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.

Sunday, February 27, 2022

Lenticulostriate artery length and middle cerebral artery plaque as predictors of early neurological deterioration in single subcortical infarction

 This prediction does ABSOLUTELY NOTHING to help survivors recover.  I would have you all fired. USELESS!

Lenticulostriate artery length and middle cerebral artery plaque as predictors of early neurological deterioration in single subcortical infarction

First Published February 4, 2022 Research Article 

Background: 

Early neurological deterioration (END) is not a rare phenomenon in single subcortical infarction (SSI; traditionally known as lacunar infarction) patients. Predictors of END in SSI patients are uncertain.  

Aims: 

We aimed to investigate the association between infarct lesion characteristics, penetrating artery morphology, carrier artery plaque features and END using whole-brain vessel-wall imaging.

 Methods: 

We prospectively collected data from SSI patients without stenosis of the corresponding carrier artery. The infarct lesion size and location, lenticulostriate artery (LSA) morphological characteristics, features of the middle cerebral artery (MCA) plaques involving M1 segment adjacent to LSA origin on the symptomatic side were compared between patients with or without END.  

Results: 

A total of 74 participants were enrolled, of whom 23 cases (31.1%) showed END. Multivariable logistic regression analysis adjusted for baseline National Institutes of Health Stroke Scale score and axial maximal diameter of infarct lesion revealed that the patients with MCA plaques adjacent to the LSA origin were more likely to develop END (odds ratio [OR] 3.87, 95% confidence interval [CI] 1.21-12.33), while with longer average length of LSAs were less likely to occur END (OR 0.21, 95% CI 0.05-0.92).  

Conclusions: 

MCA plaques located adjacent to the LSA origin and average length of LSAs on the symptomatic side were independent predictors of END in SSI patients. This finding might provide new insights into the mechanisms of the neurological progression in SSI and facilitate therapeutic interventions.

 

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