Update on the ME/CFS Tissue and Post Mortem Tissue Bank | ME Association | 24 August 2012

August 24, 2012

The MEA receives regular queries about the initiative to set up a formal UK tissue and post-mortem tissue bank where muscle, gastrointestinal and nervous system tissue samples can be collected, stored and made available for research.

The current situation is as follows:

This work has been running in parallel with the ME Biobank, which is collecting and storing blood samples for research. Work on the first phase of the Biobank is now well underway at University College London/Royal Free Hospital and The MEA Ramsay Research Fund has committed £40,000 towards the joint charity costs of funding this work for a further year starting in November 2012.

Plans to establish a tissue and post-mortem bank were initiated by setting up a steering group that looked at the complex ethical, legal, practical and financial issues that would be involved in establishing such a facility. A report of the work that was done by this group has been published in The Journal of Clinical Pathology.

Exploring the feasibility of establishing a disease-specific post-mortem tissue bank in the UK: a case study in ME/CFS
Eliana M Lacerda, Luis Nacul, Derek Pheby, Charles Shepherd, Peter Spencer J Clin Pathol doi:10.1136/jcp.2010.082032

The plan to set up a formal ‘bricks and mortar' tissue and post-mortem facility are currently on hold – mainly due to the enormous cost of setting this up and then maintaining it.

In the meantime, I am continuing to work with our consultant neuropathologist at Addenbrooke’s Hospital in Cambridge in arranging post mortems when we are notified that someone has died and the person has made it clear that they want to donate their body to ME/CFS research

The MEA does not at present hold a database of people who want to donate body tissues. However, this is something that may now be incorporated into the blood sample donor database – which should be in operation before the end of the year.

In the absence of a database, anyone who wants to donate post mortem tissues for ME research needs to make this clear in writing in a Statement of Intent which can be kept with their Will, or in a Codicil to their Will. Next of kin will need to know about this instruction and where it is kept.

More information on this procedure, as well as a Statement of Intent, can be downloaded from the MEA website.

One of the most important practical aspects in the whole process of post-mortem tissue collection is for someone (ie next of kin or solicitor) to notify The MEA as soon as possible after a death has occurred. This is because the sort of research that is being done at present requires removal and fixation of very specific tissues as soon as possible, preferably within 24 hours – and this obviously requires consent and co-operation from relatives, coroners, pathologists at a very sensitive tine.

A number of post-mortems have now taken place and some interesting findings reported – including the presence of dorsal root ganglionitis (= inflammation in bundles of nerve cells in the nerve roots that transmit sensory information back to the brain via the spinal cord).  

Those of us who are involved in various stages of this post mortem process have produced a preliminary summary of the findings in the form of a conference abstract:

Pathology of Chronic Fatigue Syndrome: Pilot Study of Four Autopsy Cases

DG O’Donovan(1,2), T Harrower(3), S Cader(2), LJ Findley(2), C Shepherd(4), A Chaudhuri(2)
(1) Addenbrooke’s Hospital Cambridge UK
(2) Queen’s Hospital Romford Essex UK
(3) Royal Devon & Exeter Hospitals UK
(4) Honorary 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.

Summary prepared by:
Dr Charles Shepherd, Hon Medical Adviser, ME Association
24 August 2012

6 thoughts on “Update on the ME/CFS Tissue and Post Mortem Tissue Bank | ME Association | 24 August 2012”

  1. Now this is the kind of excellent research I am very happy to invest in. If you get to the stage where post mortem donor cards become available for donation of organs, please let me know.

    Thank you VERY much to Dr Shepherd and his medical colleagues/pathologists in the UK who collaborated in researching and publishing/publicising these findings.
    I consider publication of these important research discoveries in medical journals or publicising the discoveries at medical conferences to be a very vital step forward.

    We are hugely in debt to the patients and their families who have endured immense suffering and have paid the ultimate price in order for this research to take place. We are deeply grateful to you and you are always in our thoughts. Thank you.

  2. It is correct that for this biobank the criteria to be applied to all patients in an initial screening will be the Fukuda criteria?

  3. “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.”

    Deceased ME patients have been found to have dorsal root ganglionitis, a feature in a number of different diseases. Studies have shown a link of ME to cancer.

    “A high incidence of severe B-cell immunodeficiency and chronic reactivated Epstein-Barr virus (EBV) infection in patients with chronic fatigue syndrome (CFS) is reported herein.”

    “Low NK activity in this family may be a result of a genetically determined immunologic abnormality predisposing to CFS and cancer.”

    But to be included in the tissue and post mortem bank you have said that patients with paraneoplastic sensory ganglionopath will be excluded.

    Paraneoplastic sensory ganglionopath is dorsal root ganglionitis. Is dorsal root ganglionitis caused by cancer or ME, does ME cause cancer and dorsal root ganglionitis?

    How can these questions be answered if the banks exclude those patients?

    “Paraneoplastic sensory neuronopathy generally occurs as part of a multifocal encephalomyelitis or encephalomyeloneuritis and less often as an isolated clinical syndrome.”

    How can paraneoplastic sensory neuronopathy be excluded when it is often an isolated clinical syndrome?

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