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 28, 2026

Neural mechanisms underlying loss of functional independence after stroke: EEG evidence of impaired motor-to-sensory directed connectivity on the affected side

 Absolutely nothing here gets survivors recovered! You're all fired!

(Margaret Yekutiel wrote a whole book about this in 2001, 'Sensory Re-Education of the Hand After Stroke'. Does your incompetent? doctor and therapists even know about it?)

Neural mechanisms underlying loss of functional independence after stroke: EEG evidence of impaired motor-to-sensory directed connectivity on the affected side

    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 reorganization of the prefrontal-sensorimotor network is critical for functional recovery, yet single connectivity metrics fail to capture its multidimensional characteristics. This exploratory study investigates network reorganization patterns and their clinical relevance to motor function and daily independence using multimodal electroencephalography (EEG) connectivity analysis, including Coherence (COH), phase lag index (PLI), and Granger causality (GC).

    Methods

    Resting-state EEG from stroke patients (n = 22) and healthy controls (n = 22) was analyzed. COH, PLI, and GC metrics were computed for key regional connections involving the prefrontal (PFC), motor (MC), sensory (SC), and parietal (PC) cortices and correlated with Fugl-Meyer Assessment for Upper Extremity (FMA-UE) and Modified Barthel Index(MBI) scores. For stroke patients, hemispheres were classified as ipsilesional (i, affected) and contralesional (c, unaffected) based on the lesion side.

    Results

    Compared to healthy controls, stroke patients exhibited distinct reorganization patterns. Preliminary evidence suggests enhanced parietal-motor coherence (COH_cPC-cMC↑) in the unaffected hemisphere alongside reduced motor-to-prefrontal directed connectivity (GC_cMC→cPFC↓). Interhemispherically, the findings may indicate weakened information flow from the unaffected to affected motor/sensory areas (GC_cMC→iMC↓, GC_cMC→iSC↓), accompanied by reduced bilateral motor synchronization (PLI_iMC-cMC↓). Within the affected hemisphere, there was evidence of enhanced bidirectional parietal-motor phase transfer (PLI_iPC-iMC↑), whereas directed pathways were significantly impaired (GC_iMC→iSC↓, GC_iPC→iSC↓, GC_iPFC→iMC↓). Clinically, the affected motor-to-sensory pathway (GC_iMC→iSC) showed a strong negative correlation with the MBI (r = -0.61, P = 0.002), and both interhemispheric motor regulation (GC_cMC→iMC) and synchronization (PLI_iMC-cMC) were significantly correlated with functional deficits (P < 0.05).

    Conclusion

    Post-stroke networks may exhibit a “local compensation-global impairment” reorganization pattern. The affected motor-sensory pathway (GC_iMC→iSC) may be a biomarker for functional independence and thus allow for guided sensory integration-based precision rehabilitation.

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