MGH Researchers make a key discovery to diagnose patients with fibromyalgia
The words’ You look so good’ are often heard by fibromyalgia patients. How could you be ill? How are you?” Or perhaps the nonsensical words” all in your head is fibromyalgic. Recent and ongoing investigations, however, confirm this invisible disease’s reality. This information enables individuals with fibromyalgia and other similar invisible conditions to make sure that their complex diseases are validated. Furthermore, understanding recent research helps to guide and identify natural solutions for healthy fibromyalgia pain management.
The symptoms often change and coexist with symptoms of other diseases, as well as those of others can be clearly diagnosed by Harvard Medical School Fibromyalgia written by Marco Loggia, Ph.D. Investigator, the Main Biomedical Imaging Center, Massachusetts General Hospital Assistant Professor of radiology. Mass General and Swiss colleagues have recently found a distinct pattern of brain inflammation in patients with fibromyalgia that can be the key to the disorder’s diagnosis.
For quite a while, Fibromyalgia was a physical mystery. There is no test or scan that can detect this, unlike other chronic medical conditions. Physicians can diagnose only based on the reported symptoms of a patient and exclude other potential causes.
A team of researchers at Mass General, however, has recently identified an inflammatory pattern of patients with fibromyalgia in their brains which can be key to the diagnosis of elusive disease in a team made up of the Karolinska Institute of Sweden. They may also provide validation of the legacy of their symptoms for patients with fibromyalgia, who are often skeptical.
Fibromyalgia patients often report felt pain, fatigue, swings in moods, and difficulty sleeping throughout the body (click here to read what is fibrous sleep), and memory. These symptoms should come and go and coexist with symptoms of other conditions, which make it difficult to diagnose clearly.
The body’s healing process consists of inflammation. Infections and injuries would not cure without inflammation. However, it may also be harmful to inflammation. Inflammation is of two types, acute and chronic. Acute swelling suddenly results from injury or infection. Classic symptoms such as swelling, redness, and pain are present.
Acute inflammation, depending on the origin of inflammation, is temporary, lasts from a few days to a few weeks. Chronic inflammation is long-lasting, months and years old inflammation. It happens slowly and paves the way for chronic diseases. Heart, autoimmune disorders, and other diseases are related to chronic inflammation, including neurological conditions such as diabetes, cancer, Alzheimer’s, arthritis.
The team, led by MarcoLoggia, Ph.D., employed PET brain imaging technology to measure activity levels of a key protein in astrocytes and microglia, two types of brain cells known as Glial cells, using a strategy previously successful in identifying brain inflammation associated with chronic back pain.
When comparing the fibromyalgia patient imaging results with healthy controls, they found that in several regions of the brain fibromyalgia patients had increased inflammatory activity. Researchers suspect that the complexity of fibromyalgia symptoms can be explained by this widespread inflammation. The correlation between inflammatory activity and fibromyalgia symptoms also appears. The greater the tiredness reported, the higher the inflammation levels found by researchers.
The researchers believe it can improve the sensitivity of pain and fatigue-related receptors. The researchers could also measure the efficacy of new treatments by measuring how inflammation levels change in treatment reaction.
“Patients with fibromyalgia demonstrate inflammation of the brain, which has two consequences,” Loggia states.
“We, first of all, validate these patients that their condition is real, a claim which is often met with skepticism and social stigmatism, and even some clinicians, by demonstrating that objective neurochemical changes can be observed. Second, our findings identify a novel therapeutic goal in the case of neuroinflammation which paves the way for new treatments in this misunderstanding and complicated condition.
Studies of PET imaging show high glial activation, correlation with fatigue. A study has documented the first time in patients with a misunderstood condition called fibromyalgia a widespread inflammation of their brains.
For the first time, a study conducted by researchers from the Massachusetts General Hospital (MGH), working with a team from Sweden’s Karolinska Institute documented a widespread inflammation in the minds of poorly understood patients known as fibromyalgia. Their report was published in the Brain, Behavior, and Immunity newspapers online.
Marco Loggia, Ph.D. at the MGH-based Martinos Center for Biomedical Imaging, co-senior author, says that “we have not had good fibromyalgia treatment options and that the identification of a treatment target could lead to the development of innovative, more efficient treatments. “It should be helpful to find objective neurochemical brain changes for fibromyalgia patients to reduce the persistent stigma facing many, their symptoms are often told to be imaginary and nothing is really wrong with them.”
The present study has shown that fibromyalgia (FM) patients have high TSPO binding compared to healthy controls (HC) as measured with CPBR28 PET. In several regions of the brain involving FM pathology in previous neuroimaging studies, this marker of glial activation has been increased. In several of these regions, we also report positive associations of TSPO PET signal and subjective fatigue ratings, one of the most common signs reported by FM patients (Clauw, 2014, Wolfe et al., 2011). We note that neuroimmune/glial activation in FM pathology has a role to play.
These results conform to a series of clinical data which show that neuroinflammation and FM may have an association. Several studies have shown high CSF levels of neuroglial signaling molecules, such as fractalkine and IL‐8.
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