A recent study from the SFU Institute for Neuroscience and Neurotechnology (INN) and Rotman Research Institute at the University of Toronto points to the thalamus to help explain the long-term disabilities experienced after a stroke. Under lead author Phillip Johnston, a graduate student at SFU INN, the November 6 publication focuses on why strokes cause “a prominent slowing of neural activity.”
A stroke is the result of “blocked blood flow to the brain” or “sudden bleeding in the brain.” In both cases, this sudden change can cause damage to the brain cells. When an individual experiences a stroke, damage to axons in other parts of the brain can cause indirect injury to the thalamus. The thalamus is a part of the brain that works as a “central networking hub that regulates functions such as language, memory, attention, and movement.” It receives all sensory information (except smell) through nerve fibers, called axons, then processes this information. Next, the thalamus sends the data back through the axons to the cerebral cortex for interpretation. The cerebral cortex helps with “high-level functions” such as memory and reasoning.
The thalamus’ communication with the rest of the brain via axons “makes it susceptible to indirect damage.” This can potentially lead to corticothalamic circuit dysfunction, where the thalamus’ ability to communicate with the cerebral cortex is inhibited.
Using computer models to measure brain activity with magnetoencephalography, or “magnetic fields produced by [the] brain’s electrical currents,” researchers compared 18 chronic stroke survivors to a group of healthy individuals. SFU researchers concluded that there is “a link between the amount of indirect damage suffered to the thalamus and the level of impairment a patient experiences” after a stroke.
“If certain treatments, such as drugs or brain stimulation, could restore normal function in the thalamus, [ . . . ] researchers believe some long-term impacts of stroke could be alleviated.” — SFU news release
Specifically, researchers noted “decreased thalamic volume, altered tissue microstructure, and decreased blood flow” in those who had experienced a stroke, which “correlated significantly with poorer cognitive and language outcomes.” Researchers stated that because a stroke does not directly affect the thalamus, it can remain “somewhat intact.” Inversely, there is still “brain tissue that dies due to direct damage from the stroke lesion,” Johnston told SFU News. This key difference provides researchers “some hope that new treatments could promote recovery by restoring [the thalamus’] function, or preventing its disruption in the first place.
“If certain treatments, such as drugs or brain stimulation, could restore normal function in the thalamus [ . . . ] researchers believe some long-term impacts of stroke could be alleviated,” noted SFU’s press release.
“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,” said Dr. Randy McIntosh, SFU biomedical physiology and kinesiology professor, who was quoted in the press release. McIntosh also noted that “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,” he added.
