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Syc-Mazurek, Stephanie B

0000-0002-9549-6648

Mayo Clinic

Department of Neurology, Mayo Clinic College of Medicine, Rochester, MN.

Citations 14

“Railroad Track” Brain Fluorodeoxyglucose-PET Sign in Antiphospholipid Syndrome–Related Posterior Cortical Atrophy

Neurology | October 7, 2026 | Volume: 107 | Issue: 9 | Pages: No page available

10.1212/wnl.0000000000218621 | PMID 42842850

Pearls & Oy-sters: DPPX Antibody-Associated Encephalitis in a Patient With Diarrhea, Tremor, Ocular Flutter, and Cognitive-Psychiatric Changes

Neurology | September 1, 2026 | Volume: 107 | Issue: 7 | Pages: No page available

10.1212/wnl.0000000000218522 | PMID 42679339

Epiretinal membranes in multiple sclerosis: A window into glial pathobiology?

Multiple Sclerosis Journal | July 6, 2026 | Volume: No volume available | Issue: No issue available | Pages: No page available

10.1177/13524585261464504 | PMID 42405522

Psychiatric comorbidities cluster early after onset in MOGAD: a cross-sectional comparative study with MS and NMOSD

Journal of Neurology, Neurosurgery & Psychiatry | April 9, 2026 | Volume: 97 | Issue: 9 | Pages: 817-826

10.1136/jnnp-2025-338335 | PMID 41956817

Background Psychiatric comorbidities are increasingly recognised in demyelinating diseases, yet their frequency and timing in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are not well defined. We aimed to characterise the spectrum and temporal pattern of psychiatric illness in MOGAD and compare to multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD) with aquaporin-4 antibody (AQP4-IgG). Methods We conducted a cross-sectional study of patients with MOGAD (n=388), age-matched and sex-matched MS (n=257) and AQP4-IgG-positive NMOSD (n=58) evaluated at Mayo Clinic (1991–2025). Psychiatric diagnoses, timing relative to the first attack and patient-reported outcomes were extracted from electronic health records (EHRs). Complementary analyses were conducted using the NeuroBlu real-world EHR database. Results Among 388 patients with MOGAD, 54.8% had ≥1 psychiatric disorder, most commonly anxiety (47.7%), depression (36.6%) and attention-deficit/hyperactivity disorder (ADHD, 9%). After the first attack, 33.3% of patients with MOGAD developed a new psychiatric disorder, often within the first year. MOGAD showed a lower frequency of depression versus MS (36.6% vs 47.5%, p=0.02) but similar rates of anxiety and ADHD. Temporal patterns differed: psychiatric disorders often appeared years before onset in MS but clustered shortly after onset in MOGAD. NeuroBlu analyses supported high rates of psychiatric disorders across the three conditions. Conclusion Psychiatric comorbidities are common in MOGAD, particularly depression and anxiety, typically emerging close after onset, whereas in MS they often preceded onset by years. These findings underscore the need for routine psychiatric screening in MOGAD and highlight unresolved questions regarding whether, and to what extent, MOG-IgG-mediated inflammatory demyelination contributes to psychiatric vulnerability.
TRUE-MOGAD Score

Neurology Neuroimmunology & Neuroinflammation | April 1, 2026 | Volume: 13 | Issue: 3 | Pages: No page available

10.1212/nxi.0000000000200563 | PMID 41921125

MRI characteristics during attack and remission distinguish patients with MOG antibody-associated disease from multiple sclerosis

Journal of Neurology, Neurosurgery & Psychiatry | July 20, 2025 | Volume: No volume available | Issue: No issue available | Pages: jnnp-2025-336684

10.1136/jnnp-2025-336684 | PMID 40685157

Background Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) and multiple sclerosis (MS) have both overlapping and distinct MRI lesion features, which vary with imaging timing. This study identified distinguishing MRI characteristics using paired MRIs at clinical attack and remission. Methods We retrospectively identified Mayo Clinic patients with MOGAD and MS that: (1) fulfilled respective diagnostic criteria; (2) had paired attack (≤30 days) and remission MRI scans (≥12 months) without interval attacks. MRIs were compared between groups for key features. Results We included 43 patients with MOGAD (median age 31 years (range, 3–67); 63% female) and 49 patients with MS (median age 39 years (range, 17–65); 65% female). Resolution of at least one T2-lesion differentiated MOGAD from MS (sensitivity, (95% CI 77% to 100%), specificity, (95% CI 86% to 99%); Youden’s index (YI)=0.90). Resolution of at least two T2-lesions indicated MOGAD (sensitivity 62% (95% CI 41% to 79%); specificity, 100% (95% CI 94% to 100%); YI=0.62). MOGAD patients were more likely to have normal MRI scans at follow-up compared with MS (brain 14/44 (32%) vs 0/60 (0%), p<0.001; spine 21/27 (78%) vs 7/36 (19%), p<0.001). In addition, the presence of T1-hypointense, ovoid periventricular T2, and enhancing lesions were more common in MS versus MOGAD at attack and remission and in the spine, longitudinally extensive T2 lesions were more common in MOGAD attacks (8/27 (30%)). Conclusion Paired MRI at attack and remission revealed distinctive characteristics of MOGAD and MS, with greater diagnostic value at remission driven by the discriminating power of T2-lesion resolution. In MOGAD patients with initial parenchymal involvement, a 1-year follow-up MRI may aid diagnosis and serve as a new baseline.
Assessment of concurrent neoplasms and a paraneoplastic association in MOGAD

Annals of Clinical and Translational Neurology | February 11, 2025 | Volume: 12 | Issue: 4 | Pages: 861-870

10.1002/acn3.52301 | PMID 39932929

AbstractCases of myelin oligodendrocyte glycoprotein (MOG) antibody‐associated disease (MOGAD) co‐occurring with neoplasms have been reported. In this international, retrospective cohort study in South Korea and the USA, 16 of 445 (3.6%) patients with MOGAD had concurrent neoplasm within 2 years of MOGAD onset, resulting in a standardized incidence ratio for neoplasm of 3.10 (95% confidence interval [CI], 1.77–4.81; P < 0.001) when compared to the age‐ and country‐adjusted incidence of neoplasm in the general population. However, none of the nine tumor tissues obtained demonstrated MOG immunostaining. The slightly increased frequency without immunohistopathological evidence suggest with true paraneoplastic MOGAD is extremely rare.
Radiologic Lag and Brain MRI Lesion Dynamics During Attacks in MOG Antibody–Associated Disease

Neurology | May 6, 2024 | Volume: 102 | Issue: 10 | Pages: No page available

10.1212/wnl.0000000000209303 | PMID 38710000

MOG Antibody–Associated Disease in the Setting of Metastatic Melanoma Complicated by Immune Checkpoint Inhibitor Use

Neurology Neuroimmunology & Neuroinflammation | May 2, 2024 | Volume: 11 | Issue: 4 | Pages: No page available

10.1212/nxi.0000000000200249 | PMID 38696737

Timing and Predictors of T2-Lesion Resolution in Patients With Myelin Oligodendrocyte Glycoprotein Antibody–Associated Disease

Neurology | June 19, 2023 | Volume: 101 | Issue: 13 | Pages: No page available

10.1212/wnl.0000000000207478 | PMID 37336767