## Paraneoplastic Cerebellar Degeneration (PCD) ### Pathological Hallmark of PCD **Key Point:** The pathognomonic finding in PCD is **loss of Purkinje cells** with relative preservation of granule cells — the opposite of what the distractor claims. ### Histopathological Features | Cell Type | Status in PCD | Mechanism | |-----------|---------------|----------| | Purkinje cells | Severely depleted | Primary target of immune attack; express cdr1/cdr2 antigens | | Granule cells | Relatively preserved | Secondary loss due to lack of Purkinje cell input | | Molecular layer | Gliosis, inflammation | T-cell infiltration, cytotoxic response | ### Anti-Yo Antibodies and Mechanism 1. **Antigen Recognition:** Anti-Yo IgG binds to cdr1 (cerebellar degeneration-related antigen 1) and cdr2 on Purkinje cell cytoplasm 2. **Immune Mechanism:** CD8+ T-cell-mediated cytotoxic destruction of Purkinje cells 3. **Result:** Selective Purkinje cell loss → cerebellar ataxia, dysarthria, nystagmus ### Cancer Associations with PCD **High-Yield:** Anti-Yo PCD occurs predominantly in: - **Ovarian cancer** (50–80% of anti-Yo PCD cases) - **Breast cancer** (10–30% of anti-Yo PCD cases) - Rarely: endometrial, gastric, lung cancers ### Prognosis and Treatment **Clinical Pearl:** Unlike some paraneoplastic syndromes, PCD is often **irreversible** even with cancer treatment or immunotherapy. However, early aggressive immunosuppression (corticosteroids, IVIG, plasmapheresis) may slow progression if initiated within weeks of symptom onset. **Warning:** Delayed diagnosis and treatment lead to permanent neurological disability. The window for intervention is narrow.
Sign up free to access AI-powered MCQ practice with detailed explanations and adaptive learning.