The clinical presentation of FMD is highly variable. Common motor symptoms of FMD include tremors, dystonia, myoclonus, gait disturbances jerks, and paresis (11). One of the key characteristics of FMD is its abrupt onset, often triggered by physical or psychological stressors (12). Table 1 summarizes the clinical features of FMD.

Functional dystonia is characterized by unusual postures or abnormal muscle contractions, but unlike organic dystonia, these symptoms can change over time or even reverse spontaneously. Symptoms often improve when patients are distracted, but they may worsen when attention is focused on the movement. For example, during a neurological examination, a patient's tremor might decrease or disappear when they are asked to perform a cognitive task, such as counting backwards (13).

Patients with FMD may experience a range of non-motor symptoms, including sensory disturbances, cognitive difficulties such as memory loss, and dissociative experiences (14).

Emotional factors, such as anxiety and depression, are frequently linked to FMD, complicating its clinical presentation. Psychiatric comorbidities can intensify symptoms, leading to a more severe and chronic expression of the disorder (15).

The true prevalence of FMD remains difficult to estimate due to factors such as underdiagnosis and misdiagnosis. Recent studies suggest that FMD accounts for 2%–20% of patients seen in movement disorder clinics, although this varies based on location and diagnostic criteria applied (16). Epidemiological studies have consistently shown that FMD is more prevalent in women, with a female-to-male ratio of approximately 4:1 (17). The prevalence of FMD phenotypes varies depending on the specific presentation and population. In Western countries, studies report that functional tremor is the most common phenotype, accounting for approximately 36% of cases, followed by functional dystonia at around 34% (18).

FMD typically presents in midlife, between the ages of 35 and 45 years, though this likely underestimates cases in pediatric and elderly populations (19). In pediatric populations, FMD may emerge after acute stressors, such as school-related pressures or family conflicts, while in older adults, it may be misdiagnosed as age-related conditions like Parkinsonism (20). Socioeconomic factors also contribute to the prevalence of FMD, with higher rates observed among individuals from lower socioeconomic backgrounds (21).

The etiology of FMD is complex, involving interactions between several contributing factors, including genetic predispositions, alterations in brain networks, and psychosocial stressors (22).

An emerging area of interest is the role of genetic predisposition. Studies suggest that certain individuals may be more susceptible to FMD due to genetic factors that affect the brain's regulation of motor control and emotional responses (23). For example, variations in genes associated with neurotransmitter systems, particularly those regulating dopamine and serotonin, may increase vulnerability to abnormal movement patterns when exposed to stress or trauma. These findings point to a potential heritable component in FMD, though further research is needed to clarify the specific genetic factors involved (24).

Neurobiological findings also emphasize disruptions in the brain's reward system, particularly involving the dopaminergic pathways. Abnormal dopamine signaling may lead to the reinforcement of abnormal movement patterns, contributing to the persistence of symptoms even after the initial stressor has passed (25).

Social and cultural factors can play a significant role in the development of FMD. Research indicates that societal expectations, cultural norms, and familial influences may shape how symptoms are expressed and perceived (19, 26). In some cultures, certain types of emotional distress may be more likely to manifest as physical symptoms like abnormal movements, reflecting a form of somatization (27). A recent study highlights that prevalence of FMD has increased in recent years, particularly in young individuals, possibly due to socio-environmental factors (28). For instance, the COVID-19 pandemic and increased exposure to social media platforms have been linked to the rise in cases of functional tic-like behaviors, especially in adolescents (29). This suggests that sociocultural and psychological factors may significantly influence the presentation and prevalence of FMD in specific populations. A summary of etiology and risk factors associated with FMD are found on Table 2.

The diagnosis of FMD is based on recognizing positive clinical signs, rather than through a process of exclusion (30). A key diagnostic feature is symptom inconsistency, where abnormal movement patterns vary over time in terms of amplitude, frequency, and distribution (31, 32). Additionally, distractibility is an important indicator; abnormal movements often resolve when the patient's attention is directed elsewhere (33).

Functional neuroimaging, particularly fMRI, has become a key tool in diagnosing FMD. Studies have revealed abnormalities in brain regions associated with motor control, most notably the premotor cortex and thalamus, where FMD patients show reduced volume and connectivity (34).

Beyond the premotor cortex and thalamus, research has identified altered activity in regions such as the supplementary motor area (SMA) and basal ganglia, both of which are critical for voluntary motor control (35). Additionally, hyperactivity in emotional processing centers, including the amygdala and cingulate cortex, has been observed in FMD patients, linking emotional dysregulation to movement dysfunction. The increased functional connectivity between motor regions and the emotion-processing areas suggests that FMD arises from a combined disruption of motor and emotional networks (36).

Electrophysiological testing, including electroencephalogram (EEG) and electromyography (EMG), plays an essential role in diagnosing FMD and distinguishing it from other neurological conditions. These tests assess the electrical activity of muscles and nerves, offering valuable insights into movement abnormalities (37). For example, in cases of psychogenic tremor, EMG can detect co-activation of antagonist muscles—a pattern uncommon in organic movement disorders but characteristic of FMD. This simultaneous contraction of opposing muscles results in inefficient or erratic movement, pointing to a functional, rather than structural, abnormality (38).

Management for FMD incorporates a multidisciplinary approach, blending physical, psychological, neuromodulation, and pharmacological therapies (39).

Physiotherapy plays a pivotal role in the management of FMD. The core components of effective intervention include gaining a comprehensive understanding of the patient's symptoms, assessing the impact on daily function, evaluating the patient's perception and confidence in the established diagnosis, and collaboratively setting clear goals for physiotherapy (40). Research has shown that targeted physiotherapy can be effective in providing sustained symptom relief. In one study, an intensive short-term rehabilitation program led to a 73.5% improvement rate (41).

Occupational therapy, with its holistic approach that addresses physical, mental, and social determinants of health, is also well-suited to assist patients with FMD in maximizing functional outcomes. As in physiotherapy, occupational therapy interventions should be tailored to meet the specific goals of FMD treatment (42).

Neuromodulation therapy represents an exciting and innovative approach for treating complex and challenging cases of FMD, particularly those for whom evidence-based treatment options remain limited. As a novel therapeutic strategy, neuromodulation has the potential to influence key brain networks, positioning it as a promising candidate for addressing the needs of these patients (43).

Transcranial magnetic stimulation (TMS) has long been studied for its ability to noninvasively assess cortical excitability and connectivity (44). Repetitive TMS (rTMS), in particular, has shown potential to produce lasting neuromodulatory effects through mechanisms like long-term potentiation. A recent study involving 33 FMD patients compared TMS applied over the motor cortex contralateral to symptoms against TMS over spinal roots in a control group (45). The observed symptom improvement suggests that nonspecific factors, including behavioral changes or placebo effects, may contribute to the therapeutic response.

Recently, Intermittent Theta Burst Stimulation (iTBS), a form of transcranial magnetic stimulation, has emerged as a potential treatment for FMD. iTBS is a non-invasive brain stimulation technique that involves delivering short bursts of high-frequency magnetic pulses, used to modulate cortical activity in various neurological disorders, including FMD, resulting in reduction of symptoms (46).

The pharmaceutical approach for managing FMD has evolved to encompass a diverse array of agents that target both the symptomatic and underlying neurophysiological abnormalities. By employing various medications, clinicians can tailor interventions to alleviate pain and modulate muscle activity, while improving functional outcomes (47).

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) are commonly prescribed for pain related to muscular, temporomandibular joint (TMJ) issues, migraines, and trauma (48, 49). They work by inhibiting prostaglandin synthesis, reducing inflammation and pain, but may also slow tooth movement at high doses by affecting bone resorption (50–52).

Selective Serotonin Reuptake Inhibitors (SSRIs) are used to treat depressive and anxiety-related disorders, including those linked to movement issues (53). However, they may alter muscle tone and reduce osteoblastic activity, potentially compromising dental enamel and orthodontic tooth movement (54–57).

Botulinum Toxin (BoNT-A) is utilized for a range of hyperkinetic movement disorders such as cervical dystonia, hemifacial spasm, and tics (58, 59). It reduces muscle hyperactivity in the head and neck but may impact craniofacial growth and mandibular development, especially in children (60–63).

Lastly, dopaminergic and anticholinergic agents, used in conditions like Parkinson's disease, dystonia, and tardive dyskinesia, help improve muscle coordination and oral hygiene (64–67). However, they can also cause xerostomia, increasing the risk for dental caries and tooth structure loss (68, 69).

Dental professionals should be well-prepared and adequately trained to recognize and differentiate the symptoms of FMD, allowing them to develop and implement tailored treatment plans for these patients. Overlapping symptoms, such as jaw pain, restricted mouth opening, and chewing difficulties are common in both temporomandibular disorders (TMD) and OMD. However, TMD is typically characterized by localized joint pain, often accompanied by clicking or popping sounds during joint movement. It arises primarily from mechanical or structural disturbances affecting the TMJ and associated musculature, frequently linked to parafunctional habits like bruxism (87). Conversely, OMD is a functional movement disorder involving dysfunction in motor control pathways, particularly within the basal ganglia (88). It is marked by involuntary, sustained muscle contractions and abnormal movements, with less emphasis on joint dysfunction.

A distinguishing feature of OMD is the presence of a sensory trick, or geste antagoniste, where simple tactile stimuli, such as touching the chin, can momentarily suppress the dystonic movement (89). This phenomenon is absent in TMD and serves as a valuable clinical indicator to differentiate it from OMD. Additionally, while TMD is predominantly pain-driven, OMD patients primarily experience uncontrollable movements, with discomfort emerging as a secondary consequence of muscle fatigue or joint stress. Importantly, these conditions may coexist or influence one another. The repetitive, involuntary jaw movements in OMD can impose abnormal forces on the TMJ, leading to secondary TMD symptoms such as joint pain or disc displacement (90). On the other hand, chronic TMD-related pain and dysfunction may increase muscle tension and, in susceptible individuals, trigger or exacerbate dystonic patterns (91). Unlike TMD, which follows predictable biomechanical patterns of pain and movement restriction, FMD symptoms may fluctuate with psychological stressors and often lack a clear anatomical basis. The hallmark of FMD includes task-specific manifestations that can transiently improve with distraction or simple maneuvers, further distinguishing them from structural TMJ disorders (92, 93).

FMD is often associated with heightened pain sensitivity, making routine orthodontic adjustments more uncomfortable for patients. It can also cause changes in occlusion due to involuntary muscle contractions, spasms, and abnormal tongue movements, leading to dental misalignment such as open bites, cross bites, and shifting teeth. Parafunctional habits like bruxism and tongue thrusting may further cause enamel wear, tooth mobility, and malocclusion.

To effectively accommodate patients with FMD, dental professionals should begin by establishing clear treatment goals and setting realistic expectations. It is essential to explain any potential risks and complexities in a calm, reassuring manner, while also maintaining thorough and accurate documentation.

During treatment, consider using shorter appointment durations to help prevent fatigue and reduce the risk of overstimulation, both of which can exacerbate functional symptoms. Scheduled breaks can further improve patient tolerance and comfort. Additionally, incorporating distraction techniques such as light, reassuring conversation, calming background music, or sensory tools like stress balls may help reduce anxiety and support a more relaxed experience. Additionally, the use of nitrous oxide sedation during appointments can be an effective option when other pain management techniques prove insufficient.

The sustained or repetitive contractions of the jaw muscles make it difficult for patients to maintain a stable jaw posture during dental treatment (5).

Abrupt head movements and spasms commonly associated with FMD may compromise traditional impression-taking, often requiring multiple attempts due to movement-induced errors. To mitigate this challenge, clinicians may consider alternative modalities, such as intra-oral scanning and cone-beam computed tomography, which offers reduced acquisition time and improved accuracy (94, 95).

Involuntary tongue movements, jaw spasms, and other motor disturbances can dislodge wires, accelerate appliance wear, and require frequent adjustments or replacements, thereby prolonging treatment duration and increasing the risk of dental complications. Similarly, extraoral appliances, such as reverse pull headgear, maybe poorly tolerated by FMD patients. Involuntary movements can destabilize these appliances, causing discomfort and placing excessive stress on dental and craniofacial structures, potentially compromising treatment outcomes.

Given these challenges, fixed appliances may be more suitable for FMD patients, as they provide greater stability and are less affected by involuntary movement-related disruptions.

Indirect bonding techniques can provide significant advantages for FMD patients by reducing chair time during bonding procedures. This approach lowers the risk of accidental events, such as self-inflicted oral injuries or broken brackets from involuntary jaw movements.

Orthodontists should frequently reassess occlusal stability and consider adjustments like occlusal splints. Splints may exert therapeutic effects by modulating sensory signals transmitted via the trigeminal nerve to the sensory trigeminal nucleus (96–99). This nucleus spans from the cervical spinal cord to the mesencephalon and interfaces with reticular interneurons across various levels of the central nervous system. The structural and functional integration of this trigeminal complex may explain the observed overlap between sensory tricks and the use of oral appliances in managing OMD (96). However, the precise mechanisms by which the trigeminal nucleus modulates dystonic movements remain poorly understood. While oral appliances show promise as an adjunct to medical treatments, further research is necessary to clarify their role and optimize their design.

Overall, careful appliance selection and regular monitoring are critical to ensure optimal care and minimize side effects.

Physiologic orthodontic tooth movement relies on forces of appropriate magnitude and vector to induce bone remodeling on both the compression and tension sides of the periodontal ligament (100). Any disruption in this process can impair orthodontic mechanics and result in imprecise tooth movement. In patients with OMD, unbalanced forces from peri-oral muscles and the masseteric apparatus may counteract the vector-specific forces applied by orthodontic appliances.

Furthermore, high-frequency tremors and unpredictable repetitive forces resulting from orofacial tics may introduce uncontrolled micro forces on teeth, potentially accelerating root resorption in susceptible patients, further complicating orthodontic treatment (101, 102).

Retention is important for patients with FMD, as involuntary muscle forces can lead to relapse even after achieving satisfactory occlusion during orthodontic treatment (103).

Fixed lingual retainers are commonly utilized to counteract the undesirable forces associated with muscle hyperactivity, providing continuous stabilization of the dental arches.

Pharmacologic approaches, such as botulinum toxin (BoNT-A) injections, have shown promise in reducing abnormal muscular activity, which can help improve stability after active orthodontic treatment (104).

These interventions may be beneficial during the retention phase, as they can mitigate the impact of involuntary muscle forces. By integrating appropriate retention strategies and considering adjunctive therapies like BoNT-A, orthodontists can enhance treatment stability and minimize the risk of relapse in FMD patients.

Medications used to manage FMD can significantly influence orthodontic treatment outcomes by affecting tooth movement, dentoalveolar and craniofacial growth, retention, and relapse. These effects often result from mechanisms such as altered bone remodeling, muscle activity regulation, and oral health changes like xerostomia and dental attrition (105).

Some medications may slow tooth movement by inhibiting bone turnover, while others can compromise retention by increasing the risk of enamel wear or muscle hyperactivity (106). Understanding these interactions is crucial for orthodontists to make adjustments to treatment plans, minimize complications, and ensure long-term stability, especially in patients requiring prolonged medication use. Table 4 summarizes various medication classes used in managing FMD and their effects on OTM, dentoalveolar growth, retention, and relapse.