Our very elderly stroke population’s overall PSD rate, assessed a mean of ∼4 months post-stroke, reached 44.8%, with no significant difference for those evaluated before or 3 months post-event. Our PSD patients’ MADRS-assessed depression intensity was moderate/severe for 39%. Stroke-attributable ≥ 1 mRS-point gain was the only independent PSD predictor.
Study-population neurological parameters (relatively small parenchymal lesion volume, mean admission NIHSS = 2.25, mean mRS = 1.8 post-stroke) highlighted relatively low overall stroke severity, keeping in mind that patients with communication impairment or severe disability were excluded, which represents an important limitation.
However, our results reflect real-world stroke in the very elderly, as < 20% can be assessed for PSD after the acute phase. Nonetheless, considering post-stroke functional disability as the main PSD predictor, we think our results probably underestimate the real PSD rate. Indeed, PSD was common after minor strokes, but its cumulative rate was lower than for all-type–stroke survivors.9
Despite diverse screening methods used to detect PSD, a meta-analysis showed a relatively constant ∼30% PSD rate, regardless of the time-to-assessment until 10 years.2 Those patients’ mean age was 65–71 years, ∼15 younger than our specifically geriatric PSD population. The relatively high PSD rate in very old stroke survivors might be explained by the elderly’s overall high vulnerability to depression, and their relatively low capacity for mental readjustment to their new acute stroke-generated state.4 Also, their relatively short life expectancy and low probability of returning to their pre-stroke state can contribute to frequent loss of morale. Depression prevalences for the elderly in the general population are 4.4% (75–84 years) and 5% (≥ 85 years) ;10 its risk is multiplied by ∼10 for aged stroke victims.
PSD impact on our patients’ quality of life (QOL) is difficult to evaluate and represents another limitation. However, even a mild mood disorder has been shown to negatively affect stroke survivors’ long-term QOL,2,9 meaning clinical detection of even a mild morale dip could improve their QOL.
What do our results bring to clinical practice? The recent large, randomized FOCUS, AFFINITY and EFFECTS trials did not confirm the initially positive effect of fluoxetine, an SSRI, on stroke recovery.11–13 Although their results clearly demonstrated fluoxetine efficacy against PSD, it was unfortunately offset by the doubled bone-fracture risk. 11–13 Therefore, post-stroke patients at-risk of PSD must be identified instead of systematically prescribed preventive antidepressants. Our observations suggest that a ≥ 1 mRS-point gain after the stroke’s acute phase, regardless of the final functional grade, can identify very elderly patients at high risk of developing PSD, for whom depression screening or even preventive antidepressant therapy could be justified.