A recent study by 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 the 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.

"Our findings suggest that indirect damage to the thalamus plays an important and under-explored role in the abnormal brain activity and long-term disability that often follow stroke," says Phillip Johnston, lead author of the study and a graduate student working with Randy McIntosh at the SFU Institute for Neuroscience and Neurotechnology. "But unlike the brain tissue that dies due to direct damage from the stroke lesion, the thalamus appears to be disrupted but still somewhat intact, offering some hope that new treatments could promote recovery by restoring its function, or preventing its disruption in the first place."

For the study, researchers recorded the brain activity of 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, the 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.

Johnston explains 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 traveling to the thalamus and keep it operating normally, researchers believe some long-term impacts of stroke could be alleviated.

"These findings also raise many new questions about which facets of post-stroke disability are due to indirect thalamus disruption, and which are due to direct damage from the lesion itself," says McIntosh. "The thalamus could undergo several types of damage following stroke and we don't know if one type in particular, or a combination, produces the abnormal brain activity observed in this study. A crucial next step will be investigating how indirect thalamus damage and related abnormal brain activity develops over time, particularly in the first hours and days after the stroke."