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. Did your doctor somehow miss the recovery protocol that Pedro Bach-y-Rita used to recover fully back in 1958 with only a partial brain?

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.

Sunday, October 25, 2026

Depression, Not Anxiety, Linked to Poorer Cognition After Stroke

 It doesn't make a damn bit of difference what causes that poor cognition! SOLVE THE DAMN PROBLEM!

Prevent that cognition problem from occurring! Luckily my cognition remained intact since my doctor would have failed at that like he failed at my motor recovery and spasticity!

Depression, Not Anxiety, Linked to Poorer Cognition After Stroke

TOPLINE

Depression, but not anxiety, was independently linked to poorer executive function over 5 years after ischaemic stroke. The association between depression and visuospatial function was less robust. Anxiety was present in 27%-36% of patients at each assessment. 

METHODOLOGY

  • Researchers analysed data from the single-centre, observational STROKDEM cohort, which included 191 patients with ischaemic stroke (119 men and 72 women) assessed at 6, 12, 36, and 60 months after stroke.
  • Data on anxiety were available for 157 patients at 6 months and 85 patients at 60 months; patients with poorer baseline cognition were more likely to be lost to follow-up.
  • Patients completed neuropsychological testing across five domains (memory, executive function, attention, visuospatial abilities, and language), with results expressed as domain-specific z-scores.
  • Anxiety was measured using the Hamilton Anxiety Rating Scale (scores ≥ 8 indicated clinically relevant anxiety), depression was assessed using the Center for Epidemiologic Studies Depression Scale (scores ≥ 16 indicated clinically relevant depression), and stroke severity was evaluated using the National Institutes of Health Stroke Scale.
  • Researchers fitted two models, each using one affective score as the outcome and the five cognitive domains as predictors, with adjustment for the other affective score, time, sex, age, education, and stroke severity. Sensitivity analyses used multiple imputation and pattern-mixture models to address attrition.

TAKEAWAY

  • After mutual adjustment and false discovery rate correction, depression was independently associated with executive function (standardised regression coefficient [b], -0.167; P = .021) and visuospatial abilities (b, -0.208; P = .043). 
  • No cognitive domain was independently associated with anxiety after adjustment for depression. 
  • The association between depression and executive function held across all sensitivity analyses, including multiple imputation (b = -0.178; P = .015) and pattern-mixture analysis (P = .008 to .025). The association between depression and visuospatial abilities was not significant after multiple imputation (P = .195). 
  • Anxiety prevalence ranged from 26.6% to 36.1% across assessments (28.7% at 6 months and 31.8% at 60 months), whereas depression prevalence declined from 27.1% to 17.8%. 

IN PRACTICE

"Distinguishing between [depression and anxiety] requires joint modelling; failing to do so risks misattributing depression-related cognitive impairment to anxiety. For clinical practice, screening for depression is the more informative route for identifying stroke survivors at cognitive risk," the authors wrote. 

"This does not diminish the importance of anxiety, which is prevalent, persistent, and detrimental to quality of life and rehabilitation participation in its own right," they added. 

SOURCE

The study was led by Florine Ruthmann, Université de Lille, Inserm, Lille, France. It was published online on October 12 in the Journal of Affective Disorders.

LIMITATIONS

Attrition was substantial, and patients with poorer baseline cognition were more likely to be lost to follow-up; the COVID pandemic further contributed to the loss to follow-up at 60 months. Few patients had persistent anxiety. Psychiatric history was not available, psychotropic medication use was not adjusted for, and education was the only measure of cognitive reserve. The study was observational and conducted at a single centre, and the cohort included mostly men; effect sizes were modest.DISCLOSURES

Hauts-de-France Regional Council funded the study. The authors reported having no conflicts of interest.

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