Bruxism

The prevalence of chronic bruxism is unknown, because no large, probability-based, random sample study has been performed using polysomnography (which is needed to measure bruxism). Based on a combination of attrition assessment and reports by parents, spouses, or roommates, it is estimated that 5% to 21% of the population has substantial sleep bruxism . Many bruxers do not have substantial attrition and many do not make tooth-grinding sounds during sleep, so sleep partner or parental reports are not always accurate. The pathophysiology of bruxism is unknown. The most cogent theory describes bruxism as a neuromotor dysregulation disorder. This theory proposes that bruxism occurs because of the failure to inhibit jaw motor activity during a sleep state arousal. There are numerous clear-cut neuromotor diseases that exhibit bruxism as a feature of the disease (eg, cerebral palsy). The disorder of periodic limb movements is similar to an OMD, except that it occurs in the leg muscles . There are many articles that describe the clinical presentation and consequences of bruxism; most agree that the single most effective way to protect the teeth from progressive attrition, fracture, or clenching-induced pulpitis is to fabricate an occlusal appliance and have the patient use it at night . The problem with an occlusal-covering appliance is that it does little or nothing to stop the bruxism in the long term. Most alter the behavior for a few weeks when first used, but this only offers a brief respite from some headaches and bruxism-induced TMJ derangement or arthritis problems. In cases in which the disorder is severe and the damaging consequences are well beyond the teeth, one option is to inject the masseter or temporalis about every 3 to 6 months to minimize the power of the bruxism activity. The literature supports this concept; one of the first reports was by Van Zandijcke and Marchau in 1990 who provided a brief note on the treatment of a brain-injured patient who exhibited severe bruxism with botulinum toxin type-A injections (100 U total into the masseter and temporalis). Seven years later, Ivanhoe and colleagues described the successful treatment of a brain-injured patient who had severe bruxism with botulinum toxin type-A. In this case, the patient was injected with a total of 50 U to each of four muscles (right and left masseter and temporalis) for a total of 200 U. Of course, the successful treatment of a single case of brain injury–induced bruxism does not make a compelling story for its routine use in managing bruxism. The story was extended by a more recent report . The investigators reported on the long-term treatment of 18 cases of severe bruxism with botulinum toxin type-A. These patients all had severe bruxism, which had been causing symptoms for an average of 14.8 ± 10.0 years and all had no success with previous medical or dental treatment. Similar to previous reports, the masseter muscle was injected with a mean dose of 61.7 ± 11.1 U per side. The efficacy of these injections was rated by the subjects as a 3.4 on a scale from 0 to 4 (with 4 being equal to total cessation of the behavior). The investigators described one subject who experienced dysphagia as a side effect of the injections. Finally, another investigator described a young child (age 7) who had severe brain injury–induced bruxism that was treated successfully with botulinum toxin . The primary management method for strong bruxism and clenching is still a full-arch occlusal appliance, which does not stop the behavior but limits its dental damage . Fortunately, the most severe cases of bruxism and clenching now have several motor suppressive medications; in extreme cases, botulinum toxin injections can be added to occlusal appliance treatment.

Oromandibular dystonia

Oromandibular dystonia is one form of a focal dystonia that affects the orofacial region and involves the jaw openers (lateral pterygoids and anterior digastrics), tongue muscles, facial muscles (especially orbicularis oris and buccinator), and platysma. When this occurs in association with blethrospasm (focal dystonia of the orbiculares oculi muscles), it is called Meige’s syndrome . Dystonia is considered present when repeated, often asynchronous spasms of muscles are present. Most dystonias are idiopathic and the focal form of dystonia occurs 10 times more often than does the generalized systemic form . The prevalence of all forms of idiopathic dystonia ranges between 3 and 30 per 100,000 . Focal dystonias can be primary or secondary; the secondary form of dystonias occurs as a result of a trauma (peripheral or central), brainstem lesion, systemic disease (eg, multiple sclerosis, Parkinson’s disease), vascular disease (eg, basal ganglia infarct), or drug use . Most dystonias are primary or “idiopathic” and demonstrate no specific CNS disease. Of course, various pathophysiologic mechanisms have been proposed to explain dystonia (eg, basal ganglia dysfunction, hyperexcitability of interneurons involved in motor signaling , reduced inhibition of spinal cord and brainstem signals coming from supraspinal input and dysfunction of neurochemical systems involving dopamine, serotonin, and noradrenaline ). All dystonias are involuntary but tend to be more intermittent than dyskinesias (see later discussion) and are compromised of short, but sustained, muscle contractions that produce twisting and repetitive movements or abnormal postures .

One interesting aspect of the involuntary motor disorders is that patients can control or suppress the movement partially with the use of tactile stimulation (eg, touching the chin in the case of orofacial dystonia or holding an object in their mouth). This suppressive effect has been called “geste antagonistique” . These tactile maneuvers may lead physicians to the erroneous diagnosis of malingering or hysteria. Other examples of sensory tricks include placing a hand on the side of the face, the chin, or the back of the head, or touching these areas with one or more fingers, which, at times, will reduce the neck contractions that are associated with cervical dystonia. With some dystonias, patients have discovered that placing an object in the mouth (eg, toothpick, piece of gum) may reduce dystonic behaviors of the jaw, mouth, and lower face (oromandibular dystonia). Finally, most of the focal and segmental dystonias only occur during waking periods and disappear entirely during sleep.

For treatment, there are several medications that can be used to suppress hyperkinetic muscles (see later discussion). After medications, the other primary method for treating dystonia is chemodenervation using botulinum toxin. In 1989, Blitzer and colleagues first described the injection of botulinum toxin for oromandibular dystonia. They described injecting many of the orofacial muscles in oromandibular dystonia and claimed that masseter and temporalis injections helped with suppressing the overall oromandibular dystonia. These early reports did not specifically look at tongue movement changes nor were tongue botulinum toxin injection performed. In 1991, Blitzer and colleagues described the first use of botulinum toxin in patients who had lingual dystonia, but cautioned clinicians that dysphagia was a problem in some of their cases; unfortunately, doses and injections sites were not described carefully. In 1997, Charles and colleagues reported on nine patients who had repetitive tongue protrusion that resulted from oromandibular dystonia or Meige’s syndrome. They were treated with botulinum toxin injections into the genioglossus muscle at four sites by way of a submandibular approach. Six of these patients were helped, and the average dose injected was 34 U, which produced a 3- to 4-month effect. Clearly, there is a need to explore when, where, and to what degree botulinum toxin may become useful in the management of the patient who has galloping tongue or tongue-based severe dyskinesia. There are many variations of oromandibular dystonia, but one common one is involuntary jaw-opening dystonia. One complication of jaw-opening dystonia is that the TMJ can become locked physically in the wide-open position, so that even after the dystonic contraction stops, the jaw will not close easily. In 1997, Moore and Wood described the treatment of recurrent, involuntary TMJ dislocation using botulinum toxin A. The injected target was the lateral pterygoid muscle, and they injected each lateral pterygoid using electromyographic guidance. The investigators described that the effect lasted for 10 months. The lateral pterygoid is the muscle that is most responsible for opening; it is a difficult injection, which has a high potential for misplacement of the solution into other adjacent muscles.

Dyskinesia

Risk factors for the development of tardive dyskinesia are older age, female sex, and the presence of affective disorders . For spontaneous dyskinesias, the prevalence rate is 1.5% to 38% in elderly individuals, depending on age and definition. Elderly women are twice as likely to develop the disorder . When this disorder is associated with a drug use, the medications that are implicated most commonly are the neuroleptic medications that are now in widespread use as a component of behavioral therapy. The prevalence of drug-induced dyskinesia (tardive form) is approximately 15% to 30% in patients who receive long-term treatment with neuroleptic medications . These medications chronically block dopamine receptors in the basal ganglia. The result would be a chemically-induced denervation supersensitivity of the dopamine receptors which leads to excessive movement; however, other neurotransmitter abnormalities in γ-aminobutyric acid (GABA)ergic and cholinergic pathways have been suggested. There are isolated reports in the literature that implicate dental treatment as a factor in the onset of spontaneous orofacial dyskinesia. Orofacial dyskinesia occurs as involuntary, repetitive, stereotypical movement of the lips, tongue, and sometimes the jaw during the day . Sometimes the dyskinesia is induced by medication (tardive) or it can occur spontaneously. The spontaneous form of dyskinesia often affects the elderly. Typically, the tardive form of dyskinesia occurs in mentally ill patients who have a long-term exposure to medications that are used to treat the mental illness . By definition, tardive dyskinesia requires at least 3 months of total cumulative drug exposure, which can be continuous or discontinuous. Moreover, the dyskinesia must persist more than 3 months after cessation of the medications in question. Most dopamine receptor antagonists cause oral tardive dyskinesia to one degree or another. The typical antipsychotics—and in recent years, even the atypical antipsychotics—including clozapine, olanzapine, and risperidone were reported to cause tardive dystonia and tardive dyskinesia. No adequate epidemiologic data exist regarding whether any particular psychiatric diagnosis constitutes a risk factor for the development of tardive reactions to medications; however, the duration of exposure to antipsychotics that is required to cause tardive reaction is from months to years. Exposure to antipsychotics need not be long, and a minimum safe period is not apparent. This duration of neuroleptic exposure seems to be shorter for women. A longer duration of exposure to neuroleptics does not correlate with the severity of the reaction. Treatment of orofacial dyskinesia is largely with medications (see later discussion).

Drug-induced dystonic-type extrapyramidal reactions

There are patients who have developed a medication-induced oral motor hyperactivity that does not fit into the dyskinesia category . These medications and illegal drugs produce a motor response that is classified better as an unspecified extrapyramidal syndrome (EPS) reaction. EPS responses typically have three presentations: dystonia, akathisia, and parkinsonism. Dystonic reactions consist of involuntary, tonic contractions of skeletal muscles . Akathisia reactions occur as a subjective experience of motor restlessness . Patients may complain of an inability to sit or stand still, or a compulsion to pace or cross and uncross their legs. Parkinsonian reactions manifest themselves as tremor, rigidity, and akinesia, which shows as a slowness in initiating motor tasks and fatigue when performing activities that require repetitive movements (bradykinesia). When a medication or drug induces a dystonic EPS reaction, it typically involves the muscles of the head, face, and jaw that produce spasm, grimacing, tics, or trismus. Most of the literature has focused on the more severe acute dystonic EPS reactions that occur with use of antipsychotic medications. In addition to the antipsychotics, several antiemetics with dopamine receptor–blocking properties have been associated with tardive dystonia. These include prochlorperazine, promethazine, and metoclopramide. Of course, other less severe reactions do occur that vary in intensity and even wax and wane over time. The most commonly reported offending agents that are not neuroleptics are the selective serotonin reuptake inhibitors (SSRIs) and the stimulant medications and illegal drugs.

Serotonergic agents that cause extrapyramidal reactions

SSRIs (eg, fluoxetine, fluvoxamine, paroxetine, sertraline, citalopram, escitalopram) are used for depression and a variety of other mental illnesses. Unfortunately, these drugs are reported to produce the side effect of increased clenching and bruxism . Actually the term “SSRI-induced bruxism” may not be accurate in that the actual motor behavior does not present as brief, strong, sleep state–related contractions as seen in bruxism, but more of an increased sustained nonspecific activation of the jaw and tongue musculature. Patients generally describe an elevated headache and tightness in their jaw, tongue, and facial structures. The best information available about the effect of SSRI class medications on oromandibular structures comes from a study in 1999, which examined the acute effects of paroxetine on genioglossus activity in obstructive sleep apnea . It found that paroxetine, 40 mg, produced a clear augmentation of peak inspiratory genioglossus activity during non-rapid eye movement (NREM) sleep. Of course, the recent widespread use of SSRIs is based on a perception that these drugs have a lower side effect profile than do other categories of antidepressant medications (eg, tricyclics and monoamine oxidase inhibitors). Unfortunately, only case-based literature exists at this time; further polysomnographic studies on the motor effects of SSRIs are necessary to define prevalence and risk factors and to establish a causal relationship between SSRI use and oral motor disorders.

Stimulant drugs and other medications that cause extrapyramidal reactions

Illegal drugs, such as methamphetamine cocaine and 3,4-methylenedioxymethamphetamine (Ecstasy), and legal prescription stimulants, such as methylphenidate, phentermine, pemoline, dextroamphetamine, amphetamines, and diethylproprion, have been reported to induce bruxism and dystonic extrapyramidal reactions . All stimulant drugs have the potential to cause extrapyramidal reactions and they are being used in greater numbers to treat obesity or as stimulants for children who have attention deficit hyperactivity disorder or narcolepsy and even for severe depression .