MRI Prognostic Factors in Multiple Sclerosis, Neuromyelitis Optica Spectrum Disorder, and Myelin Oligodendrocyte Antibody Disease

Abstract

Several MRI measures have been developed in the last couple of decades, providing a number of imaging biomarkers that can capture the complexity of the pathological processes occurring in multiple sclerosis (MS) brains. Such measures have provided more specific information on the heterogeneous pathologic substrate of MS-related tissue damage, being able to detect, and quantify the evolution of structural changes both within and outside focal lesions. In clinical practise, MRI is increasingly used in the MS field to help to assess patients during follow-up, guide treatment decisions and, importantly, predict the disease course. Moreover, the process of identifying new effective therapies for MS patients has been supported by the use of serial MRI examinations in order to sensitively detect the sub-clinical effects of disease-modifying treatments at an earlier stage than is possible using measures based on clinical disease activity. However, despite this has been largely demonstrated in the relapsing forms of MS, a poor understanding of the underlying pathologic mechanisms leading to either progression or tissue repair in MS as well as the lack of sensitive outcome measures for the progressive phases of the disease and repair therapies makes the development of effective treatments a big challenge. Finally, the role of MRI biomarkers in the monitoring of disease activity and the assessment of treatment response in other inflammatory demyelinating diseases of the central nervous system, such as neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte antibody disease (MOGAD) is still marginal, and advanced MRI studies have shown conflicting results. Against this background, this review focused on recently developed MRI measures, which were sensitive to pathological changes, and that could best contribute in the future to provide prognostic information and monitor patients with MS and other inflammatory demyelinating diseases, in particular, NMOSD and MOGAD.

Imaging of Central Nervous System Demyelinating Disorders

“…In ADEM, MRI lesions completely or partially resolve for up to 90% of patients 51 . A 2021 article nicely summarized the currently known factors on imaging for MS, NMO, and MOG-associated disease, 52 as shown in figure 11-6 . Asymptomatic lesions are seen in MS, whereas in NMOSD, this only rarely occurs 53 …”

Case Report: Neuromyelitis Optica Spectrum Disorder With Progressive Elevation of Cerebrospinal Fluid Cell Count and Protein Level Mimicking Infectious Meningomyelitis: A Diagnostic Challenge

“…The delayed diagnosis and treatment might be the critical factors. Previous studies found that tetraparesis and long spinal cord lesions were associated with long-term disability ( 12 , 13 ). Since our case presented with these poor prognostic factors, follow-up is required to define the long-term prognosis.…”

ATP line splitting in association with reduced intracellular magnesium and pH: a brain 31P MR spectroscopic imaging (MRSI) study of pediatric patients with myelin oligodendrocyte glycoprotein antibody‐associated disorders (MOGADs)

“…The frequency-domain 31 P spectra were analyzed by lineshape fitting (Figure S2, Supporting Information) using an in-house program written in MATLAB (MathWorks, Natick, MA, USA). Typically all 31 P peaks were fitted using a single-Gaussian lineshape model with inclusion of prior knowledge of metabolite chemical shifts and resonance patterns as soft constraints when approperiate 17,[43][44][45] Lineshape deconvolution was performed for P i and β-ATP signals with asymmetric appearance or line splitting, using two separate Gaussian components with different chemical shifts. The average chemical shift of such signal was determined by the population-weighted chemical shift δ = c 1 δ 1 + c 2 δ 2 , where c 1 and c 2 are the relative populations of the two components (c 1 + c 2 = 1).…”

“…This study is carried out on a cohort of pediatric patients with myelin oligodendrocyte glycoprotein antibody‐associated disorders (MOGADs)—an idiopathic, inflammatory, demyelinating condition of the central nervous system (CNS), with high prevalence in young adults and heterogeneity in individual symptoms, radiological manifestations and clinical course 40–42 . MOGAD lesions are often non‐specific on conventional MRI; the diagnosis at the initial presentation requires an accurate serum antibody test 42,43 . Currently, there is still a lack of understanding of the molecular, biochemical, and cellular mechanisms that cause specific lesions to form, though several energy abnormalities are considered to be present at the sites of demyelination 44–46 .…”

“…[40][41][42] MOGAD lesions are often non-specific on conventional MRI; the diagnosis at the initial presentation requires an accurate serum antibody test. 42,43 Currently, there is still a lack of understanding of the molecular, biochemical, and cellular mechanisms that cause specific lesions to form, though several energy abnormalities are considered to be present at the sites of demyelination. [44][45][46] Herein, we present evidence of the presence of two β-ATP peaks in this cohort, and report their corresponding Mg 2+ levels, based on the δ β-ATP -to-[Mg 2+ ] conversion formula previously established by Iotti et al 23 The cerebral heterogeneity in Mg 2+ and the correlation between intracellular pH and [Mg 2+ ] are revealed by high-spatial-resolution 3D 31…”