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 Recrudescence. Show all posts
Showing posts with label Recrudescence. Show all posts

Saturday, October 5, 2024

Everything You Need to Know About Stroke Recrudescence

 Did your competent? doctor inform you of this possible problem? I'm sure your doctor knew of all this earlier research if they were competent at all!


Post-Stroke Recrudescence: A Case Report and Literature Review  August 2023


Post-stroke recrudescence from infection: an immunologic mechanism?  July 2018

The latest here:

Everything You Need to Know About Stroke Recrudescence

Stroke recrudescence is the temporary return of previous stroke symptoms, without new stroke damage. It’s possible to mistake them for a new stroke, so it’s best to seek emergency care.

Post-stroke recrudescence (PSR), or simply “stroke recrudescence,” is when old stroke symptoms temporarily come back. Factors such as infection, dehydration, or certain medications often trigger it.

Understanding stroke recrudescence is important for accurate diagnosis and proper care, preventing unnecessary interventions.

Stroke recrudescence, or post-stroke recrudescence (PSR), typically various physiological stressors trigger it. Some common causes include:

PSR can occur after both ischemic and hemorrhagic strokes and is more common in people who have had larger strokes. The condition is fairly common, affecting about 10% of people seeking medical attention for transient neurological issues.

One study looked at 153 participants who experienced PSR years after their initial stroke. The symptoms usually came back about 4 years after the first stroke, lasted less than a day, and were generally mild. The study found that females, African Americans, and people with certain health conditions like diabetes and high cholesterol were more likely to experience PSR.

What is the difference between recrudescence and relapse?

  • Recrudescence is the temporary return of stroke symptoms that were previously resolved, often triggered by factors like infections or stress. It doesn’t involve new brain damage and typically improves once you address the trigger.
  • Relapse refers to the recurrence or worsening of stroke symptoms after a period of relief. This often suggests a new stroke or progression of the underlying condition and may require intensified treatment.

While “recrudescence” specifically describes the return of old symptoms without new damage, “relapse” is sometimes used more broadly and less precisely, especially in informal contexts.

The symptoms of stroke recrudescence typically include the temporary reappearance or worsening of neurological deficits that were present after the original stroke.

These symptoms can vary depending on the area of the brain that was affected by the original stroke but generally include:

  • Weakness or numbness: Often on one side of the body (e.g., face, arm, leg).
  • Speech difficulties: Difficulty speaking or understanding speech (e.g., slurred speech, difficulty finding words).
  • Vision problems: Temporary vision changes (e.g., blurred vision, loss of vision in one or both eyes).
  • Coordination problems: Difficulty with balance, walking, or coordination.
  • Sensory changes: Altered sensation (e.g., tingling or loss of sensation on one side of the body).

These symptoms are usually mild, abrupt, and resolve within a short period, often less than 24 hours. They mimic the symptoms of the initial stroke but don’t indicate a new stroke or brain injury.

Experts consider recrudescence as a common stroke mimic, meaning it can look like a new stroke but isn’t. Stroke mimics makeup about 30% of stroke-related cases, with 42% of these people having a history of previous strokes.

Diagnosing PSR is challenging because there are no specific blood tests or imaging results for it. Additionally, since PSR symptoms are temporary and can appear in individuals with existing vascular risk factors, distinguishing them from those of a new stroke, a transient ischemic attack (TIA), or other conditions can be difficult.

Key features of PSR include a worsening of old stroke symptoms, identifiable stressors (e.g., dehydration, stress, infection), and a history of chronic (long-term) stroke on brain scans, with no new acute lesions visible on imaging.

Diagnosis involves several steps to distinguish it from other conditions that may appear similar. Here’s how healthcare professionals typically do it:

  • Review medical history and symptoms: They examine past stroke history and current symptoms, focusing on the return of previously resolved deficits and recent triggers.
  • Neurological exam: They assess symptoms to see if they match prior deficits.
  • MRI or CT scan: They check for new lesions or changes.
  • Diffusion-weighted imaging: They rule out new acute ischemic events, which should show no new abnormalities in recrudescence.
  • Rule out other conditions: They differentiate from conditions like TIAs, seizures, or migraine. Unlike TIAs, people with PSR generally have fewer cardiovascular problems.
  • Identify triggers: They look for recent factors such as infections, stress, or medication changes that might have caused symptom recurrence.

How long does recrudescence last?

Stroke recrudescence typically lasts a short time, usually resolving within hours to a day. Symptoms often start suddenly but ease completely once you receive treatment for an underlying trigger, such as an infection or electrolyte imbalance.

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.

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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Monday, February 25, 2019

Recrudescence of Old Stroke Deficits Among Transient Neurological Attacks

No clue, my doctor never warned me of this, but then he knew absolutely nothing about stroke, managed to tell me I had a CVA(had to ask what that was), nothing on recovery, he did warn me about fainting taking warfarin.  My OT was the only person that seemed to know anything. With a 10% occurrence rate your doctor is responsible for a protocol to prevent that problem. Which will never happen.

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.