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Wake-up stroke: From pathophysiology to management. Wake-up strokes (WUS) are strokes with unknown exact time of onset as they are noted on awakening by the patients. They represent 20% of all ischemic strokes. The chronobiological pattern of ischemic stroke onset, with higher frequency in the first morning hours, is likely to be associated with circadian fluctuations in blood pressure, heart rate, hemostatic processes, and the occurrence of atrial fibrillation episodes. The modulation (...) of stroke onset time also involves the sleep-wake cycle as there is an increased risk associated with rapid-eye-movement sleep. Furthermore, sleep may have an impact on the expression and perception of stroke symptoms by patients, but also on brain tissue ischemia processes via a neuroprotective effect. Obstructive sleep apnea syndrome is particularly prevalent in WUS patients. Until recently, WUS was considered as a contra-indication to reperfusion therapy because of the unknown onset time
Perioperative stroke: pathophysiology and management Although perioperative stroke is uncommon during low-risk non-vascular surgery, if it occurs, it can negatively impact recovery from the surgery and functional outcome. Based on the Society for Neuroscience in Anesthesiology and Critical Care Consensus Statement, perioperative stroke includes intraoperative stroke, as well as postoperative stroke developing within 30 days after surgery. Factors related to perioperative stroke include age, sex (...) , a history of stroke or transient ischemic attack, cardiac surgery (aortic surgery, mitral valve surgery, or coronary artery bypass graft surgery), and neurosurgery (external carotid-internal carotid bypass surgery, carotid endarterectomy, or aneurysm clipping). Concomitant carotid and cardiac surgery may further increase the risk of perioperative stroke. Preventive strategies should be individualized based on patient factors, including cerebrovascular reserve capacity and the time interval since
Pathophysiology of Long Non-coding RNAs in Ischemic StrokeStroke is a neurological disease with high disability and fatality rates, and ischemic stroke accounts for 75% of all stroke cases. The underlying pathophysiologic processes of ischemic stroke include oxidative stress, toxicity of excitatory amino acids, excess calcium ions, increased apoptosis and inflammation. Long non-coding RNAs (lncRNAs) may participate in the regulation of the pathophysiologic processes of ischemic stroke (...) as indicated by altered expression of lncRNAs in blood samples of acute ischemic stroke patients, animal models of focal cerebral ischemia and oxygen-glucose deprivation (OGD) cell models. Because of the potentially important role, lncRNAs might be useful as biomarkers for the diagnosis, treatment and prognosis of ischemic stroke. This article reviews the functions of lncRNAs in different pathophysiology events of ischemic stroke with a focus on specific lncRNAs that may underlie ischemic stroke
Motor Overflow and Spasticity in Chronic Stroke Share a Common Pathophysiological Process: Analysis of Within-Limb and Between-Limb EMG-EMG Coherence The phenomenon of exaggerated motor overflow is well documented in stroke survivors with spasticity. However, the mechanism underlying the abnormal motor overflow remains unclear. In this study, we aimed to investigate the possible mechanisms behind abnormal motor overflow and its possible relations with post-stroke spasticity. 11 stroke patients (...) of the resting muscles. The severity of motor impairment was quantified through reflex torque (spasticity) and weakness. EMG-EMG coherence was calculated between the contracting muscle and each of the resting muscles. During elbow flexion on the impaired side, stroke subjects exhibited significant higher motor overflow to the iFDS muscle compared with healthy subjects (ipsilateral or intralimb motor overflow). Stroke subjects exhibited significantly higher motor overflow to the contralateral spastic muscles
Advances in Understanding the Pathophysiology of Lacunar Stroke: A Review. Stroke is the second leading cause of death in the world, and nearly one-third of ischemic strokes are lacunar strokes (LSs) or small subcortical infarcts. Although smaller in size, they create large problems, leaving many patients with intellectual and physical disabilities. Because there are limitations in understanding the underlying pathophysiology of LS, the development of novel therapies has been slow.When the term (...) lacune was described in the 1800s, its underlying pathophysiological basis was obscure. In the 1960s, C. Miller Fisher, MD, performed autopsy studies that showed that vessels supplying lacunes displayed segmental arteriolar disorganization, characterized by vessel enlargement, hemorrhage, and fibrinoid deposition. For these pathologic changes, he coined the term lipohyalinosis. Since that time, few attempts have been made to reconcile this pathologic description with modern mechanisms of cerebral
Post-Stroke Sleep-Disordered Breathingâ€”Pathophysiology and Therapy Options Sleep-disordered breathing (SDB), encompassing both obstructive and central sleep apnea, is prevalent in at least 50% of stroke patients. Small studies have shown vast improvements in post-stroke functional recovery outcomes after the treatment of SDB by continuous positive airway pressure. However, compliance to this therapy is very poor in this complex patient group. There are alternative therapy options for SDB (...) that may be more amenable for use in at least some post-stroke patients, including mandibular advancement, supine avoidance, and oxygen therapy. There are few studies, however, that demonstrate efficacy and compliance with these alternative therapies currently. Furthermore, novel SDB-phenotyping approaches may help to provide important clinical information to direct therapy selection in individual patients. Prior to realizing individualized therapy, we need a better understanding of the pathophysiology
Nonsustained Atrial Fibrillation in Ischemic Stroke Patients and Strokeâ€Free Controls From the Perspective of StrokePathophysiology Short-lasting (<30 s), nonsustained episodes of atrial fibrillation (NS-AF) are considered a risk factor for future development of paroxysmal or persistent AF. Nonetheless, their causal role in stroke pathogenesis is currently unknown. In this study we determined the frequency of NS-AF, together with the associated clinical and imaging features, in stroke-free (...) controls and ischemic stroke patients.A total of 332 controls, ≥50 years of age and no prior history of stroke or AF, were evaluated with 24-hour Holter monitoring for the presence of <30-s-long AF episodes. The demographic and cardiovascular features of this cohort, together with imaging finding on magnetic resonance imaging, were compared to a consecutive series of ≥50-year-old ischemic stroke patients without AF (n=498). The prevalence of NS-AF was significantly higher among ischemic stroke patients
PR interval prolongation in coronary patients or risk equivalent: excess risk of ischemic stroke and vascular pathophysiological insights. Whether PR prolongation independently predicts new-onset ischemic events of myocardial infarction and stroke was unclear. Underlying pathophysiological mechanisms of PR prolongation leading to adverse cardiovascular events were poorly understood. We investigated the role of PR prolongation in pathophysiologically-related adverse cardiovascular events (...) , P < 0.001) and combined cardiovascular endpoints (HR 2.4, 95% CI: 1.30-4.43, P = 0.005). PR interval predicts new-onset MI at the exploratory cut-off >162 ms (C-statistic 0.70, P = 0.001; HR: 8.0, 95% CI: 1.65-38.85, P = 0.010).PR prolongation strongly predicts new-onset ischemic stroke, MI, cardiovascular death, and combined cardiovascular endpoint including CHF in coronary patients or risk equivalent. Adverse vascular function may implicate an intermediate pathophysiological phenotype
Pathophysiology and Risk of Atrial Fibrillation Detected After Ischemic StrokePathophysiology and Risk of Atrial Fibrillation Detected After Ischemic Stroke - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more (...) . Pathophysiology and Risk of Atrial Fibrillation Detected After Ischemic Stroke (PARADISE) The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our for details. ClinicalTrials.gov Identifier: NCT03275155 Recruitment Status : Active, not recruiting First Posted : September 7, 2017 Last Update Posted : November 19, 2018 Sponsor: Lawson Health Research Institute
B cells do not have a major pathophysiologic role in acute ischemic stroke in mice Lymphocytes have been shown to play an important role in the pathophysiology of acute ischemic stroke, but the properties of B cells remain controversial. The aim of this study was to unravel the role of B cells during acute cerebral ischemia using pharmacologic B cell depletion, B cell transgenic mice, and adoptive B cell transfer experiments.Transient middle cerebral artery occlusion (60 min) was induced (...) argue against a major pathophysiologic role of B cells during acute ischemic stroke.
Pathophysiology and Neuroprotective Strategies in Hypoxic-Ischemic Brain Injury and Stroke Hypoxic-ischemic brain injury and stroke are closely related and devastating conditions that can affect individuals of all ages.[...].
NADPH Oxidase-Related Pathophysiology in Experimental Models of Stroke Several experimental studies have indicated that nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox) exert detrimental effects on ischemic brain tissue; Nox-knockout mice generally exhibit resistance to damage due to experimental stroke following middle cerebral artery occlusion (MCAO). Furthermore, our previous MCAO study indicated that infarct size and blood-brain barrier breakdown are enhanced in mice (...) previous study, we examined the effects of Nox activity on focal ischemic injury in a novel congenic rat strain: stroke-prone spontaneously hypertensive rats with loss-of-function in Nox. In this review, we summarize the current literature regarding the role of Nox in focal ischemic injury and discuss critical issues that should be considered when investigating Nox-related pathophysiology in animal models of stroke.
Correlates of Post-Stroke Brain Plasticity, Relationship to Pathophysiological Settings and Implications for Human Proof-of-Concept Studies The promotion of neurological recovery by enhancing neuroplasticity has recently obtained strong attention in the stroke field. Experimental studies support the hypothesis that stroke recovery can be improved by therapeutic interventions that augment neuronal sprouting. However plasticity responses of neurons are highly complex, involving the growth (...) and differentiation of axons, dendrites, dendritic spines and synapses, which depend on the pathophysiological setting and are tightly controlled by extracellular and intracellular signals. Thorough mechanistic insights are needed into how neuronal plasticity is influenced by plasticity-promoting therapies in order not to risk the success of future clinical proof-of-concept studies.
Pathophysiology of Stroke in the Contralateral Posterior Cerebral Artery Distribution from a Tentorial Herniation 27730772 2018 11 13 1738-6586 13 1 2017 Jan Journal of clinical neurology (Seoul, Korea) J Clin Neurol Pathophysiology of Stroke in the Contralateral Posterior Cerebral Artery Distribution from a Tentorial Herniation. 101-102 10.3988/jcn.2017.13.1.101 Ansari Mustafa M Department of Neurology, UC Davis Medical Center, Sacramento, CA, USA. Chang Gregory Youngnam GY Department
Diabetes and Stroke: Epidemiology, Pathophysiology, Pharmaceuticals and Outcomes There has been a significant increase in obesity rates worldwide with the corresponding surge in diabetes. Diabetes causes various microvascular and macrovascular changes often culminating in major clinical complications, 1 of which, is stroke. Although gains have been made over the last 2 decades in reducing the burden of stroke, the recent rise in rates of diabetes threatens to reverse these advances (...) . Of the several mechanistic stroke subtypes, individuals with diabetes are especially susceptible to the consequences of cerebral small vessel diseases. Hyperglycemia confers greater risk of stroke occurrence. This increased risk is often seen in individuals with diabetes and is associated with poorer clinical outcomes (including higher mortality), especially following ischemic stroke. Improving stroke outcomes in individuals with diabetes requires prompt and persistent implementation of evidence-based
StrokePathophysiologyStrokePathophysiology Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 StrokePathophysiologyStroke (...) Pathophysiology Aka: StrokePathophysiology , CVA Causes , Transient Ischemic Attack Causes , TIA Risk Factors , Cerebrovascular Accident Risk Factors , CVA Risk Factors From Related Chapters II. Risk Factors (increased systolic ) (with or ) significantly lowers the risk of CVA African American or Hispanic Race Sedentary lifestyle of CVA or Age over 65 years Increased Apolipoprotein-a Consider in cryptogenic stroke if suspected with aura Especially in women over age 35, abuse or use smoking ( abuse