Watching conference too long triggered PEM.
There was some rehash of information along with some new findings.
The broadest perspective suggests ME/CFS is a heterogeneous disease involving neurologic and autonomic nervous system perturbation. It is unclear to me whether mitochondrial dysfunction is an independent abnormality triggered by immune system dysregulation vs the result of microcirculation dysfunction.
NIH intramural study will eventually provide trove of data for many years. Preliminary results interesting. What is causing low B Cells in CSF?
I suspect that the greatest strength of NIH intramural approach will turn out to be their fairly narrow inclusion criteria.
In my opinion, the most fruitful areas of research that need further investigation are:
- metabolic, neurologic, and immunologic response to exercise challenge in ME/CFS patients (I suspect the muscle biopsies collected will be prove to be valuable). What is it about exercise that triggers PEM? Is it just exacerbation of low volume state? Does exercise trigger neuroinflammation? Does exercise trigger abnormal immune response?
- go beyond looking at data from "omics" to finding tissue level pathphysiology (Ron Davis's team may be particularly helpful in developing new technologies to measure in vivo organism level biologic processes)
- validate MRI spectroscopy data. What does MRI spectroscopy look like in other disease states (Alzheimer's, Parkinson's, Depression, Mitochondrial disease, Multiple sclerosis)
Lastly, the NIH intramural study of ME/CFS points out the inherent difficulty of evaluating patients who suffer with debilitating fatigue. Much work still needs to be done to help clinicians work through the methodical steps of determining the etiology of often non specific symptoms. The ultimate diagnosis may be ME/CFS but there are other disease states such as undiagnosed cancer and myositis that are often not apparent in initial workup. Perhaps this an avenue to pursue in at least introducing ME/CFS as a topic to teach in medical schools and residency programs.
There was some rehash of information along with some new findings.
The broadest perspective suggests ME/CFS is a heterogeneous disease involving neurologic and autonomic nervous system perturbation. It is unclear to me whether mitochondrial dysfunction is an independent abnormality triggered by immune system dysregulation vs the result of microcirculation dysfunction.
NIH intramural study will eventually provide trove of data for many years. Preliminary results interesting. What is causing low B Cells in CSF?
I suspect that the greatest strength of NIH intramural approach will turn out to be their fairly narrow inclusion criteria.
In my opinion, the most fruitful areas of research that need further investigation are:
- metabolic, neurologic, and immunologic response to exercise challenge in ME/CFS patients (I suspect the muscle biopsies collected will be prove to be valuable). What is it about exercise that triggers PEM? Is it just exacerbation of low volume state? Does exercise trigger neuroinflammation? Does exercise trigger abnormal immune response?
- go beyond looking at data from "omics" to finding tissue level pathphysiology (Ron Davis's team may be particularly helpful in developing new technologies to measure in vivo organism level biologic processes)
- validate MRI spectroscopy data. What does MRI spectroscopy look like in other disease states (Alzheimer's, Parkinson's, Depression, Mitochondrial disease, Multiple sclerosis)
Lastly, the NIH intramural study of ME/CFS points out the inherent difficulty of evaluating patients who suffer with debilitating fatigue. Much work still needs to be done to help clinicians work through the methodical steps of determining the etiology of often non specific symptoms. The ultimate diagnosis may be ME/CFS but there are other disease states such as undiagnosed cancer and myositis that are often not apparent in initial workup. Perhaps this an avenue to pursue in at least introducing ME/CFS as a topic to teach in medical schools and residency programs.
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