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, July 7, 2026

Eye-tracking phenotypes reveal clinically meaningful heterogeneity of attention and executive control dysfunction after stroke

 How EXACTLY will this get survivors recovered? Oh, nothing, so fucking useless? You're all fired! 'Assessments' have NEVER GOTTEN SURVIVORS RECOVERED! You need EXACT REHAB PROTOCOLS for that! This has none, so fucking useless!

Eye-tracking phenotypes reveal clinically meaningful heterogeneity of attention and executive control dysfunction after stroke

    We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.

    Abstract

    Background

    Post-stroke impairments in attention and executive control are common and clinically relevant, whereas conventional neuropsychological tests mainly capture task outcomes and provide limited information about process-level task behavior. Eye tracking can quantify fixation behavior, saccadic activity, and visual sampling, but whether integrated eye-tracking features can reveal clinically interpretable heterogeneity after stroke remains insufficiently defined.

    Objective

    This study examined whether integrated multi-paradigm eye-tracking features could identify exploratory eye-movement phenotypes in individuals with stroke and whether these phenotypes were associated with behavioral, clinical, lesion-related, and functional characteristics.

    Methods

    In this single-center exploratory case-control study, 72 subacute stroke participants (14–90 days post-onset) and 36 matched healthy controls completed five tasks of attention and executive control and six eye-tracking paradigms. Group differences in behavioral and eye-tracking measures were examined with false discovery rate correction. Within the stroke group, K-means clustering was performed using four nonredundant integrated eye-tracking features: total fixation duration, first-fixation duration, number of fixations, and total saccade distance. Cluster stability and sensitivity analyses were conducted using bootstrap resampling, alternative feature sets, and combined clustering with healthy controls. Post-clustering comparisons and exploratory regression analyses were used to evaluate the clinical relevance of the identified phenotypes.

    Results

    Compared with healthy controls, participants with stroke showed lower performance across attention/executive-control tasks and altered eye-tracking metrics across paradigms. The most consistent eye-movement pattern was shorter total fixation duration and a higher number of fixations across the six paradigms, whereas total saccade distance differed most clearly during the antisaccade task. K-means clustering identified two exploratory eye-movement phenotypes: a High-Fixation/Low-Saccade phenotype and a Low-Fixation/High-Saccade phenotype. The two-cluster solution remained stable across bootstrap and sensitivity analyses. The Low-Fixation/High-Saccade phenotype showed poorer cognitive performance, greater neurological and functional impairment, higher emotional symptom burden, and more frequent frontal involvement and bilateral or multifocal involvement. In exploratory hierarchical regression, eye-movement phenotype explained additional variance in Barthel Index scores beyond demographic variables, post-stroke timing, neurological severity, and conventional attention/executive-control performance.

    Conclusions

    Integrated multi-paradigm eye-tracking features identified two exploratory eye-movement phenotypes in individuals with subacute stroke. The Low-Fixation/High-Saccade phenotype was associated with broader clinical burden. These findings suggest that eye tracking may provide process-level information complementary to conventional assessment of post-stroke attention and executive-control dysfunction. Given the single-center and cross-sectional design, these preliminary phenotypes require validation in longitudinal and multicenter studies.

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