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Authors : Dr. Suraj Agarwal .


Orofacial movement disorders are often misdiagnosed as temporomandibular disorders, hence understanding these conditions is pertinent for the practitioner treating orofacial pain. Aspects of epidemiology, etiology, pathophysiology, clinical presentation, and diagnosis are discussed along with treatment considerations for these orofacial movement disorders.


OMD involves the motor aspects of cranial nerves V, VII, and XII and may present as hyper activity or hypo activity of the masticatory, facial, and tongue musculature or combinations of these voluntary muscles. These movement disorders are centrally mediated pathologic conditions involving the basal ganglia (the caudate, putamen, globuspallidus, subthalamus, and substantianigra) and their communication with other areas of the brain. Along with the cerebral cortex, the basal ganglia are responsible for the performance of fine motor functions. OMD may present in many forms, common presentations of hyperactive OMD: oromandibular dystonia, orofacial dyskinesia, and drug-induced extra pyramidal syndrome reactions.

Oromandibular Dystonia

Oromandibular Dystonia (OD) is a focal dystonia whereby repetitive or sustained spasms of the masticatory, facial, or lingual muscles result in involuntary and possibly painful jaw opening closing, deflecting, or retruding movements, or a combination of these movements. Compared with dyskinesia, ODs are intermittent and present as short, sustained muscle contractions resulting in abnormal muscle movements and posturing. Focal dystonias may be primary (idiopathic) or secondary. The primary form is more common and does not involve underlying central nervous system pathology, such as infarctions and tumors.

In particular, the diagnosis is elusive in selected patients who have unrecognized triggers and present during periods of quiescence. Validity of the diagnosis for the different types of focal dystonias cannot be assessed because there is no available gold standard (a diagnostic test or biomarker) as yet. Misdiagnosis commonly includes TMD or spontaneous condylar dislocation, hemimasticatory or hemifacial spasms and psychologic manifestations. Currently, OD affects approximately 3 to 30 per 100,000 persons in the United States. Some studies suggest that OD affects more women than men, with a mean age of symptom onset between 31 and 58 years. Dental and oral and maxillofacial surgical procedures and orofacial trauma have been temporally and anatomically related to the onset of dystonia. In studies by Tanand Jankovic, most ODs are idiopathic in etiology, accounting for 63% of cases reported. Other possible causes include drug-induced OD (22.8%), peripheral-induced OD (9.3%), post anoxic OD (2.5%), neurodegenerative disorder–associated OD (1.8%), and head injury–associated OD (0.8%).

Pathophysiology for OD is unknown; however, it probably has multi-factorial mechanisms involving basal ganglia dysfunction, hyper excitability of motor neurons involved in signalling, reduced inhibition of spinal cord and brainstem signals coming from supra spinal input, and dysfunction of neurochemical systems involving dopamine, serotonin, and nor adrenaline. The clinical characteristics of OD are classified according to the affected muscles.

The muscles involved may be the muscles of mastication, muscles of facial expression, or the muscles of the tongue. Patients may present with jaw-opening, jaw-closing, jaw-deflecting, or jaw retruding dystonia, or a combination of any of these. The uncontrolled or involuntary mandibular movements may be repetitive or sustained. The combination of OD and blepharospasmis known as Meige syndrome. Similarly, dystonic spasms may result in nasal contractions, facial grimacing, lip pursing, lip sucking or smacking, chewing, tooth clenching and grinding, tongue movements, retractions of corners of mouth, and plasma contractions.

Involvement of the laryngeal muscle groups may lead to dysarthria, dysphagia, dysphonia, breathing difficulties, and alteration in vocalization. For unknown reasons, patients often report triggers or exacerbating factors, such as stress, depression, glaring light, watching television, driving, reading, talking, praying, fatigue, and chewing. Likewise for reasons unknown, patients also report that they have learned certain sensory tricks, or ‘‘gesteantagonistique,’’ which are typically tactile stimulations of the orofacial region to control and suppress movements. Sensory tricks are more prevalent among jaw opening OD. Other means to help control the dystonia, such as sleeping, relaxing, talking, singing, humming, lip biting, tongue posturing, swallowing, chewing gum, and in some instances, alcohol intake, may be reported by patients.

Orofacial Dyskinesia

Orofacial dyskinesia (Dock) is defined as involuntary, repetitive, stereotypical movement of the face, tongue, and jaw that may be painful. Dyskinesia may be spontaneous (idiopathic) or tardive (medication-induced). Oral and maxillofacial surgeons should be aware of well-known complications of ODk, namely tooth wear and fracture, prosthesis damage and displacement, accelerated bone loss among edentulous patients, orofacial pain, temporomandibular joint degeneration, ulcers secondary to tongue and cheek biting, dysarthria, dysphagia, chewing difficulties, inadequate food intake and weight loss, and social embarrassment secondary to compromised facial aesthetics .

Spontaneous orofacial dyskinesia

The less common spontaneous form of dyskinesia typically affects the elderly. The prevalence of spontaneous ODk varies depending on the population studied, ranging from 1% to 38%. Specifically, it affects 1.5% to 4% of the healthy elderly 18% to 31.7% of the elderly living in retirement homes and 3.7% of the elderly in day care centres. It has been suggested that antipsychotic drugs, which are often used in the elderly, may merely unmask dysfunctional sub cortical circuits that predisposes the individual to ODk. Previous studies have suggested a two- to three fold higher female to male ratio; however, this is likely attributable to the over representation of females in these study populations. The presence of spontaneous ODk occurring in various central nervous system conditions is well established and includes chronic schizophrenia, Alzheimer disease, dementia, autism, mental retardation and Rett syndrome.

The clinical presentation of spontaneous ODk is typically milder in intensity compared with tardive ODk and involves various combinations of tongue, lips, and jaw movements. Spontaneous ODk is also strongly associated with ill-fitting removable prosthesis, so-called ‘‘prosthetic stereotypies,’’ oral pain, and perception of inadequate oral hygiene. Whether ill-fitting prostheses are the cause or the effect of ODk is yet to be determined. It has been suggested that wearing ill-fitting prostheses is a greater risk factor for oral stereotypies than not wearing prostheses. It has also been suggested that ODk and tardive dyskinesia (TD) are associated with edentulism. One study reported 16% of subjects who had mild ODk, half of whom did not wear prostheses, questioning the association between ill-fitting prostheses and spontaneous ODk.

Tardive dyskinesia

TD represents rapid, repetitive, non-random, stereotypic movements involving the tongue, lips and jaw areas. Combinations of tongue twisting and protrusion, lip smacking and puckering, and chewing movements occur secondary to exposure to an offending drug, typically conventional antipsychotic drugs, such as chlorpromazine, haloperidol and perphenazine. Other areas of the body may be involved, typically extremities and trunk. The diagnosis of TD requires a minimum of 3 months of cumulative exposure to the offending drug. Also, TD must persist for 3 months after withdrawal of the offending medication. Patients are often able to voluntarily suppress involuntary orofacial movements through activities such as eating or talking. Alternatively, TD can be exacerbated by stimulants, neuroleptic medication withdrawal, anticholinergic medications, emotional arousal, and distraction of other unaffected areas of the body during voluntary movements.

TD can be socially embarrassing and result in dysphagia and dysarthria in some cases. The incidence and prevalence of TD varies with age (greater in the elderly) and sex (greater in females). Other known risk and predisposing factors for TD include greater drug exposure (specifically to conventional antipsychotics), poor response to treatment, genetics, affective disorders, brain damage and cognitive impairment, parkinsonism, diabetes mellitus, and alcohol and substance abuse. The annual incidence for TD is 5% in the younger population (mean 28 years) to 12% in the older population (mean 56 years). Reportedly, more than 20% of patients treated with neuroleptic medications develop TD.

The prevalence of TD has doubled over 20 year’s inpatients who have schizophrenia and were treated with newer atypical antipsychotics, such as risperidone and olanzapine that promised fewer extra pyramidal side effects, suggesting other mechanisms for the development of TD. In a recent study involving hospitalized patients who had schizophrenia, TD occurred in 40% of those treated with antipsychotics, 39% of those treated with atypical antipsychotics and 47% treated with both typical and atypical antipsychotics. The cause of TD is chronic exposure to dopamine receptor–blocking drugs (i.e. conventional antipsychotics) used in the treatment of psychosis and schizophrenia.

The clinical course of TD is difficult to predict because it may persist improve or recur after a brief period of quiescence despite withdrawal of the offending drug. The pathophysiology of TD remains elusive. The current theory states that chronic blockade of dopamine D2 receptors in the striatum results in increased receptor sensitivity and hence elevations of dopamin function. This concept fails to explain why the majority of patients are not afflicted by TD despite exposure to dopamine receptor–blocking drugs. One possible explanation for susceptibility to TD among select patients is the association between a serine-to-glycine polymorphism in exon 1 of the DRD3 gene and TD. The effect of dopamine receptor–blocking agents on g-aminobutyric acid (GABA), cholinergic and nor epinephrine systems and oxy-radical production causing neuronal degeneration are other possible explanations for TD. Drug-induced extra pyramidal syndrome (DiEPS) reactions are movement disorders that are commonly reported with use of prescribed medications and illicit or stimulant drugs. DiEPS reactions usually present as dystonia, akathisia and parkinsonism.


The clinician should be well aware of the efficacy and limitations of these options and must educate the patient as to the underlying disorder, the available treatment modalities, and the expected outcome of the therapy. The first step is to take a thorough history, including a medication and illicit drug history. If the examination findings indicate a movement disorder, MRI should be performed to rule out a central degenerative, demyelinating, or sclerotic lesion of the nervous system. For those cases of hemi facial spasm, a magnetic resonance angiography may be performed to rule out vascular compression of the facial nerve.
Diagnostic Work-Up for Orofacial Movement

Management of OMD can be broadly divided into medical management, chemo denervation using botulinum neurotoxin (BoNT), and surgical management. Medical management involves the use of various centrally acting medications. The surgical management may range from myectomy to a pallidotomy. Of all these approaches, injecting BoNT into the affected musculature has proved to be the most effective means of managing OMD.





Trihexyphenidyl hydrochloride (Artane)
Biperiden (Akineton)


GABAergics Oral baclofen (Lioresal)
Intrathecal baclofen


Clonazepam (Klonopin)
Diazepam (Valium)
Lorazepam (Ativan)




Buspirone (BuSpar)


Amantadine (Symmetrel)
Benztropine (Cogentin)

Table: Drugs for Orofacial Movement


  1. Ramesh Balasubramaniam et al. Orofacial Movement Disorders. Oral Maxillofacial Surg Clin N Am 20 (2008) 273–285.
  2. Glenn T. Clark et al. four oral motor disorders. Dent Clin N Am 51 (2007) 225-243.

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