syndrome after traumatic head injury tried to apply a toothbrush to his tongue instead of to his teeth (180). In contrast, in ideomotor apraxia, an object selected for a desired action may be correctly selected, but the action itself only approximately resembles the correct action. For example, body-part-as-object errors involve the hand taking the place of the object when the patient is asked to simulate operating a tool for a requested activity, such as using scissors (207). These examples demonstrate that semantically approximate errors are not unusual in brain disease, and not specific to Ganser syndrome.
Functional seizure disorder is more often termed psychogenic nonepileptic seizures or PNES. Functional seizure is the most commonly recognized among paroxysmal functional disorders; functional syncope or drop attack also can occur (122). Functional seizure involves abrupt, episodic, stereotyped movements, often with interruption of awareness, without epileptic waveforms on EEG (09). Eye closure is common and characteristic (61). Because functional seizure can occur spontaneously without evident increased self-attention and even during sleep (118), this should raise the question of whether such nonepileptic seizures qualify as a form of functional neurologic disorder. For this reason, functional seizure is not further discussed in this article. Further information on functional seizures can be read in the MedLink article, “Functional or psychogenic nonepileptic seizures.”
Mass psychogenic illness is the preferred term for what was formerly called mass hysteria or mass sociogenic illness. Mass psychogenic illness is distinguished from other forms of functional disorder by its being contagious. Mass psychogenic illness has been extensively documented over the centuries (84). Mass psychogenic illness occurs among individuals who are spatially closely grouped, including in school and the workplace (18). The symptoms that have been reported include tics, perceived low-frequency sounds, vertigo, syncope, headache, tachypnea, tremor, astasia-abasia, disinhibited emotion, and inattention (19). Although many reports of mass psychogenic illness have involved populations that may be considered to be not well educated (children, people from developing countries), a notorious and controversial incident involved half of the American embassy staff in Havana, Cuba, between 2016 and 2017. This included auditory disturbances, imbalance, and headache (17), now commonly termed as anomalous health incidents. In the initial report, the authors excluded mass psychogenic illness but did not adduce a convincing alternate explanation. A review of persons with such symptoms excluded specific brain trauma (55). The authors also did not appear to be familiar with how functional neurologic disorder can present (260; 35).
There has been an increase in mass psychogenic illness since 2019 as social media became more widely used. In particular, young women and teenage girls are prone to functional movement disorder following their observing charismatic women (“influencers”) on TikTok or YouTube who demonstrate what they refer to as tics (125; 192; 185). Highly unusual in the history of research on mass psychogenic illness is that this variant is precipitated by exposure to visual media without the afflicted persons sharing physical space with other similar individuals. In the largest study thus far of diagnosed “functional” tics (involving 294 individuals), this movement disorder overwhelmingly occurred in girls and largely followed observing internet media (170). The prognosis is favorable: peak severity is at one month, then decline; spontaneous remission occurs in 20%. Although medications are not efficacious, psychological care can benefit.
Dissociative identity disorder deserves special mention. In this controversial illness, formerly termed multiple personality disorder, for the most part, the symptoms do not involve neurologic deficits, but rather the presentation of entire “personalities,” ie, a coherent array of habits and emotional patterns that characterize a distinct “identity” that is different from the patient’s original personality (40). The core personality is often unaware, or incompletely aware, of the other personalities, extending to amnesia of the experiences of the other personalities, thus overlapping functional cognitive disorder (described above). Dissociative identity disorder shares etiology with functional neurologic disorder in that it appears to be a response to severe stress. Moreover, dissociative identity disorder can include objective neurologic changes, including personality-specific suppressed visual evoked potentials (257), nystagmus (27), EEG (30), and cerebral perfusion patterns (220).
Whereas functional neurologic disorder involves primarily one symptom, the complaints in somatization disorder (or Briquet syndrome) involve multiple, typically autonomic neurologic dysfunctions and do not suggest well-defined neurologic or other medical disorders. Examples of such complaints include nonfocal abdominal pain, nonspecific chest pain, dysuria, backache, erectile dysfunction, food intolerance, and fatigue (138). However, the distinction between functional neurologic disorder and somatization disorder has not been clear.
Factitious disorder is the fabrication of illness within oneself for gaining personal attention rather than monetary or material gain. An unmet need to feel in control may be responsible for some instances. Neurologic illnesses that may be feigned include meningoencephalitis, epilepsy, loss of consciousness, visual loss, speech disorder, limb paresis (21), unilateral neglect during clock drawing (137), quadriplegia (87), or irregular breathing (282). Personality disturbances can attend factitious disorder, including aggressivity, impaired impulse control, suicidal threats, and self-destructive behavior. A history of aliases and changing of hospitals or physicians may occur. Factitious disorder imposed on self may be triggered in children by a sudden change in lifestyle or other psychosocial trauma (74).
Factitious disorder associated with repeated hospitalization, particularly when the patient presents to a multitude of medical centers, had been termed Munchausen syndrome (10), but the preferred term for the disorder is now factitious disorder imposed on self (04). Pseudologia fantastica is a characteristic finding (ie, excessive lying without delusion) (197; 139). Not uncommonly, such patients endure repeated invasive procedures for diagnosis or treatment, to no avail. Factitious disorder imposed on self has been reported to present as complex regional pain syndrome (formerly termed reflex sympathetic dystrophy) (58), hemiplegia (32), status epilepticus (219; 59), neurogenic bladder (117), paraparesis (155; 146), meningitis (165), metabolic encephalopathy (258), or syncope (264).
In contrast to factitious disorder, malingering is the fabrication of symptoms to obtain personally favorable changes in environmental conditions such as employment or financial gain (98).
Factitious disorder imposed on another is the fabrication of medical complaints in a dependent individual by another, usually by a mother for her underage child (177). The behavior allows the caregiver to have the social attention or improved feeling of importance that he or she feels otherwise not to be able to obtain, while also placing the child's health in peril. This is child abuse. The dependent undergoes needless evaluation that can be invasive, loses time from school or other activities necessary for maturation, suffers psychological trauma from chronically being in a sick role, and may be harmed by unnecessary medication. To achieve the deception, the caregiver must have detailed medical knowledge. Non-neurologic manifestations of factitious disorder imposed on another may include applying iodine to the dependent’s skin to simulate jaundice and adding menstrual blood to the dependent’s urine to suggest hematuria (15). Unfortunately, the diagnosis has been carelessly applied in the medical literature, extending to instances where the mother has sincere but mistaken beliefs concerning disease in the child (244).
The most common neurologic manifestation of factitious disorder imposed on another is alleged epileptic seizures because serious medical action may be prompted simply by false eyewitness testimony rather than from physical evidence or abnormal clinical exam. In a variation of factitious disorder imposed on another, a lawsuit in the United States has alleged that a pediatric neurologist fabricated the diagnosis of epilepsy in several hundred of his underage patients, with concomitant needless prescription of antiepileptic medications and implantation of seizure-control devices, to reap profits for himself and his hospital (77). Other neurologic manifestations can include apnea, loss of consciousness, and, in one instance, myalgic encephalomyelitis (161). In contrast to the usual victim being a child, however, several case reports have indicated similar abuse of adults (230; 111), often involving covert poisoning by the caregiver. In one of these cases, a 71-year-old man had recurrent stupor for two decades that was reversed by intravenous flumazenil. The clinicians had initially become convinced that the patient had an exotic disorder that released an endogenous benzodiazepine until they discovered that the patient’s wife had confessed to surreptitiously intoxicating him (as well as her mother) with lorazepam. The investigators themselves confessed to having easily been misled by a beguiling, but ultimately false, hypothesis.
Legal cases that contest the erroneous diagnosis of factitious disorder imposed on another have surfaced in recent years. In one case, a young woman’s mother falsely reported her as having leg paralysis, digestive disorder, and cancer to the child’s physicians (212). This abuse entailed many forms and years of unnecessary medical treatment. After such extended abuse, the daughter conspired with her boyfriend to murder her mother. The boyfriend, who fatally stabbed the mother, was sentenced to life in prison; the daughter was released after serving 8 years of the 10-year sentence. In another instance, a children’s hospital accused a mother of factitious disorder imposed on another due to her daughter’s inexplicable pain (114). The hospital kept the child away from the family out of concern that the mother was inflicting physical child abuse, even though an outside pain expert diagnosed the child with complex regional pain syndrome. The mother became hopeless about having any further contact with her daughter and, thus, took her own life. The then-17-year-old girl was awarded a legal settlement against the hospital after the misdiagnosis and false imprisonment were found.
Prognosis and complications
Because diverse factors may be responsible for functional neurologic disorder, a simple statement concerning prognosis is not possible. Furthermore, research studies have used (and probably continue to use) inconsistent diagnostic methods for functional neurologic disorder (Kirkwood and 166), thus confounding meta-analysis for prognosis.
Functional movement disorder may endure for years and disrupt daily living activities and employment (243; 101). Only about half of patients with functional tremor or paresis improve, generally in response to eliminating stressors and cultivating the patient’s trust in the physician (127; 101). Prognosis for improvement from functional dystonia is poor, but combined psychotherapy and physical therapy may be efficacious and, therefore, should be tried (222). Functional movement disorder is also costly, with an estimated annual cost of care exceeding $100 billion in the United States (05).
The presentation of hemiparesis becomes potentially dangerous if emergency medical personnel are unable to recognize the functional source of symptoms and fibrinolytic therapy is administered (eg, rtPA). However, research has shown no harm from fibrinolytics given to persons presenting with acute stroke symptoms with unremarkable neuroimaging, including persons who were later diagnosed with functional stroke (57).
Functional tics in persons who watched tics on electronic media have shown a 20% spontaneous resolution rate (170).
Under present medical evaluation and treatment, functional neurologic disorder incurs more costs than other neurologic disorders of similar extent of disability (242). The authors note that the extent of federal research funding for functional neurologic disorder in the United States is disproportionately low compared to the extraordinary amount of cost for care.
Factitious dystonia of a limb can persist for years, to an extent that it can be painful, and the dystonic posture may be maintained even while the patient is asleep (20). This published case report suggests that an illness that starts with voluntary and sustained abnormal limb posture can progress through neurologic reorganization to an involuntary disorder. In one instance of factitious epilepsy, discovering the absence of epileptic signs in the patient led to referral for psychiatric hospitalization. The patient committed suicide (219). In other instances, patients with factitious disorder may be lost to follow-up through voluntary self-removal from approved medical care (165). Voluntary overdosage with electrolytes can induce metabolic encephalopathy (258).
Factitious disorder imposed on another has a fatality rate of from 9% to 30% for involved children (15).
Clinical vignette
The 29-year-old right-handed hospital administrator complained of acute neck pain without a clear cause. After a nerve anesthetic block was given, his left arm became numb. This was treated with a neurosurgical C5-C6 fusion, which was followed by marked right arm pain, which spread into his right leg. He felt that his right leg unexpectedly lost control while walking at times. For an unspecified time, he also developed an inability to open his right eye, which gradually recovered. He tended to avoid using the right arm for spontaneous self-care, in part because he had developed a right-arm tremor with voluntary movements. Hospitalization determined that the brain MRI, limb electromyography, and lumbar puncture studies were normal. He took leave from his employment and later decided not to continue working.
He also reported word-finding difficulty, slowed thinking, and episodic memory loss. When he extended his right arm, an uncontrollable proximal tremor occurred. This could be aborted by having him clench and unclench his left hand.
Over the years, his symptoms reduced after he had undergone a course of cognitive behavioral therapy. Brain MRI at that time was again unremarkable.
Over 6 years of follow-up, the complaints continued, but he managed with the behavioral techniques. Of note, the patient has incurred episodes of bilateral limb erythema following emotional upset. In the clinic, formal examination was associated with upper limb piloerection.
Comment. The patient incurred multiple, variably occurring neurologic complaints shortly after he developed spontaneous neck pain and cervical spinal surgery. The finding that was most often evident in the clinic was the right-arm tremor, which was always produced with right-arm elevation. This could be abolished by having him perform voluntary competing movements of his left hand. This technique assisted with his activities of daily living, though he felt unable to continue his administrative work or safely drive. His examination supports the diagnosis of functional neurologic disorder because of his ability to suppress the right arm tremor by redirecting self-attention to the other side of the body. In addition, there were intermittent autonomic neurologic disturbances that followed increased self-attention or emotional upset, including limb color change and piloerection. As discussed below in this article, autonomic disturbances are not unusual in functional neurologic disorder. These findings argue against a psychiatric etiology or a contrived cause.
Biological basis
Anatomic localization
Although structural MRI studies of functional neurologic disorder have reported significant structural changes, they have not been consistent across various studies and were identified only at the group level using advanced quantitative methods (167). Thus, depending on the study, there were either focal volume increases or decreases, or both. At present, no signature structural brain MRI finding characterizes functional neurologic disorder. It is unclear whether the focal tissue losses may result from neurodegeneration or whether focal increases may follow from compensatory behavior.
According to a comprehensive review of the literature, there is no preponderant symptom involvement of one side of the body or the other (251), thus not implicating a deficit for a particular side of the brain.
Pathophysiology
The etiology, if there can be only one, for functional neurologic disorder is highly controversial. The past century of thought about functional neurologic disorder centered on the hypothetical mechanism of “conversion” that was purported by Freud and Breuer (43; 96). According to this hypothesis, repressed psychological distress is ameliorated by subconscious conversion to an involuntary bodily symptom. There is, however, no scientific evidence for this process, and indeed, the hypothesis is untestable (54).
A major difficulty with positing a single pathophysiological etiology is that among all patients with functional neurologic disorder, there are many exceptions to “rules” or patterns that have been recognized. Thus, for example, psychiatric disorder has been invoked as a precondition for functional neurologic disorder because this is common among patients. However, many patients do not have psychiatric complaints (133; 273; 268; 269; 154). Similarly, psychiatric disorder is common in stroke, Parkinson disease, multiple system atrophy, dystonia, and epilepsy (92; 157; 179; 294), but there is no plausible mechanism that a psychiatric disorder would cause these neurologic disorders. The absence of distinct biomarkers in functional neurologic disorder that are available on a clinically ordered brain MRI scan is also true for many other neurologic disorders, such as Parkinson disease, essential tremor, dystonia, amblyopia, and migraine.
Functional neurologic disorder is frequently preceded either immediately or within a few weeks by either emotional or physical trauma. Seldom recognized in the research literature, but pertinent, is that functional disorder can appear in other animals following emotional or physical trauma (06; 119; 217; 135). These reports involved reversible neurologic changes that were not associated with macroscopic neuroanatomical changes. A related response to a threat to survival is tonic immobility in humans, as observed in animals inside and outside of the laboratory setting, which can also include tremor (172).
A valuable insight by Kretschmer was that the recourse by various vertebrates to hyperactivity or appearing to simulate death (thanatosis) as an instinctive antipredator mechanism could be the basis for diverse functional neurologic disorder in humans in response to perceived threat (144; 63).
A comprehensive literature review by Edwards and colleagues has suggested that for certain individuals, a trauma, either psychological or physical, markedly disrupts the patient’s predictions or anticipation for the quality of the external or internal world with respect to the patient’s activities (75). Such a distorted prediction of sensory experience may thus apply to functional blindness, anesthesia, or pain. Furthermore, the altered expectation for sensory input may change kinesthesis (proprioception) as well, and thus, cause patients to anticipate that part of their body will have either reduced proprioception (the situation following paralysis) or fluctuating proprioception (eg, following tremor or dystonia). According to the “Bayesian” hypothesis, as termed by Edwards and colleagues, the patient may then unconsciously and involuntarily adjust limb movement to match prediction. This would automatically resolve the perceptual mismatch and reduce “surprise.” Support for this comes from the observation that patients with idiopathic unilateral facial paresis (Bell palsy) may also show ipsilateral limb hemiparesis (134), even though the peripheral locus of injury is physiologically incompatible with hemiparesis. Keane suspected that hemiparesis with Bell palsy arises because patients assume that they have a stroke, so ipsilateral weakness is to be expected. Keane reported that such patients’ hemiparesis can be resolved simply with counseling. In everyday life, involuntary adjustment of perceptual physiological gain may occur when, for example, we “ignore” pain from an injury when we have to focus on escaping danger. As another example, we may become so preoccupied with our thoughts as to fail to recognize familiar passersby who technically happen within their visual field. On the other hand, Edwards and colleagues cite experimental evidence that ordinary perception of a mildly noxious stimulus may be aggravated by a preceding aversive stimulus (75). Hence, the revision of perceptual gain may not be all that unusual. In the case of functional illness, however, such resetting is greater, enduring, and difficult to voluntarily reset.
A difficulty with the Bayesian hypothesis is that it posits that the pathologic voluntary activity results from a recurrent cycle of mismatched sensory input and abnormal expectation. This process is beyond experimental validation; thus, the hypothesis is not testable. Moreover, unexplained is why some functional neurologic symptoms involve just one part of the body, rather than enveloping the entire body. It is not clear, for example, why a distorted prediction by the patient may involve only one arm or leg with functional tremor or paresis, while sparing the other side of the body. In addition, Edwards and colleagues predicted that patients with functional movement disorder will have abnormal somatic sensation (75). Contrary to the hypothesis, patients with functional neurologic disorder are not exceptional in their sensory experiences when compared to healthy individuals or individuals afflicted by other neurologic disorders (210; 268; 269).
As noted above, physical trauma can precipitate functional neurologic disorder, including following the COVID-19 illness vaccination (described under the “Clinical manifestations” section). A possible mechanism involves the release of proinflammatory cytokines after physical injury. The clue comes from the release of cytokines (inflammatory kinds of protein that are widely released in the body by macrophages and helper T cells after neural injury) early in complex regional pain syndrome (CRPS) (293; 31). Complex regional pain syndrome, in turn, often involves functional movement disorder (222; 223; 277; 136). Consequently, proinflammatory cytokines may be instrumental to the onset of functional neurologic disorder, at least following limb tissue injury. Further research will be needed to determine how cytokines may elicit variable limb motor control, for example, by inducing neuroplastic changes in the brain or spinal cord sensorimotor structure directly connected to the specific limb.
Of note is that individuals who are homozygous for the catechol-O-methyltransferase gene (Val158Met) have heightened somatosensory perceptions (285). Such individuals may be prone to complex regional pain syndrome and functional neurologic disorder following physical injury, though at this stage this can only be speculative. Familial functional movement disorder has been reported, which further supports a genetic basis (240).
Marshall and colleagues evaluated a patient with functional hemiparesis following unspecified trauma (169). Attempted movement of the hemiparetic limb was associated with increased metabolic activity of the contralateral orbitofrontal and anterior cingulate areas, which are thought to be involved with motor inhibition. The affective response to painful stimuli can be modulated by hypnotic suggestion. This response has been associated with altered activity of the anterior cingulate area in human volunteers (206). Patients with functional hemiparesis, regardless of symptom laterality, may show decreased activity in the left dorsolateral prefrontal cortex on PET scanning during voluntary movements (238). The failure by such patients to activate motor-related frontal cortical areas while observing a moving hand (unlike healthy individuals) suggests a deficit of motor imagery (47). Another study has reported decreased thalamic and caudate nucleus metabolism contralateral to the side of functional hemiparesis, which resolved when the hemiparesis resolved (279). This observation may be related to the structural imaging finding of bilateral thalamic atrophy in chronic functional hemiparesis (11; 187). In contrast, functional limb paresis has been found to be associated with hypertrophy of the premotor cortices, which may reflect the effects of increased motor inhibitory activity (12).
Similarly, reduced contralateral somatosensory cortical activity to peripheral tactile stimulation was demonstrated on fMRI in patients with unilateral functional somatosensory loss (102). In contrast, cortical activity in the deficient areas occurred when the patients underwent bilateral tactile stimulation; the authors speculate that this was because the patients were distracted from maintaining inhibited awareness of stimulation on the affected side. This evidence suggests that the frontal cortex may activate the nucleus reticularis of the thalamus, which secondarily inhibits primary somatosensory cortex processing in individuals with functional somatosensory loss (116).
Increased metabolic activity in frontal and subcortical areas may appear in patients with suspected functional hemianopia, which suggests a focal cerebral inhibitory process in functional visual loss similar to that postulated for functional somatosensory loss (286). An interesting case report indicated psychic blindness associated with specific personalities in dissociative personality disorder. Visual evoked responses were absent only in the personalities that were blind (281). The authors suggested that strong, “top-down” cerebral inhibition (perhaps mediated by the thalamus) could have this remarkable neurophysiological effect. Similarly, healthy subjects can become experimentally trained to forget emotionally upsetting scenes (71). Such forgetfulness is associated with right inferior frontal increased metabolism, coupled with decreased metabolism in memory-associated and vision-associated brain areas. A related case report of a woman with selective loss of autobiographical memories from childhood demonstrated different areas of brain activity on fMRI when well-recalled episodes were probed compared to poorly recalled episodes (38). Combined, these results suggest that circumstances that lead to psychological repression (either of memories, voluntary movements, or sensations) involve direct participation of inhibitory brain areas.
Increased functional connectivity on fMRI evaluations has been observed between emotionally related brain areas and motor-associated areas in persons with either functional dyskinesia or functional gait disturbance (278; 274). These results suggest, in contrast to the inhibitory mechanisms above, a vulnerability to excessive activation of motor areas by emotional stimuli. Consequently, it is presently unclear whether a unitary hypothesis regarding regional cerebral activation patterns and functional neurologic disorder can be advanced.
Mal de debarquement involves a variable sensation of bodily oscillation without overt physical signs. The cause of this experience is not understood. Possibly relevant is that illusory bodily tremor in a patient who incurred the COVID-19 illness improved after intravenous saline perfusion but not oral supplementation (33). The cause was uncertain, but this was suggested to result from an interaction among the patient’s concurrent small fiber neuropathy, postural orthostatic tachycardia syndrome, and hypovolemia. These findings may be a clue to the source of the discomfort in mal de debarquement.
Factitious disorder imposed on self, while superficially suggesting intact cognitive function by the patient’s glib presentation, can occur with executive dysfunction, specifically, disturbances with conceptual organization, management of complex information, and judgment following formal neuropsychological testing (197). Indirectly, this finding suggests aberrant cerebral physiology, though this requires further investigation. Leukoaraiosis (nonspecific white matter hyperintensities) has been observed with brain MRI in factitious disorder, whose relationship with disease etiology is uncertain (88). Regional cerebral hypoperfusion has been reported in factitious disorder (184).
Factitious disorder imposed on self generally does not cause sustained peripheral tissue changes apart from incision of the skin. In an exceptional instance, a woman who had repeatedly covertly self-administered intravenous insulin had developed reactive Langerhans cell hypertrophy in her pancreas (nesidioblastosis), which was found on partial pancreatectomy, and initially led to the diagnosis of noninsulinoma pancreatogenous hypoglycemia syndrome (263). Repeated hypoglycemia led to physicians’ reassessment, which then led to discovering that the patient had harbored ampules of insulin. In another form of tissue damage, self-inflicted (or inflicted on a dependent individual) skin lesions generally have irregular borders and occur symmetrically on the body (36).
Epidemiology
The prevalence of functional neurologic disorder has been estimated to be 1% to 15% of all presentations at neurologic clinics (288; 02; 53). Pediatric manifestations are relatively uncommon, especially before the age of 8 years (193); however, they may account for up to 15% of patients seen in pediatric neurologic clinics (89). The youngest onset of functional neurologic disorder was reported at age 4 years (287).
In one epidemiologic study of 405 patients with functional neurologic disorder, the leading manifestations were pain, negative motor symptoms (eg, astasia, paresis), vertigo, and somatosensory disturbances (158). Peak incidence of onset is in young adulthood, and there is a high association with anxiety disorders and depression (158; 195; 03; 29). Nonetheless, psychosocial stressors are not invariably associated with functional neurologic disorder, whereas preceding physical trauma is frequently identified (199). Moreover, the lack of a gold standard for diagnosing functional neurologic disorder complicates the determination of the disorder’s epidemiology (140).
There is a substantial predilection of functional neurologic disorder for women (158; 56; 213). The gender bias for females is not evident in children under 13 years of age (89).
Functional neurologic disorder can appear during pregnancy. A review of case reports finds that the diverse symptoms (weakness, amnesia, among others) occurred most often in the final trimester (49).
Tonic immobility occurs in the vast majority of women who have been raped (183).
Research has emerged showing that associated specific genotypes have predicted forms of functional neurologic disorder. A tryptophan hydroxylase 2 gene polymorphism--G703T--has been shown to predict early onset of functional neurologic disorder (237).
Epidemiology studies on factitious disorders are few. In a single hospital over several years, the prevalence of factitious disorder imposed on self was 0.4%, whereas factitious disorder imposed on another was 0.5% (90). There is a slight female bias, and the mean age of onset is at 48 years (25). According to a national survey in Norway, a female predominance occurred in factitious disorder imposing on self, whereas a male predominance occurred in malingering (221). Factitious disorder imposed on another is almost invariably caused by a woman and the patient’s mother. Most were married; the mean age of onset is 28 years (291).
Ganser syndrome has been rarely reported in part because of a lack of a gold standard for diagnosis. As of 2022, 117 cases had been published (245).
Differential diagnosis
Confusing conditions
Although functional neurologic disorder resembles highly deleterious medical illnesses, examination for which should routinely be conducted in the work-up, functional neurologic disorder should not be considered a diagnosis of exclusion (73; 246). Instead, the well-trained and insightful clinician should be highly suspicious of such disease in the presentation of attentionally-modifiable disorder or of a disorder that superficially resembles conventional neurologic disease but that shows markedly atypical characteristics (eg, astasia-abasia, concentric visual field loss that changes visual angle when testing with stimuli at different distances from the patient). A history of psychiatric disturbance or concurrent personality disorder raises the suspicion for functional disorder, but these do not by themselves rule out structural, physiologic, or infectious pathologic processes, nor do they conversely rule in functional neurologic disorder.
The summary below can be considered only an incomplete overview of conditions that may be confused with functional disorder, as new examples are frequently published. An extensive list of differential diagnoses for functional neurologic disorder has been provided (247).
Functional neurologic disorder is suggested in part by the variability of the symptoms, particularly for impairments that are chronic, such as paralysis or visual loss. Nonetheless, the clinician must recall that "traditional" neurologic disorders, even if chronic and "stable," may also variably appear. Thus, for example, the comprehension deficit in aphasia may vary in relation to how often the patient is tested: it is usually at its best on initial evaluation and then worsens, suggesting vulnerability to fatigue (26). Tremor (as in Parkinson disease or essential tremor) typically abates during sleep; thus, it is clearly influenced by the extent of conscious arousal. Moreover, tremor can be dampened through voluntary reaching. A remarkable instance of voluntary, nonfunctional palatal tremor has been described (28). Postanoxic action myoclonus and Parkinsonian tremor may be aggravated by anxiety and may abate when the individual is emotionally calm (211; 08). Tics may be voluntarily suppressed, but only for a limited period (142). Fatigue, intoxication, medication effects, or systemic infection may aggravate nearly any central nervous system disorder. Such disturbances are distinguished from functional disorder by their adherence to a replicable association with toxic agents, fatigue, or sleep deprivation. In contrast, functional disorder fluctuates over several seconds to minutes and sometimes in relation to who is observing (including the patient himself) or if the patient is aware of being observed.
Resignation syndrome involves the gradual restriction of voluntary activity to the point of stupor and needing feeding support (216). This disorder appears primarily in individuals who are refugees from war-torn countries, and for whom social support by the accommodating country has been withdrawn. Because this disorder is not noted to recur or to be reversed, it does not qualify as functional neurologic disorder but should be considered in the assessment of individuals who have acquired immobility.
Primary progressive aphasia is a dementing illness that involves gradual, irreversible impairment in language, with comparative retention of other cognitive functions. This may be mistaken for functional neurologic disorder but can be recognized by abnormal brain SPECT imaging (203). Acute aphasia due to neurosyphilis has been mistaken for functional illness due to the absence of corroborative CT scan abnormalities (39).
Complex regional pain syndrome is a controversial disorder that was formerly termed “reflex sympathetic dystrophy,” “shoulder-hand syndrome,” “Sudeck dystrophy,” or “algodystrophy.” It is frequently mistaken for malingering. In this disorder, a usually catastrophic physiologic event (traumatic limb injury, spinal cord injury, stroke, myocardial infarction, or extensive burns) precipitates severe pain in a limb, sometimes associated with focal autonomic changes (altered perspiration, hair growth, skin color, or edema) and, in late stages, with focal osteomalacia. In a strange alternation of cause and effect, one case of complex regional pain syndrome included unilateral leg edema and was apparently triggered by acute severe emotional distress (110), rather than the behavioral change occurring in response to somatic illness. The disorder responds to the combination of physical therapy and behavioral therapy, which should be provided by hospitalization with the care of a multidisciplinary team (228). However, in one case, the present topic’s author has found substantial pain reduction following implantation of a spinal cord stimulator. Although the present author’s perspective is that complex regional pain syndrome is not itself a form of functional neurologic disorder, it should be noted that complex regional pain syndrome often includes functional movement disorder, ie, varying involuntary movements in relation to self-attention (222; 223; 277; 136).
A wide variety of perceptual disorders associated with brain injury may show a "covert" recognition of stimuli under special circumstances, despite the overt denial of awareness. The existence of intact but unconscious processing is indicated by autonomic changes (altered heart rate, respiration, skin conductance, pupillary size, etc.) for certain stimuli (eg, familiar faces or voices), despite overt denial. This has been termed "guilty knowledge" due to its similarity to the autonomic signs of criminality during polygraphy in legal investigations (22). Nonautonomic behaviors may also signify retained sensory processing despite an overt failure of recognition. Disorders with dissociations between conscious and unconscious sensory processing include prosopagnosia (impaired face recognition) (22), cortical deafness (78), visual agnosia (181), acquired alexia (inability to read meaningfully), in which patients may still have intact lexical decision (eg, intact ability to categorize uncomprehended words) (62), and unilateral neglect, where stimulus size may affect bisection judgments despite unawareness of peripheral stimulus extent (168). Such findings demonstrate that overt disability may coexist with covert ability, due to the failure of intact cognitive processes to attain conscious awareness following certain forms of brain injury. These disturbances are almost invariably associated with focal structural brain lesions.
Increasing attention has been drawn to the diagnostic confusion that can attend antibody-mediated epilepsies, in particular, NMDA-receptor (or NMDAR) encephalitis. In the latter disorder, there is a frequent occurrence of rapidly fluctuating behavioral disturbances that may include paranoia, delusions, hallucinations, suicidality, and apparent seizures, despite generally unremarkable standard structural brain imaging and video EEG recording. The predominant occurrence of such findings in young women, which in many cases is associated with an ovarian teratoma, may lead to the mistaken impression of functional seizures (147; 52). When a teratoma is present, the disorder often markedly improves with surgical removal of the tumor and immunosuppressant medication.
Opposite to functional neurologic disorder is anosognosia, the unawareness of neurologic deficit (eg, hemiparesis, amnesia, aphasia) (13). A classic example of anosognosia is Anton syndrome, the denial of blindness (94). Although a psychological defense mechanism is plausible in certain cases following cerebral injury, the associated cognitive deficits suggest that such a lack of awareness more often results from defective cognitive functions essential for self-monitoring (176). In addition, the present author has often encountered facial motor disturbances that occurred without the patient’s awareness, and yet were instigated with either emotional disturbance or direct neurologic examination (in contrast to spontaneous facial movements not during direct examination). These disturbances include excess blinking, orbicularis oris quivering, and tongue deviation when the patient is asked to protrude the tongue. Acute brain injury may rarely be associated with denial of intact ability (eg, vision) (113). Such “inverse anosognosia” is more often observed in functional neurologic disorder, a distinction being that persons who are afflicted with functional neurologic disorder are emotionally disturbed by their deficits, in contrast to the denial of intact visual ability in structural brain damage.
Associated or underlying disorders
Functional neurologic disorder may occur with or without another concurrent neurologic disorder. Consequently, diagnosing traditional neurologic disorder (eg, stroke, Parkinson disorder) does not mean excluding functional neurologic disorder.
Although there is a high co-occurrence of psychiatric disorders in persons with functional neurologic disorder, most persons with functional disorder do not have mood disorder (273). Consequently, the clinician should not assume that persons with functional neurologic disorder have mood disorder, but instead should inquire of them directly.
More than half of the patients with functional neurologic disorder also have hypermobile Ehlers-Danlos syndrome and hypermobile spectrum disorders, ie, they are double-jointed (55).
Various forms of autonomic neurologic disorder commonly occur in persons with functional neurologic disorder. As far back as World War I, dusky limb changes have been reported in functional neurologic disorder (07). Sustained tachycardia or postural orthostatic tachycardia syndrome have been observed recurrently in persons diagnosed with functional neurologic disorder (01; 143; 171; 60). About 40% of patients with functional movement disorder have restless legs syndrome as well (224). In another small sample, the incidence of irritable bowel syndrome was twice as much (36%) in persons with functional movement disorder than in control subjects (253).
Emerging evidence also suggests that functional neurologic disorder involves elevated inflammatory blood biomarkers (226; 272; 198). Thus, emerging literature implies widespread bodily disorder beyond the central nervous system in persons with functional neurologic disorder.
Diagnostic workup
There is no gold standard method for diagnosing functional movement disorder (140). Three leading methods are used: (1) variants of the Fahn and Williams criteria (85); (2) the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-V) approach (04); and (3) clinician-determined. The lack of consensus on diagnostic criteria likely hampers research progress on assessment and management. Stone has advocated for abolishing the widely used criterion for diagnosing functional neurologic disorder based on its presumed “incongruence” with other, more familiar neurologic disorders, owing to our still limited understanding of the diverse manifestations of more familiar neurologic disorders (248).
As with any complaints of bodily disorder or functional disability, or the observation of behavioral changes that suggest specific neurologic disorders, patients should undergo the usually indicated workups, unless the patient has been recognized by staff to have presented frequently with the same complaints without objectively confirmed abnormal biomarkers (eg, lesions on brain MRI, epileptiform waves on EEG). In such instances, the reliability of previous workups should be reviewed before deciding that the illness is functional. Otherwise, the suspicion of functional disorder should not preclude a conventional medical workup because functional disorder does not in itself exclude concurrent medically treatable disorders.
In the clinic or hospital, functional neurologic disorder should be diagnosed when noting the patient’s complaint of a persisting neurologic symptom that disrupts everyday activities, and which varies with self-attention. Supportive findings include variability of neurologic signs during history taking and formal examination. The specific conditions that elicit or aggravate symptoms should be tested, for example, during formal neurologic motor limb or oculomotor assessment. In addition, techniques that may distract the patient from the symptoms could be administered to determine whether the symptoms can be ameliorated. For example, after noting that formal limb power or coordination testing may aggravate tremor or paresis, the patient’s limb control should be reassessed when asking the patient to perform naturalistic, whole-body maneuvers without drawing attention to the particular part of the body. This can include asking the patient to transfer between a chair or wheelchair to the examination bed, or to walk backwards.
Another common feature is the patient’s unawareness or diminished awareness of periods of normalcy (200). This can be demonstrated during clinical examination, including examining the patient with distracting methods as referred to above. This should be used to show to the patient that the condition is intermittent and reversible.
On the other hand, the clinician’s failure to change the symptoms or signs during examination should raise the possibility of an alternative, nonfunctional diagnosis.
Functional neurologic disorder may be suspected with a history of frequent changes in the involvement of medical practitioners, particularly when workups failed to identify the disorder, or if historical details are vague. Multiple surgical scars may suggest factitious disorder imposed on self (10). Fluctuation of a deficient function, such as limb use or vision, suggests functional disorder (208; 249). Similar concerns apply to malingering or factitious disorder imposed on self (21). The suspicion for factitious disorder imposed on self should be raised in patients who present themselves for diagnostic workup despite a longstanding history of repeated invasive diagnostic measures (as evidenced by multiple surgical scars). A history of using aliases should also raise suspicion for factitious disorder.
Although studies have indicated a high incidence of a history of sexual abuse in persons with functional neurologic disorder (275; 218), Stone and colleagues advise deferring inquiry for sexual abuse to an expert in this area because of the considerable amount of skillful evaluation and discussion that would be needed (249).
Several clinical neurologic tests may improve diagnosis of functional neurologic disorder, specific to the presenting complaint. Stone and colleagues offer a brief overview of these tests and their degree of reliability (250). The following provides some considerations for diagnosing specific functional neurologic phenomena.
Functional neurologic disorder is suggested by fluctuating manifestations during examination. Nonetheless, tremors that are commonly thought not to have a functional etiology may also diminish with distraction (173). This observation suggests that nonspecific tremor may have a functional basis. Variable muscle recruitment during contractions or irregular intervals from stimulus to jerk onset are consistent with functional myoclonus or functional startle (267). Dystonia accompanied by pain and variable presentation suggests functional neurologic disorder (150). In a large study, 37% of patients with fixed-hand dystonia fulfilled diagnostic criteria for functional etiology (222). This was considered by the authors to be underestimated, owing to the presumed difficulty with distracting the patient from maintaining the fixed posture of the limb.
Because asynchronous rhythmic oscillations in different parts of the body (eyes, neck) can be self-induced through practice (156), this does not exclude functional tremor or nystagmus. In contrast, entrainment is a well-recognized and reliable sign for unilateral functional upper limb tremor (81). After recognizing the characteristic frequency of the functional tremor, the patient is asked to copy the examiner’s demonstrated tremor with the other hand and at a frequency different from the functional tremor. Entrainment is demonstrated if the functional hand becomes synchronized with the copied tremor.
During tilt-table testing, individuals who are considered to have functional syncope are highly likely to close their eyes at the onset of apparent syncope, in marked contrast to persons who have cardiovascular syncope (262).
Commonly seen in functional coma are normal vital signs, toxicology, complete blood count, and serum electrolytes, with normal tendon, pupillary, and vestibulo-ocular reflexes, normal muscular tone, and flexor plantar responses. In coma following demonstrable structural brain disease or metabolic dysfunction, the patient does not prevent his hand from striking his face when it is released from grasp above the face. In contrast, in functional coma (or mildly impaired arousal), the patient’s hand misses the face when released from above. In the presence of such findings, cerebral neuroimaging is unlikely to be necessary. In functional coma, ice-water caloric vestibular testing (after ascertaining the integrity of the tympanic membrane) may induce nausea so severe as to provoke well-integrated limb or postural movements or arousal. Similar defensive maneuvers may follow presentation of concentrated ammonia ("smelling salts") to the nose. Failure to demonstrate integrated responses to noxious environmental stimuli should prompt evaluation with an EEG to rule out nonconvulsive status epilepticus.
Assessing functional visual disorder must be tailored to the presenting symptom. Helpful tests for evaluating functional visual loss include observing the patient's pupillary and facial responses in reaction to silently presenting a mirror. Patients with functional blindness often attend the clinic wearing sunglasses, which may be a useful sign (23). Blink to visual threat may signify integrity of visual awareness (as long as one prevents corneal stimulation through gusts of air). However, the absent blink to threat does not strictly imply visual loss but may be due to inattention (70). It is conceivable that patients who anticipate testing methods for functional visual loss may willfully prevent reflexive eye movements, such as blink to threat. Further recommendations for assessment are available (37). Unfortunately, automated assessment of visual fields does not distinguish between functional and structural visual disorders (233). Similarly, visual evoked responses can be episodically inhibited in dissociative personality disorder in individuals with personality-dependent visual loss, which suggests that this technique is not reliable when evaluating suspected mechanisms of visual loss (281).
Functional hemianesthesia may be suspected when a vibrating tuning fork applied to the forehead is not felt past the midline (137; 104).
Functional hemiparesis of the lower extremities has been traditionally diagnosed through examining for the Hoover sign, which applies distraction away from the paretic limb (123). This is tested by having the patient supine in bed or on the examination table while the examiner places both hands beneath the patient's heels. When asked to force the feet down (essentially, hip extension), only one leg moves. Then the examiner tests leg elevation in the nonparetic side while keeping the hand beneath the paretic heel. In true hemiparesis, upward mobility of the nonparetic leg causes no forceful movement of the paretic limb. In contrast, in functional hemiparesis, the "paretic" leg will move down forcefully to stabilize the upward movement of the other leg (256). Although useful, this sign is subjective and, thus, may be difficult to assess reliably. This difficulty may be overcome through using strain gauges attached to the lower extremities and even the upper extremities and calculating the ratio of voluntary activation versus involuntary activation (through mobilizing the opposite limb) (297). Although more objective, this measure is elaborate and, thus, unlikely to become popular. It should also be noted that concurrent pain with leg movement may confound interpretation of the test, the test’s reliability has not been assessed, and test performance among individuals with defined neurologic disease (eg, multiple sclerosis) has not been evaluated (256).
In contrast to the Hoover sign, a reportedly more reliable test is to assess whether there is voluntary stabilization of the “paretic” leg while the unimpaired leg is actively abducted against the examiner’s resistance (236). In nonfunctional hemiparesis, the paretic limb hyperabducts when the opposite leg abducts against resistance. In functional hemiparesis, the unimpaired leg hyperadducts when the “paretic” leg is required to abduct against resistance. A blinded study is needed to confirm the validity of this method.
The suspicion of functional paraparesis may be confirmed with the Spinal Injuries Center (SIC) test (292). In this test, patients who demonstrate an inability to elevate their legs have their knees passively flexed while they are recumbent. The examiner gently removes contact. The maintenance of flexed posture is a positive test and has a reported 100% sensitivity and 98% specificity.
Unilateral functional sensorimotor deficit (resembling stroke) may be associated with increased N140 component of the event-related potential following somatic stimulation on the affected side (164). This asymmetry can remit following therapeutic hypnotic suggestion.
Functional paraplegia is frequently accompanied by dense sensory loss that does not respect dermatomal boundaries but rather the "underwear line" (249). Lower extremity tendon reflexes, cremasteric reflexes, plantar responses, anal sphincter tone, and limb muscle tone are usually normal. Case studies demonstrate that normal motor evoked potentials support the diagnosis of functional paraplegia (205). Integrity of muscle tone (and, hence, some degree of voluntary muscle control) can be demonstrated by flexing the hip and knee while the patient is supine and noting whether the leg slowly falls to one side, if at all. The clinician may surreptitiously monitor for subtle postural adjustments of the lower extremities while redirecting attention to the patient's upper body. Monitoring during sleep (eg, by direct observation, video monitoring, or accelerometry) can disclose lower extremity movements that are asynchronous with upper extremity movements and, hence, not reflexive (153).
The science of statistics can help uncover factitious amnesia. Subjects with true amnesia should have about a 50/50 chance of recalling whether individual test stimuli were present on a 20-item list they have been shown. In contrast, subjects with malingered amnesia, who are naive to the principles of probability, may fail to recall items correctly at greater than 50% probability (41), thereby indicating covert recognition of list items.
Factitious disorder imposed on another may be suspected for unexplained pediatric illnesses in which a parent (usually a mother) shows obsessive concern with the illness and is medically astute while developing close social relationships with clinical staff. Frequently, the father is unaware of the child's disorder and may not accompany the child to the clinic (15). Confirmation of the fabrication of the illness in hospitalized children may be obtained through surreptitious video recording. However, the legality of this measure may vary with the jurisdiction serving the particular hospital, so legal counsel is needed when entertaining this approach. If a clinical program adopts this approach, a well-defined plan for taking action to protect the child must be in place (244). Careful monitoring of the child's visitors and objects taken to the child or left in the room with them may aid in the diagnosis. Monitoring of physiologic functions such as respiration may also be beneficial.
Management
Common treatment approaches include the following:
• Empathetic support by the clinician
• Psychiatric management for co-occurring mood disorder
• Cognitive behavioral therapy or other behavioral treatments
• Physical rehabilitation
• Hypnosis
• Other approaches
Empathetic support. In general, the clinician who diagnoses functional neurologic disorder should explain why another neurologic disorder is unlikely to explain the symptoms. Reassurance while conveying sincere interest in the patient's welfare will prove valuable (208; 202; 254). Conveying that the disorder is nonetheless a neurologic disorder can improve symptoms (101). Praise given by clinicians or therapists for functional gains, however small, can help to accelerate recovery while allowing the patient to maintain dignity (69). Rather than conveying a lack of understanding, the clinician should positively diagnose “functional neurologic disorder.” The terms "hysteria" and "malingering" should not be used (234). Patients must never be told that they are "faking" the disorder, or they will almost surely seek medical treatment elsewhere, including from unqualified and potentially harmful practitioners, or they may bring legal action. Although hospitalized patients with functional disorder may provoke resentment among staff, the clinician must always maintain a calm, professional, respectful attitude and be in charge. Avoid describing patients as "manipulative" because this amounts to admitting the clinician's failure to maintain control of a vexing clinical presentation and may deter hospital staff from acting in the best interests of the patient's long-term health. The clinician above all needs to be a team leader to maintain a coherent staff approach to the patient. Private meetings with hospital or clinic staff, conducted with complete respect for the patient and acknowledgment that functional presentations are common experiences, may help to unify the staff approach and maintain an empathetic attitude.
Psychiatric management. Patients with functional neurologic disorder commonly refuse psychiatric referral because they do not believe that they have a psychological disturbance (131). In contrast, co-occurring psychiatric disturbances that are acknowledged by functional patients, such as depression or anxiety, should be treated according to the standard of care, which may include psychiatric or psychological referral.
Behavioral intervention. Clinical trials preliminarily suggest that cognitive behavioral therapy is efficacious for functional disorder (149; 107; 254). The approach includes relaxation training and teaching patients to control their illness, rather than being passive. Combining sertraline with cognitive behavioral therapy may reduce functional seizures considerably more than cognitive behavioral therapy by itself (148). Inpatient treatment with cognitive behavioral therapy, for functional paresis at least, may be more efficacious than outpatient treatment (174).
In contrast, an outpatient clinical trial that used only cognitive behavioral therapy and required that patients be told they had a psychological disorder resulted in only a 50% success rate (190). This finding suggests that invoking a psychological disorder undermines the patient’s confidence with improvement and should not be used. In a comparable study of outpatient cognitive behavioral therapy combined with physical therapy, the success rate was only 34% (162). This result suggests that treatment outcomes would be more successful when behavioral intervention is given as part of a patient program, as shown by the MoRe program.
The behavioral intervention program ReACT (Retraining and Control Therapy), given to children with functional seizures, has been shown to have an 82% success rate for reducing episodes at 60-day follow-up (276).
In a small outpatient cognitive behavioral therapy trial for unilateral functional tremor, tremor reduction occurred in 73% of the patients at 12 weeks (82). However, in contrast to the other cognitive behavioral therapy trials, there was no indication of whether the patients’ self-reported clinical global impression had changed.
Physical rehabilitation. Physical therapy trials for functional neurologic disorder have been ongoing since 2002 and have generally been successful (167). Physical therapy for functional restricted bodily movement has been reported to have enduring benefit (186). The therapeutic process included establishing rapport with the patient. It is conceivable that such intervention is a form of psychotherapy itself, as it provides the patient reassurance, empathy, feedback, and encouragement. Similarly, compassionate visual training exercises applied over weeks to months can improve functional blindness (93).
A clinical trial of the Movement Retraining, or MoRe, method obtained outstanding improvement for functional movement disorder (126). This method involved a 5-day hospital admission (after having failed outpatient therapy), providing daily symptom-oriented physical or occupational therapy, with daily assessments and management by a staff psychologist, including elements of cognitive behavioral therapy. At the end of treatment, 87% of the patients improved on the patient-rated Clinical Global Impression Scale. Comparable gains were demonstrated on a patient-reported outcome, the Canadian Occupational Performance Measure (51).
Hypnosis. Hypnosis was first applied in the late 19th century (34) and may be therapeutically successful in the hands of a skillful practitioner, at least when motor disturbances occur (182).
Other approaches. A preliminary report of virtual reality exposure training showed feasibility (46). In this approach, patients view themselves as cartoon depictions of themselves, or “avatars,” while they are encouraged to comply with various video-based motoric gaming. Further results are pending.
One case report observed resolution of functional itch with topiramate, suggesting a potential role for pharmacologic treatments for functional diseases (50).
An exciting development is the application of repetitive transcranial magnetic stimulation to the motor-associated cortex in individuals with functional movement disorder. A literature review found that transcranial magnetic stimulation for functional movement disorder can be beneficial (194). Further research is needed to exclude placebo effects.
The basis for post-treatment improvement is unknown. Chastan and colleagues suggested that patients with functional paresis may be helped by observing their involuntary limb contractions that are induced by stimulation. However, this would not explain improvement for active, dyskinetic movement disorders. Instead, the improvement of interhemispheric inhibition that can follow transcranial magnetic stimulation may possibly be responsible (152). Such treatment has already been shown to have ample success for depression that is refractory to medication (284). Thus, it may also be possible that functional disturbances may improve following transcranial magnetic stimulation, secondary to improving an underlying mood disorder. One may expect to observe further exciting developments in this line of investigation.
A limitation in comparing these trials of either cognitive behavioral therapy, physical therapy, or both for functional movement disorder is the inconsistency in using outcome measures. In addition, the field of managing functional neurologic disorder lacks outcome measures that are more specific to the particular symptom, particularly regarding the impact of such therapy on everyday self-care abilities in the community.
The diagnosis of factitious disorder imposed on another requires assembling the involved clinical staff and legal counsel to review evidence supporting the diagnosis and then contacting a child protection agency for the child's safety and removal. Such steps must be undertaken without informing the responsible caregiver first (15). Advice or leadership from clinicians with expertise in diagnosing and intervening in the condition is recommended (244). Psychiatric evaluation of the caregiver may be required and may involve a court order.
Outcomes
The natural history of functional neurologic disorder without treatment is not well characterized owing to inconsistent methods of diagnosing the disorder as well as limited long-term follow-up. Spontaneous recovery is not unusual.
Functional movement disorder can progress to more familiar neurologic disorders. Progression to Creutzfeldt-Jakob disease has been observed a few times (108). In a small study, 26% of persons with Parkinson disease had been initially found to have functional movement disorder (289). These findings suggest that neurodegenerative disorders and functional movement disorder have a shared pathophysiology.
Repetitive transcranial magnetic stimulation to the brain has led to a sustained reduction of functional tremor as much as 12 months subsequently, unlike patients who underwent sham treatment (261).
Physical therapy combined with physical retraining has been demonstrated, and 69% retained gains at 6-month (126) and 12-month follow-up (115). Comparable findings were obtained in the management of functional gait disorder (130). A similar, 5-day inpatient program of physical therapy, but without cognitive behavioral therapy, obtained an impressive 72% improvement at 6 months’ follow-up on a clinical global impression scale (188). Entrainment treatment (in which unilateral functional tremor is trained to match an imposed, different tremor in the opposite arm) was efficacious in 60% of participants at 6-month follow-up, though relapses were also noted (81). Four to 6 days of psychotherapy led to improved symptom control in persons with either functional movement disorder or functional seizures (124). Clinical trials to establish the replicability of treatment outcomes are much needed.
Media
References
- 01
- Aboudrar S, Benjelloun H, Benazzouz A, et al. Evaluation de l'activité vagale par le test de la respiration profonde (Deep-Breathing) [Evaluation of the vagal activity by the Deep-Breathing test]. Neurophysiol Clin 2007;37(1):41-6. PMID 17418357
- 02
- Ahmad O, Ahmad KE. Functional neurological disorders in outpatient practice: an Australian cohort. J Clin Neurosci 2016;28:93-6. PMID 26754851
- 03
- Aldenkamp AP, Mulder OG. Behavioural mechanisms involved in pseudo-epileptic seizures: a comparison between patients with epileptic seizures and patients with pseudo-epileptic seizures. Seizure 1997;6:275-82. PMID 9304718
- 04
- American Psychiatric Association. Conversion disorder (functional neurological symptom disorder) [review]. Diagnostic and Statistical Manual of Mental Disorders (5th ed). Arlington, Virginia: American Psychiatric Association, 2013:318-21.
- 05
- Anderson KE, Gruber-Baldini AL, Vaughan CG, et al. Impact of psychogenic movement disorders versus Parkinson’s on disability, quality of life, and psychopathology. Mov Disord 2007;22:2204-9. PMID 17876850
- 06
- Anonymous. Hysteria in animals. N Engl J Med 1898;139:95-7.
- 07
- Anonymous. Sections of psychiatry and neurology: special discussion on shell shock without visible signs of injury. Proc R Soc Med 1916;9(Sect Psych Neurol):i-xliv. PMID 19979447
- 08
- Apartis E. Clinical neurophysiology of psychogenic movement disorders: how to diagnose psychogenic tremor and myoclonus. Neurophysiol Clin 2014;44:417-24. PMID 25306082
- 09
- Asadi-Pooya AA. Psychogenic nonepileptic seizures: a concise review. Neurol Sci 2017;38:935-40. PMID 28275874
- 10
- Asher R. Munchausen's syndrome. Lancet 1951;i:339-41. PMID 14805062
- 11
- Atmaca M, Aydin A, Tezcan E, Poyraz AK, Kara B. Volumetric investigation of brain regions in patients with conversion disorder. Prog Neuropsychopharmacol Biol Psychiatry 2006;30:708-13. PMID 16600450
- 12
- Aybek S, Nicholson TR, Draganski B, et al. Grey matter changes in motor conversion disorder. J Neurol Neurosurg Psychiatry 2014;85:236-8. PMID 23236016
- 13
- Babinski J. Contribution à l'étude des troubles mentaux dans l'hémiplégie organique cérébrale (Anosognosie). Rev Neurol 1914;22:845-8. Translated in Rottenberg DA, Hochberg FH (eds.) Neurological classics in modern translation. New York: Hafner Press, 1977:131-5.
- 14
- Baguley DM, Cope TE, McFerran DJ. Functional auditory disorders [review]. Handb Clin Neurol 2016;139:367-78. PMID 27719856
- 15
- Baldwin MA. Munchausen syndrome by proxy: neurological manifestations. J Neurosci Nurs 1994;26:18-23. PMID 8195645
- 16
- Barbagallo G, Nisticò R, Vescio B, et al. The placebo effect on resting tremor in Parkinson's disease: an electrophysiological study. Parkinsonism Relat Disord 2018;52:17-23. PMID 29551396
- 17
- Bartholomew RE, Perez DFZ. Chasing ghosts in Cuba: is mass psychogenic illness masquerading as an acoustical attack? Int J Soc Psychiatry 2018;64:413-6. PMID 29607716
- 18
- Bartholomew RE, Wessley S. Protean nature of mass sociogenic illness: from possessed nuns to chemical and biological terrorism fears. Br J Psychiatry 2002;180:300-6. PMID 11925351
- 19
- Bartholomew RE, Wessely S, Rubin GJ. Mass psychogenic illness and the social network: is it changing the pattern of outbreaks? J R Soc Med 2012;105:509-12. PMID 23288084
- 20
- Batshaw ML, Wachtel RC, Deckel AW, et al. Munchausen's syndrome simulating torsion dystonia. N Engl J Med 1985;312(22):1437-9. PMID 3990745
- 21
- Bauer M, Boegner F. Neurological syndromes in factitious disorder. J Nerv Ment Dis 1996;184:281-8. PMID 8627273
- 22
- Bauer RM. Autonomic recognition of names and faces in prosopagnosia: a neuropsychological application of the Guilty Knowledge Test. Neuropsychologia 1984;22:457-69. PMID 6483172
- 23
- Bengtzen R, Woodward M, Lynn MJ, Newman NJ, Biousse V. The "sunglasses sign" predicts nonorganic visual loss in neuro-ophthalmologic practice. Neurology 2008;70:218-21. PMID 18195266
- 24
- Benson DF. Alexia and the neural basis of reading. Ann Dyslexia 1984;34(1):1-13. PMID 24243291
- 25
- Berar A, Balusson F, Allain JS. Factitious disorder imposed on self: a retrospective study of 2232 cases from health insurance databases. Gen Hosp Psychiatry 2023;85:114-9. PMID 37862960
- 26
- Beyn ES. Peculiarities of thought in patients with sensory aphasia. Lang Speech 1958;1:233-49.
- 27
- Bhuvaneswar C, Spiegel D. An eye for an I: a 35-year-old woman with fluctuating oculomotor deficits and dissociative identity disorder. Int J Clin Exp Hypn 2013;61:351-70. PMID 23679117
- 28
- Biller J, Espay AJ. Nosography of the “essential”: volitional palatal tremor. Neurology 2013;81:772-3. PMID 23960194
- 29
- Binzer M, Andrsen PM, Kullgren G. Clinical characteristics of patients with motor disability due to conversion disorder: a prospective control group study. J Neurol Neurosurg Psychiatry 1997;63:83-8. PMID 9221972
- 30
- Birnbaum MH, Thomann K. Visual function in multiple personality disorder. J Am Optom Assoc 1996;67:327-34. PMID 8888853
- 31
- Birklein F, Schlereth T. Complex regional pain syndrome-significant progress in understanding [review]. Pain 2015;156:S94-S103. PMID 25789441
- 32
- Biver F, Delvenne V, Hirsch D, Lotstra F. Factitious hemiplegia and Munchausen's syndrome. Acta Neurol Belg 1992;92:289-95. PMID 1471466
- 33
- Blitshteyn S, Ruhoy IS, Natbony LR, Saperstein DS. Internal tremor in long COVID may be a symptom of dysautonomia and small fiber neuropathy. Neurol Int 2024;17(1):2. PMID 39852767
- 34
- Bogousslavsky J, Walusinski O. Gilles de la Tourette's criminal women; the many faces of fin de siècle hypnotism. Clin Neurol Neurosurg 2010;112:549-51. PMID 20413214
- 35
- Bokat-Lindell S. Is ‘Havana syndrome’ an ‘act of war’ or ‘mass hysteria’? New York Times. Accessed October 26, 2021. https://www.nytimes.com/2021/2010/2026/opinion/havana-syndrome-disorder.html.
- 36
- Bonamonte D, Foti C, De Marco A, et al. Self-inflicted pathological cutaneous disorders. Part II. Ital J Dermatol Venerol 2022;157:480-8. PMID 36177780
- 37
- Bose S, Kupersmith MJ. Neuro-ophthalmologic presentations of functional visual disorders. Neurol Clin 1995;13:321-39. PMID 7643828
- 38
- Botzung A, Denkova E, Manning L. Psychogenic memory deficits associated with functional cerebral changes: an fMRI study. Neurocase 2007;13:378-84. PMID 18781436
- 39
- Boyle A, Zafar R. Neurosyphilis presenting with dissociative symptoms. J Neurol Neurosurg Psychiatry 1995;59:452-3. PMID 7561936
- 40
- Brand BL, Sar V, Stavropoulos P, et al. Separating fact from fiction: an empirical examination of six myths about dissociative identity disorder. Harv Rev Psychiatry 2016;24:257-70. PMID 27384396
- 41
- Brandt J, Rubinsky E, Lassen G. Uncovering malingered amnesia. Ann N Y Acad Sci 1985;444:502-3. PMID 3860110
- 42
- Breen DP, Rohani M, Moro E, et al. Functional movement disorders arising after successful deep brain stimulation. Neurology 2018;90:931-2. PMID 29653985
- 43
- Breuer J, Freud S. Studien über Hysterie. Leipzig: Franz Deuticke, 1895 [in German].
- 44
- Bridges KE, Corballis PM, Spray M, Bagrie J. Testing failure-to-identify hunting incidents using an immersive simulation: is it viable? Appl Ergon 2021;93:103358. PMID 33485071
- 45
- Buckingham HW, Rekart DM. Semantic paraphasia. J Commun Disord 1979;12(3):197-209. PMID 438359
- 46
- Bullock K, Won AS, Bailenson J, Friedman R. Virtual reality-delivered mirror visual feedback and exposure therapy for FND: a midpoint report of a randomized controlled feasibility study. J Neuropsychiatry Clin Neurosci 2020;32:90-4. PMID 31687867
- 47
- Burgmer M, Konrad C, Jansen A, et al. Abnormal brain activation during movement observation in patients with conversion paralysis. Neuroimage 2006;29:1336-43. PMID 16213162
- 48
- Butler M, Coebergh J, Safavi F, et al. Functional neurological disorder after SARS-CoV-2 vaccines: two case reports and discussion of potential public health implications. J Neuropsychiatry Clin Neurosci 2021;33:345-8. PMID 34261345
- 49
- Cabreira V, McLoughlin C, Shivji N, et al. Functional neurological disorder in pregnancy, labour and the postpartum period: systematic review. BJPsych Bull 2024:1-11. PMID 39391946
- 50
- Calabro RS, Bramanti P, Digangi G, Mondello S, Italiano D. Psychogenic itch responding to topiramate. Psychosomatics 2013;54:297-300. PMID 23274005
- 51
- Callister MN, Klanderman MC, Boddu SP, et al. Outpatient motor retraining for functional movement disorder: predictors of a favorable short-term response. Mov Disord Clin Pract 2023;10:1377-87. PMID 37772308
- 52
- Caplan JP, Binius T, Lennon VA, Pittock SJ, Rao MS. Pseudopseudoseizures: conditions that may mimic psychogenic non-epileptic seizures. Psychosomatics 2011;52:501-6. PMID 22054618
- 53
- Carson A, Lehn A. Epidemiology. Handb Clin Neurol 2016;139:47-60. PMID 27719864
- 54
- Carson A, Ludwig L, Welch K. Psychologic theories in functional neurologic disorders. Handb Clin Neurol 2016;139:105-20. PMID 27719831
- 55
- Chan L, Hallett M, Zalewski CK, et al. Clinical, biomarker, and research tests among US government personnel and their family members involved in anomalous health incidents. JAMA 2024;331:1109-21. PMID 38497797
- 56
- Chastan N, Parain D. Psychogenic paralysis and recovery after motor cortex transcranial magnetic stimulation. Mov Disord 2010;25:1501-4. PMID 20568093
- 57
- Chernyshev OY, Martin-Schild S, Albright KC, et al. Safety of tPA in stroke mimics and neuroimaging-negative cerebral ischemia. Neurology 2010;74:1340-5. PMID 20335564
- 58
- Chevalier X, Claudepierre P, Larget-Piet B, Lejonc JL. Münchausen's syndrome simulating reflex sympathetic dystrophy. J Rheumatol 1996;23:1111-2. PMID 8782150
- 59
- Christensen RC, Szlabowicz JW. Factitious status epilepticus as a particular form of Munchausen's syndrome. Neurology 1991;41:2009-10. PMID 1745368
- 60
- Chudleigh C, Savage B, Cruz C, et al. Use of respiratory rates and heart rate variability in the assessment and treatment of children and adolescents with functional somatic symptoms. Clin Child Psychol Psychiatry 2019;24(1):29-39. PMID 30354283
- 61
- Chung SS, Gerber P, Kirlin KA. Ictal eye closure is a reliable indicator for psychogenic nonepileptic seizures. Neurology 2006;66:1730-1. PMID 16769949
- 62
- Coslett HB, Saffran EM. Evidence for preserved reading in ‘pure alexia.’ Brain 1989;112:327-59.
- 63
- Cretton A, Brown RJ, LaFrance WC, Aybek S. What does neuroscience tell us about the conversion model of functional neurological disorders? J Neuropsychiatry Clin Neurosci 2020;32:24-32. PMID 31619119
- 64
- Crommelinck M. Neurophysiology of conversion disorders: a historical perspective. Neurophysiol Clin 2014;44:315-21. PMID 25306072
- 65
- Crozier WJ. Reflex immobility and the central nervous system [review]. Exp Biol Med 1923;21:55-6.
- 66
- Dabholkar PD. Ganser syndrome. A case report and discussion. Br J Psychiatry 1987;151:256-8. PMID 3690119
- 67
- Dalfen AK, Feinstein A. Head injury, dissociation and the Ganser syndrome. Brain Inj 2000;14:1101-5. PMID 11147582
- 68
- de la Torre Laso J. The reality of tonic immobility in victims of sexual violence: "I was paralyzed, I couldn't move." Trauma Violence Abuse 2024;25(2):1630-7. PMID 37555259
- 69
- Delargy MA, Peatfield RC, Burt AA. Successful rehabilitation in conversion paralysis. BMJ 1986;292:1730-1. PMID 3089374
- 70
- Denny-Brown D. Disintegration of motor function resulting from cerebral lesions. J Nerv Ment Dis 1950;112:1-45. PMID 15422381
- 71
- Depue BE, Curran T, Banich MT. Prefrontal regions orchestrate suppression of emotional memories via a two-phase process. Science 2007;317:215-9. PMID 17626877
- 72
- Dieterich M, Staab JP. Functional dizziness: from phobic postural vertigo and chronic subjective dizziness to persistent postural-perceptual dizziness. Curr Opin Neurol 2017;30:107-13. PMID 28002123
- 73
- Drapier S, Vérin M. Psychogenic movement disorders [Article in French]. Rev Neurol (Paris) 2012;168:662-7. PMID 22898562
- 74
- Eden OB, McNinch AW. Voodoo, videos and fits: another presentation of truancy. Eur J Ped 1992;151:918. PMID 1473548
- 75
- Edwards MJ, Adams RA, Brown H, Pareés I, Friston KJ. A Bayesian account of ‘hysteria’. Brain 2012;135:3495-512.** PMID 22641838
- 76
- Edwards MJ, Bhatia KP. Functional (psychogenic) movement disorders: merging mind and brain. Lancet Neurol 2012;11:250-60.** PMID 22341033
- 77
- Egan NM. Misdiagnosed for greed. People 2010;74:145-7.
- 78
- Engelien A, Huber W, Silbersweig D, et al. The neural correlates of ‘deaf-hearing’ in man. Conscious sensory awareness enabled by attentional modulation. Brain 2000;123:532-45. PMID 10686176
- 79
- Ercoli T, Lutzoni L, Orofino G, Muroni A, Defazio G. Functional neurological disorder after COVID-19 vaccination. Neurol Sci 2021;42:3989-90. PMID 34324120
- 80
- Espay AJ, Aybek S, Carson A, et al. Current concepts in diagnosis and treatment of functional neurological disorders. JAMA Neurol 2018;75:1132-41.** PMID 29868890
- 81
- Espay AJ, Edwards MJ, Oggioni GD, et al. Tremor retrainment as therapeutic strategy in psychogenic (functional) tremor. Parkinsonism Relat Disord 2014;20:647-65. PMID 24679736
- 82
- Espay AJ, Ries S, Maloney T, et al. Clinical and neural responses to cognitive behavioral therapy for functional tremor. Neurology 2019;93(19):e1787-98. PMID 31586023
- 83
- Espiridion ED, Valent K, Qatanani A, Adesina O, Oladunjoye AO. A rare case of Ganser syndrome: psychogenic or organic? Cureus 2020;12(8):e10144. PMID 33014642
- 84
- Evans H, Bartholomew R. Outbreak! The Encyclopedia of Extraordinary Social Behavior. San Antonio, TX: Anomalist Books, 2009.**
- 85
- Fahn S, Williams DT. Psychogenic dystonia [review]. Adv Neurol 1988;50:431-55. PMID 3400501
- 86
- Fasano A, Daniele A. Functional disorders after COVID-19 vaccine fuel vaccination hesitancy. J Neurol Neurosurg Psychiatry 2022;93:339-40. PMID 34408004
- 87
- Feldman MD, Duval NJ. Factitious quadriplegia. A rare new case and literature review. Psychosomatics 1997;38:76-80. PMID 8997120
- 88
- Fenelon G, Mahieux F, Roullet E, Guillard A. Munchausen's syndrome and abnormalities on magnetic resonance imaging of the brain. BMJ 1991;302:996-7. PMID 2039898
- 89
- Ferrara J, Jankovic J. Psychogenic movement disorders in children. Mov Disord 2008;23:1875-81. PMID 18709677
- 90
- Ferrara P, Vitelli O, Bottaro G, et al. Factitious disorders and Munchausen syndrome: the tip of the iceberg. J Child Health Care 2013;17(4):366-74. PMID 23411659
- 91
- Ferreira JJ, Trenkwalder C, Mestre TA. Placebo and nocebo responses in other movement disorders besides Parkinson's disease: how much do we know? Mov Disord 2018;33:1228-35. PMID 30230626
- 92
- Fiest KM, Dykeman J, Patten SB, et al. Depression in epilepsy: a systematic review and meta-analysis. Neurology 2013;80:590-9. PMID 23175727
- 93
- Fischer M, Kattah J, Eggenberger E, Pula J. Babinski's other legacy: treating hysterical blindness with persuasion [abstract]. Neurology 2013;80:P06.019.
- 94
- Forstl H, Owen AM, David AS. Gabriel Anton and "Anton's Symptom": on focal diseases of the brain which are not perceived by the patient (1898). Neuropsychiatr Neuropsychol Behav Neurol 1993;6:1-8.
- 95
- Foster KR, Garrett DC, Ziskin MC. Can the microwave auditory effect be "weaponized"? Front Public Health 2021;9:788613. PMID 35004589
- 96
- Freud S. Über den psychischen Mechanismus hysterische Phänomene: vorläufige Mittelung. In: Studien über Hysterie und anderen Werke aus den Jahren 1892-1899. Frankfurt: S. Fischer Verlage, 1899:81-98 [in German].
- 97
- Frykman GK, Wood VE, Miller EB. The psycho-flexed hand. Clin Orthopaed Rel Res 1983;174:153-7. PMID 6831798
- 98
- Galli S, Tatu L, Bogousslavsky J, Aybek S. Conversion, factitious disorder and malingering: a distinct pattern or a continuum? Front Neurol Neurosci 2018;42:72-80. PMID 29151092
- 99
- Ganser SJ. Ueber einen eigenartigen hysterischen Dämmerzustand. [In German.] Arch Psychiatrie Nervenkrankh 1898;30:633-40.
- 100
- Gbahabo DD, Duma SE. I did not scream. i could not; i was terrified. i just followed them. . .i blocked my mind. then they all raped me: a narrative inquiry on the onset of tonic immobility among women rape victims in Nigeria. PLoS One 2024;19(2):e0278810. PMID 38315681
- 101
- Gelauff J, Stone J, Edwards M, Carson A. The prognosis of functional (psychogenic) motor symptoms: a systematic review. J Neurol Neurosurg Psychiatry 2014;85:220-6. PMID 24029543
- 102
- Ghaffar O, Staines WR, Feinstein A. Unexplained neurologic symptoms: an fMRI study of sensory conversion disorder. Neurology 2006;67:2036-8. PMID 17159115
- 103
- Giambalvo E. Simone Biles said she got the 'twisties." Gymnasts immediately understood. Washington Post. Accessed July 28, 2021. https://www.washingtonpost.com/sports/olympics/2021/07/28/twisties-gymnastics-simone-biles-tokyo-olympics/.
- 104
- Gilman S. Joint position sense and vibration sense: anatomical organisation and assessment. J Neurol Neurosurg Psychiatry 2002;73:473-7. PMID 12397137
- 105
- Goetz CG. Charcot, hysteria, and simulated disorders. Handb Clin Neurol 2016;139:11-23. PMID 27719832
- 106
- Goetz CG, Leurgans S, Raman R, Stebbins GT. Objective changes in motor function during placebo treatment in PD. Neurology 2000;54:710-4. PMID 10680808
- 107
- Goldstein LH, Chalder T, Chigwedere C, et al. Cognitive-behavioral therapy for psychogenic nonepileptic seizures: a pilot RCT. Neurology 2010;74:1986-94. PMID 20548043
- 108
- Gomez-Mayordomo V, Kojović M, López-Valdés E, et al. Functional neurological symptoms as initial presentation of Creutzfeldt-Jakob disease: case series. J Neurol 2023;270(2):1141-6. PMID 36175672
- 109
- Graham JD. Static tremor in anxiety states. J Neurol Neurosurg Psychiatry 1945;8(3-4):57-60. PMID 20984306
- 110
- Grande LA, Loeser JD, Ozuna J, Ashleigh A, Samii A. Complex regional pain syndrome as a stress response. Pain 2004;110:495-8. PMID 15275803
- 111
- Granot R, Berkovic SF, Patterson S, Hopwood M, Mackenzie R. Idiopathic recurrent stupor: a warning. J Neurol Neurosurg Psychiatry 2004;75:368-9. PMID 14966147
- 112
- Harrison NA, Johnston K, Corno F, et al. Psychogenic amnesia: syndromes, outcome, and patterns of retrograde amnesia. Brain 2017;140:2498-510. PMID 29050391
- 113
- Hartmann JA, Wolz WA, Roeltgen DP, Loverso FL. Denial of visual perception. Brain Cogn 1991;16:29-40. PMID 1854468
- 114
- Hauser C. Family in 'Take Care of Maya' documentary is awarded $261 million. New York Times. www.nytimes.com/2023/11/10/us/take-care-of-maya-trial-damages-kowalski.html. Accessed November 10, 2023.
- 115
- Hebert C, Behel JM, Pal G, Kasi R, Kompoliti K. Multidisciplinary inpatient rehabilitation for functional movement disorders: a prospective study with long term follow up. Parkinsonism Relat Disord 2021;82:50-5. PMID 33248393
- 116
- Heilman KM, Watson RT. Conversion hemianesthesia: possible mechanism. J Neuropsychiatry Clin Neurosci 2009;21:99-100. PMID 19359461
- 117
- Heimbach D, Bruhl P. Munchhausen's syndrome in urology. Int Urol Nephrol 1995;27:539-45. PMID 8775036
- 118
- Higgins S, Koutroumanidis M. Psychogenic non-epileptic seizures arising almost exclusively from sleep. Seizure 2022;99:43-7. PMID 35588647
- 119
- Higier H. Hysterie bei einer Katze und einem Kanarienvogel. [In German.] Neurol Centralbl 1898;17:597-9.
- 120
- Hinson VK, Cubo E, Comella CL, Leurgans S, Goetz CG. Rating scale for psychogenic movement disorders: a study of interrater agreement [abstract]. Neurology 2003;60:A212.
- 121
- Hoagland H. Quantitative aspects of tonic immobility in vertebrates. Proc Natl Acad Sci U S A 1927;13(12):838-43. PMID 16587289
- 122
- Hoeritzauer I, Carson AJ, Stone J. 'Cryptogenic Drop Attacks' revisited: evidence of overlap with functional neurological disorder. J Neurol Neurosurg Psychiatry 2018;89:769-76. PMID 29436489
- 123
- Hoover CF. A new sign for the detection of malingering and functional paresis of the lower extremities. J Am Med Assoc 1908;51:746-7.
- 124
- Hubschmid M, Aybek S, Maccaferri GE, et al. Efficacy of brief interdisciplinary psychotherapeutic intervention for motor conversion disorder and nonepileptic attacks. Gen Hosp Psychiatry 2015;37:448-55. PMID 26099544
- 125
- Hull M, Parnes M. Tics and TikTok: functional tics spread through social media. Mov Disord Clin Pract 2021;8:1248-52. PMID 34765689
- 126
- Jacob AE, Kaelin DL, Roach AR, Ziegler CH, LaFaver K. Motor retraining (MoRe) for functional movement disorders: outcomes from a 1-week multidisciplinary program. PM R 2018;10:1164-72. PMID 29783067
- 127
- Jankovic J, Vuong KD, Thomas M. Psychogenic tremor: long-term outcome. CNS Spectr 2006;11:501-8. PMID 16816790
- 128
- Jankovic J. "Psychogenic" versus "functional" movement disorders? That is the question. Mov Disord 2014;29(13):1697-8. PMID 25255973
- 129
- Jones E, Fear NT, Wessely S. Shell shock and mild traumatic brain injury: a historical review. Am J Psychiatry 2007;164:1641-5. PMID 17974926
- 130
- Jordbru AA, Smedstad LM, Klungsøyr O, Martinsen EW. Psychogenic gait disorder: a randomized controlled trial of physical rehabilitation with one-year follow-up. J Rehabil Med 2014;46:181-7. PMID 24248149
- 131
- Kanner AM, Parra J, Frey M, Stebbins G, Pierre-Louis S, Iriarte J. Psychiatric and neurologic predictors of psychogenic pseudoseizure outcome. Neurology 1999;53:933-8. PMID 10496249
- 132
- Kaski D, Bronstein AM, Edwards MJ, Stone J. Cranial functional (psychogenic) movement disorders. Lancet Neurol 2015;14:1196-205.** PMID 26581970
- 133
- Kathol RG, Cox TA, Corbett JJ, Thompson HS. Functional visual loss: follow-up of 42 cases. Arch Ophthalmol 1983;101(5):729-35. PMID 6847460
- 134
- Keane JR. Hysterical hemiparesis accompanying Bell's palsy. Neurology 1993;43:1619. PMID 8351026
- 135
- Keehn JD. Psychopathology in animals. NZ Psychol 1982;11:37-44.
- 136
- Kempert H. Clinical overlap of functional neurologic symptom disorder and complex regional pain syndrome in pediatrics: a case report. J Pediatr Rehabil Med 2021;14:113-120. PMID 33720859
- 137
- Khan I, Fayaz I, Ridgley J, Wennberg R. Factitious clock drawing and constructional apraxia. J Neurol Neurosurg Psychiatry 2000;68:106-7. PMID 10671119
- 138
- Khouzam HR, Field S. Somatization disorder: clinical presentation and treatment in primary care. Hosp Phys 1999;35:20-4.
- 139
- King BH, Ford CV. Pseudologia fantastica. Acta Psychiatr Scand 1988;77:1-6. PMID 3279719
- 140
- Kirkwood B, Mark VW. Consistency of inclusion criteria for functional movement disorder clinical research studies: a systematic review. NeuroRehabilitation 2022;50:169-78. PMID 35213329
- 141
- Knibb JA, Hodges JR. Semantic dementia and primary progressive aphasia: a problem of categorization? Alzheimer Dis Assoc Disord 2005;19 Suppl 1:S7-14. PMID 16317259
- 142
- Koller WC, Biary NM. Volitional control of involuntary movements. Mov Disord 1989;4:153-6. PMID 2733707
- 143
- Kozlowska K, Palmer DM, Brown KJ, et al. Reduction of autonomic regulation in children and adolescents with conversion disorders. Psychosom Med 2015;77(4):356-70. PMID 25954919
- 144
- Kretschmer E. Instinct and hysteria. Br Med J 1937;2:574-8. PMID 20780908
- 145
- Krooks JA, Weatherall AG, Holland PJ. Review of epidemiology, clinical presentation, diagnosis, and treatment of common primary psychiatric causes of cutaneous disease. J Dermatolog Treat 2018;29:418-27. PMID 29052453
- 146
- Kwan P, Lynch S, Davy A. Munchausen's syndrome with concurrent neurological and psychiatric presentations. J R Soc Med 1997;90:83-5. PMID 9068438
- 147
- Labate A, Irani SR, Vincent A, et al. Anti-NMDA receptor encephalitis: a video case report. Epileptic Disord 2009;11:267-9. PMID 19713171
- 148
- LaFrance WC, Baird GL, Barry JJ, et al. Multicenter pilot treatment trial for psychogenic nonepileptic seizures: a randomized clinical trial. JAMA Psychiatry 2014;71:997-1005. PMID 24989152
- 149
- LaFrance WC, Miller IW, Ryan CE, et al. Cognitive behavioral therapy for psychogenic nonepileptic seizures. Epilepsy Behav 2009;14:591-6. PMID 19233313
- 150
- Lang AE. Psychogenic dystonia: a review of 18 cases. Can J Neurol Sci 1995;22:136-43. PMID 7627915
- 151
- Lang AE, Koller WC, Fahn S. Psychogenic parkinsonism. Arch Neurol 1995;52:802-10. PMID 7639632
- 152
- Lanza G, Bella R, Giuffrida S, et al. Preserved transcallosal inhibition to transcranial magnetic stimulation in nondemented elderly patients with leukoaraiosis. Biomed Res Int 2013;2013:351680. PMID 23984349
- 153
- Lauerma H. Nocturnal limb movements in conversion paralysis. J Nerv Ment Dis 1993;181:707-8. PMID 8228956
- 154
- Lawlor M, Huynh B, Humphreys K, Ogunbowale L, Kopelman MD, Plant GT. Observational cohort study of 100 patients presenting with functional visual loss: clinical characteristics and comparison with other functional neurologic disorders. Can J Ophthalmol 2024;59(6):e727-e736. PMID 38580217
- 155
- Lazar RB. Munchausen syndrome presenting as acute spinal cord injury. Arch Phys Med Rehabil 1986;67:568-9. PMID 3741084
- 156
- Lee J, Gresty M. A case of "voluntary nystagmus" and head tremor. J Neurol Neurosurg Psychiatry 1993;56:1321-2. PMID 8270936
- 157
- Lehn A, Mellick G, Boyle R. Psychiatric disorders in idiopathic-isolated focal dystonia. J Neurol 2014;261:668-74. PMID 24449065
- 158
- Lempert T, Dieterich M, Huppert D, Brandt T. Psychogenic disorders in neurology: frequency and clinical spectrum. Acta Neurol Scand 1990;82:335-40. PMID 2281751
- 159
- Lenka A, Jankovic J. Sports-related dystonia. Tremor Other Hyperkinet Mov (N Y) 2021;11:54. PMID 35036047
- 160
- Linden SC, Jones E. German battle casualties: the treatment of functional somatic disorders during World War I. J Hist Med Allied Sci 2013;68:627-58. PMID 22492735
- 161
- MacDonald TM. Myalgic encephalomyelitis by proxy [letter]. BMJ 1989;299:1030.
- 162
- Maggio JB, Ospina JP, Callahan J, Hunt AL, Stephen CD, Perez DL. Outpatient physical therapy for functional neurological disorder: a preliminary feasibility and naturalistic outcome study in a U.S. cohort. J Neuropsychiatry Clin Neurosci 2020;32:85-9. PMID 31564236
- 163
- Malik MF. Ganser states as functional cognitive disorder. Asian J Psychiatr 2023;79:103366. PMID 3647328
- 164
- Maldonado JR, Jasiukaitis P. Selective attention as possible mechanism of symptom production in conversion disorders [abstract]. J Psychosom Res 2003;55:140.
- 165
- Marchant B, Brown J. Munchausen meningitis. J Roy Soc Med 1990;8:532-3. PMID 2231587
- 166
- Mark VW. Functional neurological disorder: extending the diagnosis to other disorders, and proposing an alternate disease term—Attentionally-modifiable disorder. NeuroRehabilitation 2022;50:179-207.** PMID 35253784
- 167
- Mark VW. Biomarkers and rehabilitation for functional neurological disorder. J Pers Med 2024;14(9):948. PMID 39338202
- 168
- Marshall JC. Line bisection and neglect severity. Brain Cogn 1998;38:275-80. PMID 9853103
- 169
- Marshall JC, Halligan PW, Fink GR, Wade DT, Frackowiak R. The functional anatomy of a hysterical paralysis. Cognition 1997;64:B1-8. PMID 9342933
- 170
- Martino D, Hedderly T, Murphy T, et al. The spectrum of functional tic-like behaviours: data from an international registry. Eur J Neurol 2023;30:334-43. PMID 36282623
- 171
- Maurer CW, Liu VD, LaFaver K, et al. Impaired resting vagal tone in patients with functional movement disorders. Parkinsonism Relat Disord 2016;30:18-22. PMID 27334304
- 172
- Marx BP, Forsyth JP, Gallup GG, Fuse T, Lexington JM. Tonic immobility as an evolved pradator defense: implications for sexual assault survivors [review]. Clin Psychol Sci Pract 2008;15:74-90.
- 173
- McAuley JH, Rothwell JC, Marsden CD, Findley LJ. Electrophysiological aids in distinguishing organic from psychogenic tremor. Neurology 1998;50:1882-4. PMID 9633751
- 174
- McCormack R, Moriarty J, Mellers JD, et al. Specialist inpatient treatment for severe motor conversion disorder: a retrospective comparative study. J Neurol Neurosurg Psychiatry 2014;85:895-900. PMID 24124043
- 175
- McDaniel KD, Cummings JL, Shain S. The "yips": a focal dystonia of golfers. Neurology 1989;39:192-5. PMID 2915788
- 176
- McGlynn SM, Schacter DL. Unawareness of deficits in neuropsychological syndromes. J Clin Exp Neuropsychol 1989;11:143-205. PMID 2647781
- 177
- Meadow R. Munchausen syndrome by proxy. The hinterland of child abuse. Lancet 1977;ii:343-5. PMID 69945
- 178
- Meek H. Medical men, women of letters, and treatments for eighteenth-century hysteria. J Med Humanit 2013;34:1-14. PMID 23192402
- 179
- Mele B, Holroyd-Leduc J, Smith EE, Pringsheim T, Ismail Z, Goodarzi Z. Detecting anxiety in individuals with Parkinson disease. A systematic review. Neurology 2018;90:e39-e47. PMID 29212828
- 180
- Miller P, Bramble D, Buxton N. Case study: Ganser syndrome in children and adolescents. J Am Acad Child Adolesc Psychiatry 1997;36:112-5. PMID 9000788
- 181
- Milner AD, Perrett DI, Johnston RS, et al. Perception and action in 'visual form agnosia'. Brain 1991;114:405-28. PMID 2004249
- 182
- Moene FC, Spinhoven P, Hoogduin KA, van Dyck R. A randomized controlled clinical trial of a hypnosis-based treatment for patients with conversion disorder, motor type. Int J Clin Exp Hypn 2003;51:29-50. PMID 12825917
- 183
- Moller A, Söndergaard HP, Helström L. Tonic immobility during sexual assault–-a common reaction predicting post-traumatic stress disorder and severe depression. Acta Obstet Gynecol Scand 2017;96:932-8. PMID 28589545
- 184
- Mountz JM, Parker PE, Liu HG, Bentley TW, Lill DW, Deutsch G. Tc-99m HMPAO brain SPECT scanning in Munchausen syndrome. J Psychiatry Neurosci 1996;21(1):49-52. PMID 8580117
- 185
- Müller-Vahl K, Pisarenko A, Jakubovski E, Fremer C. Stop that! It's not Tourette's but a new type of mass sociogenic illness. Brain 2022;145:476-80. PMID 34424292
- 186
- Ness D. Physical therapy management for conversion disorder: case series. J Neurol Phys Ther 2007;31:30-9. PMID 17419887
- 187
- Nicholson TR, Aybeck S, Kempton MJ, et al. A structural MRI study of motor conversion disorder: evidence of reduction in thalamic volume. J Neurol Neurosurg Psychiatry 2014;85:227-9. PMID 24039028
- 188
- Nielsen G, Buszewicz M, Stevenson F, et al. Randomised feasibility study of physiotherapy for patients with functional movement symptoms. J Neurol Neurosurg Psychiatry 2017;88:484-90. PMID 27694498
- 189
- Nutt JG, Bloem BR, Giladi N, Hallett M, Horak FB, Nieuwboer A. Freezing of gait: moving forward on a mysterious clinical phenomenon. Lancet Neurol 2011;10:734-44. PMID 21777828
- 190
- O’Connell N, Watson G, Grey C, Pastena R, McKeown K, David AS. Outpatient CBT for motor functional neurological disorder and other neuropsychiatric conditions: a retrospective case comparison. J Neuropsychiatry Clin Neurosci 2020;32:58-66. PMID 31466518
- 191
- Okun MS, Koehler PJ. Paul Blocq and (psychogenic) astasia abasia. Mov Disord 2007;22:1373-8. PMID 17516452
- 192
- Olvera C, Stebbins GT, Goetz CG, Kompoliti K. TikTok tics: a pandemic within a pandemic. Mov Disord Clin Pract 2021;8:1200-5. PMID 34765687
- 193
- Ouss L, Tordjman E. Conversive disorders among children and adolescents: towards new "complementarist" paradigms. Neurophysiol Clin 2014;44:411-6. PMID 25306081
- 194
- Oriuwa C, Mollica A, Feinstein A, et al. Neuromodulation for the treatment of functional neurological disorder and somatic symptom disorder: a systematic review. J Neurol Neurosurg Psychiatry 2022;93(3):280-90. PMID 35115389
- 195
- Pakalnis A, Drake ME, Phillips B. Neuropsychiatric aspects of psychogenic status epilepticus. Neurology 1991;41:1104-6. PMID 2067641
- 196
- Pankratz L. Münchhausen versus Munchausen [letter]. Med J Aust 1986;145:301. PMID 3528781
- 197
- Pankratz L, Lezak MD. Cerebral dysfunction in the Munchausen syndrome. Hillside J Clin Psychiatry 1987;9:195-206. PMID 3428878
- 198
- Paredes-Echeverri S, Maggio J, Begue I, Pick S, Nicholson TR, Perez DL. Autonomic, endocrine, and inflammation profiles in functional neurological disorder: a systematic review and meta-analysis. J Neuropsychiatry Clin Neurosci 2022;34:30-43. PMID 34711069
- 199
- Parees I, Kojovic M, Pires C, et al. Physical precipitating factors in functional movement disorders. J Neurol Sci 2014a;338:174-7. PMID 24439198
- 200
- Parees I, Saifee TA, Kassavetis P, et al. Believing is perceiving: mismatch between self-report and actigraphy in psychogenic tremor. Brain 2012;135:117-23. PMID 22075068
- 201
- Parker N. Ganser syndrome [letter]. Aust N Z J Psychiatry 1989;23:308. PMID 2803138
- 202
- Peckham EL, Hallett M. Psychogenic movement disorders. Neurol Clin 2009;27:801-19, vii. PMID 19555832
- 203
- Philbrick KL, Rummans TA, Duffy JR, Kokmen E, Jack CR. Primary progressive aphasia. An uncommon masquerader of psychiatric disorders. Psychosomatics 1994;35:138-41. PMID 8171172
- 204
- Pierpaoli C, Nayak A, Hafiz R, et al. Neuroimaging findings in US government personnel and their family members involved in anomalous health incidents. JAMA 2024;331(13):1122-34. PMID 38497822
- 205
- Pillai JJ, Markind S, Streletz LJ, Field HL, Herbison G. Motor evoked potentials in psychogenic paralysis. Neurology 1992;42:935-6. PMID 1565257
- 206
- Rainville P, Duncan GH, Price DD, Carrier B, Bushnell MC. Pain affect encoded in human anterior cingulate but not somatosensory cortex. Science 1997;277:968-71. PMID 9252330
- 207
- Rapcsak SZ, Croswell SC, Rubens AB. Apraxia in Alzheimer's disease. Neurology 1989;39(5):664-8. PMID 2710357
- 208
- Reuber M, Mitchell AJ, Howlett SJ, Crimlisk HL, Grunewald RA. Functional symptoms in neurology: questions and answers. J Neurol Neurosurg Psychiatry 2005;76:307-14. PMID 15716517
- 209
- Reynolds JR. Paralysis and other disorders of motion and sensation dependent on idea. Br Med J 1869;2:483-5. PMID 20745663
- 210
- Ricciardi L, Nisticò R, Andrenelli E, et al. Exploring three levels of interoception in people with functional motor disorders. Parkinsonism Relat Disord 2021;86:15-8. PMID 33819899
- 211
- Rollinson RD, Gilligan BS. Postanoxic action myoclonus (Lance-Adams syndrome) responding to valproate. Arch Neurol 1979;36:44-5. PMID 369491
- 212
- Rubenstein J. “I’m ready for freedom.” People 2024;101:36-41.
- 213
- Sadan O, Neufeld MY, Parmet Y, Rozenberg A, Kipervasser S. Psychogenic seizures: long-term outcome in patients with and without epilepsy. Acta Neurol Scand 2016;133:145-51. PMID 26177156
- 214
- Sadnicka A, Rosset-Llobet J. A motor control model of task-specific dystonia and its rehabilitation. Prog Brain Res 2019;249:269-83. PMID 31325986
- 215
- Saha K, Cha YH. Mal de debarquement syndrome. Semin Neurol 2020;40:160-4. PMID 31986543
- 216
- Sallin K, Lagercrantz H, Evers K, Engström I, Hjern A, Petrovic P. Resignation syndrome: catatonia? Culture-bound? Front Behav Neurosci 2016;10:7. PMID 26858615
- 217
- Sanger VL, Handy AH. A strange fright-flight behavior pattern (hysteria) in hens. J Am Vet Med Assoc 1962;140:455-9. PMID 14496931
- 218
- Sar V, Akyüz G, Dogan O, Oztürk E. The prevalence of conversion symptoms in women from a general Turkish population. Psychosomatics 2009;50:50-8. PMID 19213973
- 219
- Savard G, Andermann F, Teitelbaum J, Lehmann H. Epileptic Munchausen's syndrome: a form of pseudoseizures distinct from hysteria and malingering. Neurology 1988;38:1628-9. PMID 3419607
- 220
- Schlumpf YR, Reinders AATS, Nijenhuis ERS, Luechinger R, van Osch MJP, Jäncke L. Dissociative part-dependent resting-state activity in dissociative identity disorder: a controlled fMRI perfusion study. PLoS One 2014;9:e98795. PMID 24922512
- 221
- Schrader H, Bohmer T, Aasly J. The incidence of diagnosis of Munchausen syndrome, other factitious disorders, and malingering. Behav Neurol 2019;2019:3891809. PMID 30944662
- 222
- Schrag A, Trimble M, Quinn N, Bhatia K. The syndrome of fixed dystonia: an evaluation of 103 patients. Brain 2004;127:2360-72. PMID 15342362
- 223
- Schwartzman RJ, Kerrigan J. The movement disorder of reflex sympathetic dystrophy. Neurology 1990;40:57-61. PMID 2296383
- 224
- Serranova T, Slovák M, Kemlink D, Šonka K, Hallett M, Růžička E. Prevalence of restless legs syndrome in functional movement disorders: a case-control study from the Czech Republic. BMJ Open 2019;9:e024236. PMID 30670516
- 225
- Shafiq F, Mitsikostas DD, Zis P. Nocebo in motor neuron disease: systematic review and meta-analysis of placebo-controlled clinical trials. Amyotroph Lateral Scler Frontotemporal Degener 2017;18:576-82. PMID 28593798
- 226
- Sharma AA, Szaflarski JP. Neuroinflammation as a pathophysiological factor in the development and maintenance of functional seizures: a hypothesis. Epilepsy Behav Rep 2021;16:100496. PMID 34917920
- 227
- Sheehy MP, Marsden CD. Writer's cramp-a focal dystonia. Brain 1982;105:461-80. PMID 7104663
- 228
- Sherry DD, Wallace CA, Kelley C, Kidder M, Sapp L. Short- and long-term outcomes of children with complex regional pain syndrome type I treated with exercise therapy. Clin J Pain 1999;15:218-23. PMID 10524475
- 229
- Sigal M, Altmark D, Alfici S, Gelkopf M. Ganser syndrome: a review of 15 cases. Compr Psychiatry 1992;33:134-8. PMID 1544298
- 230
- Sigal MD, Altmark D, Carmel I. Munchausen syndrome by adult proxy: a perpetrator abusing two adults. J Nerv Ment Dis 1986;174:696-8. PMID 3772359
- 231
- Simmons BP, Vasile RG. The clenched fist syndrome. J Hand Surg 1980;5:420-7. PMID 7430578
- 232
- Skidmore F, Anderson K, Fram D, Weiner W. Psychogenic camptocormia. Mov Disord 2007;22:1974-5. PMID 17712851
- 233
- Smith TJ, Baker RS. Perimetric findings in functional disorders using automated techniques. Ophthalmology 1987;94:1562-6. PMID 3431827
- 234
- Solyom C, Solyom L. A treatment program for functional paraplegia/Munchausen syndrome. J Behav Ther Exp Psychiatry 1990;21:225-30. PMID 2086607
- 235
- Song IU, Kim JS, Kim HT, Lee KS. Task-specific focal hand dystonia with usage of a spoon. Parkinsonism Relat Disord 2008;14:72-4. PMID 17287140
- 236
- Sonoo M. Abductor sign: a reliable new sign to detect unilateral non-organic paresis of the lower limb. J Neurol Neurosurg Psychiatry 2004;75:121-5. PMID 14707320
- 237
- Spagnolo PA, Norato G, Maurer CW, et al. Effects of TPH2 gene variation and childhood trauma on the clinical and circuit-level phenotype of functional movement disorders. J Neurol Neurosurg Psychiatry 2020;91:814-21. PMID 32576619
- 238
- Spence SA, Crimlisk HL, Cope H, Ron MA, Grasby PM. Discrete neurophysiological correlates in prefrontal cortex during hysterical and feigned disorder of movement. Lancet 2000;355:1243-4. PMID 10770312
- 239
- Srivastava A, Gupta A, Kumar R, Gangadhar BN, Murali T. A rare case of psycho-flexed hand. Acta Neuropsychiatr 2008;20:157-8.
- 240
- Stamelou M, Cossu G, Edwards MJ, et al. Familial psychogenic movement disorders. Mov Disord 2013;28:1295-7. PMID 23568243
- 241
- Stathis P, Smpiliris M, Konitsiotis S, Mitsikostas DD. Nocebo as a potential confounding factor in clinical trials for Parkinson's disease treatment: a meta-analysis. Eur J Neurol 2013;20:527-33. PMID 23145482
- 242
- Stephen CD, Fung V, Perez DL, Espay AJ. Comparison of inpatient and emergency department costs to research funding for functional neurologic disorder: an economic analysis. Neurology 2025;104(6):e213445. PMID 39999398
- 243
- Steriopoulos V, Fine J, Lang A, Feinstein A. Psychiatric outcome in patients with a psychogenic movement disorder [abstract]. Neurology 2000;54:A419.
- 244
- Stirling J Jr; American Academy of Pediatrics Committee on Child Abuse and Neglect. Beyond Munchausen syndrome by proxy: identification and treatment of child abuse in a medical setting. Pediatrics 2007;119:1026-30. PMID 17473106
- 245
- Stokes YH, Jahangiri M, Ochoa JG. A case of Ganser syndrome presenting as a stroke alert: fact or factitious? Cureus 2024;16(10):e71736. PMID 39553138
- 246
- Stone J. Functional neurological disorders: the neurological assessment as treatment. Neurophysiol Clin 2014;44:363-73. PMID 25306077
- 247
- Stone J. Lessons from a neurologist after 25 years of functional neurological disorder subspeciality practice [review]. Neurol Clin 2023;41:569-82.** PMID 37775191
- 248
- Stone J. Incongruence in FND: time for retirement. Pract Neurol 2024;24:163-5. PMID 38212112
- 249
- Stone J, Carson A, Sharpe M. Functional symptoms and signs in neurology: assessment and diagnosis. J Neurol Neurosurg Psychiatry 2005;76:i2-12. PMID 15718217
- 250
- Stone J, LaFrance WC Jr, Brown R, Spiegel D, Levenson JL, Sharpe M. Conversion disorder: current problems and potential solutions for DSM-5. J Psychosom Res 2011;71:369-376. PMID 22118377
- 251
- Stone J, Sharpe M, Carson A, et al. Are functional motor and sensory symptoms really more frequent on the left. A systematic review. J Neurol Neurosurg Psychiatry 2002a;73:578-81. PMID 12397155
- 252
- Stone J, Smyth R, Carson A, Warlow C, Sharpe M. La belle indifference in conversion symptoms and hysteria: systematic review. Br J Psychiatry 2006;188:204-9. PMID 16507959
- 253
- Stone J, Warlow C, Deary I, Sharpe M. Predisposing risk factors for functional limb weakness: a case-control study. J Neuropsychiatry Clin Neurosci 2020;32:50-7. PMID 31466514
- 254
- Stone J, Warlow C, Sharpe M. The symptom of functional weakness: a controlled study of 107 patients. Brain 2010;133:1537-51. PMID 20395262
- 255
- Stone J, Wojcik W, Durrance D, et al. What should we say to patients with symptoms unexplained by disease? The "number needed to offend". BMJ 2002b;325:1449-50. PMID 12493661
- 256
- Stone J, Zeman A, Sharpe M. Functional weakness and sensory disturbance. J Neurol Neurosurg Psychiatry 2002c;73:241-5. PMID 12185152
- 257
- Strasburger H, Waldvogel B. Sight and blindness in the same person: gating in the visual system. Psych J 2015;4:178-85. PMID 26468893
- 258
- Strobel M, Chevallier J, de la Vareille B, Lacave J, Real JL. Encéphalopathie métabolique à rechutes, autolavages gastriques et syndrome de Munchausen. [Article in French]. Rev Méd Intern 1994;15:663-5. PMID 7800986
- 259
- Suarez SD, Gallup GG. Tonic immobility as a response to rape in humans: a theoretical note. Psychol Rec 1979;29:315-20.
- 260
- Swanson RL, Hampton S, Green-McKenzie J, et al. Neurological manifestations among US government personnel reporting directional audible and sensory phenomena in Havana, Cuba. JAMA 2018;31:1125-31. PMID 29450484
- 261
- Taib S, Ory-Magne F, Brefel-Courbon C, et al. Repetitive transcranial magnetic stimulation for functional tremor: a randomized, double-blind, controlled study. Mov Disord 2019;34:1210-9. PMID 31180620
- 262
- Tannemaat MR, van Niekerk J, Reijntjes RH, Thijs RD, Sutton R, van Dijk JG. The semiology of tilt-induced psychogenic pseudosyncope. Neurology 2013;81:752-8. PMID 23873974
- 263
- Teixeira M, Santos P, Bastos Furtado A, Delgado Alves J. When a histologic diagnosis becomes factitious: a case of Munchausen syndrome. Cureus 2022;14:e28876. PMID 36225520
- 264
- Tellioglu T, Oates JA, Biaggioni I. Munchausen's syndrome presenting as baroreflex failure [letter]. N Engl J Med 2000;343:581. PMID 10979787
- 265
- Teodoro T, Edwards MJ, Isaacs JD. A unifying theory for cognitive abnormalities in functional neurological disorders, fibromyalgia and chronic fatigue syndrome: systematic review. J Neurol Neurosurg Psychiatry 2018;89:1308-19. PMID 29735513
- 266
- Thaut MH, McIntosh GC, Rice RR, Miller RA, Rathbun J, Brault JM. Rhythmic auditory stimulation in gait training for Parkinson's disease patients. Mov Disord 1996;11:193-200. PMID 8684391
- 267
- Thompson PD, Colebatch JG, Brown P, et al. Voluntary stimulus-sensitive jerks and jumps mimicking myoclonus or pathological startle syndromes. Mov Disord 1992;7:257-62. PMID 23571302
- 268
- Tinazzi M, Geroin C, Marcuzzo E, et al. Functional motor phenotypes: to lump or to split? J Neurol 2021a;268(12):4737-43. PMID 33961091
- 269
- Tinazzi M, Marotta A, Zenorini M, Riello M, Antonini A, Fiorio M. Movement perception of the tonic vibration reflex is abnormal in functional limb weakness. Parkinsonism Relat Disord 2021b;87:1-6. PMID 33895678
- 270
- Tonogai I, Sairyo K. Psychogenic equinovarus caused by dislocation of the Chopart joint complex. Case Rep Orthop 2018;2018:2736917. PMID 29854518
- 271
- Tyrer PJ, Lader MH. Tremor in acute and chronic anxiety. Arch Gen Psychiatry 1974;31(4):506-9. PMID 4423027
- 272
- van der Feltz-Cornelis C, Brabyn S, Ratcliff J, et al. Assessment of cytokines, microRNA and patient related outcome measures in conversion disorder/functional neurological disorder (CD/FND): the CANDO clinical feasibility study. Brain Behav Immun-Health 2021;13:100228. PMID 34589743
- 273
- van der Hoeven RM, Broersma M, Pijnenborg GH, et al. Functional (psychogenic) movement disorders associated with normal scores in psychological questionnaires: a case control study. J Psychosom Res 2015;79:190-4. PMID 26113484
- 274
- van der Kruijs SJ, Bodde NM, Vaessen MJ, et al. Functional connectivity of dissociation in patients with psychogenic non-epileptic seizures. J Neurol Neurosurg Psychiatry 2012;83:239-47. PMID 22056967
- 275
- van Merode T, Twellaar M, Kotsopoulos IA, et al. Psychological characteristics of patients with newly developed psychogenic seizures. J Neurol Neurosurg Psychiatry 2004;75:1175-7. PMID 15258225
- 276
- Vassilopoulos A, Mohammad S, Dure L, Kozlowska K, Fobian AD. Treatment approaches for functional neurological disorders in children. Curr Treat Options Neurol 2022;24:77-97. PMID 35370394
- 277
- Verdugo RJ, Ochoa JL. Abnormal movements in complex regional pain syndrome: assessment of their nature. Muscle Nerve 2000;23:198-205. PMID 10639611
- 278
- Voon V, Brezing C, Gallea C, et al. Emotional stimuli and motor conversion disorder. Brain 2010;133:1526-36. PMID 20371508
- 279
- Vuilleumier P, Chicherio C, Assal F, Schwartz S, Slosman D, Landis T. Functional neuroanatomical correlates of hysterical sensorimotor loss. Brain 2001;124:1077-90. PMID 11353724
- 280
- Waddell KJ, Lang CE. Comparison of self-report vs. sensor-based methods for measuring the amount of upper limb activity outside the clinic. Arch Phys Med Rehabil 2018;99:1913-6. PMID 29408483
- 281
- Waldvogel B, Ullrich A, Strasburger H. Sighted and blind in one person: a case report and conclusions on the psychoneurobiology of vision. Nervenarzt 2007;78:1303-9. PMID 17611729
- 282
- Walker FO, Alessi AG, Digre KB, McLean WT. Psychogenic respiratory distress. Arch Neurol 1989;46:196-200. PMID 2916958
- 283
- Walusinski O. A case of Charcotian grande hystérie: observation by Julien Offray de La Mettrie in 1738. Eur Neurol 2012;67:98-106. PMID 22236737
- 284
- Wani A, Trevino K, Marnell P, Husain MM. Advances in brain stimulation for depression. Ann Clin Psychiatry 2013;25:217-24. PMID 23926577
- 285
- Wendt L, Albring A, Benson S, et al. Catechol-O-methyltransferase Val158Met polymorphism is associated with somatosensory amplification and nocebo responses. PLoS One 2014;9:e107665. PMID 25222607
- 286
- Werring DJ, Weston L, Bullmore ET, Plant GT, Ron MA. The neural mechanisms of visual conversion disorder: a functional magnetic resonance imaging study [abstract]. J Neurol Neurosurg Psychiatry 2001;71:139-40.
- 287
- Williams DT, Ford B, Fahn S. Phenomenology and psychopathology related to psychogenic movement disorders. Adv Neurol 1995;65:231-57. PMID 7872143
- 288
- Williams DT, Ford B, Fahn S. Treatment issues in psychogenic-neuropsychiatric movement disorders. Adv Neurol 2005;96:350-63. PMID 16383231
- 289
- Wissel BD, Dwivedi AK, Merola A, et al. Functional neurological disorders in Parkinson disease. J Neurol Neurosurg Psychiatry 2018;89:566-71. PMID 29549192
- 290
- Witek N, Stebbins GT, Goetz CG. What influences placebo and nocebo responses in Parkinson's disease? Mov Disord 2018;33:1204-12. PMID 30132980
- 291
- Yates G, Bass C. The perpetrators of medical child abuse (Munchausen Syndrome by Proxy): a systematic review of 796 cases. Child Abuse Negl 2017;72:45-53. PMID 28750264
- 292
- Yugué I, Shiba K, Ueta T, Iwamoto Y. A new clinical evaluation for hysterical paralysis. Spine 2004;29:1910-3. PMID 15534415
- 293
- Zhang JM, An J. Cytokines, inflammation and pain. Int Anesthesiol Clin 2007;45:27-37. PMID 17426506
- 294
- Zhang LY, Cao B, Zou YT, et al. Depression and anxiety in multiple system atrophy. Acta Neurol Scand 2018;137:33-7. PMID 28748633
- 295
- Ziegler JS, von Stauffenberg M, Vlaho S, Bohles H, Kieslich M. Dystonia with secondary contractures: a psychogenic movement disorder mimicking its neurological counterpart. J Child Neurol 2008;23:1316-8. PMID 18984843
- 296
- Zimmer C. Beyond the ivory tower. A distant mirror for the brain. Science 2004;303:43-4. PMID 14704413
- 297
- Ziv I, Djaldetti R, Zoldan Y, Avraham M, Melamed E. Diagnosis of "non-organic" limb paresis by a novel objective motor assessment: the quantitative Hoover's test. J Neurol 1998;245:797-802. PMID 9840352
Contributors
All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.
Author
-
Victor W Mark MD
Dr. Mark of the University of Alabama at Birmingham has no relevant financial relationships to disclose.
See Profile
Patient Profile
- Age range of presentation
-
- 4 to 73 years
ICD & OMIM codes
- ICD-10
-
- Conversion disorder: F44.4
- Extrapyramidal and movement disorder, unspecified: G25.9
- Malingering: F68.1
- ICD-11
-
- Functional neurological disorder and, or conversion disorder, are re-termed Dissociative Neurological Symptom Disorder in ICD-11: 6B60
- Factitious disorder imposed on self: 6D50
- Factitious disorder imposed on another: 6D51
- Malingering: QC30
This is an article preview.
Start a Free Account
to access the full version.
-
Nearly 3,000 illustrations, including video clips of neurologic disorders.
-
Every article is reviewed by our esteemed Editorial Board for accuracy and currency.
-
Full spectrum of neurology in 1,200 comprehensive articles.
-
Listen to MedLink on the go with Audio versions of each article.
Questions or Comment?
MedLink, LLC
3525 Del Mar Heights Rd, Ste 304
San Diego, CA 92130-2122
Toll Free (U.S. + Canada): 800-452-2400
US Number: +1-619-640-4660
Support: service@medlink.com
Editor: editor@medlink.com
ISSN: 2831-9125
Also in This Category
-
-
Neurogenetic Disorders
GM2 gangliosidoses
Apr. 30, 2026
-
General Child Neurology
Developmental delay in children: evaluation and management
Apr. 29, 2026
-
Neuropharmacology & Neurotherapeutics
Levacetylleucine
Apr. 23, 2026
-
Infectious Disorders
Whipple disease
Apr. 08, 2026
-
Neurogenetic Disorders
Mucopolysaccharidoses
Apr. 01, 2026
-
Stroke & Vascular Disorders
Primary CNS angiitis
Mar. 10, 2026
-
Neuro-Ophthalmology & Neuro-Otology
Cortical blindness
Mar. 02, 2026