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.

Showing posts with label secondary problem. Show all posts
Showing posts with label secondary problem. Show all posts

Monday, October 5, 2026

Comparative evaluation of diffusion models for detecting gray matter microstructural alterations in post-stroke depression patients

 Useless! What you should be doing is creating EXACT 100% recovery protocols, thus preventing depression the correct way! No need to treat this secondary problem if you were to solve the primary problem of 100% recovery! Don't understand that? Get the hell out of stroke! A hell of a lot of mentors and senior researchers need to be removed!

Comparative evaluation of diffusion models for detecting gray matter microstructural alterations in post-stroke depression patients


  • F

    Fang Zhang

  • J

    Jing Zhang

  • L

    Lei Zhang

  • H

    Hengjun Jin

  • D

    Daqing Li

  • Wei Zhao

    Wei Zhao *

  • Department of Radiology, Huaibei People's Hospital, Huaibei, Anhui, China

Abstract


Background: 


Post-stroke depression (PSD) is often underdiagnosed because its gray matter microstructural abnormalities can be subtle.(This is incredibly easy! One question! Are you fully recovered? Y/N? No would likely mean is depressed! You are totally overthinking this.) This study compared four diffusion models (DTI, DKI, MAP, and NODDI) to identify objective imaging biomarkers for the early detection of PSD.


Methods: 

Sixty-four participants were enrolled, including 23 age- and sex-matched healthy controls (HC), 26 patients with acute cerebral infarction without PSD (non-PSD; HAMD-21 < 7), and 15 patients with PSD (HAMD-21 ≥ 7). Clinical assessments (HAMD-21, ADL, MoCA, and MMSE) and diffusion spectrum imaging were performed. Intergroup differences in gray matter microstructure, diagnostic performance based on the area under the curve (AUC), and partial correlations adjusted for age, sex, and years of education were analyzed. Infarct location was not included as a covariate.


Results: 


Significant differences among the three groups were observed in age, years of education, and all clinical scale scores (p < 0.05). Altered gray matter microstructure was primarily identified in the middle frontal gyrus, posterior cingulate gyrus, paracingulate gyrus and amygdala. For group discrimination, the left anterior cingulate DKI MD_p10 demonstrated the best performance for distinguishing HC from non-PSD (AUC = 0.916). The left putamen NODDI ODI_p10 showed the highest AUC (0.916) for distinguishing HC from PSD, whereas the left putamen NODDI ODI_p50 yielded the highest AUC (0.856) for distinguishing non-PSD from PSD. After FDR correction, multiple diffusion metrics were significantly correlated with MMSE and MoCA scores, whereas no imaging parameter showed a significant correlation with HAMD-21.


Conclusion: 


Multimodal diffusion MRI detects microstructural abnormalities within emotion- and cognition-related circuits, particularly the amygdala and cingulate cortex, across the three groups. Temporolimbic NODDI parameters showed relatively higher AUC values in distinguishing PSD from HC, whereas anterior cingulate DKI metrics showed relatively higher AUC values in differentiating non-PSD stroke patients from HC. Combining multiple diffusion models may aid in the identification of PSD; however, these findings require further validation because infarct location was not adjusted for in the analyses.