Deans' stroke musings: A SYSTEMATIC REVIEW OF CEREBRAL ATROPHY IN ISCHEMIC STROKE

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, February 23, 2026

A SYSTEMATIC REVIEW OF CEREBRAL ATROPHY IN ISCHEMIC STROKE

This review DOES NOTHING TO GET SURVIVORS RECOVERED! Only EXACT REHAB PROTOCOLS DO!

Maybe if you were to read up on all this earlier research you could actually do some good!

cerebral atrophy (3 posts to April 2016)
Cortical atrophy (1 post to Gebruary 2019)
Entorhinal Cortex Atrophy (1 post to October 2017)
Frontal Cortical Atrophy (1 post to June 2016)
hippocampal atrophy (1 post to October 2019)
Posterior cortical atrophy (1 post to October 2024)
Thalamic atrophy (2 posts to March 2021)
atrophy (27 posts to January 2012)

A SYSTEMATIC REVIEW OF CEREBRAL ATROPHY IN ISCHEMIC STROKE

E Fahad Somaa1*, Azka Khan2, Anna Podlasek3,4 and Faraz Ahmed Bokhari5

1 King Abdulaziz University, Occupational Therapy Department, Faculty of Medical Rehabilitation Sciences, Jeddah, Saudi Arabia

2 Riphah International University, Faculty of Rehabilitation and Allied Health Sciences Islamabad, Pakistan

3 NIHR Nottingham BRC, University of Nottingham, Nottingham, UK

4 Clinical Radiology, Queens Medical Centre - Nottingham University Hospitals NHS Trust, Nottingham, UK

5 Department of Physiology, Shaikh Zayed Federal FPGMI, Lahore, Pakistan.

SUMMARY –

Background:

Stroke, a neurological condition, ranks as the second leading cause of death and disability worldwide, resulting in sensory, motor and cognitive impairments. Post-stroke cerebral atrophic changes in various brain regions, both ipsilesional and contralesional, carry significant clinical implications. This systematic review and meta-analysis aims to explore structural (volume and cortical thickness) and functional deficits induced by post-ischemic stroke cerebral atrophy.

Methods:

The review encompassed studies conducted from January 2010 to October 2021, result ing in the inclusion of 33 articles sourced from PubMed/Medline, Cochrane/EMBASE and PEDro databases. Keywords such as ‘stroke’, ‘cortical atrophy’, ‘cerebral atrophy’, ‘motor’, ‘sensory’ and ‘cognitive disability’ were utilized in the search process.

Results:

Notably, the temporal lobe emerged as the most commonly affected site for atrophic volume changes, followed by the thalamic areas, hippocampus, cerebellum and sensory cortex. Cortical thinning was observed in frontotemporal, inferior parietal, primary motor cortex (M1) and superior frontal gyrus regions of the stroke hemisphere. Regarding functional outcomes, gray matter volume (GMV) was found to correlate with motor function, with severe GMV atrophy hindering clinical re covery, while increased GMV was linked to better outcomes. Additionally, GMV was associated with cognitive functions. Notably, changes in total and regional brain tissue volume were observed early post stroke and continued at an accelerated rate compared to normal age-related atrophic changes.

Conclusion:

This underscores the potential of brain atrophy as a prognostic marker for identifying regions of structural plasticity and as a therapeutic target.

Keywords: Stroke; Cortical atrophy; Cerebral atrophy; Motor, sensory and cognitive impairment