Abstract

Anti-Yo antibodies are the antibodies most frequently identified with paraneoplastic cerebellar degeneration (PCD). They are detected above all in PCD associated with breast and gynaecologic malignancies. Here, we report a third case of PCD with cerebellar contrast enhancement findings at MRI. In fact, AYA cross anti-cerebellar cortex immune reaction leads mainly to hyperintensity signals in T2-weighted MRI sequences, followed by cerebellar atrophy. As such, meningeal contrast enhancement could lead to a diagnostic pitfall as it can be considered a carcinomatosis—above all in serum antibody–negative cases as well as when a metastatic tumour is found. Our patient had no tumoural cells in the cerebrospinal fluid and her neurological syndrome remained stable after immunoglobulin treatment. Anti-Yo antibody serum finding was diriment for PCD diagnosis.

Highlights

  • Paraneoplastic Cerebellar Degeneration (PCD) is a rare syndrome characterized by cerebellar dysfunction, typically with a subacute onset, associated with the presence of specific onconeural auto-antibodies

  • Anti Yo antibodies (AYA) are the antibodies most frequently identified with Paraneoplastic Cerebellar Degeneration (PCD)

  • We looked for and found anti-Yo antibodies in the serum, fulfilling the diagnostic criteria for definite Paraneoplastic Neurological Syndrome (PNS) [6]

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Summary

Introduction

Paraneoplastic Cerebellar Degeneration (PCD) is a rare syndrome characterized by cerebellar dysfunction, typically with a subacute onset, associated with the presence of specific onconeural auto-antibodies (aAb). The vast majority of patients with anti-Yo antibodies (AYA) have a breast or gynaecological cancer that develops over months to years after the neurological onset of symptoms. Contrast enhancement of the cerebellar cortex is very rare, having been described only in a patient with nonHodgkin's lymphoma and PCD with anti-Tr antibodies [4]. Brain MRI showed a meningeal cerebellar intensive contrast enhancement, associated with micro nodulations of the cerebellar hemisphere cortex (Fig. 1). The patient was advised to have a surgical treatment of ovariectomy with the intention of achieving maximum recovery of the neurological syndrome. She refused the surgery and her neurological condition was unchanged 6 months after the onset

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