Not sure if Dr Shepherd is around but he made a post on the MEA website:
http://www.meassociation.org.uk/201...yalgic-encephalopathy-on-the-new-mea-website/
Was quite interesting but I noted that in the medical world they dont feel there is enough evidence for an encaphalomyelitis - ie inflammation...and also some comments seemingly about the recent japanese study...
my question would be to him -is the japanese study is not sufficient enough to be regarded as 'robust'...? Too small? Im curious what is good enough evidence beyond the various cytokine abnormalities we've seen and the inflammation seen in above study...
Reply:
I suspect that you may have missed one of my fairly regular responses in relation to neuroinflammation and the relationship to a diagnosis of encephalomyelitis
Neuroinflammation occurs in a number of inflammatory and infective diseases. Examples include hepatitis C, HIV and lupus. Neuroinflammation also occurs in other neurological diseases which do not involve an encephalomyelitis.
The presence of neuroinflammation in the well publicised Japanese study does NOT mean that these patients have what neurologists and neuropathologists would recognise or define as an encephalomyelitis.
Encephalomyelitis refers to widespread and significant inflammation involving both the brain and spinal cord.
From a clinical point of view, encephalomyelitis presents with severe neurological symptoms and signs, which may be life threatening.
There is, at present, no pathological or neuroradiological evidence to show that people with ME/CFS have an encephalomyelitis, and that incudes the findings from the post mortem research group that I am a member of.
Like everyone else, I want to establish what the neuropathology of ME actually is - but there is no point in coming to flawed conclusions about cause unless there is sound scientific evidence to demonstrate what you are claiming.
Abstract from our paper in the Journal of Neurological Sciences on post-mortem findings which have also
demonstatred neuroinflammation in the form of dorsal root ganglionitis:
Pathology of Chronic Fatigue Syndrome: Pilot Study of Four Autopsy Cases
DG O’Donovan1, 2, T Harrower3, S Cader2, LJ Findley2, C Shepherd4, A Chaudhuri2
1Addenbrooke’s Hospital Cambridge UK
2Queen’s Hospital Romford Essex UK
3Royal Devon & Exeter Hospitals UK
4Honorary Medical Advisor to ME Association UK
Chronic Fatigue Syndrome / Myalgic Encephalomyelitis is a disorder characterised by chronic exercise induced fatigue, cognitive dysfunction, sensory disturbances and often pain. The aetiology and pathogenesis are not understood.
We report the post mortem pathology of four cases of CFS diagnosed by specialists.
The causes of death were all unnatural and included: suicidal overdose, renal failure due to lack of food and water, assisted suicide and probable poisoning.
Selected portions of tissue were made available by the various Coroners in the UK and with the assent of the persons in a qualifying relationship.
The cases were 1 male, and 3 female. Ages (years) M32, F32, F43 & F31.
One case showed a vast excess of corpora amylacea in spinal cord and brain of unknown significance but Polyglucosan Body Disease was not supported by clinicopathologial review. No ganglionitis was identified.
One case showed a marked dorsal root ganglionitis and two other cases showed mild excess of lymphocytes with nodules of nageotte in the dorsal root ganglia.
This raises the hypothesis that dysfunction of the sensory and probably also the autonomic nervous system may lead to abnormal neural activity eg hyperalgesia & allodynia rather than anaesthesia and may explain some of the symptoms of CFS / ME such as pain, hypotension, hyperacusis and photophobia. However, the syndrome may be heterogeneous.
Nevertheless, the precise relationship of fatigue, which may be either peripheral or central, to abnormalities in the peripheral nervous system (PNS) needs to be studied.
The differential diagnosis of ganglionitis should be investigated in CFS / ME patients hence Varicella Zoster, Lyme disease, HIV, Sjogren’s disease, paraneoplastic sensory ganglionopathy should be excluded by appropriate history and tests.
Thorough histopathological study of cases coming to autopsy may help to confirm or refute the hypothesis, that CFS is a disease process, and whether the symptomatology may be explained by inflammation of the sensory and autonomic divisions of the PNS.
A specific CFS / ME brain and tissue bank in the UK is proposed.
Further CS notes:
The dorsal root ganglia (DRG) are, in very simple terms, minute bundles of nerve cell bodies that lie outside the spinal cord - and so form part of the peripheral nervous system.
So inflammation of the DRG is not the same as myelitis in ME. Myelitis refers to inflammation of the spinal cord.
The DRG appear to be involved in the transmission of sensory information, and so disturbances in function may result in sensory disturbances and pain
Dorsal root ganglionitis, inflammation of the DRG, can be caused by infection such as chickenpox
But it can be associated with specific conditions such as Sjogren's Syndrome - which has some interesting overlaps with ME/CFS, including debilitating fatigue.
In the case of SS, the presence of DRG-itis has been linked to the sensory neuropathy that occurs.
As far as ME/CFS is concerned, we just don't know at this stage whether DRG-itis is part of the disease process, or whether it could just be the result of a triggering infection such as herpes
As we do more post mortems the position may become more clear.
Dr Charles Shepherd Hon Medical Adviser, MEA