Emily Harrington, MD, PhD, physician-scientist at The Ohio State University Wexner Medical Center, provided thoughts on the importance of World MS Day and the issues that plague the MS community.
On May 30 every year, individuals and organizations across the globe unite for World MS Day, a day dedicated to raising awareness toward multiple sclerosis (MS), a disease that impacts nearly 2.3 million people worldwide. The theme for this year’s event is “I Connect, We Connect” and uses the social hashtag #MSConnections as a way to highlight building community connection, self-connection, and connections to quality care.
The first World MS Day was initiated in 2009 by the Multiple Sclerosis International Federation, and since then, the campaign has focused on a different theme each year. Although highly unpredictable, patients with MS may face a range of symptoms, most common of which include fatigue, numbness and tingling, blurred vision, double vision, weakness, imbalance, pain, and problems with memory and concentration, among others. The life expectancy of the disease has increased in recent years, mainly due to the advancements in disease-modifying therapies.
Although there has been an influx of therapeutics for relapsing forms of MS, there are still several unmet needs for the MS community, including treatment options for those with progressive MS. In honor of World MS Day, NeurologyLive® sat down with Emily Harrington, MD, PhD, a physician-scientist at The Ohio State University Wexner Medical Center who specializes in caring for patients with MS. Harrington provided insight into a number of MS-related topics, including aspects of the disease that need more recognition and the ongoing battle to tackle neurodegeneration.
Emily Harrington, MD, PhD: MS is a fairly heterogenous disease, meaning that people are impacted in very different ways. People have different severity in terms of their disease presentation and chronic symptoms. If a single treatment approach doesn’t work for you, we can’t blanket treatments across different patients. It’s very individualized and some patients may be well-controlled on some of our lower efficacy, older therapies, whereas some patients may need stronger patients from the get-go. The more we learn about MS, the more than becomes apparent. I would also say that with some of the older strategies of treating less aggressively with older medications, this may not be the best approach in terms of preventing long-term disability and relapses. Treatment paradigms are changing within the field as well.
By increasing awareness and talking about it in public, it can elevate these diseases. People who don’t have MS, or the general public, can appreciate the number of people that are affected and just elevate the recognition that there are so many people in the US and around the world. Also, we hope this will bring funding for support, resources for patients, and research as well. Maybe provide opportunities for different patient groups to make new connections.
Because the fact that it tends to affect women, oftentimes younger at the onset, I hear stories from patients that they feel kind of ignored by the medical community or brushed off for a while. Those two groups tend to be more marginalized in the medical system. In terms of the way we treat, it’s important to investigate and take each case seriously. When people come in with a presentation for neurological systems, they may get someone who doesn’t have the expertise in MS or a general neurologist when they should be referred to an MS specialist. If there’s a concern for MS, it’s better to treat it early. That’s how I think about it in terms of affecting those two groups.
The benefit of treating MS is that MRI is a pretty good indicator, although some things can look a bit like MS. But if we have good high-quality MRI, we can usually give a good opinion of what those lesions look like. That’s nice that we have good diagnostic tests. If there is a question, we can always good a lumbar puncture and spinal fluid assessment. That can also help differentiate if something different is happening. Over time, people tend to declare themselves. Meaning, if we’re not sure at the beginning and we follow them for six months, by that time, we probably have a better idea. There are some disorders that are demyelinating and somewhat similar to MS, but they have a slightly different appearance on MRI with different clinical features. We definitely need some better biomarkers in terms of helping us guide treatment, diagnose early, and diagnose progressive MS. Overall, most MS specialists are comfortable with MRI diagnosis and clinical reports as well.
This is a hard question to ask. For the community, one of the main issues is that our animal models don’t do a good job of mimicking human image. They’re either characterized by a strong period of inflammation with no remission or relapses. Some of our remyelinating animal models don’t have a lot of inflammation. We’re challenged at the bench to study these models that would mimic more human MS. When talking about how we study neurodegeneration and progression in our animal models, a lot of therapies that are neuroprotective or remyelinating have been tested in animal models that don’t have a lot of inflammation, which has limited their capacity to show benefit in terms of progressive MS or repair, in my opinion. In terms of clinical trials, we need more sensitive markers to determine repair. Following someone’s type walk or their EDSS (Expanded Disability Status Scale) score is probably not a great measure for more prepared remyelinating strategies. People are thinking about this more—types of biomarkers such as neurofilament or looking at visual evoked potentials that may be more slightly finer tuned to study these therapies. We may not be measuring them in the right way once we get them into clinical trials.
One is progressive MS space and repairing myelin, which we’ve made possible in relapsing remitting when there is ongoing inflammation. We need to target more of these inflammatory niches. This includes meningeal follicles in areas where immune cells are still hanging out and are not well-targeted by our current therapies, as well as making therapies that don’t have as many systemic targets and side effects that are homing in on the mechanisms that are mediating either relapse or continued disease progression. Those are in better biomarkers—ways to determine if the therapy that we pick for an individual patient is controlling their disease—not just by looking at MRI in their clinical report but having things that can make better treatment decisions and also determine if there’s ongoing neurodegeneration happening.
Transcript edited for clarity.