Seasonal and atypical depression — structured clinical viva

This is recurrent winter-pattern major depression with atypical features (mood reactivity should be confirmed; reverse vegetative signs and rejection sensitivity are already suggested). Frame SAD as a seasonal pattern specifier, not a freestanding exotic disease. Confirm multi-year onset/remission, exclude nonseasonal episodes that would break the specifier narrative, and always bipolar-screen.[6]

Mechanisms. Discuss photoperiod reduction, retinohypothalamic input to the SCN, melatonin phase markers, and the phase-delay model in which morning bright light phase-advances circadian timing. This justifies why night-time light is usually the wrong default for classic winter SAD.[1]

Light therapy is scientific. Cite meta-analytic support for light therapy in mood disorders and Can-SAD equivalence of light and fluoxetine for winter SAD. Give parameters: ~10,000 lux, morning, ~20–30 minutes, eyes open toward the box, ocular cautions, switch monitoring.[1][2]

MAOIs. Acknowledge classic phenelzine-over-imipramine teaching in atypical depression, then explain modern stepped care: SSRI/SNRI/bupropion and psychotherapy first for most patients; irreversible MAOIs reserved for specialist refractory pathways with diet and interaction infrastructure. Cognitive therapy also has controlled evidence in atypical depression.[4]

Prevention now (autumn, currently well). Anticipatory bupropion XL started before expected onset and continued through winter is evidence-based prevention; April in southern-hemisphere autumn can be an appropriate planning/start window depending on her historical onset month. CBT-SAD is an alternative or complement with durability signals across later winters.[3][5]