Drug-induced parkinsonism (DIP) and tardive dyskinesia (TD) are movement disorders associated with antipsychotic drugs (APDs). In fact, up to one-third of patients taking APDs have TD or DIP. It is important to evaluate and treat these disorders because if left unrecognized, they can cause negative attitudes toward the patient’s treatment with antipsychotics. This can lead to reduced adherence and impact their function and quality of life.
In the case of DIP, the slowness of movements, the tremor, all those are very detrimental to the patient's well-being and quality of life.
TD is very important to evaluate and treat because it is an irreversible movement disorder. With other movement disorders, we can reduce the dosage of the antipsychotic or discontinue the medication to treat it since they are not permanent. However, with TD, APD reduction or complete withdrawal may fail to improve the symptoms of TD or might even induce withdrawal dyskinesia.
It has been very harmful using the term "EPS." By definition, any movement disorder other than spasticity is an EPS. However, it does not make sense to lump everything together as extrapyramidal because it can mean too much movement, too little movement, too fast, or too slow. When one term means different things to different people, it creates ambiguity, which is not ideal when it comes to medical documentation. The classification of EPS can obscure actual important clinical differences.
It is equivalent to referring a patient to a cardiologist for "heart problems" without specifying if there's an arrhythmia, stroke, myocardial infarction, or peripheral vascular disease. The diagnosis matters because the prognosis and treatment are different for each one. Similarly, with EPS, identifying the movement disorder is important because the prognosis and treatment are different for each movement disorder.
A major reason goes back to the use of "EPS" to categorize all movement disorders into one single diagnosis. As a result, patients usually received a single treatment, which historically was only anticholinergics until the approval of vesicular monoamine transporter 2 (VMAT2) inhibitors for TD. Also, with the first-generation APDs, there was a high percentage of patients who had early dystonia or parkinsonism. Many providers prescribed anticholinergics to prevent painful dystonia and improve adherence.
TD should be thought of as its own separate disorder instead of a side effect of antipsychotics. TD requires its own specific treatment, and it doesn't go away by discontinuing the antipsychotic. Back in 2017, I reevaluated all of my patients on benztropine. It is important to ask yourself, is this indicated and am I using it correctly for the right diagnosis? By doing this, I identified patients who actually had TD and worked on putting them on a VMAT2 inhibitor and then slowly transitioned them off the anticholinergics.
Many providers are willing to use rescue medications for movement disorders that are reversible; however, they are unwilling to treat irreversible movement conditions like TD. Providers should be encouraged to use a VMAT2 inhibitor to treat TD if it has an impact on the patient. The American Psychiatric Association (APA) recommends that patients who have moderate to severe or disabling TD associated with antipsychotic therapy be treated with a reversible inhibitor of the VMAT2. The APA guidelines also state that even patients with mild TD should be considered for VMAT2 inhibitor treatment based on factors such as patient preference, associated impairment, or effect on psychosocial functioning.
The misdiagnosis of TD and DIP is very common because many psychiatrists have gotten to be a little hyperfocused on looking for hand movements and lip movements because those two are very common symptoms of TD. They concentrate on lip puckering, lip smacking, tongue thrusting, and then piano playing movements for the hands. However, those are also the same places that patients with DIP can have tremors. Patients with DIP can have the rapid tremor of the lower lip, and there can be the classic pill-rolling tremor. If the psychiatrist hyperfocuses on just hand and lip movements, DIP may at first glance look similar to TD. Thus, it is important to evaluate the rest of the body for markedly diminished amounts of movement. It is important to also check the patient's blinking, facial expressions, arm movement, and gait.
The difference between TD and DIP is still confusing to some providers, and many are not using the activation maneuvers or assessing for rigidity as well. Historically, psychiatry providers have been taught that we don’t touch patients or that we only treat above the neck. Both of those harm our ability to make this differential because you have to look at the whole body and think about the whole body. You have to be hands-on and assess for rigidity, at least at the elbow. Other joints should be assessed as best practice, but at the minimum we should assess for both cogwheel and lead pipe rigidity at the elbow.
The key is to assess routinely. The screening for drug-induced movement disorders should not be seen as something heroic. The APA recommends assessment with a structured instrument such as the Abnormal Involuntary Movement Scale (AIMS), upon initiation of an APD, at a minimum of every 6 months in patients at high risk of TD, and at least every 12 months in other patients, as well as if a new onset or exacerbation of preexisting movements is detected at any visit. In my own practice, I made it routine to screen for movement disorders at every visit. It is unrealistic to do an AIMS assessment at every visit; however, I conduct semistructured exams at every visit. For instance, one exam that can be done at every visit is having patients tap their fingers to see if it elicits any movement. This takes approximately 10 to 15 seconds; it is a screening I can do for TD with every patient every time. After a few visits, it becomes routine for patients, and if I forget, a patient will say "Aren't you going to make me tap my fingers this time?" A semistructured assessment should be informed by a baseline AIMS and should include asking about and observing abnormal movements.
It is important to explain to patients what you're doing and why you're doing it and make the assessment simple. It should be as routine as weighing a patient every visit. A high index of suspicion along with consistency in screening is the best way to find drug-induced movement disorders because they are very prevalent. These movement disorders are subtle and insidious; especially early on, we may miss them, and they can cause the patient problems. They can disrupt the treatment of the patient's underlying illness.
We designed a survey that included healthcare providers who are treating patients with approved VMAT2 inhibitors. The survey included psychiatrists, primary care providers, psychiatric physician assistants (PAs) and nurse practitioners (NPs), as well as nonpsychiatric NPs and PAs to cover different disciplines that treat patients with drug-induced movement disorders. We also did a retrospective claims analysis among patients with evidence of benztropine initiation with a 3-year time frame of January 2017 through March 2020 to assess treatment patterns and healthcare resource utilization.
There were several findings, most notably a lot of use of anticholinergic medication that is not consistent with guideline recommendations. It was surprising that a large percentage of healthcare professionals reported that they specifically would use one particular anticholinergic, benztropine, to treat TD, not just to treat movement disorders in general. This was surprising because in the prescribing information for benztropine, it states that it is not recommended to treat TD and that it can even worsen TD.
There were a number of participants in the survey who reported that they used benztropine prophylactically not just to prevent movement disorders, but also to specifically prevent TD. The Diagnostic and Statistical Manual of Mental Disorders, 5th Edition, Text Revision (DSM-5-TR) and APA guidelines highlight that anticholinergic treatment can worsen the symptoms of TD. The APA guidelines note that anticholinergic therapy can impair quality of life and cognition; therefore, they should not be administered prophylactically.
It is important to first assess the patient's thoughts about the medication. I've noticed some patients are very attached to benztropine, as it can be mood elevating. This can cause a physiologic dependence, and patients are concerned about how they will feel if the anticholinergic is discontinued. If you approach them by just saying, "I want to take you off the anticholinergic," they will react negatively. By understanding their feelings toward the medication, you can mention that you don't think they need the medication and that you would like to help them slowly taper off of it to avoid withdrawal symptoms. I have had success with slow and steady tapers in practice, and patients can benefit by no longer experiencing the negative consequences of anticholinergics.
When patients have TD, I start the VMAT2 inhibitor first, monitor for progress, and then start to taper the anticholinergic. I have observed that patients are more convinced of the utility of decreasing the anticholinergic once they experience initial benefit with VMAT2 inhibitors. Then I explain that they could improve even more if we decrease and eventually taper off the anticholinergic because that can worsen the TD.
