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.

Friday, April 5, 2024

Brain changes and associated cognitive deficits evident in patients with neurological long COVID

 Luckily my bout with COVID was short, probably because I was well vaccinated. I didn't want any more brain damage than I already have.

Brain changes and associated cognitive deficits evident in patients with neurological long COVID


Brain changes associated with cognitive deficits were observed in individuals with neurological long COVID, according to a study published in the journal Brain.

“Our data indicate a specific profile of cognitive dysfunction in neurological long COVID characterised by impairment in episodic memory, attention, processing speed, and verbal fluency,”

reported Víctor M. Serrano del Pueblo, University of Castilla-La Mancha, Albacete, Spain, and colleagues. “This altered cognitive performance is associated with reduced integrity of specific white matter regions involved in the interconnection of distal regions responsible for these cognitive functions.”

The study included 83 patients with persistent neurological symptoms after COVID-19 and 22 patients with COVID-19 who had recovered without neurological sequelae. The mean age (50.50 vs 50.82 years) and mean duration from acute infection to neuropsychological and MRI assessments (15 vs 16 months) were similar in the 2 groups. The majority (>90%) of participants were vaccinated after their acute COVID-19 infection.

Overall, the mean global cognitive function of patients with neurological long COVID, assessed by the Addenbrooke’s Cognitive Examination 20 (ACE III) screening test, was significantly lower compared with those who had recovered (overall cognitive level [OCLz] = -0.39 vs 0.32; P < .01). Of the patients with long COVID, 27% had an impaired overall cognitive function (OCLz ≤ -0.7), with cognitive severity spanning from severe impairment (12%) to relatively mild deficit (15%).

Furthermore, 48% of patients scored below the 24th percentile in the Rivermead Behavioural Memory Test (RBMT) for episodic memory assessment (global index), with 50% of them exhibiting a severe deficit. Of the 14 RBMT subtests, 8 were significantly below normal, including delayed object recognition, delayed face recognition, delayed spatial route recall, and delayed story recall. 

In addition, specific cognitive functions and executive domains were significantly below the population norms and controls for attention (ACE IIIz < 0; P < .001), verbal fluency (ACE IIIz < 0; P < .006), processing speed (trail making test-Az< 0; P = .005), and verbal working memory (Wechsler Adult Intelligence Scale IV Digit spanz< 0; P < .017), with 24% to 34% of patients having some degree of deficit and up to 20% showing severe impairment.

MRI examination, including grey matter morphometry and whole brain structural connectivity, showed that patients with long COVID had thinner cortex in a specific cluster centred on the left posterior superior temporal gyrus compared with patients who had recovered.

In addition, lower fractional anisotropy and higher radial diffusivity were observed in widespread areas of the patients’ cerebral white matter relative to controls. Correlations between cognitive status and brain abnormalities revealed a relationship between altered connectivity of white matter regions and impairments of episodic memory, overall cognitive function, attention and verbal fluency.

“To the best of our knowledge, this is the first study involving cognitive testing and neuroimaging from both patients with neurological long COVID and previously SARS-CoV-2-infected subjects who no longer present persistent neurological symptoms (our control group),” the authors noted. “It allows us, therefore, to argue that the neuropsychological and brain alterations found in our long COVID patients are specific to this syndrome, and responsible for chronic cognitive dysfunction.”

“Our study supports the now-increasing evidence for there being a diverse manifestation of neurological symptoms associated with cognitive alterations and brain changes,” the authors concluded.

Source: Brain

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