<p>Initiating therapy for tardive dyskinesia (TD) involves balancing clinical management with individual patient needs, as TD management can present unique challenges and considerations. An accurate diagnosis and personalized care that addresses both the practical aspects of treatment initiation and the impact of symptoms on the patient’s functioning and quality of life are necessary to manage TD effectively.</p>

The pathophysiology of TD is not well understood, but there are known risk factors. Older age, female sex, African ethnicity, longer illness duration, some cognitive or mood disorders, and gene alterations are all unmodifiable patient- or illness-related risk factors. There are also modifiable factors that we should consider to prevent TD from occurring. These include diabetes, smoking, and alcohol use, which all increase the likelihood of developing TD. Finally, clinicians must use DRBAs cautiously to minimize the risk of too much dopamine blockade, which could lead to parkinsonism, akathisia, and, ultimately, TD.

 

Differentiating TD from other movement disorders, such as parkinsonian side effects, Parkinson disease, Tourette syndrome, or tremors, prevents misdiagnosis and ensures appropriate treatment. The Abnormal Involuntary Movement Scale (AIMS) is an invaluable tool for assessing the severity and distribution of TD symptoms. With TD, you want to understand how long the symptoms have been present, the severity and distribution of symptoms, and the impact that these symptoms are having on the patient. So, the location of a patient’s TD symptoms can be very important, especially if their motor symptoms impact their job or ability to interact with others, which can lead to depression or social withdrawal.

 

When diagnosing TD, clinicians should first assess whether the DRBA can be reduced or replaced, especially in patients with mood disorders for whom alternative treatments might be viable. Patients with TD who are on a first-generation antipsychotic should be switched to a second-generation antipsychotic, if possible, because there is a less profound dopamine blockade with the use of second-generation agents. In the future, potential therapies, such as muscarinic receptor agonists and positive allosteric modulators, that do not block postsynaptic dopamine receptors may also be an option when switching therapies. This may help TD symptoms as well, although more research is needed.

 

If lowering the dose or stopping the potentially offending DRBA is not possible or helpful, adding a VMAT2 inhibitor such as valbenazine or deutetrabenazine is recommended to reduce the patient’s TD symptoms while maintaining the needed antipsychotic effectiveness. Close monitoring and careful dose adjustments are important during the initiation of VMAT2 inhibitor therapy. After starting treatment with a VMAT2 inhibitor, you want to follow improvements in not only the severity of the movements but also their frequency and distribution. So, I do follow-up AIMS testing each time I see a patient to have an objective assessment.

 

Clinicians should also follow up with the patient, asking them questions about how their symptoms are improving. Here, input from the patient’s family or caregiver(s) can also be helpful. How often do they have symptoms (ie, what percentage of the day or week)? Has the impact on their ability to work improved? Do they feel psychologically less stressed and more relieved? Are they able to leave the house and feel less ashamed and have more social interactions? These are all aspects that go into patient care. We are treating not only a movement and a muscle that twitches but also the entire patient, so we need to address what their TD means to them, how it interferes with their life, and what their goals are.