LAS VEGAS – When it comes to the pharmacologic treatment of patients with dysthymic disorder, the best scientific evidence points to selective serotonin reuptake inhibitors as a first-line treatment, Dr. Hagop S. Akiskal said during a psychopharmacology conference sponsored by the Nevada Psychiatric Association. This includes fluoxetine, sertraline, and citalopram, to a maximum of 40 mg/per day.
Suggested second-line interventions include mirtazapine, duloxetine, venlafaxine, and bupropion, said Dr. Akiskal, professor of psychiatry at the University of California, San Diego.
Doug Brunk/Elsevier Global Medical News
Dr. Hagop S. Akiskal
When first- and second-line interventions for dysthymic disorder fail, consider trying the tricyclic antidepressants desipramine or nortriptyline. Another option is the reversible monoamine oxidase inhibitor (MAOI) moclobemide, though this agent is not approved for use in the United States. "Don’t forget phenelzine and tranylcypromine, with certain dietary/pharmacologic restrictions," Dr. Akiskal said. "There’s also selegiline, which has been used for a long time to treat Parkinson’s disease, but it’s controversial as to whether dietary and pharmacologic restrictions should be as vigorous with this agent as with phenelzine and tranylcypromine. I would use it thinking it’s less problematic than those two agents, but still be on your guard."
He went on to highlight certain dietary and drug restrictions with irreversible MAOIs to avoid hypertensive crises. These include aged cheeses, concentrated yeast extracts, sauerkraut, broad bean pods, tap beers (though other alcoholic beverages "might be safe if consumed in moderation"), some aged meats, which "contain relatively high levels of tyramine and require closer scrutiny," pickled fish, and concomitant serotonergic antidepressants.
Dr. Akiskal, who is also editor in chief of the Journal of Affective Disorders, noted that dysthymic disorder shares many similarities to major depressive disorder, including a familial association, phase advance of REM sleep, diurnal variation, effects on thyroid-stimulating hormone and thyrotropin-releasing hormone, elevated levels of plasma corticotrophin-releasing factor, sleep deprivation response, response to antidepressants, and treatment-emergent hypomania.
On functional MRI, dysthymic patients show significantly more right amygdala, right thalamic, right fusiform gyrus, and left cerebellar activity, compared with controls for the negative-neutral contrast. "The point is, dysthymia is presented in the brain; it’s not in the ‘mind’ of the patient," Dr. Akiskal said.
Dr. Akiskal disclosed that he is a consultant for the Lilly and the Lundbeck foundations. He also is a member of the speakers bureau for AstraZeneca, BioMarin, Bristol-Meyers Squibb, Dey Pharma, GlaxoSmithKline, Merck, and Sanofi.