GUEST EDITOR IN CHIEF
Mary Ann Picone, MD, FAAN, FACP, has been the medical director of the MS Center at Holy Name Medical Center in Teaneck, New Jersey, since 1993. She is a board-certified neurologist with more than 2 decades of experience in the field of multiple sclerosis. In addition to her current position, she also is a member of the Clinical Advisory Board of the New Jersey Metro Chapter of the National Multiple Sclerosis Society and has been named a Top Doctor by Castle Connolly.
As principal investigator for numerous studies, Dr. Picone has participated in clinical research focusing on disease modification of MS, symptom management, psychosocial interventions, and quality of life improvement for patients and families. She has also authored and edited several books, including MS for the Non-Neurologist and Foot and Ankle Pain Management.
It was my pleasure to have attended the Consortium of Multiple Sclerosis Centers (CMSC) Annual Meeting, in Nashville, Tennessee, held May 29 to June 1. It is a multidisciplinary meeting that brings together neurologists, nurse practitioners, physical therapists, occupational therapists, pharmacists, and other allied health care practitioners specializing in the care of patients with multiple sclerosis (MS).I always leave this meeting with several new clinical pearls, a renewed energy in improving care for our patients, and the enjoyment of having reconnected with old friends and colleagues. This year was no different.
This year’s agenda included myriad programs and workshops, from neuroimaging and disease management to rehabilitation and psychosocial platforms.The opening John F. Kurtzke Lecture, given by Darin Okuda, MD, a professor of neurology and the director of the Neuroinnovation program at UT Southwestern Medical Center in Dallas, covered eye-opening and innovative ways of understanding changes on MRI and what we may be missing.We routinely look at 2-dimensional MRI images where MS lesions may appear to be unchanged over time. Yet Okuda and his team have been able to construct 3-dimensional images with artificial intelligence (AI)–assisted models that can show evolution of these lesions over time and be able to detect increases or decreases in size between time points that otherwise would not have been read as having changed.
A question that researchers often grapple with is, When does MS start? Okuda was first in demonstrating radiologically isolated syndrome (RIS), lesions that are suggestive of MRI before the first clinical episode. But now we are recognizing an MS prodrome of clinical symptoms—such as fatigue and cognitive changes—that may be associated with underlying central nervous system (CNS) tissue damage before we even see lesions on MRI.In short, the question becomes, What happens prior to RIS, and can AI help us detect these changes that are currently below the resolution of what we currently can detect?In his lecture, he was also able to show differences in sound between a brain not affected by MS vs a brain with demyelinating lesions.
Fred Lublin, MD, the Saunders Family Professor of Neurology and director of the Corinne Goldsmith Dickinson Center for Multiple Sclerosis at the Icahn School of Medicine at Mount Sinai in New York, New York, took us from the onset of the era of the first effective MS disease-modifying therapy—interferon beta-1b—to the now more than 20 FDA-approved therapies we have as options.We have come a long way and have been very effective in treating the inflammatory aspect of MS, but we have still not been able to prevent progression, particularly in nonrelapsing progressive MS.As Lublin pointed out, we also still have not found the cause of MS.We have, however, gotten better at diagnosing the disease earlier, and we eagerly await the newly revised McDonald diagnostic criteria this fall.
A symposium led by Jennifer Graves, MD, PhD, an associate professor of neurosciences and director of the University of California (UC)San Diego Neuro-immunology Research Program at UC San Diego School of Medicine, on aging in MS was of particular interest considering that, as our patients are doing better and living longer with MS, we find ourselves grappling with trying to determine what cognitive changes may be related to aging vs cognitive decline associated with MS.Assessment of comorbidities and lifestyle management becomes even more important with age.We need to encourage our patients to stop smoking or vaping; maintain a healthy body weight; get good sleep; and maintain mental, physical, and social stimulation.
Exercise is still the best medicine to slow cognitive decline.Robert Motl, PhD, a professor of kinesiology and nutrition and of rehabilitation sciences at the University of Illinois Chicago College of Applied Health Sciences, presented a wonderful lecture on aging forward with MS and the importance of the proper exercise training for our patients with MS.Also discussed was symptom management to decrease pain and improve quality of life for our patients, including treatment of spasticity; bowel and bladder management; and dystonia, fatigue, and cognitive evaluation and rehabilitation strategies.The growing role of randomized, controlled rehabilitation studies was another excellent workshop.
The efficacy of ocrelizumab (Ocrevus; Genentech) in diverse populations was the subject of another presentation. Riley Bove, MD, an associate professor of neurology at UC San Francisco Weill Institute for Neurosciences, discussed research on the Bcell–depleting monoclonal antibody therapies ocrelizumab and ublituximab-xiiy (Briumvi; TG Therapeutics) in breastfeeding situations and their relative safety for patients.
As I pointed out earlier, the challenge of treating primary progressive MS and nonrelapsing secondary progressive MS remains. Most of our current therapies affect the adaptive immune system, but how can we better target the innate immune system and targets such as microglia within the CNS that can contribute to smoldering inflammation with an otherwise intact blood-brain barrier?PET scan imaging may give us a better understanding of the altered homeostasis that occurs with microglia and astrocytes, and we will have more results of the Bruton tyrosine kinase inhibitor therapies later this year. Fluid biomarkers such as serum neurofilament light chains as a marker for inflammation and glial fibrillary astrocytic protein are being used more frequently in both clinical practice and research studies and can help better detect earlier worsening of disease activity and progression.
Jeffrey Cohen, MD, the director of the Experimental Therapeutics Program at Cleveland Clinic in Ohio, presented the John Whitaker Lecture and discussed autologous hematopoietic stem cell transplantation andchimeric antigen receptor T-cell therapy. Phase 1 studies are currently ongoing in patients with active relapsing and secondary nonactive progressive MS.The main advantage of this therapy is the potential for much deeper B-cell depletion within the tissues including the CNS and may provide increased potential for repair.
Leaving this year’s meeting, I felt that the future is very optimistic.We look forward to new diagnostic criteria for MS, earlier diagnosis and treatment with high-efficacy therapies for our pediatric and adult patients, greater focus on managing comorbidities, and improving exercise programs for our older patients.
Mary Ann Picone, MD, FAAN,
FEATURES IN THIS ISSUE
MULTIPLE SCLEROSIS
MS Biomarkers: Overview of Current and Emerging Markers
By Asya Wallach, MD
MS Self-Management: What Does It Mean?
By Gavin Giovannoni, PhD, MBBCh, FCP, FRCP, FRCPath
NEUROMUSCULAR
Unraveling the Therapeutic Potential of Potassium Channel Blockers: A Focus on Amifampridine and Its Role in LEMS and Beyond
By Kevin Chang, PharmD
