GRAPHICAL ABSTRACT

INTRODUCTION

Functional movement disorder (FMD) is a subtype of functional neurological disorder (FND) characterized by involuntary, unwanted movements. FMD is common and has been referred to by many names throughout the history of medicine. Descriptions of patients with this disorder are present not only in medical literature but also in other nonclinical forms, such as art, lithography, paintings, and sculptures. While functional disorders have been most commonly referred to as psychogenic or conversion disorder in the past few decades, they have historically been termed “hysteria.” [1,2] Descriptions of “hysteria” date back to as early as the late 19th century, when Paul Richer, a medical artist and colleague of Charcot, produced an illustration of back arching that has been thought to have been a FMD. The term hysteria was ultimately renamed conversion disorder (included in the DSM-V), and later on, psychogenic or FND. In recent years, the term functional movement disorder has been used more often and argued for [3]. Examples of artwork thought to illustrate FMD are shown in Figure 1.

While FMD is commonly identified in the field of neurology, this disorder continues to have a major impact on patients’ lives, as quality of life has been shown to be greatly affected [4]. It is also not uncommon for both the clinician and patient to struggle to understand or deal with this disorder effectively. Patients may also feel that they have not received a clear diagnosis and go from doctor to doctor. Physicians, on the other hand, may not feel certain about the diagnosis themselves or even when certain about the diagnosis, find patients with FMD difficult to treat, as they often require more time. Furthermore, even when patients receive a clear diagnosis from an experienced physician, treatment and recovery can remain challenging.

Much progress has been made in research on FMD, and recent work in the past 20 years has improved the understanding and management of this disorder. This review aims to provide a practical overview of this disorder and discuss new findings relevant to the pathophysiology of FMD, as well as treatment protocols found to be effective.

EPIDEMIOLOGY

There are several factors that pose a challenge in studying the epidemiology of FMD. Varying terminology and definition of FMD are major complicating factors in determining the incidence and prevalence of this disorder. Another limitation is that the majority of reports are prevalence figures from studies based on data from neurology clinic settings. Studies have reported that FMD accounts for approximately 3% to 8% of movement disorder clinic visits [5,6]. However, these numbers may not accurately reflect the entire picture, as FMD can also coexist with organic neurological disorders [7]. Other unique factors that can have an impact on public health can also play a role. For example, a recent cross-sectional study found an increased incidence of FMD in both children and adults during the relatively recent COVID-19 pandemic, highlighting the role of psychological and environmental stressors in the development of this disorder [8]. Functional symptoms occurring after war, mass vaccination or toxic exposure have also been reported [9-13]. While symptoms can involve various systems, neurological symptoms such as headache, dizziness, weakness, tremor, myoclonus and paresthesia have been reported. These reports suggest that functional neurological symptoms can occur at a societal level and highlight the role of culture in their occurrence.

The mean age at onset of FMD has been reported to range from 46 years to 53 years, with a female preponderance [5,14,15]. A retrospective analysis of 199 patients seen from movement disorders centers at academic referral sites revealed that the prevalence of FMD was 2 to 3 times higher in women than in men [15]. A recent meta-analysis of 4,905 patients revealed that FMD peaks in midlife for all phenotypes, but those with functional dystonia and weakness are younger, whereas those with gait disorders are older [16]. Several risk factors for FMD have been reported, including childhood trauma or psychiatric symptoms/illnesses such as anxiety, depression, and somatization [17,18]. However, the presence of such psychiatric factors is not required for the diagnosis of FMD [18]. Figure 2 illustrates the biopsychosocial model of FMD.

While most of the literature on FMD pertains to the adult population, there are some data on FMD in the pediatric population. Although children and adults share common features, the prevalence of childhood FMD has been reported to be lower than that of adult FMD, ranging from 2.8% to 23.1%, with a female preponderance in most studies [19]. Predisposing factors include genetic predisposition, childhood abuse, and perfectionist personality trait [20]. Psychiatric illnesses may coexist, with reports of approximately 10% of pediatric patients with FMD. Based on past reports, pediatric patients who have concurrent psychiatric comorbidities appear to have predominantly anxiety and/or attention deficit hyperactivity disorder [20].

PHENOMENOLOGY AND DIAGNOSTIC APPROACH

FMDs span a wide range of phenomena. Some common examples are functional tremor, myoclonus, dystonia, and gait disorders. Other uncommon presentations include but are not limited to parkinsonism, facial movements (e.g., blepharospasm and dystonia), and chorea [21-24]. Functional tremor has been reported to be the most common, ranging from 43%–61% of FMD patients [5,25]. FMD can also present as single or mixed phenomena, and the clinical picture can be further complicated when there is concomitant functional and organic movement disorder, often termed “functional overlay.” [26] A recent study revealed that mixed FMD is the most common phenotype following tremor [16].

History-taking when encountering a patient raising concern for FMD should be performed in a careful and detailed manner, as various details can be obtained by questioning the patient’s experience of their symptoms, which can be helpful [2]. For example, probing for the time course of the disorder and change in the nature of symptoms over time is important, as patients with FMD may often note a sudden onset of symptoms that follow a stressful incident (e.g., a car accident) that can serve as a trigger, incongruent with an organic neurological disorder. Inquiring about concurrent or past stress, anxiety, and depression is important, as patients may have ongoing stressors in their lives or have had early-life trauma.

Establishing a positive diagnosis, rather than diagnosing FMD on the basis of a diagnosis of exclusion, has been emphasized in the past decade. Therefore, it is important to look for characteristics that are commonly found in patients with FMD, which are examples of inconsistency or incongruity, the two diagnostic pillars of the disorder. Examples of inconsistency include variability, distractibility, suggestibility and selectivity [27,28]. Variability is noted, for example, when tremor appears to be present at different frequencies. Distractibility can be seen when a patient is distracted by performing various mental tasks (e.g., having the patient serially subtract 7 from 100) and the symptoms abate (e.g., tremor becomes less or absent). Suggestibility can be noted when the examiner engages in conversation with the patient about the symptom, which can either bring out the symptom or cause a noticeable change in the tremor (e.g., tremor becomes worse). A good example of selectivity is when the patient is found to have symptoms in a certain situation, such as during the exam, but is asymptomatic at other times during the clinical encounter.

Entrainability is a feature of FMD that is incongruent with tremor typically seen in an organic neurological disorder, such as Parkinson’s disease. Entrainability can be tested for by having the patient with bilateral hand tremor tap along with the examiner using one of the affected limbs. When the opposite limb that is not participating in the tapping task is found to have altered tremor frequency or adopts the tremor frequency of the tapping limb, entrainability is established [29]. Features of incongruity are also noted in a variety of functional gait disorders, such as excessive slowness, astasia-abasia, knee buckling, tightrope walking, and truncal jerking [30]. Table 1 provides a summary of clinical features of FMD.

Other signs that are examples of incongruence with organic neurologic disorder but can be seen in patients with FMD include the psychogenic toe sign, Hoover’s sign, whack-a-mole sign, and swivel chair sign. The psychogenic toe sign is seen in psychogenic toe dystonia when fixed posturing and resistance to manipulation are noted [31]. Hoover’s sign is a well-known sign of functional weakness that is found when weakness in hip extension returns to normal with contralateral hip flexion against resistance [32,33]. This sign is highly specific and moderately sensitive for the diagnosis of functional disorder in patients with unilateral limb weakness [34]. The whack-a-mole sign can be found in hyperkinetic FMD when the examiner suppresses a moving body part, only to have movement in another body part occur [35]. The swivel chair test is considered positive when a patient with functional gait difficulty can propel a chair while seated normally [36]. However, while these signs have been found to have high specificity, sensitivity is often low to moderate, so the examiner must be cautious in the application and interpretation of these clinical signs [34,37,38].

Examples of FMDs that can be particularly challenging to diagnose include functional parkinsonism, dystonia, and gait disorders. Functional parkinsonism is one of the least commonly reported subtypes of FMD but is often quite disabling [39]. Features include abrupt onset, early involvement of bilateral shaking and slowness and the absence of true bradykinesia (lack of progressive decrement on repetitive manual tasks) [40]. Dopamine transporter (DAT) imaging is often required to reach diagnostic certainty. Patients with functional parkinsonism have also been noted to develop idiopathic Parkinson’s disease later in life, further complicating matters [41]. Differentiating functional dystonia from organic dystonia is another tricky issue. Functional dystonia may be suspected when sustained fixed posturing is noted for several days, sometimes after a minor precipitating event. Other clinical hints of functional dystonia include presence of paroxysmal tremor, precipitation of attacks or an increase in symptom severity during examination, atypical and variable duration of attacks, and additional physical signs or medically unexplained symptoms suggestive of functional etiology [42]. Finally, functional gait disorders are commonly seen in clinic, but diagnosis can be challenging, as there is not a single walking pattern that leads to the diagnosis. Furthermore, patients with an organic neurological disorder such as dystonia or chorea can also fall into the incongruity category, which can lead the clinician to an erroneous diagnosis. It is also possible for patients to have concurrent functional and organic gait disorders. Therefore, various testing maneuvers, such as having the patient perform dual tasks while walking, walking in a straight line, and performing the Romberg test and pull test, can be helpful for assessing variability, distractibility, suggestibility, and incongruity, which would point toward a functional etiology [43].

While there are several scales for FND, there are many limitations, unlike those developed for organic neurological disorders (e.g., the Unified Parkinson’s Disease Rating Scale [UPDRS]). The scales developed to date may or may not have the capacity to assess all symptom types in FMD. While the initial scale developed for assessing FMD captures a variety of symptom types, there is lack of ease of use as a result [44]. For this reason, clinicians may prefer to use the Simplified Version of the Psychogenic Movement Disorders Rating Scale (S-FMDRS) [45].

While testing is not mandatory for the diagnosis of FMD, the decision regarding whether to pursue standard neurological investigations such as imaging or electrophysiology depends on various factors, such as the physician’s familiarity level affected by the length of fellowship training, healthcare costs, and medical liability claims [46]. Since the diagnosis of FMD should ideally be made on a positive basis rather than via a rule-out approach, the examination is of utmost importance, focusing on relevant features mentioned above. However, caution must be exercised, and appropriate testing methods should be utilized when necessary, as it is not uncommon for patients to have concurrent organic neurological disorders with superimposed functional symptoms.

Physicians may also misdiagnose organic neurological disorders presenting in an atypical or “bizarre” fashion as FMD. Some examples are early-onset or advanced Parkinson’s disease, dystonia, tics/Tourette’s syndrome, stiff-person syndrome, Huntington’s disease, neuroacanthocytosis, and Wilson’s disease [47-53]. For example, symptoms that occur in advanced Parkinson’s disease, such as diphasic dyskinesia, or sensory trick (improvement of symptoms when applying sensory stimuli to the affected area), and task-specificity (symptoms occurring when performing a specific task such as writing or playing a musical instrument) in dystonia can be mistaken for functional symptoms [54,55]. For this reason, some physicians are likely hesitant to diagnose FMD immediately, despite having a strong suspicion for a non-organic neurological disorder.

Phenomenologically, pediatric patients with FMD can also present with functional tremor, dystonia, myoclonus, gait dysfunction, and tics [20]. The most common types of FMD have been reported to be tremor, dystonia, and myoclonus [19]. Some common features in childhood FMD include the dominant side being more affected, functional dystonia presenting in a paroxysmal, and not fixed, pattern, and easily demonstrable features of FMD, including variability, distractibility, entrainability, and suggestibility.

NEUROPHYSIOLOGIC ASSESSMENT

Many studies have investigated the underlying neurophysiology of FMD, using a variety of techniques, such as electrophysiology, clinical neurophysiology (e.g., electromyography-electroencephalogram [EMG-EEG] and jerk-locked back-averaging), functional magnetic resonance imaging (fMRI), positron emission tomography (PET), and transcranial magnetic stimulation (TMS). Electrophysiology is particularly useful in studying functional tremor, as this method can help to differentiate functional tremor from organic tremor using surface EMG or accelerometry [56]. These methods can also help to assess for tremor frequency, variability, distractibility, and entrainability, as well as the pattern and duration of EMG bursts. Spectral and coherence analyses of tremor can also be performed via specialized software. Performing the ballistic movement test is also useful, as there is an abrupt transient pause of functional tremor when the individual is asked to perform a quick movement of another body part [57]. Effect with mass loading may also be helpful, as it has been reported that there is an increase in the tremor amplitude and frequency in 70% of patients with functional tremor [58,59].

For patients with functional myoclonus, performing jerk-locked back-averaging using EMG-EEG can reveal the presence of the Bereitschaftspotential [60,61]. This is a negative, slow-rising cortical potential that occurs before self-paced, voluntary movements. The presence of a Bereitschaftspotential suggests that the movement itself uses the mechanism of voluntary movement, despite the lacking sense of voluntariness in FMD [62]. Another way to evaluate myoclonus is to analyze reflex myoclonus; a long latency is indicative of functional myoclonus, whereas the latency of reflex myoclonus is short [63]. Finally, myoclonus can be analyzed by looking at the EMG underlying the movement and antagonist muscle as well. In functional myoclonus, the EMG burst length is longer, and there is variable antagonist muscle activity [64].

While functional tremor and myoclonus have been more readily studied using the techniques discussed above, functional dystonia is more challenging to study for several reasons. First, the diagnosis of functional dystonia may not be clear, as the clinical picture can be convincing for organic dystonia [62]. Second, physiologic abnormalities have been identified in both organic and functional dystonia, leading to difficulty in differentiating the two disorders. Third, individuals who are predisposed to developing organic dystonia may also develop functional dystonia. Nevertheless, some studies using paired associative stimulation (PAS) have shown that plasticity is abnormal in organic dystonia, whereas individuals with functional dystonia are found to have normal results [65]. TMS research has also been actively conducted in patients with dystonia to study measures of plasticity, with conflicting results [66]. Temporal discrimination has been found to be abnormal in both organic and functional dystonia [67]. Comparing the R2 blink reflex in patients with atypical blepharospasm may help in the diagnosis of functional blepharospasm [68].

UPDATES IN NEUROIMAGING RESEARCH

Neuroimaging research on FND has grown in the past 20 years, and studies have included or exclusively looked at patients with FMD. However, most studies have focused on a larger group, i.e., patients with various types of FND. Different modalities have been utilized, including task neuroimaging, resting-state functional connectivity and quantitative structural imaging [69]. Recent fMRI studies have shown that there is decreased functional connectivity between the right temporoparietal junction (TPJ) and bilateral sensorimotor regions and impaired hemodynamic responsiveness of the dorsolateral prefrontal cortex and presupplementary cortex to changes in the loss of movement control in patients with FMD [70,71]. Dysfunction of these areas, which play a role in self-agency, is thought to contribute to patients’ subjective sense of involuntariness in abnormal movements. While findings were found to be independent of depression, anxiety and childhood sexual abuse, group differences in correlation between right TPJ functional connectivity and childhood emotional abuse were found [70].

In a cross-sectional fMRI study of patients with functional tremor and essential tremor, increased activation in the right cerebellum during a motor task and increased activation in the paracingulate and left Heschl’s gyrus during a basic-emotion task were found [72]. This study was repeated in patients with functional and organic dystonia, revealing no differences between groups in motor task activation but decreased activation in the right middle temporal gyrus and bilateral precuneus and increased activation in the right inferior frontal gyrus, bilateral occipital cortex, fusiform gyrus and bilateral cerebellum in patients with functional dystonia [73]. In the intense-emotion task, patients with functional dystonia were found to have decreased activation in the left insular and left motor cortices and increased activation in the left fusiform gyrus. In summary, patients with functional dystonia were found to have stimulus-dependent altered activation in networks involved in attentional control, spatial cognition and motor preparation/execution.

More recent studies have continued to examine the neurobiological importance of early-life maltreatment (ELM) in the development of FND or FMD. A study investigating neuroimaging endophenotypes linked to ELM subtypes in patients with FND found that individual differences in reported early-life physical abuse severity correlated with motor-limbic/paralimbic connectivity strength [74]. Another study analyzed resting-state functional connectivity data from 38 patients with FMD, and tryptophan hydroxylase 2 (TPH2) gene polymorphism carriers were found to have earlier FMD age of onset and decreased connectivity between the right amygdala and middle frontal gyrus [75]. These findings highlight the effects of early-life physical or sexual abuse in the development of FMD, as well as gene‒environment interactions that may be relevant.

Studies conducted on FMD thus far support the relationship between emotional processing and this disorder on the basis of altered activation of brain regions relevant to emotional processing and increased functional connectivity between these areas and movement-related brain regions. As more recent studies have shown, there may be individual genetic or epigenetic differences predisposing certain individuals to develop FMD throughout their lifetime. More work is necessary to be able to apply these findings clinically in terms of delivering more effective treatments or predicting treatment outcomes.

SHARING THE DIAGNOSIS

There have been varying opinions on how to share the diagnosis of FMD with the affected individual. Certainly, there is not a “one-size-fits-all” approach that is always applicable, due to differences in the severity of symptoms, patients’ illness beliefs, psychosocial factors, etc. Stigma, or possible shame of experiencing symptoms with no supporting findings on conducted tests, may also add to patients’ reluctance to accept the diagnosis of FMD. Furthermore, clinicians themselves may also feel uncomfortable or at times frustrated that there is no neurological test on which one can base the diagnosis of FMD to persuade the patient, which can lead to difficulty in sharing the diagnosis. As a result, it is not uncommon for clinicians to prefer to keep the diagnosis from the patient or avoid discussion of the diagnosis itself. They may tell the patient that the tests conducted thus far have not been revealing, and that there is no concrete neurological “diagnosis” that fits. This may confuse the patient further and delay them from receiving a clear diagnosis of FMD, which may lead to poor prognosis. Ultimately, if the patient is lucky, further down the line, he or she may meet a clinician who is more straightforward, providing the patient with a direct explanation of FMD. A further complicating issue is when the clinician is not entirely certain whether the patient may also have a concurrent organic neurological disorder.

Several aspects should be considered when the diagnosis is shared with the patient. A study using a 22-item questionnaire probing diagnostic and management issues in FMD found that acceptance of the diagnosis by the patient, as well as the management of psychological stressors and concurrent psychiatric disorders, were the most important factors for predicting a favorable prognosis [46]. Therefore, the clinician should aim to achieve a strong rapport that provides a solid basis for the patient’s acceptance of the diagnosis. As trust in the patient‒doctor relationship is usually built over time, this may not always be immediately achievable; however, patients can generally determine whether or not the physician has a favorable and respectful attitude. When the patient receives the impression that this is not the case, trust between the patient and doctor is difficult to attain. Other dimensions of physician behavior patients have been found to base their trust on include competence, compassion, confidentiality, reliability and communication [76].

It has also been shown that sharing the physical signs found on the clinical examination can be helpful in accepting the diagnosis [32,77]. In addition, explaining that the symptoms are potentially common and reversible, as well as describing the issue as a software problem rather than a hardware problem, while being clear by giving the diagnosis using one of the available terms, have been emphasized. General principles to keep in mind when encountering a patient with FMD and delivering the diagnosis are listed in Table 2.

Factors that play a role in patients’ acceptance of the diagnosis also include health/illness beliefs and expectations. Examples of illness beliefs are how the patient perceives his or her symptoms and their interpretation of them. A patient, for example, may note limb weakness and interpret that as having a stroke. Beliefs about what a stroke is can lead to further thoughts, such as how symptoms affect life and what to do in order to get better [51]. It has also been shown that helping patients achieve a more accurate understanding of their illness, as well as directing them to sources of self-help, has beneficial results.

TREATMENT

While the treatment of FMD may need to be tailored to each patient, many studies have shown that physical therapy plays an important role in patient recovery [78-80]. Physical therapy is particularly helpful for patients who are experiencing involuntary movements occurring to the point that activities of daily living or gait are affected. Physical therapy can be broken down into four elements, which include first, educating the patient; second, showing the patient that normal movement can occur; third, retraining patients to move their affected body part with diverted attention; and finally, changing maladaptive behaviors related to their symptoms [78].

Physical therapy has also been found to be beneficial either on an outpatient or inpatient basis in patients with FMD. While physical therapy in the majority of these studies has been conducted as an outpatient, patients have been found to improve when physical therapy has been performed on a subacute basis (2–3 months or longer). Ideally, an inpatient program using a multidisciplinary approach may confer the most benefit, even when performed for a short duration (e.g., five days). Treatment methods vary across studies, with several core principles found to include the following: behavior shaping, avoiding reinforcement of maladaptive movements such as using a wheelchair, goal-focused rehabilitation, graded progression of task or exercise difficulty, the use of quantitative outcome measures to gauge improvement, and involving family members, etc [81]. Table 3 outlines treatment studies published in the past two decades.

While there may be underlying and concurrent psychological factors or disorders present, such as depression or anxiety, in patients with FMD, it has been reported that approximately 24% of patients do not appear to have such psychiatric factors [82]. Therefore, the absence of a psychiatric disorder or stressors during life should not lead the clinician to exclude the possibility of FMD. However, a formal neuropsychiatric evaluation has been suggested to inform diagnosis and help develop a patient-centered treatment plan in patients with FMD [47].

It has been shown that the initial clinical encounter itself, when the clinician is obtaining the history of present illness, has an impact on patients’ future acceptance of the diagnosis [46,83]. Furthermore, providing the patient with a clear and comprehensible explanation is important for acceptance of the diagnosis, which is the basis for successful treatment. The patient should even be shown the physical signs found on neurological exam, which may help them to accept the diagnosis and reassure them that their symptoms are potentially reversible [32]. Communicating with the patient in a way that assures them that the clinician believes their symptoms are genuine, as well as maintaining a respectful and sympathetic manner toward them, are certainly important points as well. Although placebo can be effective short term, deceiving the patient by administering placebo and later informing them of the diagnosis is generally not recommended, given the harmful effect this approach may have on patient-clinician rapport and trust. Educating patients on the disorder with the help of printed or online material (https://neurosymptoms.org) can also be helpful. Referring patients to psychiatrists or mental health professionals is also encouraged.

To date, there are no standardized testing methods or universal practice guidelines for the diagnosis and management of FMD [46]. While the use of electrophysiology is helpful in the diagnosis of FMD, clinicians may not always have the time or resources to conduct such testing in the real world. Moreover, physician knowledge and training in FMD has been found to be lower in countries outside the USA, which is another barrier [46]. However, as the diagnosis of FMD can often be reached clinically, emphasis should be placed on identifying positive diagnostic signs. The lack of multidisciplinary treatment programs for FMD continues to be an issue internationally, but such programs are necessary, as they have been found to be most effective in the management of this disorder.

PROGNOSIS

While the studies to date are mostly small and retrospective, determining the outcome and prognosis of FMD is somewhat limited. Overall, studies have shown that prognosis is usually poor and tends to worsen with increasing time to diagnosis [5,84]. Early diagnosis in patients with functional tremor or mixed symptoms, including functional weakness, has been found to be a good prognostic factor in multiple studies [28,85-87]. While FMD has been found to have a greater female preponderance, sex was not found to have an effect on prognosis. Some studies have shown that patients who are younger have a relatively favorable prognosis, whereas other studies have not found age to be a significant factor. Mixed results have also been shown regarding psychiatric comorbidities and prognosis.

The majority of studies on the prognosis of FMD have shown that the overall prognosis of this disorder is poor, as there is usually only transient improvement in motor symptoms, and approximately one-third of patients have similar or worse symptom severity at follow-up [84]. Factors associated with a poor prognosis differ depending on the type of symptom [84]. For example, patients with tremor have been found to have a poor prognosis when a precipitating event or psychiatric comorbidities are present. Patients with functional weakness have been reported to have a poor prognosis when the following factors are present: increased age of onset, high Beck Hopelessness Scale score, concurrent anxiety, personality disorders, pending litigation or receiving benefits at admission. Patients with FMD have also been found to have low quality of life and high levels of disability [88]. Quality of life is at least as altered in FMD as it is in organic movement disorders such as Parkinson’s disease or dystonia, with unemployment rates similar to or higher in FMD [4,88]. Quality of life may also be affected by nonmotor symptoms that cooccur in FMD, such as pain, fatigue, psychiatric issues and cognitive difficulties [89]. Surprisingly, greater severity of nonmotor symptoms, but not motor symptoms, was found to be correlated with poorer health-related quality of life [89].

Prognosis in the pediatric FMD population is difficult to assess because of the high percentage of patients lost to follow-up as a result of unwillingness of parents to accept the diagnosis [90]. While a brief duration of symptoms and presence of tremor have been found to lead to good prognosis in pediatric patients, other factors, such as age at onset, comorbidities, and stressors, do not seem to affect the prognosis [91].

CONCLUSION

It is not uncommon for patients with FMD to report that they had not received a clear diagnosis despite being evaluated by various specialists and undergoing extensive testing. While many factors may be responsible for this, it is important for clinicians, particularly neurologists, to take a proactive approach, as this disorder not only causes distress in patients, leading to poor quality of life and high levels of disability, but also incurs substantial costs to the healthcare system, as patients may go from doctor to doctor and continue to seek care at clinics, in-hospital, or even the emergency room. Therefore, educating practicing clinicians across domains, including neurology, psychiatry and rehabilitation, is crucial to increase awareness across relevant specialties that may play a role in treatment. Increased awareness will also help clinicians consider FMD as a possible diagnosis when positive signs are found during the clinical encounter.

It is encouraging to see renewed interest in this disorder and active measures being taken, such as use of the proposed terminology of FMD, as well as progress in research leading to increased understanding of the pathophysiology. Improving accessibility to treatment resources for FMD remains a challenge but is highly important. Directing patients to helpful websites or educational materials that aid in the understanding their disorder can be useful. Recent online self-help tools and self-cognitive behavioral therapy may also help, but only when used in conjunction with standard in-person treatment.

In summary, better dissemination of physician knowledge about FMD and directing patients to appropriate education resources and/or treatment programs is important in the management of this disorder. Basic principles taught in medical school, including attention, respect, understanding and compassion toward the patient, should not be forgotten; after all, receiving the diagnosis of FMD can be daunting, and the journey to recovery has just begun.

Notes

Conflicts of Interest

The author has no financial conflicts of interest.

Funding Statement

None

Acknowledgments

None

Figure 1.

Examples of artwork depicting functional movement disorder. A: Arc de cercle by Paul Richer. Etudes cliniques, 1881. Digital image source: Bibliothèques d’Universitè Paris Citè. B: The motor phase of a hysterical attack by Paul Richer. Études cliniques sur l’hystèroèpilepsie ou grand hystèrie, 1885. C: Handle as a gymnast. Roman, 0–100 CE; LFRD 3398. Freud Museum (https://stories.freud.org.uk/charcot/5/). D: Arch of Hysteria by Louise Bourgeois, 1993. Contemporary artwork interpreted as conversion disorder manifesting as involuntary arching of the back. Source: © The Easton Foundation/VAGA at ARS, New York/SACK, Seoul.

Figure 2.

Biopsychosocial model of FMD. The etiology of FMD is multifactorial and includes early life or current stress, social factors, comorbid psychiatric factors and secondary gain. FMD, functional movement disorder.

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