Scientists have found compelling evidence of brain abnormalities in patients with chronic fatigue syndrome (CFS) or myalgic encephalomyelitis (MA).
The findings, one of the most rigorous investigations to date, begin to shed light on the biological basis of the disease that can cause crippling fatigue. The study is the first to show a link between imbalances in brain activity and fatigue, and suggests that these changes may be caused by abnormalities in the immune system.
“People with ME/CFS have very real and disabling symptoms, but figuring out their biological basis has been extremely difficult,” said Walter Koroshets, director of the NIH’s National Center for Neurological Disorders and Stroke (NINDS) in the US. This in-depth study of a small group of people found several factors that may contribute to ME/CFS.
The study involved only 17 patients, and the findings need to be confirmed in a larger cohort before they can be called a roadmap for new treatments. In addition, the patients were evaluated and evaluated before the outbreak, so it is unclear how much the findings apply to long-term Covid. But scientists have described his work as a long-overdue deep dive into biology.
Professor Carl Morton, who studies ME/CFS at the John Radcliffe Hospital, University of Oxford and was not involved in the recent work, said: “This is a very important paper and I’m very pleased to have it out.” We’ve done quite a few studies that show that there might be a problem with this cell or that cell, but no one has ever really looked at what’s going on in a patient before.
The patients in the study, 300 carefully selected from the original pool, all had an infection before they got sick. During the study, they stayed at the NIH clinic for a week and were given extensive physiological evaluations.
Results from functional magnetic resonance imaging (fMRI) brain scans show that people with ME/CFS have lower activity in a brain region called the temporal-parietal junction (TPJ). . The motor cortex, the part of the brain that controls body movement, was also abnormally active during strenuous tasks. However, there were no signs of muscle fatigue.
This suggests that fatigue in ME/CFS is due to dysfunction of the brain regions that drive the motor cortex, and that changes in the brain may alter patients’ perception of energy and fatigue.
“We may have identified a physiological focal point for fatigue in this population,” said Brian Walt, an associate research physician at NINDS and first author of the study. Natural relationships. “Rather than physical fatigue or a lack of motivation, fatigue may arise from a mismatch between what one expects to achieve and what one’s body can do.”
Morton said that the presence of abnormalities in mental functioning does not indicate that patients are psychologically manipulating their illness or that they have no control over it. “The brain can respond to stimuli and influences on the body,” he said. “The brain is physically, biochemically not functioning properly and it’s the illness that’s doing that, not the patient.”
The patients also had a higher heart rate and it took longer for their blood pressure to normalize after exercise. Also, changes in the patients’ T cells, taken from cerebrospinal fluid samples, suggest that these immune cells are trying to fight something. This may indicate that the body’s immune system is not able to stop after the infection is cleared, or that there is a chronic infection in the body.
The authors identify possible events starting with an immune response that can cause changes in the central nervous system, which lead to changes in brain chemistry and ultimately affect the function of certain brain structures that control motor function and visual perception. Fatigue.
“We think that the immune system is affecting the brain in several ways, including biochemical changes and downstream effects such as motor, autonomic and cardiovascular problems,” said Avindra Nath, clinical director of NINDS and senior author of the study.
The findings were hailed by scientists as an important step towards identifying the underlying biological causes of the disease. Until now, there was no clear biological basis for the disease, leading patients to be dismissed, isolated, and to seek ineffective treatment options.