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.

Thursday, December 10, 2020

Dynamic Change in Mean Platelet Volume and Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

So you found an association between mean platelet volume and delayed cerebral ischemia. What the fuck is the solution to prevent that problem? Or are survivors supposed to solve this on their own? Useless.

Dynamic Change in Mean Platelet Volume and Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Liuwei Chen and Quanbin Zhang*
  • Department of Neurosurgery, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China

Background: The mean platelet volume (MPV) has been shown to predict short-term outcomes in patients who have experienced aneurysmal subarachnoid hemorrhage (aSAH). The purpose of this study was to explore the temporal variation of MPV in patients with aSAH and its relationship to the development of delayed cerebral ischemia (DCI).

Methods: Data from 197 consecutive aSAH patients who were treated at our institution between January 2017 and December 2019 were collected and analyzed. Blood samples to assess MPV were obtained at 1–3, 3–5, 5–7, and 7–9 d after the initial hemorrhage. Univariate and multivariate analyses were performed to investigate whether MPV was an independent predictor of DCI and the receiver operating characteristic (ROC) curve and area under the curve (AUC) were determined.

Results: The MPV values in patients with DCI were significantly higher compared to those without DCI at 1–3, 3–5, 5–7, and 7–9 d after hemorrhage (P < 0.001). The trend for MPV in patients with DCI was increased at first and then decreased. The transition from increases to decreases occurred at 3–5 d after hemorrhage. The optimal cutoff value for MPV to accurately predict DCI was 10.35 fL at 3–5 d after aSAH in our cohort. Furthermore, the MPV observed at 3–5 d was an independent risk factor for DCI [odds ratio (OR) = 4.508, 95% confidence interval (CI): 2.665–7.626, P < 0.001].

Conclusions: MPV is a dynamic variable that occurs during aSAH, and a high MPV at 3–5 days after hemorrhage is associated with the development of DCI.

Introduction

Aneurysmal subarachnoid hemorrhage (aSAH) is a critical hemorrhagic stroke with a high risk of morbidity, mortality, and associated financial costs (1, 2). The mechanism of brain injury following aSAH remains multifactorial. There is evidence that thrombosis and inflammation may be elevated following aSAH (3, 4).

Delayed cerebral ischemia (DCI) is a major cause of poor functional outcomes in patients who survive following an initial hemorrhage (5, 6). DCI has been associated with a worse prognosis, a more severe clinical course, and increased mortality in patients with aSAH (7). The pathogenesis of DCI involves micro-thrombosis, neurovascular uncoupling, perfusion mismatch, spreading depolarizations, and inflammatory responses, all of which culminate in infarction (8). Identifying patients who are at high risk of DCI will assist with the management of patients with aSAH.(Well then where are the management solutions?)

Mean platelet volume (MPV) reflects the average size of platelets, which is associated with the function and activation of platelets (9). Previous studies have demonstrated the clinical significance of MPV in many thrombotic diseases, such as acute ischemic stroke (10), acute myocardial infarction (11), and deep vein thrombosis (12). Our initial work also showed that an elevated MPV was associated with poor short-term outcomes in aSAH patients (13). However, there is few published research concerning the dynamic change in MPV during aSAH and its relationship with DCI (14). The purpose of this study was to explore the temporal variation of MPV in patients with aSAH and the relationship of MPV with the development of DCI.

 

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