Case debrief

The patient has a lengthy history of recurrent MDD, ranging from low levels to full MDEs. They appear unipolar in nature and have been responsive to antidepressant plus augmentation approaches

This case was difficult in that she did achieve remission for the first time in many years with the addition of an atypical antipsychotic Unfortunately, this class of agents are often effective in the treatment of MDD but carry the risk for TD, which she did develop

This case was also complicated in that she had PMEs, personality disorder traits, and some somatic symptoms that were difficult to navigate. However, once the MDD symptoms lessened, these complicating factors also improved

The clinician tried to pharmacodynamically re-create her aripiprazole (Abilify) by using buspirone (BuSpar), to no avail. Next, working with the patient’s desires to keep medication at a minimum, staying within a trusted class of medication (SNRI), she was able to be titrated to a significantly higher than usual but approved dose (desvenlafaxine [Pristiq] 300 mg/d), where she began a gradual and sustained response

The low-dose diazepam (Valium) also likely improved her stress-induced lability issues as well, and was a serendipitous addition by an outside provider

Take-home points

It can be difficult to determine whether certain symptoms are from depression, stress, personality, medical, or cultural variables

Working with a few medications and maximizing their doses for therapeutic effects makes clinical sense until side effects occur and change the risk/benefit analysis

Side effects ultimately make clinicians change treatments, sometimes in the face of remission, which is clinically difficult in that the next set of medications may work better, worse, or the same – or may have different or worse side effects

Often during these medication switches, patients are undertreated initially with low doses or due to new side effects and the risk of depressive relapse is high

In this case, the patient was titrated rapidly to a moderate-high SNRI dose in order to achieve a better therapeutic effect more quickly to avoid relapse. This was successful. Side effects were alleviated and depressive remission was restored on a minimum of medications

Performance in practice: confessions of a psychopharmacologist

What could have been done better here?

• – Should more pressure for psychotherapy (dynamic, dialectical, or otherwise) have been given, noting her personality traits?

• – This might have alleviated the need for an atypical antipsychotic trial and the emergence of TD

Can one really “re-create” a complex medicine like the atypical Abilify (aripiprazole)?

• – 5-HT1A partial agonism could come from buspirone (BuSpar) as in this case

• – 5-HT2A antagonism could come from nefazodone (Serzone) or trazodone ER (Oleptro)

• – Cannot easily obtain dopamine-3 (D3) partial receptor agonism from another agent (e.g., ropinirole, pramipexole)

• – Do not want to get D2 receptor antagonism from another typical or atypical antipsychotic agent, or more TD could occur

• – Perhaps it was over zealous, too theoretical, and a waste of time attempting the buspirone (BuSpar) augmentation