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.

Showing posts with label MCA. Show all posts
Showing posts with label MCA. Show all posts

Sunday, January 31, 2021

Pilot study to characterize middle cerebral artery dynamic response to an acute bout of moderate intensity exercise at 3‐ and 6‐months poststroke

What the hell was this research for? It is your doctor's responsibility to get you able to do this moderate exercise.

Pilot study to characterize middle cerebral artery dynamic response to an acute bout of moderate intensity exercise at 3‐ and 6‐months poststroke

Billinger SA, Whitaker AA, Morton A, et al.
Journal of the American Heart Association|January 27, 2021

At 3‐ and 6‐months after stroke, researchers assessed the middle cerebral artery blood velocity (MCAv) dynamic response to an acute bout of exercise in humans. Individuals were categorized according to the MCAv dynamic response to the exercise bout as responder or nonresponder(???) and they investigated if physical activity, aerobic fitness, and exercise mean arterial blood pressure differed between groups. In this analysis, MCAv was evaluated by transcranial Doppler ultrasound during a 90‐second baseline followed by a 6‐minute moderate-intensity exercise bout. A faster time delay, higher amplitude, and reported higher levels of physical activity and aerobic fitness was seen in responders vs nonresponders. An immediate rise in MCAv following exercise onset followed by an immediate decline to near baseline values was seen in the nonresponders, while the responders showed an exponential rise until steady state was reached. It was shown that patients with a greater MCAv response to the exercise stimulus reported statin use and regular participation in exercise.

Read the full article on Journal of the American Heart Association.

 

Tuesday, September 13, 2016

Changes in Middle Cerebral Artery Blood Flow Velocity During Sonolysis Using a Diagnostic Transcranial Probe With a 2-MHz Doppler Frequency in Healthy Volunteers

    It sounded good but didn't work. Better velocity of MCA blood flow would probably drive more oxygen to the localized brain tissue.

    1. David Školoudík, MD, PhD, FESO
    + Author Affiliations
    1. Department of Neurology, Hospital Třinec-Sosna, Třinec, Czech Republic (P.B.); Comprehensive Stroke Center, Department of Neurology, Ostrava University Medical Faculty and University Hospital, Ostrava, Czech Republic (M.K., D.Šk.); Comprehensive Stroke Center, Department of Neurology, Faculty of Medicine and Dentistry, Palacký University and University Hospital, Olomouc, Czech Republic (R.H., D.Ša., P.K., D.Šk.); and Department of Medical Biophysics, Faculty of Medicine and Dentistry, Institute of Molecular and Translational Medicine, Palacký University, Olomouc, Czech Republic (K.L.).
    1. Address correspondence to David Školoudík, MD, PhD, FESO, Comprehensive Stroke Center, Department of Neurology, University Hospital, 17 Listopadu 1790, CZ-708 00 Ostrava, Czech Republic. E-mail: skoloudik@hotmail.com

    Abstract

    Objectives—Ultrasound has various biological effects in the human body. The effects of continuous monitoring with ultrasound (sonolysis) on vasodilatation of the radial artery were described recently. We wanted to ascertain whether similar changes in the blood flow velocity during sonolysis could also be detected in the middle cerebral artery.
    Methods—Fifteen healthy volunteers (6 male and 9 female; age range, 23–68 years; mean ± SD, 47.1 ± 15.1 years) were subjected to 1 hour of middle cerebral artery sonolysis using a diagnostic transcranial probe with a 2-MHz Doppler frequency and measurement of the blood flow velocity at 2-minute intervals. During a second session, a flow curve was recorded for 10 seconds at 2-minute intervals. The peak systolic velocity, end-diastolic velocity, mean flow velocity, pulsatility index, and resistive index were recorded during both measurements.
    Results—Irregular changes in the measured blood flow parameters were recorded during both sessions. Changes in particular hemodynamic parameters during both measurements were similar. The changes in the peak systolic velocity, end-diastolic velocity, mean flow velocity, pulsatility index, and resistive index were not significantly different between the two measurements (P < .05 in all cases).
    Conclusions—As opposed to sonolysis of the radial artery, sonolysis of the middle cerebral artery using a diagnostic 2-MHz frequency in healthy volunteers did not lead to changes in the flow curve or peripheral vasodilatation.

Thursday, January 28, 2016

Stroke Rounds: Lesion Site Affects Reperfusion Benefit With Clot Grabber

If the ICA is blocked is it even a stroke since that is prior to entering the Circle of Willis? And if the Circle of Willis is complete then that wouldn't cause problems. Is this problem even defined correctly?
http://www.medpagetoday.com/Cardiology/Strokes/55888?xid=nl_mpt_cardiodaily_2016-01-28&eun=gd3r
The magnitude of functional outcome benefits from reperfusion with endovascular thrombectomy may depend on the site of occlusion, a meta-analysis showed.
Reperfusion was associated with 3.5-fold higher odds of a good functional outcome (0-2 on the modified Rankin Scale) at 90 days among patients with internal carotid artery (ICA) occlusions and 6.2-fold higher among those with proximal middle cerebral artery (MCA) occlusions versus persistent occlusion.
Reperfusion had no significant association with good functional outcome in distal MCA lesions (OR 1.4, 95% confidence interval 0.8-2.6), although there was a link in the M2 occlusion subset (OR 2.2, 95% CI 1.0-4.7), Robin Lemmens, MD, PhD, of University Hospitals Leuven in Belgium, and colleagues reported online in Neurology.
"The association between reperfusion and good clinical outcomes is stronger in patients with proximal(closer) occlusions compared to distal(farther) occlusions," the group concluded. "Our results, however, do not indicate that patients with distal MCA occlusions do not benefit from endovascular therapy."
"In contrast, the results underscore the need for additional clinical trial data to determine the effect of endovascular therapy in this subgroup," they continued.
Indeed, the study "is not going to change my practice," Haitham Dababneh, MD, of Doctors Hospital at Renaissance in Edinburg, Texas, told MedPage Today. He likewise called for better data from randomized controlled trials, noting differing baseline characteristics between groups in the meta-analysis and the fact that there were fewer patients with distal strokes than proximal strokes.
For now, "it's hard to compare apples to oranges," Dababneh said.
As for the reason why patients with distal MCA occlusions might show less benefit from reperfusion, the authors suggested that those individuals "have less brain tissue at risk of infarction (i.e., less brain tissue that can be salvaged with reperfusion) compared to patients with more proximal MCA or ICA occlusions."
Lemmens and colleagues pooled patient-level data from four large endovascular trials -- SWIFT, STAR, DEFUSE 2, and IMS III -- for a total of 710 patients in their analysis.
Panagiotis Papanagiotou, MD, of Hospitals Bremen-Mitte in Germany, told MedPage Today that clinicians should focus on careful patient selection, perhaps with advanced imaging techniques.
Papanagiotou, who was an investigator for SWIFT, added that the improvement of endovascular techniques -- such as "direct thrombus aspiration to achieve higher recanalization rates" -- may also be helpful for the treatment of distal lesions.

Saturday, June 13, 2015

PATHOLOGY OF ISCHEMIC INFARCTS

This course explains what occurs to the exact location of your stroke.  I would have appreciated knowing this but my doctor told me nothing about my stroke or recovery. I worried about my brain rotting from the damage. The picture from there is rather gruesome, which probably resembles my brain right now.
http://neuropathology-web.org/chapter2/chapter2bCerebralinfarcts.html
In the first day or so, the infarct appears as a poorly demarcated area of softening.
 
 

 

 
CT Imaging at this stage may be negative, especially in brain stem infarcts. MRI is much more sensitive. At the peak of edema, the infarct appears hypodense and bright on T2 MRI images. The infarcted tissue becomes sharply demarcated and softens progressively. From the second week onward, it begins to disintegrate and is gradually replaced by a cavity. The size and location of infarcts follows the anatomy of vascular territories.




Microscopical examination in the first 24 to 48 hours reveals anoxic neurons, pallor of staining and vacuolization of the white matter due to unraveling of myelin, and axonal swellings. During the first week, there is a transient inflammatory reaction, especially around blood vessels and in the meninges, due to release of arachidonic and other fatty acids. As the core of the infarct disintegrates, endothelial cells from the periphery proliferate, and capillaries grow into the dead tissue. Neovascularization (which accounts for contrast enhancement) peaks at 2 weeks. Monocytes from the blood stream enter the infarct through damaged vessels. They ingest the products of degradation of neurons and myelin and are transformed into lipid-laden macrophages. Macrophage reaction appears early and peaks at 3-4 weeks. Astrocytes from the surrounding undamaged brain proliferate and form a glial scar around the infarct. This is completed in approximately 2 months. After that, the infarct remains unchanged. With maturation of new capillaries and glial scar formation, the blood brain barrier is once again sealed. Neurons do not regenerate. So, some brain tissue is lost forever.
Old MCA infarct. A collapsed cavity.

Monday, February 9, 2015

Distance to Thrombus in Acute Middle Cerebral Artery Occlusion A Predictor of Outcome After Intravenous Thrombolysis for Acute Ischemic Stroke

This would be essential if we are ever to get an objective damage diagnosis and then we could look at the stroke protocols that solved those problems. My doctor told me almost nothing but I believe he said I had an MCA infarct. Of course none of my therapists ever saw a CT/MRI scan so there was nothing they could match up damages with exercises.
http://stroke.ahajournals.org/content/early/2015/02/03/STROKEAHA.114.008454.abstract?
  1. Donald Lobsien, MD*
+ Author Affiliations
  1. From the Department of Interventional and Diagnostic Radiology (B.F., M.G., M.R.), Department of Neuroradiology (S.S., K.-T.H., D.L.), and Department of Neurology (C.H.), University Hospital Leipzig, Germany.
  1. Correspondence to Donald Lobsien, MD, Department of Neuroradiology, University Hospital Leipzig, Liebigstr. 20, 04103 Leipzig, Germany. E-mail donald.lobsien@medizin.uni-leipzig.de
  1. * Drs Friedrich and Lobsien contributed equally.

Abstract

Background and Purpose—In patients with acute middle cerebral artery (MCA) stroke, therapeutic decisions are influenced by the location of the occlusion. This study aimed to analyze clinical outcomes in patients with acute ischemic MCA stroke treated with systemic intravenous thrombolysis (IVT) using recombinant tissue plasminogen activator, according to the location of the occlusion.
Methods—Of 621 patients screened, 136 with acute stroke and MCA occlusion confirmed by CT angiography were retrospectively included in this study. The distance from the carotid T to the thrombus (DT) on coronal maximum intensity projection images and the thrombus length were measured. The correlation between DT and the modified Rankin Scale score at 90 days was analyzed.
Results—DT was an independent predictor of clinical outcome in stroke patients treated with IVT. A long DT was significantly correlated with a good clinical outcome (modified Rankin Scale score at 90 days ≤2). A poor clinical outcome was exponentially more likely than a good outcome when the DT was <16 mm (P<0.001). The thrombus length was not correlated with the modified Rankin Scale score at 90 days. A long thrombus (>8 mm) occurred significantly more often in the proximal MCA than the distal MCA (P<0.001).
Conclusion—DT is an independent predictor of clinical outcome in patients with acute MCA occlusion treated with IVT. In acute stroke with MCA occlusion confirmed by CT angiography and DT <16 mm, the likelihood of a good clinical outcome after treatment with IVT was exponentially <50%. This might warrant the evaluation of other therapy forms than IVT in patients with proximal MCA occlusion.

Thursday, March 20, 2014

For Older Stroke Patients Cutting a Hole in the Head Helps

All I could think of was this picture
trepanned_smBut in the article they had this statement which I would love to know visually in 3d what the extent of the MCA is, that would allow me to determine what my damage is compared to the maximum a MCA could cause. It seems like an incredibly simple request but I'm sure I'll never find out with the current information out there.
and brain imaging results indicating that ischemia had affected at least two-thirds of the brain served by the middle cerebral artery.
http://www.medpagetoday.com/Neurology/Strokes/44841?