We studied 45 subjects with MRl-identified lesions limited to the basal ganglia or cerebellum. 24.4% had post-stroke secondary (2 °) DSM-llI-R depressive disorders: Major Depression (MD) 9 subjects; Depressive Disorder NOS (DDNOS) 2; Dysthymia 0. Subjects were never depressed prior to infarction. 2 ° MD was more common than ECA age-, sex-, and race-matched conlrol life prevalence: OR 3.50, 95% Ci 0.88 ,.13.92, p,,0.03). Based upon previous work, we hypothesized 2 ° MD associations with Parkinsonism, thalamic lesions, and dystunia. 2 ° MD: We compared post-stroke 2 o MD to similar controls who had depression before their stroke (n-9) using Mann-Whitney U and Fisher's Exact tests. There was more Parkinsonism (6 subjects, p-0.038) with higher PDRS scores (p-0.065) and illness stage (p-0.072), and more thalamic lesions (5 subjects, p-0.033), but no greater dystonia (5 subjects) although there was less dystonic geste (i subject, p-0.024) in 2 ° MD subjects. 2 ° MD subjects had a longer follow-up interval (42.9±22.2 vs. 21.9±!6.0 months, U-52.0, p-0.035) and more cerebellar signs on exam (6 subjects, !)-0.025). 2 ° MD did not differ from controls in regard to demographics, social factors, or depression rating scales (BDI and HRSD). These data suggest associations of late-developing post-stroke 2 ° MD with Parkinsonism and dystonic phenomena, implicating ventral striatal dopamine. Cerebellar signs and thalamic lesions suggest centromedian or pulvinar thalamocortical (glutamatergic) insufficiencies. Pallidal lesions in 7 of 9 are consistent with this, or may imply thalamo-orbitofrontal overdrive in post-stroke MD.