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

New Study Identifies Features, Triggers, and Risk Factors for Post-Stroke Recrudescence

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. 

 

New Study Identifies Features, Triggers, and Risk Factors for Post-Stroke Recrudescence

BY SARAH OWENS
The re-emergence of post-stroke symptoms and deficits after they have initially resolved is more common than previously thought and associated with a number of identifiable triggers and risk factors, according to a new study published online on August 7 in JAMA Neurology.
Risk factors for post-stroke recrudescence (PSR), defined as the transient worsening or reemergence of neurologic deficits after a stroke — including changes in consciousness levels, vision, language skills, or weakness in the face, limbs, and muscles — have not yet been well characterized. But understanding them is crucial for treating physicians, since PSR can often be confused for other conditions, such transient ischemic attack, stroke mimics, and seizure – all of which require different management.
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Findings from the present study "should enable prompt diagnosis and help [physicians] distinguish poststroke recrudescence from mimics," the study authors, led by Mehmet A. Topcuoglu, MD, of the neurology department at Hacettepe University Hospitals in Ankara, Turkey, wrote.
For their study, researchers at Hacettepe University Hospitals, Massachusetts General Hospital and Harvard Medical School retrospectively reviewed the records of 1,700 patients who'd had an ischemic or hemorrhagic stroke and who experienced PSR. The researchers used preliminary diagnostic criteria for PSR – including the presence of chronic stroke on brain imaging, no acute lesions on diffusion weighted imaging, unlikely cerebral ischemia, and no evidence of seizure at the time of the event – to identify a total of 164 who were included in the final analysis.
The mean age of patients with PSR was 67, and 60 percent were women. The average time from index stroke to PSR was 3.9 years; PSR occurred after both ischemic and hemorrhagic stroke, but was far more common after ischemic stroke. The mean duration of the deficits, documented in 131 episodes, was 18.4; of these episodes, 91 (69.5 percent) resolved on day 1, 23 (17.5 percent) resolved on day 2, 8 (6.1 percent) resolved on day 3, and 9 (6.9 percent) resolved on day 4 or beyond.
Among the triggers and risk factors for PSR they identified were infections, hypotension, and hyponatremia, and to a lesser extent insomnia or stress, benzodiazepine use, and fever. The resolution of PSR symptoms was correlated with treatment or removal of the presumed trigger. Risk factors included female gender, being African American or self-identified "other" race, diabetes, dyslipidemia, smoking, and having more severe neurologic deficits at the time of the stroke.
The findings, the study authors concluded, suggest that PSR "appears to be relatively frequent, [but] recognition of PSR remains sporadic." They hope their results will "stimulate larger validation studies and ultimately enable prompt diagnosis and distinction from mimics in medical centers across the world."
The researchers noted several limitations to their study. Among them were its retrospective design, which meant they had to rely on medical records to determine the severity and evolution of stroke; the unblinded review of medical records may have contributed to bias; and the list of possible triggers was predefined. They noted that there may be as yet unknown factors contributing to PSR, as well.
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