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 21, 2026

Effects and mechanisms of transcutaneous auricular vagus nerve stimulation on post-stroke cognitive impairment in animal studies: a systematic review and meta-analysis

 Why this animal study? Don't we have enough human research out there to create protocols with? Never mind, there aren't enough functioning neurons in your stroke medical 'professionals' to accomplish that! You all need to be fired!

Effects and mechanisms of transcutaneous auricular vagus nerve stimulation on post-stroke cognitive impairment in animal studies: a systematic review and meta-analysis


    The Affiliated Huai'an Hospital of Xuzhou Medical University, Huai'an, China

Abstract

 Background:  

Post-stroke cognitive impairment (PSCI) substantially undermines rehabilitation adherence and poses a major obstacle to functional recovery. Transcutaneous auricular vagus nerve stimulation (taVNS), a noninvasive neuromodulation technique, has the potential to improve cognitive function, as demonstrated in various clinical and preclinical studies. Against this backdrop, we performed a meta-analysis of taVNS in experimental stroke models to quantify its cognitive benefits and probe the biological mechanisms involved in its effects.


Methods: 


We systematically searched databases, including PubMed, The Cochrane Library, Embase, and Scopus, to identify controlled animal studies evaluating taVNS in PSCI models. Following eligibility screening, five studies were selected for final synthesis. The primary cognitive outcomes comprised escape latency in the Morris water maze and the Barnes maze. Data extraction was performed independently by two investigators, and statistical analyses were performed using Review Manager 5.4 software.


Results: 


Five RCTs involving 158 rodents were analyzed in this study. The meta-analysis revealed that taVNS significantly improved memory function in PSCI animals (SMD = 1.85, 95% CI: 1.06 to 2.64, p < 0.01, I 2 = 57%) and learning ability (MD = − 6.38, 95% CI: − 8.87 to − 3.89, p < 0.01, I 2 = 0%) and reduced modified neurological severity scores (MD = − 1.08, 95% CI: − 1.63 to − 0.52, p < 0.01, I 2 = 38%). Mechanistically, taVNS significantly elevated acetylcholine levels (SMD = 1.57, 95% CI: 0.85 to 2.30, p < 0.01, I2 = 0%), inhibited neuronal apoptosis (SMD = 2.29), and promoted angiogenesis (SMD = 1.63). Sensitivity analysis confirmed the robustness of the primary outcomes.


Conclusion: 


This study provides preclinical evidence confirming that taVNS can effectively improve cognitive deficits in PSCI animal models. The enhancement of Ach levels, inhibition of neuronal apoptosis, and promotion of vascular repair may be related to the non-neuronal cholinergic system (NNCS), anti-inflammatory, and antioxidant stress mechanisms. However, as only a few studies were included, more high-quality animal experiments are needed in the future to develop standardized interventions and further explore the molecular mechanisms underlying these effects.

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