Tuesday, 10 March 2015

ClinicSpeak: the need for early therapy in CIS

Isn't it time to consider early effective treatment as preventive therapy? #MSBlog #MSResearch #ClinicSpeak

"The follow-up study below in CISers indicates that those who have further attacks and develop disability have reduced quality of life at 10 years. The quality of life assessment looked at physical, mental, fatigue and pain scores. As this is the extension study of the original Avonex CIS study some of the CISers received interferon-beta from the outset and a some only received it after their second attack. Once the study was closed all were offered interferon-beta therapy. This is another piece of data supporting the early initiation of DMTs in CIS. The latter has been common practice through-out the developed world since the early 2000s, but has only recently started to be adopted by UK neurologists. In fact we are only really allowed to offer DMTs to CISers if they are at high-risk of developing a second attack. Fortunately, what constitutes high-risk is left up to the discretion of the treating MSologist. This is where the problem lies; not all CISer can access an MSologist in the UK, because many, or is some areas most, CISers are not referred to MS experts. We are trying to change this. If neurologists and ophthalmologists starting using early effective therapy as preventive therapy, to prevent or delay SPMS,  then  they may change their practice. I personally think every CISer should be referred to a MSologist for an opinion."


Kinkel et al. Disease-related determinants of quality of life 10 years after clinically isolated syndrome. Int J MS Care. 2015;17(1):26-34. doi: 10.7224/1537-2073.2013-041.

BACKGROUND: The main clinical determinants of quality of life (QOL) 5 years after clinically isolated syndrome (CIS) are Expanded Disability Status Scale (EDSS) score and conversion to clinically definite multiple sclerosis (CDMS). The aim of this study was to determine the demographic, clinical, and magnetic resonance imaging (MRI) factors associated with QOL 10 years after CIS.

METHODS: Controlled High Risk Avonex® Multiple Sclerosis Prevention Study in Ongoing Neurologic Surveillance (CHAMPIONS) 10-year MSers were assessed for CDMS, EDSS score, MRI T2 activity, brain parenchymal fraction, and MSer-reported QOL. Associations were evaluated using analysis of variance models.

RESULTS: A second clinical event consistent with CDMS and higher EDSS scores at years 5 and 10 were associated with lower 36-item Short Form Health Status Survey (SF-36) Physical Component Summary scores at year 10 (P < .01). MSers with earlier onset of CDMS had worse MSer-reported Physical Component Summary, SF-36 Mental Component Summary, fatigue, and pain scores at year 10 than MSers with later or no onset of CDMS. Neither initial randomization group nor any MRI metrics assessed at baseline or during follow-up were associated with QOL at 10 years.

CONCLUSIONS: These results support the development of therapies for CISers that significantly reduce the risk of conversion to CDMS and the progression of physical disability to milestones as low as EDSS scores of 2.0.

CoI: multiple

13 comments:

  1. I wasn't referred to neurology by ophthalmology in early 2010 and was dismayed to find a letter by an ophthalmologist to the BMJ in 2006 questioning this lack of action in the light of Macdonald's 2005 revisions.

    I was asked by the ophthalmologists at the time about any tingling but it requires expert neurologist examination to find lesser, but important, problems. Prompt action may have delayed (even prevented?) my conversion to MS.

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  2. But even if you do get seen by an MSologist, some apparently still aren't keen to offer DMTs to CISers even with a high chance of relapse. I was fortunate in that my husband had Bupa through work and so I had my initial MRI and neurologist appointment privately at the time of my CIS. He told me that my local neurologist who runs the NHS MS clinic in my area is conservative in his approach and only offers DMTs to those with CDMS. With an 80% chance of a relapse being quoted at the time and having been pointed at this blog by the MS Trust, I therefore asked my GP to refer me out of area on the NHS and am now in the system to start a DMT soon.

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  3. I think there are difficulties re what constitutes high risk of further episodes in general.

    The ABN 2009 criteria seen in the current commissioning paper refers to certain other circumstances and MRI evidence. What the circumstances are and what MRI evidence is required is open to interpretation. This differs from CDMS DMT criteria which are more specific, some would argue too specific so flexibility for clinical interpretation perhaps has pros and cons. From what I understand very few CISers are on a DMT. Is this due to a conservative approach or does the policy guidance need to be more specific? I don’t know. It doesn’t help not knowing who is likely to respond and who isn’t plus the overall impact on longer term progression seems woollier. I’ve read research on the cognitive benefits but when matched to the EDSS which focuses heavily on mobility I haven’t (unfortunately) found so much.
    Furthermore the SPC of Beta Interferon which is the only DMT referred to in the current policy for CIS has its own definition of high risk, and would I imagine be an appropriate source to refer to when considering treatment. However the SPC refers to a specific lesion load and dissemination in time which I find confusing as would assume dissemination in time would be CDMS. It also seems in keeping with the 2005 McDonald Criteria.

    I’d like to see more CISers treated at onset but I think further clarity is required in respect of when and who to treat.

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  4. Personally if I was refused something I would look elsewhere if the medical profession weren't going to help. People can't wait around for a neurologist to decided how to play god and decided someone's fate. How do they think they are? It appears to be a universal dementia of medical professionals to want to dictate. And they wonder why they get things of the internet and go abroad for treatment. If that happens then it is not their fault is it?

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  5. Can a CIS be mistaken for a TIA? An attack of slurred speech, loss of grip in right hand accompanied by a loss of arm strength , in 1992, resolved itself after about two weeks. No further distinct attacks, but a slow,steady deterioration set in about 2002. Dx MS 2005.

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  6. Here in Dubai , a lot of neurologists are keen to start DMD's at CIS, Dr. recommended Interferon at first , but I was offered Gilenya and Tysabri when I demanded more aggressive treatment (opted for Gilenya) ...

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  7. Please could someone explain to me what CIS is, in layman's terms? I always thought you had MS or not. Does everyone have it? How do doctors know?

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    1. To get a diagnosis of MS you have to have lesions in time and space. Time means having an Inflamatorry attack which can cause a Clinically isolated syndrome. However you would not call it MS until a second attack occurred (lesions in time). Furthermore the attack needs to focus on a different bit of the brain eye or spinal cord (lesions in space). So at CIS it may be MS but it may not be in a large proportion of people. However with additional information such as MRI imaging where you can see addition lesions and you can tell how old they are and you can see them in more than one place you can make diagnosis. So in brief CIS is the first symptom that gets you to see a doctor I wonder when you think back you have felt a lesion.optic neuritis is often the first CIS is of MS be uase when your vision goes you notice it.

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    2. writing this on train at the moment sorry for spellin mistakes

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    3. writing this on train at the moment sorry for spellin mistakes

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    4. Thank you Mousedoctor, actually your spelling has improved, maybe you should do all your posts on the train. When I look back, I had optic neuritis and didn't even go to the doctor when I had pins and needles and numbness from the waist down. and in my arm I thought I had dirt on my contact lenses. On the day of my first outpatients appointment, the front page headlines was that a footballer had been diagnosed with MS. I worked it out for myself. I probably never had CIS.

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  8. How many CIS incidents are diagnosed as transverse myelitis too. My son ended up in A&E as he needed help to get home from a walk we'd been on. The previous week he'd fallen over when he tried to go on a run. He was transferred to the attached NHS neurological centre where TM was diagnosed. He was tested and told he had lesions on his spine, he had oligoclonal bands, positive Hoffman's sign, all warning flags you would think. He was sent away with no treatment and told the hospital would be in touch with a follow up appointment. 5 months later he got it, and a couple of weeks after that he was diagnosed with MS

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    1. I too had the TM diagnosis, but from the neurologist seen privately. i'd already been in hospital the week before when my Gp had sent me in with suspected TM only for the hospital drs to disagree and put me in the orthoepaedic ward for a suspected trapped nerve. When I eventually got the MRI (back not neck) results they said there was no trapped nerve and discharged me. This was after I'd been told the previous evening there were possibly suspicious signs but not what they were. They refused to refer me to a neurologist before discharge - maybe as they knew I had a bupa appointment the next week anyway but it was not a great experience.

      I do think my GP however is fab and he was vindicated when I got the TM diagnosis and oral steroids from the bupa neurologist the following week.

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