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  • About altitude sickness.

    I’m all seriousness: am 8n Katmandu now. I am going 9n the Langtang trek tomorrow for 11 days.

    Apart from the ‘usual’ precautions regarding acclimatisation followed by my guide that are in place for non-acclimated trekkers, as an MS patient is there anything out of the ordinary to consider?

    Thank you.

    • You should ask our resident cat…Mountain climber….NeuroDocG. I think she had a supply of steroids to fend off the altitude sickness, which has been very serious. Luckily she made it down and back to Blighty both times…yep not content with altitude sickness once, she went again.

  • When is the research community going to be looking seriously at antivirals for treating MS?

    Prof G is thinking in that direction too?

  • Why when prof g has said more than once that he does not believe thestrength of cladribine used is sufficient enough are st. Bart’s about to embark on a groundbreaking trial for wheelchair users using the very drug which may not be potent enough to achieve the best results.
    If this fails surely people will say that they thought wheelchair users were too far gone all along when actually it was another trial simply not executed quite right.

    I predict this question will not get an answer

  • I wonder if you’d consider a suggestion for a patient-information blog post?

    My friend and I have been scouring the internet for info about lymphopenia in people on immunosuppressive drugs. There is some lack of information about people who have real problems with this – often it seems to get brushed off, almost as a side note, that the numbers affected are small. (So that’s alright then?!)

    We would very much like to know your opinion on things such as:

    – What are the implications for further treatment when a drug has been discontinued due to lymphopenia? (Sequencing of DMTs?)

    – Is it sometimes necessary to withdraw DMT treatment altogether, if immunosuppression is not tolerated? What options would be left in this case? (Copaxone?)

    – How low is it advisable to let lymphocyte levels sink on immunosuppressive drugs, and for how long? Is there any danger of long term damage?

    – Why are neutrophil levels measured as well as lymphocytes? What are the implications of this?

    – Can anything be done to bolster recovery from lymphopenia?

    My friend is very ill, in a miserable state of being unable to throw off repeated infections. Over the past year she was first on Tecfidera, followed by Ocrevus, and has become lymphopenic on both. It is terribly disheartening to finally be promised a highly effective MS therapy, only to have it destroy your quality of life completely.

    – How would you continue to manage these patients?
    (In general – we’re not asking for specific advice, of course.)

    Thank you for reading.

    • All too recognizable – lymphopenia gets attention in relation to PML, but is nothing to worry about when it comes to other (non-life-threatening) infections. But when those destroy your quality of life, you wonder about the cost-benefit of having NEDA.

      I would be very interested to see some of Sonia’s questions answered.
      I don’t know if there is any research on restoration of lymphocytes after discontinuation of DMF or other DMT? Or on switching to copaxone for such reasons?

      • Thanks, Veronique – my thoughts too.

        This article discusses lymphopenia in general, but doesn’t seem too concerned with this particular subset. https://cp.neurology.org/content/9/1/53

        It’s frustrating not to be able to follow the science – but to me it all still sounds a bit experimental. No guidelines or recommendations yet about switching DMTs in these cases. After discontinuation, at least lymphocytes seem to be expected to return to baseline levels eventually. (With a possible questionmark over DMF.)

        I don’t get the impression that a great deal of research is going into people who end up with with severe lymphopenia – and the implications for ongoing sequential treatment. I’m still wondering whether DMT treatment is sometimes simply not tolerated and has to be discontinued altogether? Why would some people react in this way and not others?

        • Can the person perhaps get Filgrastim to stimulate white blood cell production? I had late-onset neutropenia a few months after my Rituxan infusion and it was proposed as a possibility. However my neutrophils recovered right away so I did not have to do it. I would be concerned about “activating” the immune system in such a way but there was a recent article about PwMS on natalizumab who had PML and Filgrastim was deemed “beneficial” for them.

          • That’s interesting, thanks. I hadn’t heard of Filgrastim. It’s good to know that this kind of option exists, although it does sound like a bit of a last resort.

    • This post is exactly what I came onto the blog to ask, many thanks Sonia for raising it so succinctly.

      1. DMD SEQUENCING: To add to the sequencing question: would cladribine be considered a more targeted version of immune suppression/modulation than say ocrelizumab or fingolimod? I believe I’ve seen some blog posts referring to it’s very targeted approach, but I may be wrong.

      2. LYMPHOCYTE RECOVERY: info on reversibility would make the choice of DMD much easier for those that have reacted very badly to immune suppression in the past:

      i) is the suppression of the sub-type of memory B cells permanent in Cladribine, or does this sub-type population also increase back to baseline with time? (I assume 2+ or 4+ years timescale?)

      ii) is the immune suppression caused by Ocrelizumab ‘reversible’ once the DMD is stopped?

      My Quality of life went so low whilst on Fingolimod that I ended up mostly bed and housebound, often not even able to read as I felt so ill and with trouble sleeping. I had similar reactions to Rebif and Tysabri but the fingolimod was another level. I totally concur with Sonia – there are a subset of patients for whom the side effects are so much worse than the mild headaches and nausea level, and whilst the levels of lymphocytes and neutrophils are within an acceptable range, adherence to the DMDs is a very serious decision over a drastic impact on quality of life vs. MS relapse and progression.

      I have felt drastically more well on Copaxone, to the point of being able to get out and about independently, and do a few hours of work. But sadly after 1 year it is still not holding my lesions. So a terrible dilemma – risk feeling bedbound/sofabound ill for most of the day whilst taking Ocrelizumab or Cladribine, or remain on Copaxone knowing my MS is not controlled.

      Many Thanks for reading.

      • Thank you, Melly, for your story. I’m really sorry to hear about your experience on Fingolimod.

        It’s interesting that you were actually put on Copaxone for that reason. I wasn’t sure if I was completely serious in suggesting it, to be honest. Better than nothing maybe.

        Regarding sequencing – we were under the impression that Ocrelizumab would be a suitable follow on for DMF, being more targeted, whereas Cladribine wouldn’t. (Unfortunately I can’t remember where we got that info – I think I read an article about it on this site, but I can’t find it now.) I wouldn’t know about Fingolimod. It would be good to have clarification.

        About the reversibility business – I think Cladribine, like Alemtuzumab, is seen as an ‘induction therapy’. As far as I understand it, this means that recovery can happen from the initial immunosuppression, leaving a hopefully permanent alteration to the immune system so it doesn’t continue to go haywire. The others, on the other hand, rely on continual top-ups to keep the immune system surpressed. So maybe Cladribine would be a solution – if it would still be safe after the previous treatment. (Clarification on this would also be very welcome.)

        I suspect lymphopenia is a thorny issue for the scientists. However as the numbers treated with these drugs increases, so will those with adverse effects. I think it will become necessary for people to start taking a bit more notice.

        • I was just wondering whether we could still expect any response from Barts to my original question of 3 September, at some point in the future? It did provoke a certain amount of discussion, so seems to be of wider interest. (I do of course appreciate how much you all do!)

  • Hi. Two questions:

    How can a person with a cardiac condition/history of MI differentiate an MI from an MS Hug? I hate going to ER unnecessarily.

    Recently, I think I read a post about lesion load. I thought it said that above 10 lesions was probably a high lesion load. I have 13 lesions but was told moderate lesion load. How do they calculate lesion load?

  • B€g pharm$

    Big party

    Addressing the Rising Prices of Disease-Modifying Therapies for Multiple Sclerosis

    (DMT) for multiple sclerosis (MS), interferon beta-1b, was approved, and an untreatable disease that had disabled humans for hundreds of years became treatable. Since then, multiple drugs with varying mechanisms of action have been approved, and neurologists now have a palette of therapies that allows for individualizing therapy and effectively controlling relapsing MS in most patients. Regrettably, this achievement has come at a steep price. Interferon beta-1b entered the market with an annual price of approximately $10 920 ($19 313, inflation adjusted). While this price stunned many physicians at the time, the price for the first DMT for MS is now looked back at with nostalgia. The prices for DMTs for MS have risen dramatically over the last 15 years, far outpacing inflation, and now have a mean price of more than $86 000 per year

    JAMA Neurology
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    Editorial
    August 26, 2019
    Addressing the Rising Prices of Disease-Modifying Therapies for Multiple Sclerosis
    Daniel M. Hartung, PharmD, MPH1; Dennis Bourdette, MD2
    Author Affiliations Article Information
    JAMA Neurol. Published online August 26, 2019. doi:10.1001/jamaneurol.2019.2445
    related articles icon Related
    Articles
    In 1993, the first disease modifying-therapy (DMT) for multiple sclerosis (MS), interferon beta-1b, was approved, and an untreatable disease that had disabled humans for hundreds of years became treatable. Since then, multiple drugs with varying mechanisms of action have been approved, and neurologists now have a palette of therapies that allows for individualizing therapy and effectively controlling relapsing MS in most patients. Regrettably, this achievement has come at a steep price. Interferon beta-1b entered the market with an annual price of approximately $10 920 ($19 313, inflation adjusted). While this price stunned many physicians at the time, the price for the first DMT for MS is now looked back at with nostalgia. The prices for DMTs for MS have risen dramatically over the last 15 years, far outpacing inflation, and now have a mean price of more than $86 000 per year (Figure).

    Figure.
    Annual Prices of Disease-Modifying Therapies for Multiple Sclerosis
    Annual Prices of Disease-Modifying Therapies for Multiple Sclerosis
    Each observation is based on 12-month supply using the wholesale acquisition cost in December of each year. The data for 2019 are based on the wholesale acquisition cost in June 2019. The wholesale acquisition cost is from the First DataBank Drug Database. For each glatiramer acetate product, we report the median price of the 20-mg and 40-mg formulations. IFN indicates interferon.

    In this issue of JAMA Neurology, San-Juan-Rodriguez et al1 provide a description of the effects of MS DMT price growth on the US Medicare Part D program. Using a 5% random sample of Medicare Part D claims data, they analyzed how the cost of self-administered DMTs for MS changed between 2006 and 2016. The authors estimate that over the 11-year period, the annual cost to the Medicare Part D program for DMTs rose from $396.6 million to $4.4 billion, which equates to a 10.2-fold increase per Medicare beneficiary. This increase was driven primarily by the annual cost of DMT treatment, which climbed more than 4-fold from $18 660 to $75 847, or nearly 13% annually. The authors also note the disturbing trends that DMT costs increased in parallel and the entry of new products seems to only propel costs higher, phenomena previously noted2 and also apparent in the Figure. As a consequence of escalating costs and Part D benefit design, the out-of-pocket expenses to patients during this same time rose 7-fold, from $372 to $2673 per 1000 beneficiaries.

    This study by San-Juan-Rodriguez and colleagues1 is an important addition to the literature on the rising cost of DMTs for MS. Their study documents the escalating costs that patients, Medicare Part D plans, and ultimately taxpayers are paying for these irrationally priced therapies. The US Medicare program is the single largest purchaser of DMTs for MS in the United States, and DMTs for MS are among the most expensive drugs purchased by the program.3,4 In 2017, the Medicare Part D program spent more than $5 billion on 11 self-administered DMTs. Medicare spent nearly $1.5 billion on branded glatiramer acetate alone.5 To put these numbers in perspective: in 2016, Medicare paid approximately $1.4 billion to neurologists for all services and procedures through the Part B program. Medicare is thus spending more than 3 times as much for DMTs for this single illness as they pay to neurologists for all of the services that they provide.

    As has been pointed out elsewhere and documented in the current study, nearly all DMTs for MS increased in price in parallel, and the introduction of new therapies seems to only propel prices higher.2,6-8 We now have 19 US Food and Drug Administration–approved DMTs for MS in 10 different mechanistic classes. So despite the existence of multiple treatment options, the price of most DMTs for MS continues to rise. The pharmaceutical and biotechnology industries claim that the high prices reflect the expense of research and development and need to incentivize continued innovation. These claims are never backed up with transparent data. In addition, they do not explain the continuous rise in the 3 drugs originally approved for MS, interferon beta-1b (Betaseron), interferon beta-1a (Avonex), and glatiramer acetate (Copaxone). These drugs have long since recouped any cost of drug development, yet their prices have continued to rise.

    Should neurologists care about the rising cost of MS DMTs?

    Finally, neurologists should look carefully at their relationships with pharmaceutical and biotechnology companies and call them to task for unreasonable increases in prices. Remaining silent should not be an option. The development of DMT for MS has been one of the great achievements of neurology in the past 25 years. Neurologists should not allow the unfettered increases in price for these drugs hurt the health care system or patients. 👍😊

    https://jamanetwork.com/journals/jamaneurology/fullarticle/2748919?guestAccessKey=eb57a8d9-443f-4de9-9146-00fac338dc13&utm_source=silverchair&utm_medium=email&utm_campaign=article_alert-jamaneurology&utm_term=mostread&utm_content=olf-widget_09032019

  • “The colective cyborg” Bart´s team have said many time that monotheraphy is not a good strategy

    That you need an dmt and neuroprotective drug (remyelination enhancer drug)

    Aparently one could think that those oligodendrocytes are somehow impared in their function and need

    some help

    This study says otherwise all you need is to switch of the inflamation surrounding them

    Analysing intrinsic and extrinsic factors involved in an impaired differentiation of induced pluripotent
    stem cell derived-oligodendrocytes in Multiple Sclerosis patients

    Multiple Sclerosis (MS), a demyelinating and inflammatory disease, affects approximately 2.5 million people
    worldwide. The destruction of the myelin sheath results in axonal degeneration and loss of function. Although
    remyelination exists in MS patients, it is restricted during disease progression.
    The proliferation and migration of oligodendroglial precursor cells (OPCs) followed by the differentiation and
    maturation of OPCs into oligodendrocytes is crucial for successful remyelination. Even though OPCs are still
    detectable in chronic MS lesions, the reconstitution of the myelin sheath fails due to an impaired differentiation of
    OPCs into mature oligodendrocytes.
    Since the underlying process is not entirely understood, it needs to be clarified.
    To address the question whether this differentiation block is mediated by intrinsic oligodendroglial factors or
    caused by the extrinsic inflammatory milieu, we generated induced pluripotent stem cell (iPSC)-derived
    oligodendrocytes (iOL) from MS patients and sex-matched healthy control individuals. By comparing these iOL
    with respect to proliferation, migration, differentiation, myelination and stress response, we examined possible
    phenotypic differences. To see whether the inflammatory environment potentially influences iOL differentiation,
    we applied the supernatant of peripheral blood derived mononuclear cells (PBMCs) to differentiating iOL of
    healthy controls.
    On the one hand, comparison of iOL from MS patients and controls revealed a similar capability to proliferate,
    migrate and differentiate and resulted in the same cell death rate after induction of oxidative stress. Moreover, to
    see whether iOL could give rise to functional oligodendrocytes, we used an in vitro myelination assay by seeding
    the cells on nanofibers showing that iOL from MS patients and controls were able to form processes along
    nanofibers.
    On the other hand, we found a significantly impaired differentiation of iOL after application of the supernatant of
    activated PBMCs during differentiation. The application of supernatants of activated single immune cell types
    indicated that this effect was predominantly caused by T cells.

    In conclusion, our data suggest that the oligodendroglial differentiation block observed in MS is predominantly
    caused by extrinsic inflammatory mediators and is not due to intrinsic oligodendroglial factors.

    These findings
    contribute to a better understanding of MS pathogenesis and may help to develop new treatment options to
    promote remyelination in MS.

    https://www.eventclass.org/contxt_glia2019/online-program/search?search=Analysing+intrinsic+and+extrinsic+factors+involved+in+an+impaired+differentiation+of+induced+pluripotent+stem+cell+derived-oligodendrocytes+in+Multiple+Sclerosis+patients

  • This is Gold

    Myelin debris are antiinflamatory (in TBI)

    “Under pro-inflammatory conditions, myelin debris not only decreased the M1-like phenotype (inflamatory), but also promoted the M2-like phenotype (antinflamatory)

    Under anti-inflammatory conditions, myelin debris increased the M2-like(inflamatory)
    phenotype. Phagocytosis inhibition reduced myelin debris effects

    Conclusion: Our study shows that myelin debris do not induce a M1-like phenotypic shift, but on the contrary,
    identifies, for the first time, myelin debris as potential endogenous antiinflammatory components following TBI.
    Moreover, their beneficial effect is partly mediated by their phagocytosis by microglia. Future work will have to
    identify (1) which phagocytosis pathway(s) is(are) particularly involved, and/or (2) other mechanism(s) such as
    those triggered by myelin debris lipid components.

    Eating myelin debris makes microglia happy

    https://www.eventclass.org/contxt_glia2019/online-program/search?search=Eating+myelin+debris+makes+microglia+happy

    • Interesting, if it works in monkeys will it work in humans? Why not do the human study. It is a molecule that block hylouronidase so blocking break down of hyalouronic acid….so we will have the ever lasting filler if it gets used in people with a bit of cosmetic filler

  • This will make the “colective cyborg” mad 🙁

    B cell in the brain ?

    Are good 🙂

    B cell-derived IL-10 modulates the inflammatory response of microglia and astrocytes

    Conclusion: B cell-derived IL-10 diminished the inflammatory response of microglia and astrocytes. Our
    findings indicate a potential disease-relevant interaction between B cells and resident microglia and astrocytes in
    the CNS, which may influence the progression of the disease and thus provide an innovative target for
    therapeutic modulation.

    https://www.eventclass.org/contxt_glia2019/online-program/search?search=B+cell-derived+IL-10+modulates+the+inflammatory+response+of+microglia+and+astrocytes

    Strange world

  • Microglia are the main phagocytes in the CNS.
    Constantly scavenging the CNS for plaques, damaged or unnecessary neurons and synapses, and infectious agents

    What happens when you kill microglia? How´s going to clean( phagocytosis) the mess?

    Astrocytes 🙂

    Astrocytic phagocytosis as a compensated function of microglial dysfunction

    Microglia are the main phagocytes in the CNS. We recently established microglial ablation model without
    affecting other CNS-related mononuclear cells, usingmicroglia-specific diphtheria toxin receptor-knockin mice. In
    this model, microglial debris were rapidly removed even under absence of functional microglia, raising a question
    how the debris were cleared. The microglial ablation did not cause infiltration of mononuclear phagocytes, such
    as the perivascular macrophages and circulating monocytes, in CNS parenchyma, suggesting that the other cell
    populations were involved in the clearance. We found that astrocytes became activated with GFAP upregulation
    upon microglial ablation, and extended their processes to microglial debris. Confocal and electron microscopy
    showed that activated astrocytes contained a significant number of microglial debris in their cell bodies as well
    as processes. Furthermore, the microglial debris were observed in the lysosome of cultured astrocytes, when
    astrocytes were co-cultured with apoptotic microglia. Gene knockdown experiments revealed that TAM family of
    phagocytic receptors expressed by astrocytes participated in the clearance. We confirmed that the astrocytic
    phagocytosis could be observed as well in some mutant mice, in which microglial phagocytic activity was
    suppressed. Taken these results together, astrocytes have a potential to compensate for the dysfunction of
    microglial phagocytic activity.

    https://www.eventclass.org/contxt_glia2019/online-program/search?search=Astrocytic+phagocytosis+as+a+compensated+function+of+microglial+dysfunction

    Strange world

  • Dengue Fever – a little bit random I realise!

    I am in Nepal until 22nd Sept. There is quite a serious mosquito borne Dengue fever outbreak. I am on Ocrelizumab. It concerns me that I may be at greater risk to health if I got it.

    My intention is to get overly keen with the mosquito repellant. Better safe, and stinking of DEET, than sorry.

    The reason for the post is not humble bragging (though it is a great trip!) but to ask if there is anything else that I ought to be doing or particularly concerned about or indeed early warnings if I do get infected?

    I have good insurance.

    Thank you and enjoy ECTRIMS.

    • Dengue fever is a mosquito-borne tropical disease caused by the dengue virus.[1] Symptoms typically begin three to fourteen days after infection.[2] This may include a high fever, headache, vomiting, muscle and joint pains, and a characteristic skin rash.[1][2] Recovery generally takes two to seven days.[1] In a small proportion of cases, the disease develops into severe dengue, also known as dengue hemorrhagic fever, resulting in bleeding, low levels of blood platelets and blood plasma leakage, or into dengue shock syndrome, where dangerously low blood pressure occurs

      A vaccine for dengue fever has been approved and is commercially available in a number of countries.[4][9] The vaccine, however, is only recommended in those who have been previously infected.

      Typically, people infected with dengue virus are asymptomatic (80%) or have only mild symptoms such as an uncomplicated fever.[15][21][22] Others have more severe illness (5%), and in a small proportion it is life-threatening.[15][22] The incubation period (time between exposure and onset of symptoms) ranges from 3 to 14 days, but most often it is 4 to 7 days.[23] Therefore, travelers returning from endemic areas are unlikely to have dengue if fever or other symptoms start more than 14 days after arriving home.[

      Severe disease is more common in babies and young children, and in contrast to many other infections, it is more common in children who are relatively well nourished.[13] Other risk factors for severe disease include female sex, high body mass index,[25] and viral load

      Dengue can be life-threatening in people with chronic diseases such as diabetes and asthma.[33]

      https://en.wikipedia.org/wiki/Dengue_fever

      • Aparently work in the mouses to

        Promotion of white matter repair by treatment with Metformin in a mouse model of demyelination with
        cuprizone/rapamycin

        Pharmacologic stimulation of endogenous stem cells has become an attractive alternative to cellular
        transplantation. Metformin, a drug widely used for type 2 diabetes, has previously been shown to stimulate adult
        neurogenesis and to promote expansion, migration and differentiation of neural stem cells as well as functional
        recovery in a model of hypoxia/ ischemia of newborn mice (Wang et al., 2012; Dadwal et al., 2015).
        Here we ask whether Metformin promotes remyelination when given after a 6 week regimen of cuprizone plus
        rapamycin to produce demyelination in the CNS, in particular the corpus callosum. Genetic fate mapping of
        oligodendrocytes in PDGFRaCreERT2: :ROSAmTomato/ mGFP mice allowed us to unequivocally identify areas
        of remyelination within the corpus callosum. Tamoxifen was given 4x during week 5 of intoxication to induce
        recombination. Metformin was injected (200mg kg-1 day-1) i.p. for seven days starting at the end of the cuprizone
        regimen. On day 8 the mice were perfused and processed for immunohistochemistry of Myelin Basic Protein
        (MBP), Green Fluorescent Protein (GFP) and axons (SMI-312 antibody). Four squares (100 microns x
        100 microns) within the area of remyelination in the corpus callosum anterior to the fornix were imaged at 63x
        magnification on a confocal microscope and immuno-reactivity quantified by thresholding using Image
        J. Metformin treatment almost doubled MBP immunoreactivity (p=0.012) while the axonal signal (SMI312
        immunoreactivity) remained the same. GFP immunoreactivity was also significantly higher in the Metformin
        group suggesting a stimulation of the oligodendrocyte precursor pool. We are presently performing cell counts
        of OPCs and mature oligodendrocytes in these regions of interest. Quantifications of myelinated axons in plastic
        sections of the contralateral brain hemispheres of the same mice by electron microscopy will be presented.
        Taken together, our data indicate that metformin stimulates oligodendrocyte turnover and remyelination and may
        be suited for clinical promotion of white matter repair.

        Glia 2019

        (Where you were 😉

  • Just heard on the news JK Rowling has donated some 15million to the Edinburgh centre named after her mum. Really hope they have same approach as Bart’s – inverting the pyramid, time is brain etc

      • Agree! Tho maybe she feels compelled due to use of mum’s name for the place. 🤞something good emerge as a result or that one of us wins the lottery and can hand Bart’s several million quid.

        • I have to be diplomatic but I can’t help feeling a tinge of jealousy as there is so much more that we could achieve with funding on this scale. However, JK Rowling is entitled to donate her money wherever she chooses.

      • “Not the wisest thing to do”
        JK Rowling is entitled to donate her money where she wants to. There are research centres all over the country looking at different areas of MS. Her mother, like my friend and his sister died in their forties and no one should have this outcome. It’s time to be open minded about research not give a generous donation negative comments.

  • Hsct

    Ectrims 2019

    ” The trial confirmed the earlier reports on NEDA, which after treatment with AHSCT was considerably higher (78.5% at five years) than with DMD treatment (2.97% at five years). Furthermore, one in two patients treated with AHSCT improved in EDSS, whereas only one in thirteen improved with DMD”

    https://onlinelibrary.ectrims-congress.eu/ectrims/2019/stockholm/279382/joachim.burman.hsct.for.ms.-.we.are.ready.for.prime.time.html?f=listing%3D0%2Abrowseby%3D8%2Asortby%3D1%2Asearch%3Dhsct%2Bstem+cell+treatment%2Bms

  • Any pwMS taking sertraline, for depression?

    “Most common antidepressant barely helps improve depression symptoms, ‘shocking’ trial finds”.

    ” The most commonly prescribed antidepressant barely relieves symptoms of modern depression, a major study reveals”.

    ” The largest independent investigation ever undertaken found patients taking sertraline experienced negligible improvements in mood.
    Published in the Lancet Psychiatry, the study comes amid mounting controversy over increased use of antidepressants by GPs in recent decades, with roughly 7.3 million people in England issued a prescription each year “.

    https://www.telegraph.co.uk/science/2019/09/19/common-antidepressant-barely-helps-improve-depression-symptoms/ 19/09/2019.

  • Is there any research into vaping and its impact on MS?
    With the increase in death numbers and lung illness from vaping currently mentioned in the news, it would be interesting to know.

  • Hsct
    Ectrims 2019

    Progression free survival was 93 % (95% CI, 85 – 100%): relapse free survival was 87% (95% CI, 78 – 97%); MRI event free survival was 74% (95% CI, 69 – 89%); and event free survival (no EDSS progression, no relapses and no new MRI lesions) was 68 % (95% CI, 54 – 84%) at five years. The annualized relapse rate post-AHSCT was 0.022. At end of follow-up, 62% of patients had improved in their expanded disability status scale (EDSS) score; 35% were unchanged and 3.3% worsened

    Efficacy of autologous hematopoietic stem cell transplantation for MS. A single-centre report of 81 patients

    Uppsala University, Uppsala, Sweden

    Palavras para que

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