1. Devic disease: clinical course, pathophysiology, and management
Alireza Minagar, J.Steven Alexander, Marjorie R Fowler, Ann C Long, Roger E Kelley 
Pathophysiology 
Volume 9, Issue 1, Pages (October 2002)
DOI: /S (02)

2. Fig. 1
Transverse myelitis in Devic disease showing cavitation, numerous foamy macrophages and small hyalinized arteries (arrows) [Hematoxylin and Eosin, original magnification 200×].
Pathophysiology 2002 9, 33-40DOI: ( /S (02) )

3. Fig. 2
Spinal cord in Devic disease showing mild cavitation and numerous foamy macrophages particularly surrounding small blood vessels. Gemistocytes are seen in the adjacent neuropil (arrow) [Hematoxylin and Eosin, original magnification 400×].
Pathophysiology 2002 9, 33-40DOI: ( /S (02) )

4. Fig. 3
The hypothetical pathophysiology of Devic disease. Disruption of the BBB facilitates transendothelial extravasation of autoreactive T cells, macrophages and demyelinating antibodies. Up-regulation of expression of endothelial cell adhesion molecules (ECAMs) during the inflammatory process assists in the inward movement of these inflammatory cells and mediators derived from them. Pro-inflammatory cytokines released by the activated T cells, like tumor necrosis factor-β (TNF-β) and interferon-γ (IFN-γ) modulate the expression of cell-surface molecules on antigen-presenting cells (APC) and their activity. The role of matrix metalloproteinases (MMPs) and other proteases is suspected in Devic disease, similar to MS, but the overall injury in Devic disease remains controversial. In addition, why only the optic nerves and spinal cord are affected, and the unique antigens that distinguish them from the rest of the CNS remain to be established.
Pathophysiology 2002 9, 33-40DOI: ( /S (02) )

5. Fig. 4
MRI appearance of acute myelitis in Devic disease. T1-weigthed post-contrast sagittal image of cervical spine. There is a linear enhancing lesion in the cervical spinal cord, extending from C2 to C6 vertebral level.
Pathophysiology 2002 9, 33-40DOI: ( /S (02) )