Asia, which holds 60% of the world's population, comprises some developing countries which are in economic transition. This paper reviews the epidemiology of stroke in South, East and South-East Asia. Data on the epidemiology of stroke in South, East, and South-East Asia were derived from the Global Burden of Disease study (mortality, disability-adjusted life-years [DALYs] lost because of stroke), World Health Organization (vascular risk factors in the community), and publications in PubMed (incidence, prevalence, subtypes, vascular risk factors among hospitalized stroke patients). Age- and sex-standardized mortality is the lowest in Japan, and highest in Mongolia. Community-based incidence data of only a few countries are available, with the lowest rates being observed in Malaysia, and the highest in Japan and Taiwan. The availability of prevalence data is higher than incidence data, but different study methods were used for case-finding, with different age bands. For DALYs, Japan has the lowest rates, and Mongolia the highest. For community, a high prevalence of hypertension is seen in Mongolia and Pakistan; diabetes mellitus in Papua New Guinea, Pakistan, and Mongolia; hypercholesterolemia in Japan, Singapore, and Brunei; inactivity in Malaysia; obesity in Brunei, Papua New Guinea, and Mongolia; tobacco smoking in Indonesia. Hypertension is the most frequent risk factor, followed by diabetes mellitus and smoking. Ischemic stroke occurs more frequently than hemorrhagic stroke, and subarachnoid hemorrhages are uncommon. There are variations in the stroke epidemiology between countries in South, East, and South-East Asia. Further research on stroke burden is required.

Mixed vascular and neurodegenerative dementia, such as Alzheimer’s disease (AD) with concomitant cerebrovascular disease, has emerged as the leading cause of age-related cognitive impairment. The brain white matter (WM) microstructural changes in neurodegeneration well-documented by diffusion tensor imaging (DTI) can originate from brain tissue or extracellular free water changes. The differential microstructural and free water changes in AD with and without cerebrovascular disease, especially in normal-appearing WM, remain largely unknown. To cover these gaps, we aimed to characterize the WM free water and tissue microstructural changes in AD and mixed dementia as well as their associations with cognition using a novel free water imaging method. We compared WM free water and free water-corrected DTI measures as well as white matter hyperintensity (WMH) in patients with AD with and without cerebrovascular disease, patients with vascular dementia, and age-matched healthy control subjects. The cerebrovascular disease groups had higher free water than the non-cerebrovascular disease groups. Importantly, besides the cerebrovascular disease groups, patients with AD without cerebrovascular disease also had increased free water in normal-appearing WM compared with healthy control subjects, reflecting mild vascular damage. Such free water increases in WM or normal-appearing WM (but not WMH) contributed to dementia severity. Whole-brain voxel-wise analysis revealed a close association between widespread free water increases and poorer attention, executive functioning, visual construction, and motor performance, whereas only left hemispheric free water increases were related to language deficits. Moreover, compared with the original DTI metrics, the free water-corrected DTI metric revealed tissue damage-specific (frontal and occipital) microstructural differences between the cerebrovascular disease and non-cerebrovascular disease groups. In contrast to both lobar and subcortical/brainstem free water increases, only focal lobar microstructural damage was associated with poorer cognitive performance. Our findings suggest that free water analysis isolates probable mild vascular damage from WM microstructural alterations and underscore the importance of normal-appearing WM changes underlying cognitive and functional impairment in AD with and without cerebrovascular disease. Further developed, the combined free water and tissue neuroimaging assays could help in differential diagnosis, treatment planning, and disease monitoring of patients with mixed dementia.

Stroke is a major cause of death and disability in Indonesia. Stroke requires high-quality, fast, and precise management to prevent and avoid disability and death. Stroke can be prevented by adequately controlling the risk factors and encouraging healthy lifestyles. Efforts are needed to organize health promotion programs at the community level. More and a better distribution of neurologists and neurointerventionalists is needed. All hospitals should have a CT scan machine and stroke units. Telemedicine for stroke patients is a very promising endeavor for an integrated acute stroke management system.

Malaysia is located in the heart of South East Asia with two land masses, Peninsular Malaysia and East Malaysia which are separated by the South China Sea. Stroke or cerebrovascular disease is Malaysia’s third leading cause of death. There were 47, 911 incident cases, 19,928 deaths, 443,995 prevalent cases, and 512,726 DALYs lost due to stroke in 2019. Successive national health and morbidity surveys from 2006 demonstrated a continuous rise in the prevalence of risk factors such as diabetes, hyperlipidaemia, and obesity. These risk factors are implicated in an increase in stroke incidence in those under 65 years of age, the largest increase of 53.3% and 50.4% in men and women, respectively, from the age strata of 35–39 years. The neurologist-to-patient ratio is 1:323,000 with the majority of neurologists working in urban centres. The healthcare system is provided predominantly by the public and private sectors. Concurrent use of traditional and complementary medicine is common and widely accepted. Challenges include delivering adequate care to rural communities, the low overall ischaemic stroke thrombolysis rates, and the high cost of thrombectomy devices for use in large vessel occlusions which have to be borne out-of-pocket by patients and their families. Effort is required to continue improving stroke care services in parallel with primary and secondary prevention strategies in the future, given the ageing population and the rising number of strokes in young adults nationally. Strategies include careful planning, inter-hospital cooperation, and increased allocation of resources from the government.

Background: Coronavirus disease 2019 (COVID-19) has placed a tremendous strain on healthcare services. This study, prepared by a large international panel of stroke experts, assesses the rapidly growing research and personal experience with COVID-19 stroke and offers recommendations for stroke management in this challenging new setting: modifications needed for prehospital emergency rescue and hyperacute care; inpatient intensive or stroke units; posthospitalization rehabilitation; follow-up including at-risk family and community; and multispecialty departmental developments in the allied professions. Summary: The severe acute respiratory syndrome coronavirus 2 uses spike proteins binding to tissue angiotensin-converting enzyme (ACE)-2 receptors, most often through the respiratory system by virus inhalation and thence to other susceptible organ systems, leading to COVID-19. Clinicians facing the many etiologies for stroke have been sobered by the unusual incidence of combined etiologies and presentations, prominent among them are vasculitis, cardiomyopathy, hypercoagulable state, and endothelial dysfunction. International standards of acute stroke management remain in force, but COVID-19 adds the burdens of personal protections for the patient, rescue, and hospital staff and for some even into the postdischarge phase. For pending COVID-19 determination and also for those shown to be COVID-19 affected, strict infection control is needed at all times to reduce spread of infection and to protect healthcare staff, using the wealth of well-described methods. For COVID-19 patients with stroke, thrombolysis and thrombectomy should be continued, and the usual early management of hypertension applies, save that recent work suggests continuing ACE inhibitors and ARBs. Prothrombotic states, some acute and severe, encourage prophylactic LMWH unless bleeding risk is high. COVID-19-related cardiomyopathy adds risk of cardioembolic stroke, where heparin or warfarin may be preferable, with experience accumulating with DOACs. As ever, arteritis can prove a difficult diagnosis, especially if not obvious on the acute angiogram done for clot extraction. This field is under rapid development and may generate management recommendations which are as yet unsettled, even undiscovered. Beyond the acute management phase, COVID-19-related stroke also forces rehabilitation services to use protective precautions. As with all stroke patients, health workers should be aware of symptoms of depression, anxiety, insomnia, and/or distress developing in their patients and caregivers. Postdischarge outpatient care currently includes continued secondary prevention measures. Although hoping a COVID-19 stroke patient can be considered cured of the virus, those concerned for contact safety can take comfort in the increasing use of telemedicine, which is itself a growing source of patient-physician contacts. Many online resources are available to patients and physicians. Like prior challenges, stroke care teams will also overcome this one. Key Messages: Evidence-based stroke management should continue to be provided throughout the patient care journey, while strict infection control measures are enforced.

Patients with amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease (AD) show functional and structural connectivity alterations in the default mode network (DMN) while cerebrovascular disease (CeVD) shows functional and structural connectivity changes in the executive control network (ECN). Such disruptions are associated with memory and executive function impairment, respectively. Concurrent AD and CeVD pathology is associated with a higher rate of cognitive decline and differential neurodegenerative patterns. Together, such findings are likely reflective of different underlying pathology in AD with and without CeVD. However, few studies have examined the effect of CeVD on network functional connectivity (task-free functional magnetic resonance imaging (fMRI)) and structural connectivity (diffusion MRI) of the DMN and ECN in aMCI and AD using a hypothesis-driven multiple seed-based approach. We examined functional and structural connectivity network changes in 39 aMCI, 50 aMCI+CeVD, 47 AD, 47 AD+CeVD, and 65 healthy controls (HCs) and their associations with cognitive impairment in the executive/attention and memory domains. We demonstrate divergent DMN and ECN functional connectivity changes in CeVD and non-CeVD subjects. Compared with controls, intra-DMN hippocampal functional connectivity reductions were observed in both AD and AD+CeVD, while intra-DMN parietal and medial prefrontal-parietal functional connectivity was higher in AD+CeVD and aMCI+CeVD, but lower in AD. Intra-ECN frontal functional connectivity increases and fronto-parietal functional connectivity decreases occurred in CeVD but not non-CeVD subjects. Such functional connectivity alterations were related with cognitive impairment in a dissociative manner: intra-DMN functional connectivity changes were associated with worse cognition primarily in non-CeVD groups, while intra-ECN functional connectivity changes were associated with worse cognition primarily in CeVD groups. Additionally, CeVD and non-CeVD groups showed overlapping and distinct alterations in inter-network DMN-ECN functional connectivity depending on disease severity. In contrast to functional connectivity, CeVD groups had greater network structural connectivity damage compared with non-CeVD groups in both aMCI and AD patients. Network structural connectivity damage was associated with worse cognition. We demonstrate differential functional and structural network changes between aMCI and AD patients with and without CeVD through diverging and deleterious network-based degeneration underlying domain-specific cognitive impairment.