Neuropathology for the Neuroradiologist: Palisades and Pseudopalisades
F.J. Wippold, IIa,b,c,
M. Lämmlea,b,
F. Anatellid,
J. Lennerzd and
A. Perryd
a Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, Mo
b Department of Radiology, Barnes-Jewish Hospital South, St. Louis, Mo
c Department of Radiology/Nuclear Medicine, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Md
d Neuropathology Division, Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO

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Fig 1. Photograph of the reconstructed 18th century Fort Massac in southern Illinois, demonstrating walls made of log palisades (courtesy of James P. Rowen).
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Fig 2. Drawing of a Verocay body illustrating the parallel rows of fusiform nuclei (modified with permission from Springer-Verlag1).
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Fig 3. Photomicrograph of Verocay bodies in a schwannoma characterized by linear arrangements of elongated tumor nuclei (hematoxylin-eosin [H&E], original magnification x400).
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Fig 4. Spongioblastic tumor showing rhythmic palisades (linear waves of tumor nuclei) or spongioblastic pattern. This feature is now considered a relatively nonspecific pattern, and other regions of this tumor showed classic histologic features of anaplastic oligodendroglioma (H&E, original magnification x400).
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Fig 5. Drawing of pseudopalisading, illustrating the garlandlike array of nuclei surrounding a region of necrosis (modified with permission from Springer-Verlag1).
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Fig 6. Pseudopalisading necrosis in a glioblastoma characterized by a garlandlike arrangement of hypercellular tumor nuclei (arrows) lining up around irregular foci of tumor necrosis (n) containing pyknotic nuclei (arrowheads). Note tumor vessel (v) (H&E; original magnification x200).
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Fig 7. Schematic representation of the formation of a pseudopalisade. Growth of the glioblastoma stimulates neo-angiogenesis. Expression of ang 2 causes endothelial damage, which, in turn, produces vascular occlusion and hypoxia. Cells unable to survive the hypoxia succumb and form the nidus of coagulation necrosis. Other cells, however, migrate to the periphery of the hypoxic field in waves forming pseudopalisades. The migrating hypoxic cells secrete VEGF, proteases, and other factors that cause further microvascular proliferation and enhanced invasiveness in regions ringing the hypoxic field. These latter effects prompt further aggressive outward expansion of the glioblastoma cells (modified with permission from Brat et al42).
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