To investigate the prevalence and behavior of sleep-related breathing disorders (SRBDs) associated with a first-ever stroke or transient ischemic attack (TIA), we prospectively studied 161 consecutive patients admitted to our stroke unit. Complete neurological assessment was performed to determine parenchymatous and vascular localization of the neurological lesion. Stroke subtype was categorized as TIA, ischemic (IS), or hemorrhagic (HS). A portable respiratory recording (PRR) study was performed within 48–72 h after admission (acute phase), and subsequently after 3 mo (stable phase). During the acute phase, 116 patients (71.4%) had an apnea–hypopnea index (AHI) > 10 events/h and 45 (28%) had an AHI > 30. No relationships were found between sleep-related respiratory events and the topographical parenchymatous location of the neurological lesion or vascular involvement. Cheyne–Stokes breathing (CSB) was observed in 42 cases (26.1%). There were no significant differences in SRBD according to the stroke subtype except for the central apnea index (CAI). During the stable phase a second PRR was performed in 86 patients: 53 of 86 had an AHI > 10 and 17 of 86 had an AHI > 30. The AHI and CAI were significantly lower than those in the acute phase (16.9 ± 13.8 versus 22.4 ± 17.3 and 3.3 ± 7.6 versus 6.2 ± 10.2, respectively) (p < 0.05) while the obstructive apnea index (OAI) remained unchanged. CSB was observed in 6 of 86 patients. The prevalence of SRBD in patients with first-ever stroke or TIA is higher than expected from the available epidemiological data in our country. No correlation was found between neurological location and the presence or type of SRBD. Obstructive events seem to be a condition prior to the neurological disease whereas central events and CSB could be its consequence. Parra O, Arboix A, Bechich S, García-Eroles L, Montserrat JM, López JA, Ballester E, Guerra JM, Sopeña JJ. Time course of sleep-related breathing disorders in first-ever stroke or transient ischemic attack.

This article provides the reader with an overview and up-date of clinical features, specific cardiac disorders and prognosis of cardioembolic stroke. Cardioembolic stroke accounts for 14-30% of ischemic strokes and, in general, is a severe condition; patients with cardioembolic infarction are prone to early and long-term stroke recurrence, although recurrences may be preventable by appropriate treatment during the acute phase and strict control at follow-up. Certain clinical features are suggestive of cardioembolic infarction, including sudden onset to maximal deficit, decreased level of consciousness at onset, Wernickes aphasia or global aphasia without hemiparesis, a Valsalva manoeuvre at the time of stroke onset, and co-occurrence of cerebral and systemic emboli. Lacunar clinical presentations, a lacunar infarct and especially multiple lacunar infarcts, make cardioembolic origin unlikely. The more common high risk cardioembolic conditions are atrial fibrillation, recent myocardial infarction, mechanical prosthetic valve, dilated myocardiopathy, and mitral rheumatic stenosis. Transthoracic and transesophageal echocardiogram can disclose structural heart diseases. Paroxysmal atrial dysrhyhtmia can be detected by Holter monitoring. In-hospital mortality in cardioembolic stroke (27.3%, in our series) is the highest as compared with other subtypes of cerebral infarction. In our experience, in-hospital mortality in patients with early embolic recurrence (within the first 7 days) was 77%. Patients with alcohol abuse, hypertension, valvular heart disease, nausea and vomiting, and previous cerebral infarction are at increased risk of early recurrent systemic embolization. Secondary prevention with anticoagulants should be started immediately if possible in patients at high risk for recurrent cardioembolic stroke in which contraindications, such as falls, poor compliance, uncontrolled epilepsy or gastrointestinal bleeding are absent.

The aim of the present study was to assess the impact of nasal continuous positive airway pressure (nCPAP) in ischaemic stroke patients followed for 2 yrs.Stroke patients with an apnoea–hypopnoea index ≥20 events·h⁻¹were randomised to early nCPAP (n = 71; 3–6 days after stroke onset) or conventional treatment (n = 69). The Barthel Index, Canadian Scale, Rankin Scale and Short Form-36 were measured at baseline, and at 1, 3, 12 and 24 months.The percentage of patients with neurological improvement 1 month after stroke was significantly higher in the nCPAP group (Rankin scale 90.9versus56.3% (p<0.01); Canadian scale 88.2versus72.7% (p<0.05)). The mean time until the appearance of cardiovascular events was longer in the nCPAP group (14.9versus7.9 months; p = 0.044), although cardiovascular event-free survival after 24 months was similar in both groups. The cardiovascular mortality rate was 0% in the nCPAP group and 4.3% in the control group (p = 0.161).Early use of nCPAP seems to accelerate neurological recovery and to delay the appearance of cardiovascular events, although an improvement in patients’ survival or quality of life was not shown.

Timely diagnosis and control of cardiovascular risk factors is a priority objective for adequate primary and secondary prevention of acute stroke. Hypertension, atrial fibrillation and diabetes mellitus are the most common risk factors for acute cerebrovascular events, although novel risk factors, such as sleep-disordered breathing, inflammatory markers or carotid intima-media thickness have been identified. However, the cardiovascular risk factors profile differs according to the different subtypes of ischemic stroke. Atrial fibrillation and ischemic heart disease are more frequent in patients with cardioembolic infarction, hypertension and diabetes in patients with lacunar stroke, and vascular peripheral disease, hypertension, diabetes, previous transient ischemic attack and chronic obstructive pulmonary disease in patients with atherothrombotic infarction. This review aims to present updated data on risk factors for acute ischemic stroke as well as to describe the usefulness of new and emerging vascular risk factors in stroke patients.

Only very little is know about the neurovascular niche after cardioembolic stroke. Three processes implicated in neurorepair: angiogenesis, neurogenesis and synaptic plasticity, would be naturally produced in adult brains, but also could be stimulated through endogen neurorepair phenomena. Angiogenesis stimulation generates new vessels with the aim to increase collateral circulation. Neurogenesis is controlled by intrinsic genetic mechanisms and growth factors but also ambiental factors are important. The leading process of the migrating neural progenitor cells (NPCs) is closely associated with blood vessels, suggesting that this interaction provides directional guidance to the NPCs. These findings suggest that blood vessels play an important role as a scaffold for NPCs migration toward the damaged brain region. DNA microarray technology and blood genomic profiling in human stroke provided tools to investigate the expression of thousands of genes. Critical comparison of gene expression profiles after stroke in humans with those in animal models should lead to a better understanding of the pathophysiology of brain ischaemia. Probably the most important part of early recovery after stroke is limited capacity of penumbra/infarct neurones to recover. It became more clear in the last years, that penumbra is not just passively dying over time but it is also actively recovering. This initial plasticity in majority contributes towards later neurogenesis, angiogenesis and final recovery. Penumbra is a principal target in acute phase of stroke. Thus, the origin of newly formed vessels and the pathogenic role of neovascularization and neurogenesis are important unresolved issues in our understanding of the mechanisms after stroke. Biomaterials for promoting brain protection, repair and regeneration are new hot target. Recently developed biomaterials can enable and increase the target delivery of drugs or therapeutic proteins to the brain, allow cell or tissue transplants to be effectively delivered to the brain and help to rebuild damaged circuits. These new approaches are gaining clear importance because nanotechnology allows better control over material-cell interactions that induce specific developmental processes and cellular responses including differentiation, migration and outgrowth.

Background and Purpose— Statins may be beneficial for patients with acute ischemic stroke. We tested the hypothesis that patients pretreated with statins at the onset of stroke have less severe neurological effects and a better outcome. Methods— We prospectively included consecutive patients with ischemic stroke of <24-hour duration. We recorded demographic data, vascular risk factors, Oxfordshire Classification, National Institutes of Health Stroke Scale (NIHSS) score, admission blood glucose and body temperature, cause (Trial of Org 10172 in Acute Treatment [TOAST] criteria), neurological progression at day 3, previous statin treatment, and outcome at 3 months. We analyzed the data using univariate methods and a logistic regression with the dependent variable of good outcome (modified Rankin Scale [mRS] 0 to 1, Barthel Index [BI] 95 to 100). Results— We included 167 patients (mean age 70.7±12 years, 94 men). Thirty patients (18%) were using statins when admitted. In the statin group, the median NIHSS score was not significantly lower and the risk of progression was not significantly reduced. Favorable outcomes at 3 months were more frequent in the statin group (80% versus 61.3%, P =0.059 with the mRS; 76.7% versus 51.8%, P =0.015 with the BI). Predictors of favorable outcome with the BI were: NIHSS score at admission (OR: 0.72; CI: 0.65 to 0.80; P <0.0001), age (OR: 0.96; CI: 0.92 to 0.99; P =0.017), and statin group (OR: 5.55; CI: 1.42 to 17.8; P =0.012). Conclusions— Statins may provide benefits for the long-term functional outcome when administered before the onset of cerebral ischemia. However, randomized controlled trials will be required to evaluate the validity of our results.