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Multiple sclerosis types. Neuromyelitis optica (NMO). Syndrome presentations. Precision medicine advances often lead to an interesting discovery. Dr. Anton Titov, MD. A disease was considered to be a single entity. But it may consist of several distinct molecular entities. Even though there is a common final pathway of clinical manifestations for that disease. It can make this disease entity to look the same. This is especially true for many cancers. There is a similar view about multiple sclerosis. Dr. Paul M. Matthews, MD. Multiple sclerosis might also represent several distinct pathophysiological entities. Perhaps that can explain a very wide heterogeneity in clinical course of multiple sclerosis. It may also explain the challenges in treatment strategy selection for patients with multiple sclerosis. Dr. Anton Titov, MD. Is there any evidence for multiple sclerosis’ heterogeneity? What do advanced MRI imaging clinical trials show? You conduct many clinical trials in your multiple sclerosis research. Dr. Anton Titov, MD. How to personalize therapy selection for multiple sclerosis patients? Dr. Paul M. Matthews, MD. Well, multiple sclerosis is diagnosed as a syndrome. It is a collection of a particular type of clinical presentation symptoms. Typically, these days, symptoms are supported by laboratory evidence for inflammatory disease in the white and gray matter. In some cases, multiple sclerosis appears in particular anatomical distributions. MRI abnormalities may also exist in the absence of evidence for other potential causes. Dr. Paul M. Matthews, MD. We don’t diagnose multiple sclerosis by a specific type of biomarker. within the syndrome of multiple sclerosis we also observe a range of clinical presentations. Some patients with multiple sclerosis have a very good prognosis. These are some very lucky patients. It is a small proportion. They may be followed for 20 more years. These patients show little progression of disability. Other patients may show rapid progression of disability of multiple sclerosis. Some patients may have infrequent relapses. Others may show frequent relapses. Dr. Paul M. Matthews, MD. Some patients may start with the progressive multiple sclerosis. It is a disability progression from the start. Others may start disability progression only in the late stages of multiple sclerosis. This heterogeneity of the multiple sclerosis syndrome can be explained in two different ways. One point is that it is a multifactorial disease. It arises from multiple genetic susceptibility factors. Dr. Anton Titov, MD. There are influences of the environment and lifestyle on multiple sclerosis. They may vary from patient to the patient. This is commonly seen with a variety of other diseases. In fact, this is amongst the most common of explanations. Interplay between genetic susceptibility and environmental factors explains different clinical symptoms in diseases with syndrome presentations. The other hypothesis is this. Within multiple sclerosis syndrome there are recognizably distinct pathophysiological processes. They may look like multiple sclerosis. But they can be defined in distinct ways. the most prominent example of this is Neuromyelitis optica [NMO]. This is really one of the only terribly clear examples of multiple sclerosis variability to date. Clinically, Neuromyelitis optica was recognized to be a syndrome that was relatively unusual within the multiple sclerosis spectrum. Dr. Anton Titov, MD. Optic neuritis and typically relatively severe spinal cord myelopathic presentations were conjoined in a group of patients. Moreover, these patients often showed relatively malignant course. Each relapse was associated with significant irreversible functional impairment. There were also ethnic differences in the frequency of this aspect of the Neuromyelitis optica syndrome. Dr. Paul M. Matthews, MD. It was found more commonly in oriental populations than in the Caucasian group. From an MRI imaging standpoint, NMO patients showed some very particular signs. The most prominent of sign of Neuromyelitis optica on MRI was longitudinally extensive T2 hyperintense inflammatory lesions in the spinal cord. There was a relatively sparser, cerebral lesions frequency in Neuromyelitis optica.