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.

Tuesday, September 10, 2019

Recrudescence of Old Stroke Deficits Among Transient Neurological Attacks

Hopefully your doctor warns you about this so you can tell the difference, and know when to get to the emergency room. 

In its literal sense, "recrudescence" is a medical word denoting a renewed outbreak of a disease.

Recrudescence of Old Stroke Deficits Among Transient Neurological Attacks 

First Published February 21, 2019 Research Article
Recrudescence of old stroke deficits (ROSD) is a reported cause of transient neurological symptoms, but it is not well characterized.
We sought to determine the prevalence, potential triggers, and clinical outcome of ROSD in a cohort of patients presenting with acute transient neurological attack (TNA) and absent acute pathology on brain imaging.
We retrospectively analyzed 340 consecutive patients who presented with TNA and no acute pathology on brain imaging that were included in an institutional stroke registry between February 2013 and April 2015. The presumed TNA cause was categorized as transient ischemic attack (TIA), ROSD, and other cause. Baseline characteristics, triggers, cardiovascular complications within 90 days, and death were recorded.
The prevalence of ROSD in the studied cohort was 10% (34/340). Infectious stressors and acute metabolite derangements were more common in ROSD compared to TIA (P < .05, each). Compared to TIA and the other TNA, ROSD was more likely to have more than 1 acute stressor (P < .001). Patients with ROSD had similar vascular risk factors compared to TIA (P > .05), including hypertension, diabetes mellitus, peripheral vascular disease, hyperlipidemia, and similarly used HMG-CoA reductase inhibitor, antihypertensive, and antiplatelet medications. Among the patients with an available 90-day follow-up (n = 233), cardiovascular events were more frequent in the TIA group as compared to other TNA (P < .05).
ROSD is common and distinct from TIA and is associated with a triggering physiologic reaction leading to transient reemergence of prior neurologic deficits. Further study of the mechanism of this phenomenon is needed to help better identify these patients.

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