Plight of youngsters struck down by ME – Sunday Express, 13 February 2011

February 13, 2011


From The Sunday Express, 13 February 2011 (story by Lucy Johnston)

MORE than 54,000 children are suffering with the debilitating condition ME.

One in 100 under-18s, including infants and toddlers, are affected by the problem, which causes chronic fatigue, a study by specialists at Bristol University reveals.

Separate research shows the condition is the biggest medical cause of long-term school absence. Researcher Dr Esther Crawley said: “Until recently we have not known the scale of the problem. There are areas of the country where parents are desperate to get treatment yet their primary care trust refuses to fund it.”

It is not known what causes myalgic encephalopathy. It is also unclear whether the increase in childhood cases is down to larger numbers developing the condition or better surveillance.

Five-year-old Ben Bazneh, of Stow market, Suffolk, developed ME after his childhood vaccinations at 14 months old. His mother Joanne said: “He was a very lively toddler but after his jab he developed a fever and his glands swelled. He became overwhelmingly tired and never recovered.

“His life is shocking. His brain is normal, he just wants to have fun, but if we let him do too much he becomes shattered and cries, ‘Stupid Mr Tired. I hate him. Tell him to leave me alone’.”

The Association of Young People with ME is on 08451 232389 and ayme.org.uk

11 thoughts on “Plight of youngsters struck down by ME – Sunday Express, 13 February 2011”

  1. We’ve had a somatic model for ME for over two decades now, and people are not getting better and the numbers suffering is growing. Men, women and children, more and more with this disease.

    It’s about time that some credence be given to the HGRV/XMRV infectious retroviral hypothesis, after all its been known for years that murine leukemia viruses cause encephalomyelitis in their host species.

    The main chance, the simple thing that can be done right now is to support the WPI so they can finish the work they’ve started.

    1. The main chance, the simple thing that can be done right now is to support the WPI so they can finish the work they’ve started.

      Blind support is unlikely to lead anywhere and anyone consider donation to a research group should take every effort to establish the scientific integrity of the host organisation. That is easily done with the partners of the MEA that CS recommends above. The position of WPI may be more equivocal: http://cfsmirror.blogspot.com/2011/02/creating-research-base-isnt-like-buying.html

      IVI

  2. Dr Charles Shepherd

    Perhaps people could also consider giving a matched donation to help some of the important research – muscle studies, biobank (= stored blood samples), tissue and post-mortem bank – that the Ramsay Research Fund is involved with.

    Dr Charles Shepherd
    Hon Medical Adviser, MEA

    1. No disrespect intended Dr. Shepherd, and I have donated to the RRF as recently as last year, but aren’t these studies really nibbling at the edges after all these decades?

      Don’t we have sufficient data from the thousands of existing biomedical research papers to go on?

      With limited funding, and patients’ running out of times after decades of illness, don’t we need to get to the root cause of this multi-systemic disease rather than looking at individual symptoms, such as listed by the MRC Expert Panel?

      You mention sub-groups in another comment on this page. We have a clear definition of one “sub-group” under the “CFS/ME” umbrella – i.e those with Myalgic Encephalomyelitis – should we not use that “sub-group” as a focus for research, considering that this is the M.E Association and that the research fund is named after Dr. Ramsay?

      If there is doubt about which patients to select for research purposes, could we not start with the 25% of those severely affected, i.e those who are most likely to have authentic organic M.E?

      May I request that the MEA re-instate the term Encephalomyelitis in place of Encephalopathy, considering post-mortem evidence has, indeed, shown inflammation in the brain of ME patients (called CFS by the coroner in Sophia Mirza’s case).

      If this is unacceptable, then could the MEA at least use the name of the disease given at WHO ICD-10 G.93.3 of PVFS/ME (or PVFS/BME for Post-Viral Fatigue Syndrome: Benign Myalgic Encephalomyeltis), until such time – if and when – as the WHO classification is changed?

      At least that indicates the usually clear viral origin of Ramsay-defined ME, which is a useful pointer to the direction biomedical ME research should take.

      In the meantime, my money is on Whittemore Peterson Institute as they have a clear focus and mission to find a cure for neuro-immune disease and that is what people with ME have. I think they are our best bet as things stand.

      It shouldn’t be a competition, in my opinion, surely the goal of all organisations that attract funding for M.E should be to find effective treatment, if not a cure? With that in mind, I would support the MEA in collaborating with and contributing financially through the RRF, with WPI.

      Thank-you for reading this.

  3. Dr Charles Shepherd

    One of the things we desperately need to find are accurate biomarkers that can differentiate sub-groups of people under the existing ME/CFS umbrella. This sub-grouping would obviously include people with Ramsay described or London criteria defined ME.

    So the biobank (= blood sample bank) will be accepting blood samples from people where we can obtain details of the person’s clinical history (obviously with their informed consent) plus a diagnosis of ME or CFS confirmed by a doctor, and follow up of health status on a regular basis. If we are able to start the biobank this year the initial samples will come from people on the MEO Disease Register – where it should be possible to pick out those with Canadian Criteria ME/CFS (which is obviously different to Ramsay ME) as well.

    The inclusion criteria for the tissue and post-mortem bank is still being discussed but it is likely to be similar. The four post-mortems reported so far in the paper I co-authored for the conference in Australia last December >> https://meassociation.org.uk/?p=3765 reported on people who had a diagnosis of either ME or CFS. Some interesting neuropathological abnormalities were found in this group (eg dorsal root ganglionitis) which we hope we will now be able to investigate in more detail if/when more tissue samples become available. There are no neuropathological findings from post-mortem tissue at present that can differentiate between Ramsay or London ME and Fukuda CFS.

    I have written a more detailed article on the current state of the biobank and tissue bank research initiatives for the February issue of ME Essential – which should be heading off to the printers fairly shortly!

    A paper describing the way in which we are hoping to set up a tissue bank has now been published in the Journal of Clinical Pathology.
    An abstract can be found here: http://jcp.bmj.com/content/early/2010/10/05/jcp.2010.082032. I’m sorry I cannot post a complete copy of this paper. This is due to copyright restrictions.

    Dr Charles Shepherd

  4. Under the NICE umbrella of CFS/ME, there is the neurological disease ME/CFS, there is idiopathic chronic fatigue and fatigue of a psychological origin. If the purpose of a biobank is to make discoveries, then those other two groups need to be excluded.

    Whether there are subgroups within ME/CFS, who knows? You cannot decide they exist based on no data. Obviously you can subgroup down to the individual too. Is there really a difference between those who meet Ramsey, or the London criteria? As the London criteria has not been officially accepted into use, nor validated or operationalised, I’m not sure how it could be used anyway. What if the biomarker(s) that differentiate between Fukuda and stricter criteria, that do not include fatigue of a psychological origin, are not to be found in neuropathological findings?

    What is the point in creating a biobank or post mortem bank if you don’t already know what definition is to be used? How can you be sure that you will be able to identify those who meet the Canadian criteria, or any other criteria?

    The only way to make this work is to have the same criteria for both banks, so why is it that this may not happen?

    I will wait and see what is finally decided, but currently it is looking a bit of a hodge podge.

    1. If, regardless of one’s personal preference, we agree that at present and in the past patients may have been placed in the same ‘pot’ even though they actually might be suffering different illnesses that are responsible for their suffering, then surely ‘we’ need to start with the ‘pot’?

      Then, depending on results, one seeks to better classify and seperate.

      Just a ‘stupid’ suggestion of mine, and who know’s it may not be particularly relevant to anyone’s research.

      1. The pot does not include those without neurological signs and symptoms. That is clearly a totally different group.

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