Cerebral changes and cognitive impairment after an ischemic heart disease: a multimodal MRI study.

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.

Cerebellum involvement in post-stroke mood: a combined ecological and MRI study.

This study evaluated a new approach combining magnetic resonance imaging and the experience sampling method in the understanding of post-stroke mood pathophysiology. Findings revealed that emotional cognition after stroke may be related to phenotypic characteristics such as cerebellar volume, thereby suggesting that this combined approach could provide new insights into the pathophysiology of post-stroke mood disorders as well as other forms of comorbidity.

Subacute default mode network dysfunction in the prediction of post-stroke depression severity.

PURPOSE: To identify patterns of rest functional connectivity (FC) in the whole brain with the default mode network (DMN) soon after stroke and to explore the predictive accuracy of the strength of rest FC in specific areas on poststroke severity of depression and anxiety symptoms. MATERIALS AND METHODS: The protocol was accepted by the local ethics board, and all patients provided informed consent to participate. Resting-state functional magnetic resonance (MR) images were acquired 10 days after a first stroke in 24 patients without a history of psychiatric illness. Independent component analysis was used to isolate the DMN in each subject. Hamilton Depression Rating Scale (HDRS) 17 and Hamilton Anxiety Rating Scale (HARS) were recorded 10 days and 3 months after the stroke. Associations between severity of anxiety or depression symptoms and DMN functional connectivity were investigated with whole-brain analyses by using statistical parametric mapping software and were adjusted for age, sex, manual laterality, and National Institutes of Health Stroke Severity scores. Correlations were considered significant if P<.001, with a cluster size of more than 50 voxels. RESULTS: Ten days after stroke, anxiety severity was correlated with functional connectivity in the middle temporal cortex and the anterior midcingulate cortex, while at 3 months after stroke, a correlation was observed with the middle temporal cortex and the posterior cingulate cortex. Poststroke depressive symptom severity did not correlate with functional connectivity changes at 10-day follow-up, while the HDRS 17 score was correlated with functional connectivity in the left middle temporal cortex and precuneus at 3-month follow-up. CONCLUSION: 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.

Evolution of depression symptoms following stroke: a prospective study using computerized ambulatory monitoring.

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.

Early temporal short-term memory deficits in double transgenic APP/PS1 mice.

We tested single APP (Tg2576) transgenic, PS1 (PS1dE9) transgenic, and double APP/PS1 transgenic mice at 3 and 6 months of age on the acquisition of a hippocampal-dependent operant "differential reinforcement of low rate schedule" (DRL) paradigm. In this task mice are required to wait for at least 10 seconds (DRL-10s) between 2 consecutive nose poke responses. Our data showed that while single APP and PS1 transgene expression did not affect DRL learning and performance, mice expressing double APP/PS1 transgenes were impaired in the acquisition of DRL-10s at 6 months, but not at 3 months of age. The same impaired double transgenic mice, however, were perfectly capable of normal acquisition of signaled DRL-10s (SDRL-10s) task, a hippocampal-independent task, wherein mice were required to emit responses when the end of the 10-second delay was signaled by a lighting of the chamber. The age-dependent and early deficits of APP/PS1 mice suggest that the appetitive DRL paradigm is sensitive to the amyloid pathology present in double APP/PS1 mice, and that this mouse line represents a good model with which to study the efficacy of therapeutic strategies against Alzheimer's disease.