Overview:
Oral tardive dyskinesia is a chronic disease involving stereotypes or uncontrolled movements of the oral cavity and even of the extremities and trunk in some cases. Tardive dyskinesia is more of a movement disorder characterized by irregular movements associated more with the use of antipsychotic medications that may be the causative. Oral tardive dyskinesia is additionally accompanied by painful sensations that are a source of profound distress for the patient. Because of its strong association with medications, oral tardive dyskinesia is also known by the name drug-induced dyskinesia. It is often reported in patients who are under long-term therapy with antipsychotic medications. However, at times the person may develop oral tardive dyskinesia even in the starting stage of antipsychotic therapy.
What Are the Causes of Oral Tardive Dyskinesia?
Although it is a rare disease, it is known more in cases of patients with first-generation antipsychotic drugs (FGAs). Sometimes the cause of the pain is also related to the use of these antipsychotic drugs, dental conditions, or often a dyskinetic tongue. The most common cause remains antipsychotic medications commonly used like Haloperidol, Fluphenazine, Risperidone, Olanzapine, etc.
Why Do These Patients Suffer Stigma?
According to clinical signs, most of the time, oral tardive dyskinesia does not cause pain or physical disabilities. But the main reason why these patients need moral, medical, and personal holistic support overall is because of the mental trauma or feelings of shame and personal stigma. The source of discomfort is when patients are conscious of their dyskinetic movements feeling that a social disability is present within them. Thus these patients often feel embarrassed, anxious, or suffer from feelings of depression due to their stereotypical dyskinetic movements.
Social stigma can also traumatize these patients, and that is because the presence of obviously odd movements can lead to feelings of inferiority and stigmatization. Feelings of shame are a common reason for seeking medical attention from psychiatrists or healthcare providers, or physicians. The core feature characterizing orofacial dyskinesia is the buccolingual-masticatory triad. This triad is basically composed of involuntary movements of the tongue, jaw, lips, or face. The twisting, curling, or protrusion of the tongue is common, along with abnormal chewing movements or lateral jaw movements. The actions like pursuing or puckering, sucking, etc., of the lips, coupled with frequent eye blinking in most cases, give an impression of anxiety and shame to the patient.
What Is the Pathogenesis of Oral Tardive Dyskinesia?
The cause of oral dyskinesia can be traced to mainly the use of antipsychotic therapy indicated in older psychotic patients, especially with the long-term use of antipsychotic drugs of the phenothiazine and butyrophenone groups used therapeutically. Several biochemical mechanisms have been accepted by researchers, including partial denervation or hypersensitivity of the brain dopamine receptors. It is also established in the literature that tardive dyskinesia in neurologic diseases like schizophrenia and Parkinson's disease (induced by L-DOPA causing oral dyskinesias) can occur accompanied by Parkinsonian symptoms in these patients.
The possible contribution by numerous oro-dental factors such as edentulism in older individuals or elderly patients can not only generate oral dyskinesia but also potentially worsen the orofacial triad of symptoms. In edentulous oral dyskinesia, it is a result often of defects in proprioceptive occurring due to loss in nerve endings and periodontal ligament of the tooth that is lost as a result of a lost tooth or an extracted tooth. The loss of periodontal ligament and limited nerve supply has been suggested in traditional literature as one plausible mechanism.
Clinical findings also support the fact that edentulous oral dyskinesia might take place in view of inadequate occlusion and over the closed vertical dimension of the jaw. This change in vertical dimension at occlusion (VDO) is associated with several factors like biomechanical factors, denture stability, masticatory muscle forces, and facial support. Also, long-standing term or chronic oral dyskinesias can definitely result in premature wear and instability of the dentures. The damage potentially either to the gingival or the underlying alveolar bone structures can cause atrophy and additional prosthetic problems.
In spite of oral dyskinesia being caused due to predisposition, the most common cause in documented cases reported is of cerebral origin. A transient chemical disruption that, in turn, leads to inhibitory signaling in the lentiform nucleus may also cause orofacial dyskinesia in clinical research studies and trials in monkeys, while a deep brain stimulation of the external globus pallidus is the cause of contralateral stereotypes involuntary muscle movements or "chores" in humans.
How Is Oral Tardive Dyskinesia Managed?
The combating strategy for the treatment of TD includes modification of the antipsychotic medication regimens. This includes drug dosage reduction if possible complete cessation of the antipsychotic drug used regularly. If the neurologist requires the patient to continue the therapy, then switching from one generation of antipsychotic medication to another, like FGA to SGA, may significantly help.
According to clinical trials and research on documented cases, that is, switching from a first-generation to a second-generation antipsychotic with a lower D2 affinity, such as Clozapine or Quetiapine, has also proven to be effective in reducing tardive dyskinesia symptoms.
Currently, recent decades have shown strong research evidence for tardive dyskinesia treatment with the use of VMAT (vesicular monoamine transporter) inhibitors. Commonly used VMAT inhibitors are Deutetrabenazine and Valbenazine, with more efficacy than tetrabenazine drugs. However, the knowledge about potential side effects for long-term clinical use is limited or elusive and needs further research.
What Are the Risks and Complications Associated With the Treatment of Oral Tardive Dyskinesia?
Individuals with psychotic disorders definitely require long-term antipsychotic therapy; however, in order to prevent a remission of their symptoms, the continuation of antipsychotic medication is indicated. The long-term impact of these medications, however, is always associated with a worsening of clinical features of the triad of oral tardive dyskinesia over time and associated with high relapse rates. In most cases, discontinuing the medication or dosage changes or switching to another antipsychotic drug should be undertaken with great caution by the physician, or else this results in a relapse of their neurologic condition.
The studies on the impact of offensive medications on dopamine and acetylcholine neurotransmission suggest that these transmitters are implicated in the process and expression of inducting oral dyskinesia. Research studies have also found that the yearly incidence of oral tardive dyskinesia remains consistent throughout the exposure to antipsychotic medications.
Research is also implicating that patients have a high probability of similar chance of developing these recurrent complications during the first year as well as even during the fifth year of treatment. Other clinical studies have reported the rise in the incidence with extended or necessitated but prolonged duration of treatment by the physician as well.
Conclusion:
Oral tardive dyskinesia is a disabling clinical disorder that has psychosocial repercussions of the mental stigma that is not only hard to manage by the physician but also challenging neurologically. Clinicians should be firstly aware of the potential risk of tardive dyskinesia occurrence in patients on long-term treatment with antipsychotic drugs. Timely recognition of clinical features of dyskinesia along with psychological and social support in these patients helps in prompt recognition and management of this seriously challenging neurologic medical condition.
