CNS findings in chronic fatigue syndrome and a neuropathological case report https://jim.bmj.com/content/65/6/97...drY5LCP4u9lC_R289wqTP3BN6vAh5T0FpCNTMc5EZUYOg Abstract Chronic fatigue syndrome (CFS) is characterized as a persistent, debilitating complex disorder of unknown etiology, whereby patients suffer from extreme fatigue, which often presents with symptoms that include chronic pain, depression, weakness, mood disturbances, and neuropsychological impairment. In this mini review and case report, we address central nervous system (CNS) involvement of CFS and present neuropathological autopsy findings from a patient who died with a prior diagnosis of CFS. Among the most remarkable pathological features of the case are focal areas of white matter loss, neurite beading, and neuritic pathology of axons in the white matter with axonal spheroids. Atypical neurons displaying aberrant sprouting processes in response to injury are observed throughout cortical gray and white matter. Abundant amyloid deposits identical to AD plaques with accompanying intracellular granular structures are observed as well. Neurofibrillary tangles are also present in the white matter of the frontal cortex, thalamus and basal ganglia. Taken together, these neuropathological findings warrant further studies into CNS disease associated with CFS
This is a single person case study? Seems this person must be atypical if they have amyloid deposits given that this hasn't shown up in other studies?
This is a N=1 study and litterature review. The patient died at age 72 following aspiration pneumonia, due to hypertensive cerebrovascular disease. She was sick with ME and FM since 1974, amongst others and had several cognitive issues. In my view I am not sure how much can be extracted from this N=1 study brain autopsy considering the advanced age and other co-morbidities. I also lack the knowledge in macro and micro-pathology to make any kind of judgement, but i would be interested to hear what our experts have to say from this case report. Edit to add: Autopsies are very seldom performed on pwME for several reasons: deaths are not that prevalent. Sudden deaths (suicide) are a shock to the family and they may not consider the possibility of an autopsy. i am uncertain whether there needs to be a window of time to collect the tissues and preserve them. Then there is a lack of a medical specialty following patients and collaborating with universities where the brain tissues are likely to end up. There is also a lack of coordination to build a brain bank and tally up data from patient who would like to donate theor brain/body to the science. It’s been discussed before, we are not there yet.
Was there any discussion about the possibility that the patient also had additional, undiagnosed AD? You mentioned the patient had cognitive issues so could it be a case of all symptoms having been attributed to CFS without looking too hard for alternative explanations?
The article is available in full at Sci-Hub. She had psychiatric manifestations and major cognitive issues. There was no big discussion on what they thought, they simply related their findings on that individual.
I don't think the diagnosis of CFS is realistic here. It seems the patient had evidence of multi-infarct (vascular) dementia over a period of 13 years with episodes of memory loss and a finally a paranoid psychosis. CFS was only diagnosed the year she died and on the basis that her symptoms were not explained by other conditions on a list in a set of criteria. Lists in sets of criteria are not going to cover everything that might lead to fatigue. She has a perfectly good reason for having episodes sounding like CFS - advanced structural brain disease with hallmarks of multi-infarct dementia.
I believe she was formally diagnosed with cfs in 1987 and also had FM, IBS, etc. But i agree with your impression that she developed ominous symptoms that were unrelated to CFS.
So this study was published 30 years after she died, aged 72 of what was probably dementia of some sort, but, was, mysteriously, diagnosed the year she died as CFS. How very confusing. I don't think this tells us anything useful about ME neurology.
Apologies for the confusion. i am still very confused and not sure why I thought this was new research. It goes on to say that more brain autopsies a companied with detailed history is very much needed.
Abundant? Well... that's interesting. Although likely to be two distinct and unrelated diagnoses, so not specifically relevant to ME. Also not very promising if it plays a role seeing how decades of attempts have failed in Alzheimer's disease.
AD and AD plaques and a potential role of infectious disease biofilms: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5008232/ This link suggests spirochetes as a possible agent, but it could be any one of several infectious diseases. The spirochete angle is supported - in addition to this author - by the likes of Alan Macdonald and Judith Miklossy. It's a curious possibility, one also suggested in MS.
Given the article says I certainly would have thought that it was recent research/case report as well.
Both of which seem to have a possible cause in latent infectious agents, possibly enteroviruses, and amyloid plaques being a protective response from the CNS to a pathogen. Some things seem to be converging. It's almost like the immune system still has many mysteries left to reveal, contrary to a weird popular belief within the medical profession that we already know everything there is to know and only have a few i's to dot and t's to cross within that sphere of known things. Which of course is a very selective belief applied only to denied diseases, but surely no harm done with insisting that a hypothesis that has failed time and time again be upheld. It's not as if it affected tens of millions of lives destructively or something like. No, we're just pouty and sour lazy overachievers, or something.
Would the white matter part be called leukoencephalopathy And the other part be due to low heat shock proteins proteopathy
