New Test Reveals Slower Signals Between Brain Regions in Patients

Signals travel slower even in regions where there's no apparent MS-related damage

Marisa Wexler, MS avatar

by Marisa Wexler, MS |

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An illustration shows neurons in the brain.

Using a new approach to track signals traveling between different brain regions, researchers found that these signals are slower in people with multiple sclerosis (MS), even in regions with no apparent disease-related damage, a new study reports.

The approach may help complement MRI findings to determine the extent of brain damage in MS patients and predict disability. It could also be used to refine virtual brain models that help tailor treatment approaches for each patient.

The study, “Whole-brain propagation delays in multiple sclerosis, a combined tractography-magnetoencephalography study,” was published in The Journal of Neuroscience.

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Brain tissue consists of ‘gray’ and ‘white matter’

Brain tissue can be broadly divided into two types: gray matter, which holds the bodies of nerve cells, and white matter, which houses nerve fibers that connect different regions of gray matter. Most complex brain processes involve the sequential activation of these areas — nerves in one gray matter region will activate, then send signals along a white matter tract to another gray matter region, and so forth.

The speed with which these signals are spread through the brain is thought to play important roles in determining brain activity. The speed of signals sent along white matter (from one gray matter region to another) is partly determined by how close the regions are to each other in physical space, but also by the thickness of the white matter fibers and their myelination state.

Myelin is a fatty wrapping around nerve fibers that helps them send electrical signals. High densities of this pale substance are how “white” matter gets its name. MS is caused by inflammation that damages the myelin sheath — but connections between observable myelin damage and resulting MS symptoms are not always clear.

“This illness is a diagnostic paradox,” Pierpaolo Sorrentino, PhD, a postdoctoral researcher at the Human Brain Project and co-author of the study, said in a project press release. “There are patients whose MRI scans show extensive degradation of myelin but do not experience a corresponding impairment, and others that show little evident damage but still experience considerable issues. Often we are not able to tell by simply looking at the [MRI] scans.”

New method measures speed of signals from one brain region to another

Sorrentino and colleagues devised a new method to measure not myelin damage itself, but the speed of signals sent from one brain region to another. Their technique involves combining tractography — assessments of brain regions and their connections based on MRI scans — with magnetoencephalography, a technique that assesses the activity of nerves by measuring the tiny magnetic fields generated by their electrical activity.

“These spontaneous bursts of activity can be used to measure the time it takes a signal to travel across the white-matter bundles connecting any two brain areas and then compare it with healthy controls without any myelinic damage,” Sorrentino said. “By not interfering directly with the signal, we can in a few minutes estimate the delay between most pairs of brain regions and then integrate it with what the MRI scans are showing us.”

The scientists used this technique to assess connective signals in the brains of 18 adults with MS and 20 control subjects without any neurological disease. In both groups, the average age was around 45 years, and most participants were female.

This illness is a diagnostic paradox. There are patients whose MRI scans show extensive degradation of myelin but do not experience a corresponding impairment, and others that show little evident damage but still experience considerable issues.

Results showed the speed of signals sent along white matter tracts tended to correlate with the length of the tract, with signals generally taking longer to move across longer tracts. This was expected, since it takes longer for signals to traverse a greater distance. However, signal speed also varied considerably among tracts of similar length, highlighting the importance of other factors such as demyelination.

Compared with controls, the average speed of signals in similar-sized tracts was significantly reduced in MS patients. Among individuals with MS, white matter tracts with lesions of myelin damage were slower at sending signals compared to tracts without visible damage, though on average both damaged and undamaged tracts in MS patients showed reduced signaling speed compared with controls.

“We observed, for both the lesioned and non-lesioned [tracts], that functional delays increased in the multiple sclerosis patients, in accordance with the hypothesis that damage to the myelin would provoke longer delays,” the researchers concluded.

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The team noted that reduced signal speed in apparently non-lesioned tracts in MS likely is reflective of broader disruptions in interconnected brain networks.

“The delays likely depend from a combination of both direct and indirect paths through which a perturbation can potentially travel between two regions,” the researchers wrote. “In this sense, one does not expect two regions that are linked by a healthy [tract] that is embedded in a diseased network to communicate as quickly as two regions that are also linked by a healthy [tract] as well as embedded in a healthy network.”

The team also noted that these patient-specific delays could help improve virtual brain models to study the disease in each patient.

“We are now able to add the time delay factor to these simulations, improving the diagnostic and predictive tools available to doctors and their patients,” Sorrentino concluded.

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