These results suggest that a dysfunction of DMN functional connectivity involved in emotional control is associated with the severity of poststroke depression. Further studies are necessary to determine the mechanisms of this functional impairment.

Background: Despite the high prevalence and impact of post-stroke depression (PSD), questions persist concerning the nature and stability of PSD over time. The current study uses state-of-the-art computerized ambulatory monitoring techniques to assess daily life depression symptoms following stroke and examines the evolution of depression levels over a three-month period. Methods: 48 patients admitted to a university hospital neurology unit for ischemic or hemorrhagic stroke participated in ambulatory monitoring of DSM-IV depression symptoms for a one-week period after hospital discharge. Clinician-administered measures of depression were also obtained at discharge and again three months later. Results: The percentage of the sample with elevated depression scores was the same at discharge and three months later, but consistency in depression profiles was low. Ambulatory monitoring revealed that elevated depression levels at hospital discharge were most strongly associated with anhedonia (t ratio = 4.840, p < 0.001) and fatigue (t ratio = 4.00, p < 0.001), whereas individuals with elevated scores at three months were predicted by daily life negative thoughts (t ratio = 4.051, p < 0.001), anxious mood (t ratio = 3.489, p < 0.01), sad mood (t ratio = 2.621, p < 0.05) and emotional reactivity (t ratio = 2.466, p < 0.05). Conclusions: The prevalence of depression may appear stable during the immediate weeks and months following stroke, but it is likely to be composed of very different symptom profiles. The immediate physical and psychological impact of stroke may induce somatic symptoms that explain elevated depression levels and which may not indicate a risk factor for later depression.

Three to 6 months after an acute coronary syndrome (ACS), cognitive impairment is observed in more than 30 % of the patients, mainly in executive functioning. The aim of this study was to investigate, using multimodal MRI, cerebral anatomo-functional substratum of executive dysfunction. Thirty-three patients were recruited 4 ± 1 months after a first ACS. Executive functions were evaluated with the Trail-Making-Test-B (TMTB) at baseline (ie 4 ± 1 months after ACS) and 6 months later (ie 10 ± 1 months after ACS). Using both time-points, we identified 3 groups of patients according to normative data based on age, gender and education level: 15 'cognitively normal' patients without impairment at each follow-up, 10 'transient impaired' patients with an impairment only at baseline and 8 'impairing' patients with an impairment only at follow-up. We explored, in the whole-brain, the structural integrity using Voxel-Based Morphometry and Tract-Based Spatial Statistics and the resting-state functional connectivity using Network-Based Statistics. No structural difference was observed between impaired and cognitively normal patients. At the functional level, compared to the 'cognitively normal' group, the 'transient impaired' patients presented an increased functional connectivity in a network centered on middle-orbito-frontal regions, whereas the 'impairing' patients presented only a non-significant decrease of functional connectivity. Executive dysfunction in ACS patients is associated to functional but no structural characteristics, particularly to an increased functional connectivity in cognitive networks in transient impaired patients. Further studies with larger sample size are needed to confirm these results and to determine if these patients could be at higher risk for developing permanent cognitive disorders.

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Novel mobile technologies provide information that is inaccessible to hospital-based tests, and allow for more complete investigations of disorder expression and etiology.