Background and Purpose-Cerebral microbleeds (CMB) are common in stroke survivors and the community-dwelling elderly. The clinical significance of CMB in the development of depression after a stroke is unknown. This study examined the association between poststroke depression (PSD) and CMB. Methods-A cohort of 235 patients with acute lacunar stroke admitted to the stroke unit of a university-affiliated regional hospital in Hong Kong was recruited. Three months after the onset of the index stroke, a research assistant administered the locally validated 15-item Geriatric Depression Scale. PSD was defined as a Genetic Depression Scale score of Ն7.The presence and location of CMB were evaluated with MRI. Results-In comparison with the non-PSD group, PSD patients were more likely to have lobar CMB (33.3% versus 19.9%; Pϭ0.022). Lobar CMB remained an independent predictor of PSD in the multivariate analysis, with an odds ratio of 2.08 (Pϭ0.032). Conclusions-The

Background: Apathy is common in stroke survivors. Unlike poststroke depression, apathy after stroke has not been extensively investigated and the significance of the location of infarcts in the development of apathy following a stroke is unknown. This study examined the association between poststroke apathy (PSA) and the location of infarcts. Methods: A cohort of 185 patients with acute ischemic stroke admitted to the Stroke Unit of a university-affiliated regional hospital in Hong Kong was recruited. Three months after the index stroke, a psychiatrist administered the Apathy Evaluation Scale (AES). PSA was defined as an AES score of 37 or above. The presence and location of infarcts were evaluated with magnetic resonance imaging. Results: Altogether 185 patients met the entry criteria and formed the study sample; 20 (10.8%) had PSA. PSA patients were older and had higher stroke severity and more depressive symptoms. The PSA group also had lower levels of physical and cognitive functioning. Compared with the non-PSA group, PSA patients were more likely to have acute pontine infarcts (35.0% vs. 11.5%; p = 0.011). They had a higher mean number (0.5 ± 0.7 vs. 0.1 ± 0.3; p = 0.003) and larger volume (0.6 ± 1.4 vs. 0.1 ± 0.3 ml; p = 0.002) of acute pontine infarcts. Six variables were entered into the predictive regression model: age, the presence, number and volume of acute pontine infarcts, the number of old infarcts and periventricular white matter hyperintensities scores. The volume of infarcts remained an independent predictor of PSA in the multivariate analysis, with an odds ratio of 3.9 (p = 0.007). The Geriatric Depression Scale, National Institutes of Health Stroke Scale, Barthel Index and Mini-Mental State Examination scores were also entered into the subsequent associative regression model; the volume of acute pontine infarcts remained a significant predictor (odds ratio = 3.8). Conclusions: This is the first report of an association between pontine infarcts and the risk of PSA. The results suggest that pontine infarcts may play a role in the development of PSA. The importance of acute pontine infarcts in the pathogenesis of PSA warrants further investigation.