Back Back
Initiating TD Management

CE / CME

eCase: Identifying TD and Initiating Management in Patients With Primary Mood Disorders

Physician Assistants/Physician Associates: 1.00 AAPA Category 1 CME credit

Nurses: 1.00 Nursing contact hour, including 1.00 hour of pharmacotherapy credit 

Social Workers: 1.00 ASWB ACE CE Credit

Pharmacists: 1.00 contact hour (0.1 CEUs)

Psychologists: 1.00 APA CE Credit

Physicians: Maximum of 1.00 AMA PRA Category 1 Credit™

Released: September 30, 2022

Expiration: September 29, 2023

Jacob Ballon
Jacob Ballon, MD, MPH
CME/CE Information

Activity

Progress
1
Course Completed

TD is a potentially disabling neurologic condition that has long been associated with chronic dopamine blockade, primarily from antipsychotic medications. It is characterized by involuntary movements, most commonly in the muscles around the face and mouth, but also can involve the trunk and extremities.1 Despite the strong association with chronic dopaminergic blockade, the precise mechanism of TD is not known.2 With the introduction of second-generation—or “atypical”—antipsychotics, there was hope that TD risk would be diminished with different presynaptic activity at the dopamine receptor.3 Unfortunately, however, these hopes have not come to fruition and TD continues to pose challenges to patients who receive long-term antipsychotic medications or other dopamine-receptor antagonists. In a meta-analysis of 41 studies of TD, the incidence of TD in people treated with second-generation antipsychotics is lower than with first-generation antipsychotics, but the incidence of TD is still significant in both groups. In patients who receive long-term second-generation antipsychotic drugs, the incidence of TD is 20%, whereas the incidence for those receiving long-term first-generation antipsychotic drugs is 30% (P = .002). The difference remained significant even after controlling for factors known to increase risk for TD including age, duration of illness, and frequency of parkinsonian symptoms (Table).4

Table. Nonmodifiable and Modifiable Risk Factors for TD5

Finding effective treatments for TD has proven elusive. Among the first observations upon the description of TD was that the antipsychotic drugs that appeared to cause TD also suppressed its symptoms—such that upon their withdrawal, the patient’s movements often worsened, especially if the cessation is not done gradually.6 Increasing the dose of the antipsychotic or switching to a different antipsychotic may appear to help, but in reality, it is likely further masking TD symptoms. Again, upon withdrawal, the symptoms often re-emerge without any diminution.7,8 Further attempts at treating TD included drugs that diminished dopaminergic transmission such as tetrabenazine and reserpine.6 However, the depletion of dopamine appeared to result in significant depressive symptoms and suicidal ideation (although in a recent large database study, these observations were not seen).9 In recent years, the FDA has approved 2 novel VMAT2 inhibitors, deutetrabenazine and valbenazine, specifically for treatment of TD. These novel options have significantly altered the treatment paradigm for patients who experience TD.10,11