Tardive Dyskinesia and How the Nervous System Works

A video from the Depression and Bipolar Support Alliance discusses information about tardive dyskinesia (TD), as well as how the nervous system works. Some people do not have enough, too much, or irregular neurotransmitters to bind to receptors that can cause irregular signaling, possibly explaining the symptoms of mental health conditions including schizophrenia, bipolar disorder, and depression. In order to treat mental health conditions, antipsychotics are often given, and much of these therapies are dopamine-receptor blocking agents. More signaling can occur when dopamine is binding to hypersensitive dopamine receptors, having an impact on areas of the brain that impact motor function, causing TD.

Using “Extrapyramidal Symptoms” in Practice: Expert Perspective

In this article, John J. Miller, MD, editor-in-chief of Psychiatric Times™, gives insight on the diversity of movement disorders that may result from the use of dopamine-2 receptor blocking agents. He explains that because the diagnosis and treatment of different movement disorders can be considerably different, treating one of them can worsen another. Therefore, he urges healthcare professionals to stray from using the term extrapyramidal symptoms, or EPS, as he has always thought that EPS was too vague and nondescript of a term, as its definition consists of various potential movement disorder adverse effects. Dr. Miller explains that drifting from this term can help improve the diagnosis and treatment of different movement disorders that can be caused by the use of dopamine-2 receptor blocking agents. He gives examples to support his point-of-view and how the community has gained a better understanding of the connection between dopamine-2 receptor blocking agents and movement disorders.

An Overview of Extrapyramidal Side Effects

One of the most common adverse effects from dopamine-receptor blocking agents are drug-induced movement disorders, or extrapyramidal side effects (EPS). The below link walks through the cause, pathophysiology, and presentation of EPS. The authors also highlight the types of drugs that are known to cause EPS and a summary a both the symptoms and treatment of EPS. The role of the healthcare team in improving outcomes for patients who have EPS is also discussed.

Video-Based Review: Differentiating Tardive Dyskinesia

It is important for an accurate diagnosis of tardive dyskinesia (TD), as well as a suitable treatment plan, as the symptoms of TD can be disruptive to both patients and caregivers. A misdiagnosis of TD can result in inaccurate interventions that may lead to harmful or poor outcomes. Researchers conducted a video-based review to help identify and differentiate TD in the psychiatric setting through looking at its clinical features and phenomenology, in addition to those of other antipsychotic-induced movement disorders. Movement phenomenology, current dose reduction or discontinuation of a dopamine-receptor blocking agent, and history of exposure to a dopamine-receptor blocking agent are how a differential diagnosis of TD is established. Challenges in diagnosing TD include other movement disorders that are linked to dopamine-receptor blocking agents, as well as abnormal behaviors and dyskinesias that are linked to older age or chronic mental illness. The duration of exposure can help in ruling out some drug-induced syndromes. Something else that the researchers note is to consider the possibility of TD presenting along with another drug-induced movement disorder. This can make diagnosis and management more complex in the same patient. Treatment options should be assessed with patients and their caregivers following documentation of the phenomenology, severity, and distribution of TD movements.

Information on Tardive Dyskinesia

UpToDate provides information on the prevention, treatment, and prognosis of tardive dyskinesia (TD). The disorder is linked to the use of dopamine receptor-blocking therapies that include first- and second-generation antipsychotics. TD commonly presents as spontaneous mouth and tongue movements. A less common feature of TD is dystonia of areas including the neck. TD has a negative impact on quality of life and psychologic wellbeing, as it may be irreversible and lifelong. Discontinuing the therapy that is causing TD is the best chance for a patient to recover.

Recognizing the Differences Between Tardive Dyskinesia and Drug-Induced Parkinsonism

Researchers conducted a literature review to locate articles on drug-induced parkinsonism (DIP) and tardive dyskinesia (TD) that related to the presentation, pathophysiology, epidemiology, and management of the disorders to note key differences between them. The presentation of DIP is often bradykinesia and rigidity, including rhythmic tremor, with the most cases seen within hours to weeks after the initiation of treatment with an antipsychotic or increase in dosage of an antipsychotic. The presentation of TD is often delayed, showing signs after at least 3 months or more of treatment with involuntary and abnormal facial movements. DIP can be resolved after discontinuing the therapy that caused it, but TD can be permanent. It is crucial for clinicians to be able to identify DIP and TD in those taking antipsychotics so that they are able to select the correct treatment and lessen adverse effects, improving patient quality of life.

Neuropsychiatric Assessment Through Telepsychiatry

A study sought to determine if the Abnormal Involuntary Movement Scale (AIMS), which relies on visual judgements, can be a reliable measurement tool through video chat. AIMS scores were examined by 2 independent raters in face-to-face contact and 2 raters assessing remotely through audio-visual transmission. Intraclass Correlation Coefficient was used to determine inter-rater reliabilities. No considerable difference was found between the raters, which may be due to the condition while examining involuntary movements using the AIMS. Researchers noted that the results were dependable to the same degree.

Meta-Analysis of Tardive Dyskinesia Prevalence With Use of Second-Generation Antipsychotics

Investigators of a meta-analysis looked to compare the prevalence of tardive dyskinesia (TD) during the use of first-generation antipsychotics (FGAs) and/or second-generation antipsychotics (SGAs). Studies were screened from January 1, 2000, to September 30, 2015. Random effects meta-analysis and meta-regression were used for 41 studies that were selected. Among these studies, global mean prevalence of TD was 25.3% (95% CI = 22.7%-28.1%). TD rates were lower in those who had current SGA treatment (20.7%; 95% CI = 16.6%-25.4%, N = 5,103) compared with current FGA treatment (30.0%; 95% CI = 26.4%-33.8%, N = 5,062; Q = 9.17, P =.002). Lower prevalence of TD (7.2%; number of studies = 4) was seen in treatment groups with those who were FGA-naïve relative to those who were treated with SGA with likely previous exposure to FGA (23.4%; P <.001; 28 studies). TD severity, that was seen in 10 studies, was of insufficient quality for the meta-analysis. Overall, higher rates of TD were seen with FGA compared with SGA therapy. Because there were insufficient reports of TD severity, the clinical impact of identified TD cases with SGAs and FGAs were not investigated. High geographical variation that was found brings a need for future research on this subject matter.

Lithium and Tardive Dyskinesia

On the Psychiatry & Behavioral Health Learning Network, Dr. Goldberg discusses the link between lithium and tardive dyskinesia (TD). While rare, Dr. Goldberg states that there is evidence of lithium causing TD in case reports. He also states what the course of action may be for someone who has taken lithium for 30 years who has suddenly developed shaking.

Drugs That Cause Tardive Dyskinesia

Tardive dyskinesia (TD) is mainly caused by the prolonged use of antipsychotic therapies. There are newer atypical antipsychotic therapies that are only sometimes linked to TD that include olanzapine, quetiapine, risperidone, paliperidone, and amisulpride. Other drugs that may cause TD include metoclopramide, antihistamines, fluoxetine, and amoxapine. When a patient is diagnosed with TD, treatment may include a reevaluation and adjustment of medications. There are available treatments to aid in counteracting the symptoms of TD. Those with schizophrenia, developmental disabilities, and other neuropsychiatric disorders may be more susceptible to TD if they are prescribed dopamine-receptor blocking therapies.