The professor of neurology at Mayo Clinic College of Medicine discussed lesser-known facets of NMOSD and how the disease evolves over time.
"We still don’t understand [NMOSD] very well. We’re getting some insights. It seems like a key substrate for the progressive disease is having extensive demyelination with viable axons.”
There are several different central nervous system demyelinating diseases, all of which have overlapping manifestations and similarities in the way they present and how they progress. Patients with neuromyelitis optica spectrum disorder (NMOSD) who are aquaporin-4 immunoglobulin G (AQP4-IgG) positive are characterized by severe attacks that typically result in major acute disability and are frequently accompanied by large MRI T2-lesions in the brain or spinal cord.
Although, over the long-term, it has been shown that the course of this disorder does not generally reflect the severity of the initial attacks. There have been an increasing number of studies which have assessed the temporal evolution of demyelinating lesions on MRI, including research recently published by Eoin Flanagan, MBBCh, et al. Despite the advancements in diagnosing NMOSD, questions remain about how the disease the continues to progress in comparison with other mimics and when patients may be more susceptible to relapse.
Brian G. Weinshenker, MD, professor of neurology, Mayo Clinic College of Medicine, has multiple research interests related to inflammatory demyelinating diseases of the CNS. He sat down with NeurologyLive to provide an update on where the space stands in understanding the complexities of NMOSD, and what remains unsolved.