Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Monday, October 18, 2021

Stroke Prevention After Cryptogenic Stroke

 You can't let your doctor get by with not figuring out THE EXACT REASON FOR YOUR STROKE. Damned difficult to prevent the next one if your doctor fails at finding the reason.

Stroke Prevention After Cryptogenic Stroke

Abstract

Purpose of Review

Cryptogenic stroke represents a heterogenous but clinically important collection of stroke etiologies for which our understanding continues to grow. Here, we review our current knowledge and most recent recommendations on secondary prevention for common causes of cryptogenic stroke including paroxysmal atrial fibrillation, atrial cardiopathy, patent foramen ovale, and substenotic atherosclerotic disease as well as the under-recognized mechanisms of occult malignancy, heart failure, and, most recently, infection with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2).

Recent Findings

The results from recent observational studies and randomized clinical trials have provided greater insight into the causal relationship and attributable risk of these suspected etiologies and have identified potential strategies to reduce the rates of recurrence. However, further clinical trials are needed to confirm the benefits of specific stroke prevention strategies, including the patient populations most likely to benefit from anticoagulation.

Summary

There is ongoing research aimed at both reducing the proportion of ischemic strokes classified as cryptogenic and resolving much of the clinical equipoise that still exists. The results of these studies have the potential to provide us with a better understanding of these occult mechanisms and allow for more targeted interventions.

Introduction

Ischemic strokes can result from several different mechanisms, the majority of which can be readily identified following a standard diagnostic evaluation. However, in about 25% of cases stroke etiology remains unknown—a clinically important point as the effectiveness of secondary prevention strategies often hinges on accurate and timely identification of the underlying cause [1]. Our understanding of cryptogenic stroke has evolved through the years and depends on the classification system used. An early and commonly used system arose from the TOAST (Trial of Org 10,172 in Acute Stroke Treatment) study which classified ischemic strokes based on five potential etiologies: [1] large artery atherosclerosis, [2] cardioembolism, [3] small vessel occlusion, [4] other determined etiology (e.g., dissection), or [5] of undetermined source (i.e., cryptogenic) [2]. According to the TOAST system, strokes could be classified as cryptogenic [1] after an extensive evaluation, [2] after an incomplete evaluation, or [3] due to the presence of multiple competing etiologies. The simplicity of the system has made it widely popular for use in both clinical practice and scientific research. However, through the years, as stroke research has evolved (along with our standards for optimal care), TOAST’s broad inclusion criteria for cryptogenic stroke has complicated efforts towards targeted medical management. Since then additional classification systems have been developed, emphasizing underlying mechanisms (causative) and/or disease manifestations (phenotypic) (Table 1) [2,3,4]. In an attempt to identify a single and therapeutically distinct subset of patients with cryptogenic stroke, Hart and colleagues proposed the concept of ESUS, or embolic stroke of undetermined source, broadly defined as nonlacunar brain infarcts occurring in the absence of [1] ≥ 50% luminal atherosclerotic stenosis of the supplying extracranial or intracranial arteries, [2] any major-risk cardioembolic source, and [3] any other specific cause of stroke (e.g., dissection, vasospasm, drug abuse) [5]. With this distinction, the authors proposed there was likely a subset of cryptogenic strokes that were more likely embolic in origin and perhaps more likely to respond to anticoagulant therapy. However, even with these new constructs, cryptogenic stroke remains a diagnostic challenge. As the 10-year risk of recurrence is estimated to be as high as 30%, investigations into potential sources of cryptogenic stroke should be focused and deliberate—guided by patient factors and clinical features aimed at increasing the yield of diagnostic studies and identifying patients who would likely benefit from targeted therapies [6].

Table 1 Summary of ischemic stroke classification systems

In the last 5 years, several clinical trials have investigated the efficacy of newer therapies for specific conditions often implicated in cryptogenic stroke. Non-vitamin K oral antagonists (NOACs), such as dabigatran, rivaroxaban, and apixaban have been explored in patients with ESUS, heart failure, and malignancy with varying degrees of success [7, 8••, 9•]. The results of these studies have inspired additional trials using these new agents in more select sub-populations. In addition, the recent CLOSE, REDUCE, and DEFENSE-PFO studies identified patients with cryptogenic stroke and PFO who may benefit most from PFO closure, prompting a recent update in the recommendations from the American Academy of Neurology [10,11,12]. Although these discoveries highlight recent progress in the area of cryptogenic stroke, their gaps and limitations emphasize the need for continued work into interventions that may further reduce the risk of recurrence in these special populations.

 More at link.

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