Multiple sclerosis with extensive leptomeningeal enhancement: a case report

Abstract

Case Presentation: A 36-year-old female baker, hypertensive, obese, and dyslipidemic, with no history of substance abuse, sought medical care in November 2025 due to low visual acuity in the left eye (LE) and severe holocranial headache, initially managed as a migraine. She progressed to LE amaurosis within 24 hours, prompting a private ophthalmological evaluation and subsequent hospitalization. Magnetic resonance imaging (MRI) confirmed severe left optic neuritis and revealed ovoid lesions (approximately 1.2 cm) in the corpus callosum and right parietal subcortical region, without contrast enhancement, suggesting a demyelinating substrate and raising the hypothesis of Multiple Sclerosis (MS). Following pulse therapy with methylprednisolone (1g/day for 5 days), she improved; however, during the same admission, she developed dizziness, headache, and intractable vomiting, requiring five sessions of plasmapheresis and a second pulse therapy. A new MRI showed lesions in the right frontal subcortical, periventricular, and posterior peritrigonal regions, along with diffuse leptomeningeal enhancement (LME). The patient showed good recovery and was discharged on oral corticosteroids with outpatient follow-up. Three days later, she returned complaining of left-hand paresthesia, ipsilateral tinnitus, vomiting, transitional dysphagia, and severe dyspnea, requiring orotracheal intubation in the ICU and a third 5-day pulse therapy. Follow-up MRI showed lesion progression (left corona radiata, right subinsular, bilateral peritrigonal). Cerebrospinal fluid analysis confirmed type 3 oligoclonal bands. She achieved an approximately 70% symptomatic improvement and was discharged on oral prednisone. Discussion: Historically, LME in MS was considered rare, reported in less than 1% of cases when evaluated by two-dimensional techniques (2D T2-FLAIR). However, recent meta-analyses demonstrate its presence in approximately 30% of patients, being more prevalent in progressive phenotypes (39%) than in relapsing-remitting forms (19%). Reliable detection of LME strongly depends on the imaging protocol, with the post-contrast 3D T2-FLAIR sequence being essential for its visualization. Histopathological studies reveal that LME corresponds to perivascular inflammatory infiltrates in the leptomeninges (composed of B cells, T cells, and macrophages). Furthermore, the presence of LME correlates with longer disease duration, higher EDSS scores, greater T1 and T2 lesion burden, and marked reduction in cortical volume. Final Comments: This case illustrates a manifestation of MS accompanied by an uncommon finding of diffuse LME. The recognition of this radiological finding requires attention and appropriate protocols, as it serves as a reliable marker of inflammatory compartmentalization, cortical damage, and greater clinical severity. Identifying it early assists the neurologist in the swift selection of highly efficacious disease-modifying therapies, aiming to mitigate the rapid accumulation of disability.