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.

Monday, September 14, 2020

Risk of Dementia in Posttraumatic Stress Disorder

You need to worry about this and your doctor is responsible for having protocols that prevent PTSD post stroke. YOUR DOCTOR'S RESPONSIBILITY.

The 23% chance of stroke survivors getting PTSD June 2012.

The latest here:

Risk of Dementia in Posttraumatic Stress Disorder

 
First Published September 10, 2020 Review Article 

Several studies have investigated the risk of dementia in posttraumatic stress disorder (PTSD) using a varying methodology. Epidemiological studies have found an increased risk of dementia with PTSD in Vietnam veterans as well as the general population. Laboratory studies reported the accelerated formation of β-amyloid and tau, which represent the primary pathology of Alzheimer’s dementia in animal models of PTSD. These investigations were conducted against a background of cognitive impairment and atrophy of the hippocampus and certain cortical areas in patients with PTSD. Very few studies have investigated the pathological basis in humans for the reported association of PTSD with dementia. This important gap in the literature has recently been partly addressed by very few studies that estimated the burden of β-amyloid and tau. The PET studies did not show an association between PTSD and the specific pathology of Alzheimer’s disease or signs of neurodegenerative diseases underlying other dementia syndromes. Another study demonstrated decreased plasma β-amyloid load and increased plasma β-amyloid 42/40 ratio in PTSD without PET evaluation. While PTSD is associated with an increased risk of dementia syndrome in general, there is no convincing evidence that it causes or accelerates the pathology of Alzheimer’s disease, which causes the most common type of dementia. Factors that may account for the association between PTSD and a clinical diagnosis of dementia are discussed in this review.

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