# Rapidly Progressive Cerebellar Syndrome Associated With Anti-Yo Antibodies Following Complete Response to Advanced Ovarian Carcinoma Treated With Olaparib: A Case Report

## TL;DR

A woman with ovarian cancer developed a rare neurological condition after treatment with olaparib, highlighting the challenge of distinguishing drug toxicity from autoimmune responses.

## Contribution

This case report describes a rare instance of anti-Yo antibody-mediated cerebellar syndrome following olaparib treatment in ovarian cancer.

## Key findings

- The patient developed neurological symptoms months after starting olaparib, with no evidence of cancer recurrence.
- Immunological treatment failed, but cancer recurrence was later detected and partially responded to chemotherapy.
- Olaparib's potential role in unmasking latent autoimmune responses is suggested but not proven.

## Abstract

Rapidly progressive cerebellar syndrome (RPCS) mediated by anti-Yo antibodies is a rare neurological manifestation of paraneoplastic syndromes, most often associated with active breast or gynecological neoplasms. Its occurrence after apparent remission of cancer is rarely described and carries a poor prognosis.

We report the case of a 47-year-old woman with stage IIIC high-grade serous ovarian carcinoma (International Federation of Gynecology and Obstetrics (FIGO)) treated with neoadjuvant chemotherapy, complete cytoreductive surgery, and maintenance treatment with olaparib. Two weeks after starting the PARP inhibitor (iPARP), she developed nausea, vomiting, and vertigo, initially attributed to drug toxicity. The dose was reduced by one level, with improvement in gastrointestinal complaints. Months later, she progressed with ataxia, dysarthria, and postural instability. An exhaustive neurological study was performed, which revealed positive anti-Yo and anti-amphiphysin antibodies. Imaging and tumor markers showed no evidence of disease recurrence. A diagnosis of paraneoplastic RPCS was made. Sequential treatment with corticosteroids, intravenous immunoglobulin, and cyclophosphamide was ineffective. It was only about six months after the diagnosis of RPCS that a locoregional recurrence was identified. The patient started carboplatin in monotherapy due to clinical frailty, with improvement in speech impairment after only one cycle.

This case highlights the diagnostic complexity in distinguishing between drug-related toxicity and immune-mediated neurological syndromes. Although there is no direct evidence linking olaparib to the induction of paraneoplastic syndromes, its immunomodulatory effects may unmask latent autoimmune responses in susceptible individuals. Anti-Yo RPCS remains a therapeutic challenge with a poor neurological prognosis. Early recognition is crucial, and further research is needed to understand the interactions between targeted therapies and paraneoplastic immunity.