Deans' stroke musings: A randomized controlled study on intermittent theta pulse stimulation for improving cognitive impairment after 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, August 25, 2025

A randomized controlled study on intermittent theta pulse stimulation for improving cognitive impairment after stroke

Didn't your competent? doctor create a protocol on this years ago? NO? So, you DON'T HAVE A FUNCTIONING STROKE DOCTOR, do you?

iTBS (12 posts to April 2016)

You 5 lost cognitive years from your stroke, will this recover that loss?

A randomized controlled study on intermittent theta pulse stimulation for improving cognitive impairment after stroke

Fei Li¹^†

Fengxia Hu¹^†

Yi Liang¹^†

Fen Liang²^*

Huiqun Tan³^*

Sisi Xing¹^*^‡

¹Department of Neurology, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Huangshi, Hubei, China
²Department of Gastroenterology, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Huangshi, Hubei, China
³Department of General Practice, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Huangshi, Hubei, China

Objective: This study evaluates the efficacy and underlying mechanisms of intermittent theta-burst stimulation (iTBS) in improving cognitive function and quality of life in post-stroke patients.

Methods: A total of 80 subacute stroke patients with cognitive deficits were randomly assigned to a control group (n = 40) receiving conventional treatment plus sham stimulation and an experimental group (n = 40) receiving conventional treatment plus iTBS over the left dorsolateral prefrontal cortex for 4 weeks.

Results: Baseline characteristics were comparable between groups. After 3 months, the experimental group demonstrated significantly greater improvements than the control group in scores for the Mini-Mental State Examination (MMSE; adjusted mean: 25.35 vs. 20.44, P < 0.001), Montreal Cognitive Assessment (MoCA; 26.49 vs. 24.57, P = 0.002), and Stroke-Specific Quality of Life (SS-QOL; 158.45 vs. 137.31, P < 0.001), and showed greater reduction in completion time for the Trail Making Test (TMT). Biochemically, the iTBS group exhibited significantly increased serum Brain-Derived Neurotrophic Factor (BDNF) and reduced levels of Tumor Necrosis Factor-alpha (TNF-α) and Interleukin-6 (IL-6) compared to the control group (all P < 0.001). Changes in BDNF levels correlated positively with improvements in MMSE scores (r = 0.58, P < 0.001).

Conclusion: iTBS is a safe and effective intervention that enhances cognitive recovery and quality of life in post-stroke patients. These benefits are associated with modulation of neuroplasticity and inflammatory markers, suggesting that iTBS may promote recovery by upregulating BDNF and attenuating neuroinflammation. Further research is needed to confirm these mechanisms.