AAN 2019 posters #1

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I discuss below two topics that we don’t understand well in MS. Firstly, the diagnosis of late onset MS (LOMS). Secondly, the occurrence of stroke in MS.

Differential diagnosis in Late Onset Multiple Sclerosis (LOMS) – Marrodan et al. Neurology Dept., Fleni, Buenos Aires, Argentina

LOMS is defined as presentation beyond the age of 50 years, accounting for less than 12% of MS cases. Diagnosis is challenging as white matter lesions could be vascular instead of demyelinating, and as a result misdiagnosis is common.

Out of 149 subjects studied by Marrodan et al., only 82 were MS (55%, Figure 1) whilst 67% had other diagnosis. Among the latter 30 had a demyelinating disorder not fulfilling the criteria for MS (20%), followed  25 defined by stroke-like lesions presenting as non-specific matter lesions (17%).

Of those who met the diagnostic criteria for LOMS , myelitis (or spinal cord involvement) was the most frequent presentation (see figure 2). Other complementary findings were MRI evidence of corpus callosum lesions (Dawson-finger sign) and black holes, as well as positive oligoclonal bands (OCBs).

It is therefore not surprising that with the predominant cord involvement LOMS cases are more likely to present with walking difficulties.

Figure 1: LOMS and differential diagnosis (or other diagnosis)
Figure 2: MS vs not MS and differences in clinical presentation, MRI and OCB patterns

Stroke diagnosis and treatment patterns in MS – Melamed et al., Montefiore Medical Center, Bronx, NY

Whilst MS is rare (US prevalence 450,000), stroke is common (US incidence 795,000 cases per year). Not surprisingly, PwMS also experience strokes, and around 1 in 10 die as a result. However, the challenge remains in the diagnosis and mistaking a stroke for an MS relapse. Moreover, co-morbidities worsen disease progression and quality of life in MS.

In a retrospective study of all strokes spanning 2009-2016 Melamed et al. identified those who had experienced a stroke with a background of MS, which amounted to 0.3%. When they compared the demographics with PwMS with stroke to non-MS with stroke, the features that stood out were that they were more likely to be women (77% vs 53%), younger (average age 63 vs 70), and in terms of risk factors were less likely to have diabetes and atrial fibrillation, but equal representation in terms of high blood pressure, high cholesterol, coronary artery disease and prior history of strokes/TIA (see Figure 3 top panel).

In terms of treatment patterns, there was no significant differences in time to presentation or receiving tPA (i.e. thrombolysis), although it looks as if they were less likely to receive the latter (see figure 3 bottom panel).

Interestingly, PwMS were more likely to have cryptogenic stroke (i.e. no identified cause) than non-MS presentations (59% vs 20%), see figure 4. In light of the complications noted in Alemtuzumab this clearly needs to be taken into consideration.

Figure 3: vascular risk factors in MS vs non-MS (top panel) and treatment patterns with acute thrombolysis (bottom panel)
Figure 4: Cryptogenic strokes in MS vs non-MS

About the author

Neuro Doc Gnanapavan

25 comments

  • Is this the only news of interest from AAN 2019? Nothing on Ocrelizumab brain atrophy? New trials, new insights into MS. Shows just how stagnant ms research.

    • I couldn’t agree more. The cost of sending the Barts team will be in the tens of thousands (it’s a seven day conference!). Makes a mockery of the claims of austerity in the NHS and academia. Also think of all the clinic appointments that aren’t taking place. Barts should make 2020 a conference free year – get on with seeing patients. Is the really no news on repair or neuroprotection at AAN 2019? I looked at the AAN conference website and was struck by “There’s no better way to combine great fun and entertainment with unparalleled networking than to attend one of these not-to-be-missed social events and meetings.“ a nice week in the US to catchup with some old pals, exchange business cards and figure out how to collaborate on some well funded research that doesn’t deliver any benefit for the patients. Call me cynical, but this is the 71st annual AAN conference and most of the disease covered are still life shortening, disabling and incurable.

      • I’d like to point out that the hospital doesn’t pay for conferences- call it cost cutting!

      • Cynical

        The NHS will not be paying for these trips and as for academia your neuros have to attend meeting to get continuing medical education points so that they are up to date with treatments. I come from Harrogate and they have a toyfair every year people go to see what toys to sell people a neurologists conference is no different, Then they have a farmers meeting called the Great Yorkshire Show where the farmer show off their pigs, dogs, wood work, cow etc. you have the Eurovision Song contest soon and people are travelling to that meeting too. As for not seeing patients you are correct that ProfG cannot see people when on a trip and so appointments shouldnt be booked, however the clinics missed get caught up I believe by doing extra clinics. As for conferences I’m from Barts why should I not travel to get educated?

    • Many things from AAN have been posted in May’s Q&A as well as in some posts comment sections, if you are interested. Nothing new on O. brain atrophy rates though. If the news were good they would have let us know.

  • Also the irony is diagnostic/chemical analysis technology has made huge strides there are no chemical/biological reactions you cannot study in full detail. Pharma know cure for MS is just around the corner and will kill the cash cow. So why not put brakes on research by reinventing b and fingolimod therapies that add completely no new benefits to Ms patient lives.

    • Of course everything will be solved by trotting out the usual conspiracy theories and “Kevin’s” regular tirades against dedicated colleagues who have the interests of pwMS at the very core of their being.
      Hey, ho, onwards and upwards 😉

      • Immunosuppressant medications clearly are not working in progressive MS according to the science, not conspiracy theories or tirades.

        Despite Pharma’s best efforts to show their effectiveness through MRIs, neurofilament levels and intrathecal IgG levels, progressive patients will never improve clinically. They will continue to spiral downhill to the same miserable endpoint, maybe slightly slower only noticeable to a statistician in selection bias trials paid by Pharma.

        Ocrevus, Tysabri, HSCT, Mavenclad, Mayzent all have failed to show any effect above placebo in “non-active” progressive MS as shown by multiple approval bodies, like the FDA.

        The only people that immunosuppressant anti-inflammatories are working for is Pharma (+shareholders) and their paid researchers and their card-carrying neurologists.

        A revolution will come and history will not be kind to these people.

        • Sorry to say but you are spot on. The inflammatory response in progressive or neurodegenerative MS is still a mystery, not only for MS but for a myriad of neurological diseases. No effective treatments until we can understand the pathology.

        • A critical finding from the Ibudilast study that demonstrated positive outcome in brain atrophy was in PPMS group not SPMS.

          • Post-hoc analysis showed that there was a marginally significant three-way interaction between the treatment
            effect and disease course (p=0.0576). After further inspection, the overall treatment effect was primarily driven by
            patients with PPMS (p=0.005), and not by patients with SPMS (p=0.97). This difference may have been driven (at
            least in part) by faster atrophy progression in the PPMS placebo group compared to SPMS placebo (p=0.016).
            Although backwards selection (p<0.05) retained age, T2 lesion volume, RNFL, and longitudinal diffusivity as
            significant baseline covariates, the adjusted difference in treatment effect was still marginally significant
            (p=0.0715) and driven by PPMS (p=0.007).
            Conclusions:
            The overall treatment effect of ibudilast on progression of brain atrophy in progressive MS appears
            to be driven by patients with PPMS, which may in part be because of their faster atrophy progression rates in
            untreated patients

            Response to Treatment According to Progressive Disease Type: Analysis from a Phase
            II Progressive MS Trial of Ibudilast

            http://indexsmart.mirasmart.com/AAN2019/PDFfiles/AAN2019-002237.pdf

            One disesase,two different responses

            🙁

  • But as with science, we need evidence. Every effective treatment has come with some serious side effects. And we have yet to see evidence of any effective neuroprotective or reparative treatments. Dedication and goodwill don’t seem a good return for the investment made to date in ms research.

  • Can some explain what it means to have Black holes. On diagnosis in 2001 was told given the 2 black holes, the neurologist considered my MS to have been active for some time. I moved neurologists and counties in 2007 and I asked about black holes and was told they are not really holes! So no real explanation. The first neuro commented that if I’d had a third that he would be quite concerned about me. So about 20 lesions and 2 holes, was ok! Now I have SPinal lesions too. I’m currently not on DMDs. I think the boat has sailed. But I focus on building my strengths and a good diet.

    • T 1 lesions(black holes)

      T-1 Weighted MRI Without Gadolinium

      This type of scan shows hypointense lesions—areas where there’s been permanent loss of myelin and/or damage to nerve fibers (axons). This is significant because when myelin and axons are damaged or destroyed, nerve cells cannot communicate with each other effectively or at all, which is what causes a person’s unique MS symptoms.

      Hypointense lesions appear as very dark areas that sometimes are called black holes. The darker the spot, the more damage has occurred. Note that in addition to permanent axonal loss, a black hole or T-1 weighted lesion may represent areas of edema (swelling) that are temporary and disappear on subsequent scans. For this reason, a neurologist often will compare current MRIs with older ones to see if lesions have resolved

      Multiple Sclerosis and MRI: T1 Black Holes & Brain Atrophy

      Aaron Boster MD

    • This abstract gives you what T1 black holes are in the first few lines https://www.ncbi.nlm.nih.gov/m/pubmed/12821527/
      They correlate with disability worsening
      Spinal cord lesions and their accrual maybe more important from the critical mass of tissue involved. But spinal cord imaging techniques are still not as good as brain imaging

      • Thank you for the replies. Since I’ve gained SC lesions my level of disability has increased. I use mobility aids but not full time wheelchair user. . So this makes sense.

  • MD2. Not saying anything against you or your colleagues. Example government is now taking full control of developing new antibiotics due to pharma lack of response due to no profit in new antibiotics. Not just conspiracy theories. Known facts. If pharma knew the cure to Ms they will never reveal it. Also doesn’t answer the question do we really need so many new b and lomod therapies. Ofatumab, Utoximab, posinmod, ozanimod, sponimod, if it wasn’t ture I’d see the funny side.

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