Association between dysphagia and symptoms of depression and anxiety after ischemic stroke.

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.

Disparities between guideline statements on acute and post-acute management of cervical artery dissection.

Even though cervical artery dissection is one of the main reasons for ischemic stroke in young patients, acute management and post-acute primary or secondary prevention of cerebral ischemia differ significantly in different centers and countries. These discrepancies are reflected by the differences in guideline recommendations of major stroke societies. Our narrative review aims to shed light on the different recommendations in guideline-statements of stroke societies and to give an overview of the current literature concerning acute management and post-acute treatment of cervical artery dissection patients. In general, intravenous thrombolysis and mechanical thrombectomy are recommended, irrespective of stroke etiology, if administered within the label. Secondary prevention of cerebral ischemia can be achieved by antiplatelet intake or anticoagulation, with, to date, neither treatment establishing superiority over the other. Duration of antithrombotic treatment, statin use as well as optimal endovascular approach are still up for debate and need further evaluation. Additionally, it is still unknown, whether the recommendations given in any of the guideline statements are similarly relevant in spontaneous and traumatic cervical artery dissection, as none of the stroke societies differentiates between the two.

No association between SARS-CoV-2 vaccination and ischaemic stroke or high-risk transient ischaemic attack.

BACKGROUND: Initiation of SARS-CoV-2 (Severe acute respiratory syndrome coronavirus type 2) vaccinations aroused scepticism within the general-public about risks including stroke. Our aim was to explore temporal associations between vaccination and cerebrovascular events through an analysis of a prospective large-scale cohort of consecutive stroke and high-risk TIA (transitory ischaemic attack) patients. METHODS: We prospectively recruited a cohort of consecutive ischaemic stroke and high-risk TIA (ABCD2-Score ≥ 4) patients treated at the Innsbruck University Hospital (STROKE-CARD Registry Study, NCT04582825) from December 2020 until February 2022. SARS-CoV-2 vaccination status and the time of administration was ascertained by electronic health-data. A Cox model with vaccination status as time-dependent co-variable was employed to examine its association with ischaemic events. RESULTS: Data on 572 participants were available with 355 (62.1%) vaccinated against SARS-CoV-2 before suffering cerebral ischaemia. In our cohort, no temporal association between vaccination and cerebrovascular event was detected (HR 1.06 [0.85-1.34; p = 0.60]) and this also applies to TIA (HR [0.82 0.37-1.85; p = 0.64]) or minor stroke (HR 1.18 [0.89-1.56; p = 0.26]) and subgroups defined by sex and age. Neither vector-based (HR 1.11 [0.79-1.56; p = 0.55]) nor mRNA-based (HR 1.06 [0.84-1.34; p = 0.61]) vaccinations were associated with the occurrence of cerebral ischaemia. CONCLUSION: Among patients with stroke or high-risk TIA, SARS-CoV-2 vaccination was not associated with cerebral ischaemia.

Sleep disorders as both risk factors for, and a consequence of, stroke: A narrative review.

BACKGROUND AND PURPOSE: Sleep disorders are increasingly implicated as risk factors for stroke, as well as a determinant of stroke outcome. They can also occur secondary to the stroke itself. In this review, we describe the variety of different sleep disorders associated with stroke and analyze their effect on stroke risk and outcome. METHODS: A search term-based literature review ("sleep," "insomnia," "narcolepsy," "restless legs syndrome," "periodic limb movements during sleep," "excessive daytime sleepiness" AND "stroke" OR "cerebrovascular" in PubMed; "stroke" and "sleep" in ClinicalTrials.gov) was performed. English articles from 1990 to March 2023 were considered. RESULTS: Increasing evidence suggests that sleep disorders are risk factors for stroke. In addition, sleep disturbance has been reported in half of all stroke sufferers; specifically, an increase is not only sleep-related breathing disorders but also periodic limb movements during sleep, narcolepsy, rapid eye movement (REM) sleep behavior disorder, insomnia, sleep duration, and circadian rhythm sleep-wake disorders. Poststroke sleep disturbance has been associated with worse outcome. CONCLUSION: Sleep disorders are risk factors for stroke and associated with worse stroke outcome. They are also a common consequence of stroke. Recent guidelines suggest screening for sleep disorders after stroke. It is possible that treatment of sleep disorders could both reduce stroke risk and improve stroke outcome, although further data from clinical trials are required.

Spreading of Beta-Amyloid in Organotypic Mouse Brain Slices and Microglial Elimination and Effects on Cholinergic Neurons.

The extracellular deposition of ß-amyloid (Aß) is one of the major characteristics in Alzheimer´s disease (AD). The "spreading hypothesis" suggests that a pathological protein (similar to prions) spreads over the entire brain. The aim of the present study was to use organotypic brain slices of postnatal day 8-10 mice. Using collagen hydrogels, we applied different Aß peptides onto brain slices and analyzed spreading as well as glial reactions after eight weeks of incubation. Our data showed that from all tested Aß peptides, human Aß42 had the most potent activity to spread over into adjacent "target" areas. This effect was potentiated when brain slices from transgenic AD mice (APP_SweDI) were cultured. When different brain areas were connected to the "target slice" the spreading activity was more intense, originating from ventral striatum and brain stem. Reactive glial-fibrillary acidic protein (GFAP) astrogliosis increased over time, but Aß depositions co-localized only with Iba1+ microglia but not with astrocytes. Application of human Aß42 did not cause a degeneration of cholinergic neurons. We concluded that human Aß42 spreads over into other "target areas", causing activation of glial cells. Most of the spread Aß42 was taken up by microglia, and thus toxic free Aß could not damage cholinergic neurons.