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1.
Figure 1

Figure 1. Morphology of normal cerebral artery. From: Varicella zoster virus vasculopathy.

Movat pentachrome stain reveals the 3 layers of a normal cerebral artery. The intima, adjacent to the lumen, is composed of a single endothelial layer (arrows indicate endothelial cell nuclei [pink]). The media is composed of smooth muscle cells, and the adventitia contains collagen and fibroblasts. An internal elastic lamina (IEL) separates the intima and media. Unlike coronary and pulmonary arteries, cerebral arteries do not have an external elastic lamina between the media and adventitia.

M.A. Nagel, et al. Neurology. 2011 Jul 26;77(4):364-370.
2.
Figure 2

Figure 2. Histologic and virologic analysis of a normal human cerebral artery and varicella zoster virus (VZV)–infected temporal and cerebral arteries of patients with VZV vasculopathy. From: Varicella zoster virus vasculopathy.

Hematoxylin & eosin (H&E) stain of a normal uninfected middle cerebral artery from subject 3 (A); Verhoeff-Van Gieson (VVG) staining shows an intact internal elastic lamina (E, arrow) devoid of VZV antigen (I). In the temporal artery of subject 1 with early VZV vasculopathy, as well as the right middle cerebral artery of subjects 2 and 3 (both of whom died of protracted VZV vasculopathy), H&E staining reveals a hyperplastic intima in all 3 arteries (B–D, vertical black lines), and VVG staining shows duplication or frank disruption of the internal elastic lamina in the arteries of all 3 subjects with VZV vasculopathy (F–H, arrows). VZV antigen (pink) in seen in the adventitia of subject 1 at 4 weeks after zoster (J, arrow), in the media of subject 2 (without a history of zoster rash) after a 45-week course of VZV vasculopathy (K, arrow), and in the hyperplastic intima of subject 3 at 48 weeks after zoster (L, arrow). Magnification = × 100 in panels A–H and × 600 in panels I–L.

M.A. Nagel, et al. Neurology. 2011 Jul 26;77(4):364-370.
3.
Figure 3

Figure 3. Immunohistochemical analyses of a normal cerebral artery and varicella zoster virus (VZV)–infected arteries from patients with VZV vasculopathy. From: Varicella zoster virus vasculopathy.

A thin layer of endothelial cells expressing CD31 is seen in the normal cerebral artery (A, brown color, arrow). The thickened intima of cerebral arteries from subjects 1–3 with VZV vasculopathy (B–D, vertical white lines) does not contain endothelial cells expressing CD31; however, a thin endothelium is seen adjacent to the lumen (B–D, brown color, arrows). In the normal artery, α–smooth muscle actin (α-SMA) is present exclusively in smooth muscle cells of the media (E, vertical black line, brown color). In the VZV-infected artery of subject 1 at 4 weeks after zoster, cells expressing α-SMA are present but less dense in the media and also seen in the hyperplastic intima (F, vertical black and white lines, brown color, respectively); in contrast, the cerebral arteries of subjects 2 and 3 with protracted VZV vasculopathy revealed a striking paucity of cells expressing α-SMA in the media (G, H, vertical black lines, brown color) and a greater abundance of such cells in the hyperplastic intima (G, H, vertical white lines, brown color). Cells expressing smooth muscle myosin heavy chain (SM-MHC) are abundant in the media of the normal artery (I, vertical black line, pink color); such cells are also present but less dense in the arterial media in subject 1 at 4 weeks after zoster (J, vertical black line, pink color) and sparse in the media of subjects 2 and 3 with protracted VZV vasculopathy (K, L, vertical black lines, pink color). Like α-SMA, SM-MHC is expressed by cells in the hyperplastic intima of the cerebral arteries of subjects 1–3 with VZV vasculopathy (J–L, vertical white lines, pink color). Magnification = × 200 in all panels.

M.A. Nagel, et al. Neurology. 2011 Jul 26;77(4):364-370.

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