Background and purpose: Dysphagia is associated with poor outcome, higher mortality, reduced quality of life, and social isolation. We investigate the relationship between swallowing impairment and symptoms of anxiety and depression after ischemic stroke.Methods: Consecutive patients with ischemic stroke participating in the prospective STROKE‐CARD Registry study from 2020 to 2022 were assessed for dysphagia on hospital admission (clinical swallowing assessment) and for persistence until discharge and 3‐month follow‐up (SINGER Independency Index). Anxiety and depression symptoms were recorded using Beck Depression Inventory (BDI) and Hospital Anxiety and Depression Scale (HADS) at 3‐month follow‐up.Results: Of 648 patients, 19.3% had dysphagia on admission, persisting in 14.8% at discharge and 6.8% at 3‐month follow‐up. With the presence or duration of dysphagia (no dysphagia, dysphagia at baseline, at discharge, at 3 months), score (mean ± SD) increased on the BDI (7.9 ± 6.7, 12.5 ± 8.7, 13.5 ± 9.0, 16.5 ± 10.2), HADS‐D (4.4 ± 3.7, 7.1 ± 4.2, 7.7 ± 4.4, 9.8 ± 4.3), and HADS‐A (4.4 ± 3.5, 5.4 ± 3.6, 6.0 ± 3.6, 7.0 ± 3.6). In linear regression analysis adjusting for age, sex, diabetes, dementia, and either functional disability or stroke severity, BDI and HADS‐D scores were significantly higher in patients with dysphagia across all points in time (admission, discharge, 3‐month follow‐up). An independent association with HADS‐A scores was only evident in patients with persisting dysphagia after 3 months. Patients with dysphagia were more likely to receive antidepressants, antipsychotics, or benzodiazepines at discharge and 3‐month follow‐up.Conclusions: Dysphagia after stroke is common and severely affects psychosocial functioning of individuals. Our results highlight swallowing impairment as an independent predictor for poststroke depressive and, to a lesser extent, anxiety symptoms.

Background: Post‐stroke dysphagia is known to have a pronounced effect on mortality and quality of life of stroke patients. Here, we investigate whether this extends to post‐stroke fatigue, a major contributor to morbidity after ischemic stroke.Methods: Patients with acute ischemic stroke (recruited consecutively in the STROKE‐CARD Registry from 2020 to 2023 at the study center Innsbruck, Austria) were examined for dysphagia via clinical swallowing examination at hospital admission. Post‐stroke fatigue was assessed using the Fatigue Severity Scale (FSS) at study specific in person follow‐up visits within the first year after ischemic stroke.Results: Among 882 ischemic stroke patients (mean age 72.4 ± 13.5 years, 36.8% females), dysphagia was present in 22.0% at hospital admission and persisted in 16.2% until hospital discharge. Post‐stroke fatigue affected 52.2% of the total cohort during follow‐up and was significantly more prevalent among those with dysphagia (68.4% vs. 49.0%, p < 0.001). The prevalence of fatigue increased with the severity of dysphagia, with the highest proportion (86.7%) in those with severe dysphagia. After multivariable adjustment for other factors associated with post‐stroke fatigue, including age, sex, pre‐stroke disability, cognitive impairment, stroke severity, inability to walk at discharge, and need for antidepressants at discharge, dysphagia remained independently associated with post‐stroke fatigue during the first year after stroke (odds ratio [OR]: 2.03, 95% confidence interval [CI]: 1.22–3.38).Conclusions: Dysphagia is common after ischemic stroke and increases the risk of post‐stroke fatigue. Patient‐tailored measures are warranted to reduce fatigue after stroke and therefore enhance quality of life.

Background: Recent advances in acute stroke therapy improved short-term outcome, but some of this benefit may be lost due to post-stroke complications, including fractures. Aims: We assessed the incidence of fractures before and after stroke and transient ischemic attack (TIA), the risk factors for fractures, and the consequences for mortality, functional outcome, and quality of life. Methods: Consecutive patients with acute ischemic stroke or TIA from the prospective STROKE-CARD Registry and the randomized controlled STROKE-CARD trial and its long-term follow-up were analyzed. We prospectively assessed all fractures using self-report and documentation, records of hospitals and general practitioners, and electronic health records with all radiographs. Results: A total of 2513 patients were included (median age = 72 years (interquartile range, IQR = 61–79), 39.2% female). In the first year after the event, 145 individuals (5.8%, 95% confidence interval (CI) = 4.9%–6.7%) experienced 152 fractures corresponding to an incidence rate of 61.87 (95% CI = 52.04–71.71) per 1000 person-years. Rates were similar after stroke and TIA (60.84 and 72.28 per 1000 person-years). The incidence of fractures was more than five times higher compared to the general population (age- and sex-adjusted hazard ratio (HR) for first fracture 5.36, 95% CI = 2.49–11.52). The risk of fractures 1 year before stroke/TIA was also increased (HR = 2.99, 95% CI = 1.39–6.42). Stroke/TIA further increased the risk of fractures as documented by a comparison between fractures 1 year before and 1 year after the event (age- and sex-adjusted risk ratio = 1.69, 95% CI = 1.10–2.58). The main risk factors for fractures were falls and osteoporosis. Fracture after stroke/TIA was associated with death (adjusted odds ratio (aOR) = 2.16, 95% CI = 1.20–3.89), inability to walk (aOR = 2.06, 95% CI = 1.08–3.93), and poor quality of life. Conclusions: Patients with ischemic stroke and TIA are at high risk for future fractures. Fracture after stroke/TIA is strongly associated with death, poor functional outcome, and reduced health-related quality of life. Therefore, there is a need to incorporate fracture prevention into post-stroke care to improve patient outcomes. Trial Registration: STROKE-CARD Registry (NCT04582825, https://clinicaltrials.gov/study/NCT04582825 ); STROKE-CARD trial (NCT02156778, https://clinicaltrials.gov/study/NCT02156778 ); STROKE-CARD long-term follow-up (NCT04205006, https://clinicaltrials.gov/study/NCT04205006 ).

Introduction: Complications may secondarily impair functional outcome after stroke and transient ischemic attack (TIA). Here, we estimated the population-level impact of complications on long-term functional outcome to describe their combined impact and identify the most impactful complications. Patients and methods: Patients admitted for acute ischemic stroke or TIA (ABCD2 score ⩾ 3) and discharged without severe disability were followed-up for occurence of 12 in-hospital and 26 post-discharge complications. Population-level impact of complications on the primary endpoint of non-excellent functional outcome (modified Rankin Scale (mRS) > 1) at end of follow-up 12 months after stroke was assessed by population attributable fraction (PAF). This cohort study was performed at a single European comprehensive stroke center and nested within a randomized controlled trial of intensified post-stroke care, STROKE-CARD. Results: Among 1705 patients aged 69.4 ± 13.6 years (59.8% male), 36.8% (95% confidence interval: 34.5, 39.2) had non-excellent outcome at 12 months, 21.3% (19.4, 23.3) had unfavorable outcome (mRS > 2), and functional worsening occurred in-hospital in 2.6% (2.0, 3.6) and post-discharge in 20.3% (18.4, 22.3). Non-excellent 1-year functional outcome was predicted in-hospital by occurrence of recurrent stroke, neurological worsening, and infections (PAF: 0.6%–3.2%). Post-discharge, 12 complications significantly predicted outcome, and pain, severe fatigue, falls, and depression were most impactful (PAF: 5.4%–13.0%). Together, in-hospital complications accounted for 7.6% and post-discharge complications for 31.8% of non-excellent outcome, whereas acute therapy (thrombolysis and/or thrombectomy) and STROKE-CARD care accounted for 8.0% and 14.5% of excellent outcomes. In moderate and severe stroke (NIHSS > 5), acute therapy was the strongest predictor of excellent outcome (PAF: 29.1%). Results were consistent or stronger in patients with TIA, without prestroke disability, or in the regional catchment area, and when focusing on unfavorable outcome or worsening in mRS. Discussion: Complications were responsible for more than one third of non-excellent 1-year functional outcome with pain, severe fatigue, depression, and falls most impactful. Complications rivaled the impact of acute therapy and determined functional outcome after TIA as well as after stroke. Conclusion: Effective prevention and treatment of complications may substantially improve long-term functional outcomes after stroke and TIA.

BACKGROUND: Poststroke dysphagia is associated with poor functional recovery and psychological consequences, including depression and fatigue, which may impede successful rehabilitation. Here, we investigate whether antidepressants may improve dysphagia recovery after acute ischemic stroke. METHODS: In this prospective cohort study, patients with acute ischemic stroke (aged ≥18 years; consecutively enrolled in the STROKE-CARD trial (Post-Stroke Disease Management) 2014 to 2019 and registry 2020 to 2023 in Innsbruck, Austria) were examined for poststroke dysphagia (by standardized clinical and instrumental examinations) and antidepressant intake at hospital admission, discharge, and inpatient 3-month follow-up. The outcome was full oral diet resumption 3 months poststroke. Associations were analyzed using multivariable logistic regression and are presented as adjusted odds ratios, adjusting for age, sex, stroke severity, dysphagia severity, depression severity, stroke localization, thrombolysis, cognitive impairment, functional disability before stroke and at hospital discharge, and study type. RESULTS: Poststroke dysphagia affected 380 (18.6%) of the total cohort of 2046 patients at hospital admission (mean age, 72.7±14.1 years; 37.8% women) and persisted in 290 (14.7%) and 95 (4.6%) patients until hospital discharge and 3-month follow-up, respectively. Among the 290 patients with persistent dysphagia at discharge included in the outcome analysis, antidepressant intake increased from 4.8% before stroke to 27.6% at hospital discharge and 49.0% at 3 months ( P <0.001). A total of 195 (67.2%) of 290 patients with persistent dysphagia regained full oral diet by 3 months, with significantly higher recovery rates in those who were discharged on antidepressants (78.8% versus 62.9%; P =0.010). Antidepressant intake at hospital discharge was independently associated with improved dysphagia recovery at 3 months (adjusted odds ratio, 2.98 [95% CI, 1.51–5.87]; P =0.002). CONCLUSIONS: Antidepressant intake was associated with better dysphagia recovery after acute ischemic stroke. As these findings are observational, randomized trials are required to clarify whether antidepressants can support dysphagia rehabilitation.