In this video, I teach you how to kick Multiple Sclerosis’ Butt. Together, we can make MS boring so you can live your best life despite the condition. Let’s jump in!
Multiple Sclerosis
Selma Blair Multiple Sclerosis Update Explained by Neurologist
I n a recent instagram post, American actor Selma Blair explains that her MS is “in remission” but that she still battles pain, fatigue, and other chronic symptoms. What is “remission,” how does MS cause pain, and what is the treatment “IVIG” that she is receiving.
Good news—Multiple Sclerosis drugs taken while breastfeeding may not affect child development.
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MS is a disease in which the body’s immune system attacks myelin, the fatty white substance that insulates and protects the nerves. Symptoms may include fatigue, numbness, tingling or difficulty walking.
“Most monoclonal antibody medications for multiple sclerosis are not currently approved for use while a mother is breastfeeding,” said study author Kerstin Hellwig, MD, of Ruhr University in Bochum, Germany. “Yet MS can develop during the childbearing years of life. Since the risk of MS relapses increases after giving birth, some mothers may need or want to restart these therapies, so it is important to determine whether these medications, through breast milk, have a negative impact on a child’s development.”
For the study, researchers used the German MS and Pregnancy Registry to identify 183 infants born to mothers taking monoclonal antibodies while breastfeeding. Of this group, 180 had mothers with MS and the three had mothers with neuromyelitis optica spectrum disease (NMOSD). NMOSD is also a demyelinating disease, but it is rare and specifically affects the optic nerve, spinal cord or brain.
The infants were compared to another 183 infants, matched for exposure to MS medications shortly before or during pregnancy, born to mothers with the same diseases who did not take monoclonal antibodies while breastfeeding.
Of those exposed to MS medications, 125 were exposed to natalizumab, 34 to ocrelizumab, 11 to rituximab and 10 to ofatumumab. Two infants were first exposed to natalizumab and then ocrelizumab. One infant was exposed to rituximab and then ocrelizumab.
The first exposures to the medications through breastfeeding ranged from the day a child was born to the ninth month of life. Infants were breastfed for an average of five-and-a-half months while their mothers took these medications.
For all infants, researchers then examined the number of hospital stays, antibiotic use, developmental delays such as problems with social and fine motor skills and delayed speech development, and the infants’ weight at follow-up visits during the first three years of life.
After comparing infants exposed to the medications to infants not exposed, researchers found no differences in their health or development.
“Our data show infants exposed to these medications through breastfeeding experienced no negative effects on health or development within the first three years of life,” Hellwig said.
A limitation of the study was that only about a third of the infants were followed for the full three years. Therefore, Hellwig said, the results for the third year of life are less meaningful than for years one and two.
Understanding genetic risk could save sight and predict multiple sclerosis earlier in young people
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Young people could be spared from going blind by a new genetic risk tool that could also help diagnose multiple sclerosis (MS) earlier, to start effective treatments.
Optic neuritis is a condition that affects people of all ages, but especially young adults, usually manifesting in blurred vision and sometimes pain when moving the eyes. Up to half of people affected in the UK eventually go on to develop MS – often many years later. Emerging evidence indicates that starting the very effective MS treatments earlier may improve long term health.
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Optic neuritis occurs because of swelling in or around the optic nerve. For those with MS-related optic neuritis, the swelling subsides on its own, and vision usually recovers. For many people whose optic neuritis does not result from MS, the optic nerve can be permanently damaged unless high doses of steroids are given quickly, resulting in loss of sight. However, steroids can result in harmful side effects. When people first develop optic neuritis, it can be difficult for patients and their doctors to decide whether the possible benefits of steroid outweigh the possible harms, when the likely cause of the optic neuritis is unclear.
Identifying whether there is an underlying cause of optic neuritis can be challenging for clinicians, with many important test results taking weeks to return. Now, new research, published in Nature Communications and led by the University of Exeter and King’s College London, has shown for the first time that combining genetic risk for MS with demographic factors significantly improves MS risk prediction in people presenting with optic neuritis.
Co-author Dr Tasanee Braithwaite, consultant ophthalmologist to the Medical Eye Unit at Guy’s and St Thomas NHS Foundation Trust, and Adjunct Senior Lecturer at King’s College London said: “As a doctor caring for many patients with optic neuritis, I’m excited by the possibility of translating this pilot research into front line clinical care in the near future. Whilst more research is needed, our study provides a strong signal that we could better identify patients at high risk of MS, perhaps enabling these people to have earlier MS treatment in the future. Whereas, if we could better identify people whose optic neuritis is very unlikely to result from MS, we could treat these people urgently to reduce irreversible vision loss and blindness.”
The team analysed more than 300 common genetic variants linked to developing MS, combining them into a genetic risk score that helps clinicians understand an individual’s chance of developing MS. They analysed data from 500,000 people in the UK Biobank, who have shared genetic samples, questionnaires and linked health information from their electronic medical records.
The researchers found 2,369 people who had MS in the UK Biobank, and 687 people with optic neuritis. Of those, 545 had no identifiable cause for their optic neuritis at the start of the study, and 124 went on to develop MS.
Applying the genetic risk score effectively helped separate those at lowest risk from those at high risk. Whilst the MS genetic risk score is not a diagnostic test, this study highlights that it could add one valuable additional piece of information to support doctors and patients to make better decisions.
Co-author Professor Richard Oram, of the University of Exeter Medical School, said: “Since the first genome was sequenced three decades ago, we’ve been working towards the promise of being able to use genetics to improve outcomes for individual patients. This research is an excellent example of precision genetic diagnosis in practice.”
Dr Clare Walton, Head of Research at MS Society, said: “Currently, 130,000 people live with MS in the UK and one in five will have experienced optic neuritis at the start of their MS journey. This research shows how using genetic scores could be a useful way to predict who will likely continue to an MS diagnosis.
“Using immunotherapies in people at high risk of MS could significantly delay the onset of the condition, but these drugs come with side effects. This exciting study opens up the possibility of finding people in which the benefits will outweigh the risks.”
The research stemmed from a summer project led by University of Exeter Medicine student Pavel Loginovic. With funding from the University of Exeter, it expanded into a research collaboration involving academics in Finland and the US. The research was further funded through Fight for Sight and the Royal College of Ophthalmologists, who awarded Dr Braithwaite a Zakarian Award to support this work.
Pavel said: “I’m elated to see this paper published, and it’s gratifying that it could have a real impact in moving research forward, ultimately aiming to get people with MS diagnosed and perhaps treated earlier. Leading this analysis while staying on top of my medical studies has been a challenge and an immense opportunity for growth, professional and personal. I’ve enjoyed the academic journey so far, and I’m excited for what’s to come.”
Normal-appearing tissue offers insights into lesion formation in Multiple Sclerosis.
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Multiple sclerosis (MS) is the result of the immune system mistakenly attacking the brain and the spinal cord, causing tissue damage (lesions) throughout. While the underlying mechanism of lesion formation is still not entirely understood, scientists at the Netherlands Institute for Neuroscience have come one step closer, focusing not on the damaged tissue but on the so-called ‘normal-appearing white matter’ tissue instead.
People with MS have clusters, or nodules, of a specific type of immune cell known as microglia. Microglia could be described as the vacuum cleaners of the central nervous system as they remove dead, redundant, or potentially dangerous particles. In the normal-appearing white matter, where no other pathology is evident, microglia (nodules) clusters are already visible. Whether these nodules are related to the progression of MS is still unclear, as they appear in almost all brain disorders and the ageing brain.
The relationship between nodules and MS
To learn more about the role of nodules in MS patients, researcher Aletta van den Bosch and her colleagues from the Huitinga group investigated the pathology of MS in brain donors at the Netherlands Brain Bank in samples with and without nodules. These samples offered insights into the severity of the MS pathology of the patients’ level of inflammation. “Patients with these nodules have a worsened pathology: they have more lesions, and the lesions are more active.”
But do the nodules play a role in the formation of lesions in MS, or are they a result of something else? For this question, van den Bosch compared their genetic profile to the nodules found in a completely different medical condition: stroke. This is because nodules in brain tissue from people who suffer from a stroke will not lead to lesion formation. Interestingly, the samples from MS patients showed vastly different genes to the nodules in Stroke patients.
Mini lesions
“We recognized many of the genes in the MS nodules quite quickly because they’re also expressed in the active lesions” van den Bosch explains. “They could almost be described as mini-lesions”. The MS nodules were activated by lymphocytes (immune cell), which were not found in the stroke tissue.
When van the team took a closer look, they found that the nodules were absorbing and processing oxidized lipids, which is known to activate these microglia. “When we looked at the axons surrounded by the high-resolution nodules, we saw they were associated with partially demyelinated axons. These nodules likely arose to clean up the oxidized myelin. Nodules activated by both the lymphocytes and these oxidized lipids may become very inflammatory, causing more damage to the tissue surrounding them, leading to a downward spiral.”
Towards a long-term solution
In the end, van den Bosch hopes this will result in new therapeutic targets to stop the progression of MS. “Now we need to explore the relationship between all these inflammatory components in the lab so we can understand exactly what leads to these early signs of breakdown. After that, we can start thinking about which steps we can remove from this process to avoid the development of new lesions altogether.”