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, December 26, 2021

Mild Luminal Stenosis of Parent Artery and Neurologic Deterioration After Acute Lacunar Stroke

 

Well congratulations, you described a problem BUT DID NOTHING TO SOLVE IT. You all need to be fired.

Mild Luminal Stenosis of Parent Artery and Neurologic Deterioration After Acute Lacunar Stroke

Originally publishedhttps://doi.org/10.1161/SVIN.121.000132Stroke: Vascular and Interventional Neurology. 2021;0:e000132

Abstract

BACKGROUND

Early neurologic deterioration (END) occurs in a quarter of acute lacunar infarcts, but the underlying pathophysiological features are poorly understood. We sought to determine the association between luminal stenosis (<50%) of the parent artery and END.

METHODS

This observational study included consecutive patients with lacunar stroke from the ischemic stroke registries of New York University Langone Health and Brown University. All included patients were admitted for acute lacunar stroke, which was defined as a subcortical infarct <1.5 cm on computed tomography or <2 cm on diffusion‐weighted imaging without significant stenosis (>50%) in the parent vessel and no cardioembolic source. We defined END as any neurologic deterioration referable to the acute lacunar stroke and not related to a medical or noncerebrovascular neurological complication. We used univariate and logistic regression analyses to determine associations between luminal stenosis (<50%) and the odds of END. Furthermore, we attempted to validate findings using the Columbia University Medical Center stroke registry and perform a meta‐analysis combining the derivation and validation groups because of the expected small samples and event rates.

RESULTS

The New York University Langone Health and Brown University sample included 205 patients, of whom 41 (20%) had END. In adjusted models, we found no definite association between luminal stenosis (<50%) and END (adjusted odds ratio [OR], 1.74; 95% CI, 0.73–4.14). From Columbia University Medical Center, 361 total patients were included, of whom 59 (16%) had END. In adjusted models, we found an association between luminal stenosis (<50%) and END (adjusted OR, 2.28; 95% CI, 1.15–4.50). Meta‐analysis of both cohorts found luminal stenosis (<50%) associated with END (relative risk, 1.69; 95% CI, 1.17–2.43).

CONCLUSIONS

In this multicenter study, luminal stenosis (<50%) may be associated with END following an acute lacunar infarct. Larger studies using vessel wall imaging are needed to validate our findings.

Early neurologic deterioration (END) can occur in about a quarter of acute lacunar strokes within hours to days after initial deficit.1 Although lacunar strokes generally have a more favorable prognosis,2 END in lacunar stroke may especially involve motor function and increase risk for long‐term disability.3, 4 Diabetes, admission motor symptom severity, higher admission National Institutes of Health Stroke Scale, and larger lacune size have been shown to be associated with progressive deficits in lacunar stroke.4, 5, 6 However, the underlying pathologic mechanisms for END after lacunar stroke remain poorly understood.

Distinct from lipohyalinosis in intrinsic cerebral small‐vessel disease, Fisher and Caplan described branch atheromatous disease (BAD) as another mechanism of lacunar‐type infarcts that involves obstruction of penetrator artery orifices by atheroma of the parent vessel or microatheroma originating at the branch point.7, 8 END is frequently reported in lacunes with BAD, but the definition for BAD‐related lacune varied across studies and is often radiographically inferred by lacune characteristics, not direct evidence of atheroma.9

Therefore, a better understanding of clinical and radiographic risk factors for END in lacunar infarct may help elucidate the underlying pathophysiological features and predict patients at high risk for deterioration. In this present study, we sought to determine the association between radiographic parent vessel luminal stenosis (<50%) and END following an acute lacunar stroke.

 

No comments:

Post a Comment