SFC ET ANOMALIES CEREBRALES

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SFC ET ANOMALIES CEREBRALES

Messagede xavier » Mer 29 Oct 2014 22:59

La fatigue chronique proviendrait-elle d'une anomalie cérébrale ?

Edité par Lorelei BOQUET-VAUTOR
le 29 octobre 2014 à 12h27
Non, être sans cesse fatigué n'est pas nécessairement un signe de fainéantise. Cela pourrait être le signe d'une maladie, dont on vient de découvrir qu'elle créait des anomalies cérébrales.

Vous passeriez bien vos journées à dormir, même après de bonnes nuits de sommeil et une hygiène de vie correcte? Vous souffrez peut-être du Syndrome de Fatigue Chronique. Aussi appelée "encéphalomyélite myalgique", cette maladie neurologique (car oui c'en est une), se caractérise par une fatigue persistante et inexpliquée qui perdure pendant des mois, voire des années, malgré le repos. Elle comprend aussi des douleurs articulaires et musculaires, des migraines, un gonflement des glandes lymphatiques, des problèmes gastro-intestinaux et une tension artérielle anormale. La fatigue chronique apparaît de façon soudaine, entraînant une détérioration rapide et importante de la santé et toucherait plus d'un million de personnes aux Etats-Unis selon les Centres de Contrôle et de Prévention des Maladies (CDC).

Si l'on connait depuis longtemps l'existence de la maladie, on en sait un peu plus sur le sujet aujourd'hui. Une étude américaine publiée mercredi dans la revue médicale Radiology, montre en effet que les personnes souffrant de fatigue chronique présentent des anomalies cérébrales, décelables par différents types de scanners et notamment les IRM (imageries par résonance magnétique). La recherche a été effectuée auprès de 15 patients, hommes et femmes, atteints du syndrome, ainsi que sur un groupe témoin de 14 personnes des deux sexes.


Des anomalies dans deux parties du cerveau

Les chercheurs se sont principalement intéressés à la taille des différents compartiments du cerveau, pour observer la substance blanche du cerveau, composée de fibres nerveuses transportant des messages entre les neurones. Le flot sanguin cérébral a aussi été analysé. La comparaison des différents résultats a révélé que les personnes souffrant du syndrome de fatigue chronique ont un volume légèrement plus faible de substance blanche et une diffusion anormale de molécules d'eau dans cette zone en particulier. Enfin, les chercheurs ont constaté des anomalies dans deux parties du cerveau qui relient le lobe frontal et le lobe temporal. "Plus ces deux parties du cerveau sont anormales, à savoir plus épaisses dans leur apparence, plus les symptômes sont sévères", souligne le Dr Michael Zeineh, professeur adjoint de radiologie à la faculté de médecine de Stanford en Californie.

"Ces résultats permettent d'envisager la possibilité d'avoir un bio-marqueur du syndrome de fatigue chronique qui pourrait aider à le diagnostiquer", estime encore le Dr Michael Zeineh. En effet, bien que la recherche ne porte que sur 15 malades, les techniques d'imagerie sont de bons outils pour déceler la maladie. Les chercheurs précisent d'ailleurs être parvenus "à un taux de détection de 80%". Reste à savoir si cette découverte permettra d'améliorer la qualité des traitements.
xavier

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Re: SFC ET ANOMALIES CEREBRALES

Messagede xavier » Mer 29 Oct 2014 23:04

Study finds brain abnormalities in chronic fatigue patients

Radiology researchers have discovered that the brains of patients with chronic fatigue syndrome have diminished white matter and white matter abnormalities in the right hemisphere.

Oct 28 2014
Michael Zeineh


Michael Zeineh and his colleagues studied the brains of patients with chronic fatigue syndrome and healthy people, and found distinct differences between the two groups.
Norbert von der Groeben

An imaging study by Stanford University School of Medicine investigators has found distinct differences between the brains of patients with chronic fatigue syndrome and those of healthy people.

The findings could lead to more definitive diagnoses of the syndrome and may also point to an underlying mechanism in the disease process.

It’s not uncommon for CFS patients to face several mischaracterizations of their condition, or even suspicions of hypochondria, before receiving a diagnosis of CFS. The abnormalities identified in the study, published Oct. 29 in Radiology, may help to resolve those ambiguities, said lead author Michael Zeineh, MD, PhD, assistant professor of radiology.

“Using a trio of sophisticated imaging methodologies, we found that CFS patients’ brains diverge from those of healthy subjects in at least three distinct ways,” Zeineh said.

CFS affects between 1 million and 4 million individuals in the United States and millions more worldwide. Coming up with a more precise number of cases is tough because it’s difficult to actually diagnose the disease. While all CFS patients share a common symptom — crushing, unremitting fatigue that persists for six months or longer — the additional symptoms can vary from one patient to the next, and they often overlap with those of other conditions.

Scientific challenge

“CFS is one of the greatest scientific and medical challenges of our time,” said the study’s senior author, Jose Montoya, MD, professor of infectious diseases and geographic medicine. “Its symptoms often include not only overwhelming fatigue but also joint and muscle pain, incapacitating headaches, food intolerance, sore throat, enlargement of the lymph nodes, gastrointestinal problems, abnormal blood-pressure and heart-rate events, and hypersensitivity to light, noise or other sensations.”

Jose Montoya


Jose Montoya
The combination of symptoms can devastate a patient’s life for 10, 20 or even 30 years, said Montoya, who has been following 200 CFS patients for several years in an effort to identify the syndrome’s underlying mechanisms. He hopes to accelerate the development of more-effective treatments than now exist.

“In addition to potentially providing the CFS-specific diagnostic biomarker we’ve been desperately seeking for decades, these findings hold the promise of identifying the area or areas of the brain where the disease has hijacked the central nervous system,” Montoya said.

“If you don’t understand the disease, you’re throwing darts blindfolded,” said Zeineh. “We asked ourselves whether brain imaging could turn up something concrete that differs between CFS patients’ and healthy people’s brains. And, interestingly, it did.”

The Stanford investigators compared brain images of 15 CFS patients chosen from the group Montoya has been following to those of 14 age- and sex-matched healthy volunteers with no history of fatigue or other conditions causing symptoms similar to those of CFS.

Three key findings

The analysis yielded three noteworthy results, the researchers said. First, an MRI showed that overall white-matter content of CFS patients’ brains, compared with that of healthy subjects’ brains, was reduced. The term “white matter” largely denotes the long, cablelike nerve tracts carrying signals among broadly dispersed concentrations of “gray matter.” The latter areas specialize in processing information, and the former in conveying the information from one part of the brain to another.

That finding wasn’t entirely unexpected, Zeineh said. CFS is thought to involve chronic inflammation, quite possibly as a protracted immunological response to an as-yet unspecified viral infection. Inflammation, meanwhile, is known to take a particular toll on white matter.

But a second finding was entirely unexpected. Using an advanced imaging technique — diffusion-tensor imaging, which is especially suited to assessing the integrity of white matter — Zeineh and his colleagues identified a consistent abnormality in a particular part of a nerve tract in the right hemisphere of CFS patients’ brains. This tract, which connects two parts of the brain called the frontal lobe and temporal lobe, is called the right arcuate fasciculus, and in CFS patients it assumed an abnormal appearance.

Furthermore, there was a fairly strong correlation between the degree of abnormality in a CFS patient’s right arcuate fasciculus and the severity of the patient’s condition, as assessed by performance on a standard psychometric test used to evaluate fatigue.

Right vs. left

Although the right arcuate fasciculus’s function is still somewhat mysterious, its counterpart in the brain’s left hemisphere has been extensively explored. The left arcuate fasciculus connects two critical language areas of the left side of the brain termed Wernicke’s and Broca’s areas, which are gray-matter structures several centimeters apart. These two structures are important to understanding and generating speech, respectively. Right-handed people almost always have language organized in this fashion exclusively in the left side of the brain, but the precise side (left or right) and location of speech production and comprehension are not so clear-cut in left-handed people. (It’s sometimes said that every left-hander’s brain is a natural experiment.) So, pooling left- and right-handed people’s brain images can be misleading. And, sure enough, the finding of an abnormality in the right arcuate fasciculus, pronounced among right-handers, was murky until the two left-handed patients and four left-handed control subjects’ images were exempted from the analysis.

This study was a start. It shows us where to look.”

Bolstering these observations was the third finding: a thickening of the gray matter at the two areas of the brain connected by the right arcuate fasciculus in CFS patients, compared with controls. Its correspondence with the observed abnormality in the white matter joining them makes it unlikely that the two were chance findings, Zeineh said.

Although these results were quite robust, he said, they will need to be confirmed. “This study was a start,” he said. “It shows us where to look.” The Stanford scientists are in the planning stages of a substantially larger study.

Additional Stanford co-authors are former medical fellow James Kang, MD, now a neuroradiologist in Hawaii; former professor of radiology and chief of neuroradiology Scott Atlas, MD, now a senior fellow at the Stanford-affiliated Hoover Institution; professor of radiology and of psychiatry and behavioral sciences Allan Reiss, MD; lead scientific programmer Mira Raman; physician assistant Jane Norris; and social-science research assistant Ian Valencia.

The study was supported by GE Healthcare and by the CFS Fund, which is housed in the Stanford Department of Medicine’s Division of Infectious Diseases.

Information about Stanford’s Department of Radiology, which also supported this work, is available at http://radiology.stanford.edu/.


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Bruce Goldman
By Bruce Goldman
Bruce Goldman is a science writer for the medical school’s Office of Communication & Public Affairs. Email him at goldmanb@stanford.Stanford Medicine integrates research,
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