1. Chapter 27 Paraneoplastic Syndromes Involving the Nervous System
Jerome B. Posner
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Figure 27-1 Axial fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI) of a patient with paraneoplastic limbic encephalopathy. There is marked hyperintensity in the medial temporal lobes bilaterally. In addition, there is slight dilatation of the temporal horns, suggesting atrophy.
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Figure 27-2 A, Normal sagittal MRI of the brain. B, T1 contrast-enhanced sagittal MRI of the brain in a patient with paraneoplastic cerebellar degeneration. The cerebellum is atrophic, but the rest of the brain is normal.
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Figure 27-3 Paraneoplastic cerebellar degeneration. A, Section of cerebellum of a patient who died of cancer without cerebellar symptoms. Multiple Purkinje cells are identified between the molecular (top) and granule cell (bottom) layers, both of which are normal. (Hematoxylin–eosin×25.) B, Section of cerebellum from a patient with autoantibody-positive paraneoplastic cerebellar degeneration. The molecular and granular cell layers are relatively normal, but Purkinje cells are absent, and there is a slight increase in Bergmann astroglia along with some inflammatory cells in the leptomeninges. (Hematoxylin–eosin×25.)
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Figure 27-4 Paraneoplastic sensory neuronopathy. A, Dorsal root ganglion obtained at autopsy from a patient without neurologic disease. B, Dorsal root ganglion obtained from a patient with paraneoplastic sensory neuronopathy and anti-Hu antibodies. Note that there are virtually no normal dorsal root ganglion neurons in the entire section. A few scattered inflammatory infiltrates are present. (Hematoxylin–eosin×40.) C, The dorsal root ganglion of another patient with anti-Hu-related subacute sensory neuronopathy. Degenerating neurons can be seen surrounded by inflammatory cells. (Hematoxylin–eosin×40.)
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