Anti-Yo paraneoplastic cerebellar degeneration presenting as Miller Fisher syndrome: a diagnostic mimic

Abstract

Case Presentation: A 73-year-old woman with a history of hypertension was admitted in December 2025 with sudden-onset dysarthria. Approximately 30 days before admission, she had developed persistent rotational vertigo and gait instability, and had been previously evaluated by otorhinolaryngology without improvement after pharmacological treatment. Neurological examination revealed mild dysarthria, ophthalmoparesis, multidirectional nystagmus, gait ataxia, and generalized areflexia, consistent with the classic triad of Miller Fisher syndrome (MFS). Cerebrospinal fluid analysis demonstrated albuminocytologic dissociation (0 cells; protein 184 mg/dL), while brain magnetic resonance imaging showed no abnormalities. Based on the suspicion of MFS, intravenous immunoglobulin was administered for five days. At the end of hospitalization, the patient developed a decreased level of consciousness, initially attributed to infectious worsening, and antibiotic therapy was initiated. She was discharged under home care, bedridden. Approximately six weeks later, she was readmitted with progressive decline in consciousness, presenting in a torporous state, non-contactable, with stereotyped “no-no” head movements and multidirectional nystagmus. Brain magnetic resonance imaging demonstrated cerebellar folia effacement and FLAIR hyperintensity suggestive of cerebellitis. Repeat cerebrospinal fluid analysis showed persistent hyperproteinorrachia (180 mg/dL) and 12 cells/mm³ (90% lymphocytes), with a negative multiplex viral panel for encephalitis. Given the suspicion of autoimmune etiology, intravenous methylprednisolone pulse therapy was administered for five days without significant clinical response. Plasma exchange was subsequently performed, totaling five sessions, after which partial improvement in consciousness and minimal spontaneous movements were observed. Further investigation with oncologic positron emission tomography–computed tomography revealed nonspecific rectal wall thickening and a hypermetabolic nodular lesion in the left iliac chain. Rectosigmoidoscopy showed no suspicious lesions. The patient underwent videolaparoscopic pelvic and retroperitoneal lymphadenectomy. Histopathological analysis demonstrated metastatic adenocarcinoma in lymph nodes. Immunohistochemistry supported Müllerian epithelial origin compatible with high-grade serous carcinoma. Discussion: Anti-Yo antibodies are a rare but well-described cause of paraneoplastic cerebellar degeneration and are most often associated with gynecological and breast malignancies. Their main target antigen is CDR2L, expressed in cerebellar Purkinje cells and tumor cells, supporting an immune-mediated mechanism of neuronal injury. Final Comments: Paraneoplastic cerebellar degeneration usually presents with subacute cerebellar ataxia, but atypical presentations may occur. In rare cases, it may mimic Miller Fisher syndrome, delaying recognition of the underlying paraneoplastic process and diagnosis of the associated malignancy.