Predictors for baseline fatigue were younger age, post-stroke depressive symptoms, and infratentorial infarctions. Baseline fatigue did predict fatigue outcome over time, suggesting that early interventions might be useful to prevent deteriorated PSF.

The pathophysiology of episodic memory dysfunction after infarction is not completely understood. It has been suggested that infarctions located anywhere in the brain can induce widespread effects causing disruption of functional networks of the cortical regions. The default mode network, which includes the medial temporal lobe, is a functional network that is associated with episodic memory processing. We investigated whether the default mode network activity is reduced in stroke patients compared to healthy control subjects in the resting state condition. We assessed the whole brain network properties during resting state functional MRI in 21 control subjects and 20 ‘first-ever’ stroke patients. Patients were scanned 9–12 weeks after stroke onset. Stroke lesions were located in various parts of the brain. Independent component analyses were conducted to identify the default mode network and to compare the group differences of the default mode network. Furthermore, region-of-interest based analysis was performed to explore the functional connectivity between the regions of the default mode network. Stroke patients performed significantly worse than control subjects on the delayed recall score on California verbal learning test. We found decreased functional connectivity in the left medial temporal lobe, posterior cingulate and medial prefrontal cortical areas within the default mode network and reduced functional connectivity between these regions in stroke patients compared with controls. There were no significant volumetric differences between the groups. These results demonstrate that connectivity within the default mode network is reduced in ‘first-ever’ stroke patients compared to control subjects. This phenomenon might explain the occurrence of post-stroke cognitive dysfunction in stroke patients.

Background: Caring for patients with dementia at home is often a long-term process, in which the independence of the patient declines, and more responsibility and supervision time is required from the informal caregiver. Objective: In order to minimize and reduce caregiver burden, it is important to explore its trajectory and the accompanying risk factors as dementia progresses; the objective of this systematic review. Methods: PRISMA guidelines were followed in this systematic review. Three databases, PubMed, PsycINFO, and EMbase, were systematically searched in November 2019 using specific keywords. Results: 1,506 hits emerged during the systematic search but only eleven articles actually met the inclusion criteria for this review. The trajectory of caregiver burden is highly variable and depends on multiple factors. Important risk factors included: patients’ behavioral and neuropsychiatric symptoms, and their decline in functioning in (I)ADL; the caregiver’s age, gender, and physical and mental health; and, within the dyads (patient/caregiver), cohabitation and kinship. Conclusion: There is no one-size-fits-all for predicting how caregiver burden will change over time, but specific factors (like being a spouse and increased behavioral impairment and decline in functional status in the patient) may heighten the risk. Other factors, not yet comprehensively included in the published studies, might also prove to be important risk factors. Future research in the field of reducing caregiver burden is recommended to integrate the patient, caregiver, and context characteristics in the trajectory of caregiver burden, and to assess more clearly the phase of the dementia progression and use of external resources.

Background: Several studies have described the frequency and risk factors of post-stroke depressive symptoms (PSDS). However, most studies did not exclude patients with depressive symptoms shortly before stroke and paid little attention to prestroke risk factors of depression, including previous depressive episodes, white matter lesions, and brain atrophy. These are potential limitations to assess the true effect of stroke on the occurrence of depressive symptoms. Our aim was to investigate the prevalence and risk factors of PSDS with adjustments for the previously mentioned prestroke factors. Methods: 420 consecutive patients with an acute clinical symptomatic transient ischemic attack or cerebral infarction were eligible for enrolment in this study. The presence of PSDS was rated by the Hospital Anxiety and Depression Scale 6–8 weeks after stroke. The relation between (pre-) stroke factors and PSDS was assessed with multivariate regression analysis. Results: The prevalence of PSDS was 13% and did not differ between stroke subtype or first-ever/ever occurrence of stroke. Higher degree of post-stroke handicap was related to PSDS (OR = 5.39; 95% CI = 2.40–12.08) and more functional independence had a protective effect on PSDS (OR = 0.88; 95% CI = 0.77–1.00). Conclusions: This is the largest study that investigated the prevalence and risk factors of PSDS by carefully excluding patients with depressive symptoms shortly before stroke. PSDS were not related to lesion side or location, but to the degree of post-stroke handicap and functional independence. Early detection of PSDS and their risk factors might help to predict long-term outcome and could promote early interventions of (behavioral) rehabilitation treatment strategies.

Background and Purpose-Poststroke memory dysfunction is a prerequisite for the diagnosis of poststroke dementia. This diagnosis is made within months after a stroke, apparently assuming a relatively stable course of the poststroke memory function. Clinical experience added to anecdotal evidence from the literature suggests that poststroke memory function may be reversible. The aim of the present study was to systematically review the available data on the time course of poststroke memory function in nondemented stroke survivors. In addition, we wanted to investigate the role of (pre-)stroke characteristics on poststroke memory function. Methods-We performed systematic literature search of PubMed with the following medical subject heading terms: memory and stroke. The search strategy yielded 798 articles of which 65 fulfilled our inclusion criteria and went on to the data extraction stage. Results-Five studies reported the prevalence of poststroke memory dysfunction at different poststroke intervals. The prevalence of poststroke memory dysfunction varied from 23% to 55% 3 months poststroke, which declined from 11% to 31% 1 year poststroke. Larger stroke volume, prestroke medial temporal lobe atrophy, and white matter lesions were related with decreased poststroke memory function. Conclusions-Not all patients with poststroke memory dysfunction 3 months after a stroke had memory dysfunction 1 year poststroke. Consequently, not all criteria for the dementia diagnosis were fulfilled any more. This may indicate that poststroke dementia may be reversible in a substantial proportion of patients with stroke. Preferably, standardized reassessment of cognitive function should be performed in each patient diagnosed with poststroke dementia. (Stroke.