Case debrief

The patient has a history of chronic MDD that ultimately became more treatment resistant and more complicated with the evolution of psychotic symptoms

Psychotic symptoms had to be differentiated from dissociative symptoms

Developed iatrogenic weight gain from her psychotropics that had to be aggressively managed in order to avoid undoing her bariatric surgery effects

Gained 30 lbs at one point, but half of this was ultimately lost due to pharmacological interventions noted earlier

This attention to side-effect mitigation allowed for a positive clinician–patient maintenance of rapport and compliance with medication polypharmacy

Developed TD after exposure to two different atypical antipsychotics that resolved completely after full antipsychotic discontinuation

This patient failed the more modern augmentation strategies where atypical antipsychotics, mood stabilizers, and stimulants were utilized

She failed psychotherapy combination treatment (supportive plus DBT strategies)

She failed one classic thyroid augmentation but has started to respond to a classic lithium augmentation

ECT would have been a reasonable acute treatment, but the patient declined

VNS or TMS might be a reasonable long-term option if lithium fails to provide complete remission in the future

Take-home points

This case emphasizes the need for full therapeutic trials of antidepressant treatments, augmentations, combinations, and psychotherapy

This case seems reasonable in that an MAOI was started after only a few antidepressant trial failures instead of waiting for several failures to occur. In this manner, the patient spent less time in a depressed state prior to MAOI therapy being utilized

Both novel and classic antidepressant augmentation strategies should be used

Rational polypharmacy is essential

• – Medications that were used serially did not overlap with regard to the antidepressant class. A mixture of trials using SNRI, MAOI, and TCA were employed

• – Augmentation strategies included drugs that operate outside the usual monoamine-enhancing agents

  • Lamotrigine (Lamictal) dampened glutamate

  • Thyroid hormone improved metabolism and perhaps provided trimonoamine facilitation, as it is theorized that this drug may increase production of NE, DA, and 5-HT in the midbrain

  • Lithium “did what lithium does,” which is largely unknown

    • Lithium might be a trimonoamine modulator and facilitate neuronal increases in available monoamines

    • It might stabilize neuronal membranes or second messenger systems via the inositol second messenger pathways

    • It might provide an increase in neurotrophic factors for better neural connectivity, improved brain circuitry, and communication with regard to its antidepressant mechanism of action

Performance in practice: confessions of a psychopharmacologist

What could have been done better here?

• – As the psychopharmacologist, seeing the patient every four to eight weeks may not have been adequate

  • She seemed to collect social stressors and become more depressed and even psychotic very quickly

  • Secondarily, increased contact with the therapist may also have provided a better alert to the pending full relapse

  • Finally, as antidepressant regimens are cross-titrated, there likely exists a time frame when overall antidepressant plasma levels are low, predisposing the patient to a depressive relapse

Possible action items for improvement in practice

• – Make sure that augmentation/combination strategies are all considered and weighed against potential for side effects, especially weight gain in this patient [pun intended]

  • Keeping this patient’s wishes to avoid weight gain in mind and having open discussions about these risks and benefits allowed her to stay involved in treatment, and even to take medications with some metabolic risks

  • The patient was more willing to maintain her medications and having achieve therapeutic dosing based on rapport developed in this manner