Multiple sclerosis (MS) and Hodgkin lymphoma (HL) share common epidemiology, genetics, and immunological factors. We report a case of a woman who presented with neurological deficits along with systemic symptoms fulfilling criteria for MS with synchronous HL. A 37-year-old woman presented with bilateral extremity weakness, numbness and urinary retention, which was preceded by three weeks of night sweats, 25-pound (11 kg) weight loss and anorexia. Neurological examinations showed spastic paraparesis, sensory deficit, and a left extensor plantar response. Magnetic resonance imaging (MRI) of the brain showed multiple non-enhancing white-matter lesions, with patchy areas of peripheral gadolinium (Gd)-enhancement in the thoracic cord. Serology was positive for JC and EBV IgG antibodies. Body imaging revealed a mediastinal mass, and lymph node biopsy confirmed classical HL. Steroid infusions resulted in mild improvements in extremity weakness and numbness. She was treated with doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) for HL. A Gd-enhanced MRI brain obtained after 4 cycles of ABVD showed resolution of enhancing lesions but new T2-FLAIR lesion consistent with active MS. Due to ongoing HL surveillance and concerns regarding immunosuppression, disease-modifying therapy for MS was not initiated. On her annual follow-up, she reported persistent fatigue, transient memory deficit, and residual bilateral feet numbness. The relationship between HL and MS has been explored in numerous studies, revealing an overlap in genetic susceptibility, shared biological pathways through lymphocyte-mediated immunity, JUN kinase activity, tyrosine phosphorylation, and common environmental factors, such as the presence of EBV. Our patient presented an atypical thoracic MRI finding of peripheral enhancement which led to further investigation and diagnosis of HL. The concurrent occurrence of MS and HL may point toward shared immune dysregulation. We report a case of co-occurrence of MS with HL and note neurological stability after treatment with ABVD chemotherapy for HL. The shared genetics and immunological interplay may explain overlaps, but MS and HL remain distinct pathologies.
Khand et al. (2026) studied this question.