Abstract
This month’s issue of International Journal of Stroke (IJS) has a particular focus on China. China represents 18% of the world’s population and consistent with its large population contributes much of the global burden of stroke. In this month’s issue of the IJS, Zhao and colleagues 1 review the prevalence, incidence, mortality, and case fatality of stroke in China. This review provides a useful benchmark of where we are at present. It emphasizes that despite improved public health policy and healthcare delivery, the burden of stroke remains high in China. The pooled annual prevalence figures obtained from a review of 26 population-based studies was 1329.5/100,000. 1 They show that in contrast to some other developed countries, the prevalence and incidence of stroke have both increased over recent decades in China, although stroke-related case fatality has declined.
A second related article, also in this month’s issue, looks at the quality of stroke care in China between 2011 and 2017. Li and colleagues 2 analyzed data from 123,259 patients diagnosed with acute ischemic stroke who were treated at 109 large tertiary hospitals in China. Twelve stroke treatment indicators were selected to calculate a process performance score. After adjusting for confounders, patients with the highest score were more likely to gain independence after stroke. A wide variation in quality of stroke care was found to exist across hospitals, and better adherence to guideline-based care was associated with improved outcomes. This work emphasizes that the more widespread adoption of best practice throughout China is likely to improve outcomes from Stroke, as it will elsewhere.
We have many IJS readers, and manuscript submissions, from China but are keen to welcome more and to be as accessible as possible. For this reason, we are very pleased to announce that IJS is now on WeChat. The name of the official WeChat account is “IntJStroke.” The logo with a QR code is provided in Figure 1. The titles and abstracts of selected accepted articles are being uploaded, having been translated by our editorial board member Xinyi (Cindy) Leng and associate editor Thomas Leung. A great thanks to Cindy. From late December 2022 when first launched to 31 January 2023, there have been over 2000 views from over 1300 readers, over 6 posts.
QR code for IJS on WeChat.
Apathy is a common and disabling symptom after stroke. 3 It shares some similarities with depression, but studies have shown it to be a separate entity and that the two can be distinguished. 4 Interestingly, recent studies have suggested that apathy relates to disruption of white-matter pathways underlying complex cortical-sub cortical circuits, while depression is not associated with similar white-matter tract damage.4,5 Therefore, one might expect the two to respond differentially to specific therapies. However, whether apathetic symptoms respond to antidepressants is uncertain. Small studies have suggested they may do, 6 but robust evidence is lacking. In this issue, Tay and colleagues 7 analyzed a large clinical trial data set to answer this question. They used data from the EFFECTS study, which randomized patients with recent stroke to fluoxetine versus placebo. They show that while fluoxetine was associated with less progression of depressive symptoms after stroke, apathetic symptoms increased after stroke, and fluoxetine had no effect on this increase. These data suggest that Selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine do not reduce apathy after stroke, and that alternative therapeutic strategies are required to treat this disabling symptom.
Post-stroke delirium (PSD) affects up to 39% of patients with ischemic stroke, is associated with inferior functional and cognitive outcome, and represents an important, but modifiable, predictor for poor recovery. Unfortunately, PSD management is often unrecognized, and initiation of pharmacological and non-pharmacological interventions is delayed. While it remains to be clarified to what extent interventional approaches can reduce the impact of manifest PSD, prevention of PSD is effective and can avert up to one-third of cases. If we are to prevent PSD, we need to know what risk factors increase its risk. In this issue, Fleischmann and colleagues 8 prospectively investigated patients with ischemic stroke admitted within 24 h, and screened them for delirium twice daily throughout the treatment period. PSD occurred in 40% of patients. Both age and male sex were significant non-modifiable risk factors. In a multivariable model adjusted for age and sex, presence of pain, urinary catheter use, and post-stroke infection were all predictors of PSD incidence. Importantly, PSD independently predicted worse National Institutes of Health Stroke Scale (NIHSS) at discharge. Interestingly, they found that insular and basal ganglia lesions increased the PSD risk about four- to eight-fold. Their results emphasize the frequency of PSD, confirm its association with worse outcome, and highlight some predictors that if treated or avoided could reduce the risk of PSD.
There has been considerable excitement about the potential of remote ischemic postconditioning (RIC) to treat acute ischemic stroke. RIC refers to an intervention where an ischemic stimulus is applied distant from the brain (e.g. a limb) within hours after an ischemic stroke, potentially resulting in neuroprotection. RIC consists of several cycles of brief periods of limb ischemia followed by reperfusion, which can be applied by inflating a simple blood pressure cuff. The presumed neuroprotective effects of RIC are hypothesized to be related to a reduction of ischemia reperfusion injury in the brain after the ischemic stroke, and are supposedly most prominent when RIC is started as soon as possible after the onset of symptoms.
The results of REPOST (The effect of REpeated rIPostC on infarct size in patients with an ischemic STroke) are published in this issue. REPOST was a randomized single-blind placebo-controlled clinical trial, performed at a single center in Nijmegen, Netherlands. 9 Adult patients admitted with an ischemic stroke in the past 24 h were randomized 1:1 to repeated RIC or sham-conditioning. Repeated RIC was performed by inflating a blood pressure cuff around the upper arm (4 × 5 min at 200 mm Hg), which was repeated twice daily during hospitalization with a maximum of 4 days. The primary outcome was infarct size after 4 days, or at discharge. The trial was prematurely stopped after 88 of the scheduled 180 patients had been included. There was no significant treatment effect; median infarct volume was 2.19 mL in RIC group and 5.90 mL in sham-conditioning, which was not significantly different (median difference: 3.71; 95% confidence interval: −0.56 to 6.09; p = 0.31). However, it was interesting that while not being significant, the infarct size trended smaller in the RIC group. Previous trials in this area have shown conflicting results, both positive and negative. A recent systematic review concluded that it appeared to be safe, and there may be a suggestion of efficacy, but whether it is really effective remains to be determined. 10 It also highlighted how previous studies had been small and underpowered and that we now need larger definitive trials to confirm whether this treatment, which is been highly effective in animal models, translates into clinical benefit. The protocol for such a trial, SERIC-IVT, in which RIC is given as an adjunct to intravenous thrombolysis is also published in this issue. 11
An interesting study in this month’s issue looks at whether attention-deficit hyperactivity disorder (ADHD) could be a risk factor for stroke. 12 The authors point out that previous observational studies have found an association between the two, but this could be because both share similar risk factors, that is, due to confounding, rather than representing a causal association. Du and colleagues applied Mendelian randomization to assess whether this relationship is indeed causal. This involves using genetic data to determine whether genetic variants predisposing to the trait in question (in this case ADHD) predispose to the outcome measure (in this case stroke). It allows an estimate of causality, because genetic variants are randomly distributed during meiosis and provide a measure of exposure since birth. Using this approach, the authors found that genetically determined ADHD was significantly associated with a higher risk of any ischemic stroke, and specifically large artery atherosclerotic stroke. These are intriguing findings, although how ADHD might increase the risk of stroke remains a mystery.