Deans' stroke musings: The Association of Glycemic Gap with Cognitive Function After Ischemic Stroke or Transient Ischemic Attack

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.

Saturday, July 19, 2025

The Association of Glycemic Gap with Cognitive Function After Ischemic Stroke or Transient Ischemic Attack

Known of the problem since May 2018; DID NOTHING TO SOLVE IT! YOU'RE FIRED!

glycemic control (5 posts to May 2018)

The Association of Glycemic Gap with Cognitive Function After Ischemic Stroke or Transient Ischemic Attack

Authors Min Y, Xu Q, Wang Y, Li Z

Received 29 January 2025

Accepted for publication 2 July 2025

Published 19 July 2025 Volume 2025:21 Pages 1425—1433

DOI https://doi.org/10.2147/NDT.S519935

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Jun Chen

Download Article [PDF]

Yan Min,¹ Qin Xu,^1,² Yongjun Wang,^{1– 3} Zixiao Li^1,^2,⁴

¹Department of Neurology, Beijing TianTan Hospital, Capital Medical University, Beijing, People’s Republic of China; ²China National Clinical Research Center for Neurological Diseases, Beijing, People’s Republic of China; ³Center of Stroke, Beijing Institute for Brain Disorders, Beijing, People’s Republic of China; ⁴Chinese Institute for Brain Research, Beijing, People’s Republic of China

Correspondence: Yongjun Wang, Beijing TianTan Hospital, Capital Medical University, Beijing, People’s Republic of China, Tel +86 010 59978351, Email yongjunwang@ncrcnd.org.cn Zixiao Li, Beijing TianTan Hospital, Capital Medical University, Beijing, People’s Republic of China, Tel +86 010 59978351, Email lizixiao2008@hotmail.com

Background: Glycemic gap (GG), as a measure of an acute derangement in glucose level in response to an active disease state, has been found to be associated with adverse outcomes in many diseases. This study aimed to determine the relationship of GG with cognitive function after ischemic stroke or transient ischemic attack (TIA).
Methods: Patients included were enrolled from a subgroup of China National Stroke Registry-III (CNSR-III). Cognitive function was assessed by the Beijing edition of the Montreal cognitive assessment (MoCA) scale. Post-stroke cognitive impairment (PSCI) was diagnosed as a MoCA score≤ 22. Post-stroke cognitive decline (PSCD) was defined as a decrease of > 2 points on the MoCA score between the 3-month and 1-year assessments. GG was calculated using admission blood glucose minus hemoglobin A1c-derived average blood glucose. Multivariable logistic regression analysis was used to evaluate the correlation between GG and cognitive function.
Results: We enrolled 767 patients with a median age of 60 years old, including 247 (32.2%) patients with PSCI in 3 months, 228 (29.73%) with PSCI in 1 year, and 166 (21.64%) patients with PSCD. The highest GG levels were related to PSCI in 3 months after adjusted for multiple potential confounders (adjusted odd ratio (OR): 2.021, 95% CI: 1.055– 3.869, P=0.0338), but not in patients with PSCI in 1 year or PSCD. No significant interactions for the impact on PSCI were observed in subgroups (P interaction > 0.05 for all).
Conclusion: Our findings show that GG is associated with acute post-stroke cognitive impairment, but not with the long-term cognitive impairment or cognitive decline.