Study Suggest Thalamus's Role in Prolonged Stroke Impact
A recent study from Simon Fraser University researchers has revealed how an overlooked type of indirect brain damage contributes to ongoing disability after a stroke.
The paper, published in Proceedings of the National Academy of Sciences, shows how the thalamus – a sort of central networking hub that regulates functions such as language, memory, attention and movement – is affected months or years after a person has experienced a stroke, even though it was not directly damaged itself. The findings may lead to new therapies that could reduce the burden of chronic stroke, which remains one of the leading causes of disability in the world.
For the study, researchers recorded the brain activity from 18 chronic stroke patients and used computer models to understand how this brain activity reflects abnormal thalamus function when compared to healthy individuals.
By studying the brain activity and anatomy of stroke survivors, SFU researchers say there appears to be a link between the amount of indirect damage suffered to the thalamus and the level of impairment a patient experiences.
Researchers explain that the thalamus communicates widely with the rest of the brain via many long connections, called axons, which makes it susceptible to indirect damage. When axons are injured by stroke in other regions of the brain, the damage can travel along the cell and damage neurons in the thalamus, causing its function to be impaired.
This impairment also has a knock-on effect of disrupting the functions that the now-damaged thalamus would normally regulate in other, undamaged parts of the brain. If certain treatments, such as drugs or brain stimulation, could restore normal function in the thalamus, or mitigate the impact of damage travelling to the thalamus and keep it operating normally, researchers believe some long-term impacts of stroke could be alleviated.
Reference: P.R. Johnston, J.D. Griffiths, L. Rokos, A.R. McIntosh, J.A. Meltzer, Secondary thalamic dysfunction underlies abnormal large-scale neural dynamics in chronic stroke, Proc. Natl. Acad. Sci. U.S.A., 121 (46) e2409345121,
https://doi.org/10.1073/pnas.2409345121 (2024).
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