The history of tardive dyskinesia (TD) is intertwined with the development and use of antipsychotic medications.  TD was first observed after the introduction of first-generation antipsychotic drugs (also known as typical antipsychotics) such as chlorpromazine (Thorazine) and haloperidol (Haldol) in the 1950s. These medications revolutionized the treatment of schizophrenia and other psychotic disorders.

Within a few years of their widespread use, clinicians began noticing abnormal, involuntary movements, particularly in patients who had been on these drugs long-term. These movements typically involved the face, tongue, and limbs.  The term “tardive dyskinesia” was introduced in the 1960s. “Tardive” means delayed, referring to the fact that the symptoms often appear after prolonged exposure to antipsychotics. “Dyskinesia” describes the involuntary movements.  It became clear that TD was more common in older patients, and those who had been on antipsychotics for extended periods. However, the exact mechanism was not fully understood.

Research linked TD to dopamine receptor hypersensitivity, particularly in the basal ganglia, caused by long-term dopamine blockade by antipsychotics.  This hypothesis makes a case for the use of new antipsychotics like pimavanserin, with no impact on the dopamine receptor.  Also, newer generation antipsychotics’ tendency to result in TD is less pronounced. Risk factors such as age, female gender, and cumulative dose of antipsychotics were recognized.  Clinicians faced a challenge: while antipsychotics were essential for managing psychosis, but prolonged use risked causing TD. There were limited treatment options available at the time.

Greater awareness of TD has led to careful monitoring of patients on long-term antipsychotics and efforts to minimize drug exposure when possible.  Rating scales like the AIMS test are required in long-term care settings to evaluate for TD and monitor for its development and progression.  

Over the past several decades the pharmaceutical industry has made significant strides in this arena.  The development of second-generation (atypical) antipsychotics was a significant milestone. These drugs have a lower risk of causing TD but do not eliminate it entirely.   New treatments for TD, such as valbenazine (Ingrezza)  and deutetrabenazine (Austedo), were approved by the FDA in the 2010s. These medications are vesicular monoamine transporter 2 (VMAT2) inhibitors and represent a significant step forward in symptom management.  Both of these medications are covered by Medicare Part D plans and may require a prior authorization process.   

In addition, there is still a great deal of reluctance in skilled nursing facilities to identify a patient as having TD.  Since it is still an adverse effect of long term antipsychotic use, facilities may shy away from identification of TD to avoid scrutiny by the department of health regarding “overuse” of antipsychotics.

However, LTC providers need to look at the big picture.  Many of the symptoms associated with TD may lead to difficulty swallowing, and an increase in risk for aspiration.  And this challenge does not even begin to address the the social stigma associated with involuntary facial and other movements.  

Lets’s do right by our patients: acknowledge the challenge of tardive dyskinesia, be on the lookout for it, and consider initiating the available treatments for our patients suffering from TD.