Occlusion of the major components of the spinal venous system is usual
ly associated with spinal arteriovenous malformations or systemic thro
mbophlebitis, Although spinal venous system dysfunction has been impli
cated in compressive cord syndromes, myelopathies from decompression s
ickness, and spinal cord trauma, its pathophysiology remains unclear,
To characterize disorders associated with spinal venous occlusion, we
developed a model in the rat produced by focally coagulating the dorsa
l spinal vein transdurally at the T7 and T10 vertebral levels, Followi
ng such occlusion, venous stasis, sludging and perivascular hemorrhage
s in the small venous branches were observed, By 1 week postocclusion,
animals developed hindlimb paralysis from which they partially recove
red over time, Histologic examination in the acute phase disclosed tis
sue necrosis, edema, and hemorrhages predominantly in the dorsal aspec
t of the spinal cord, This was gradually replaced by an intense macrop
hagic infiltration and the partial formation of a cystic cavity by 1 m
onth, These findings indicate that dorsal spinal vein occlusion in the
rat causes significant neurologic and pathologic alterations, We conc
lude that this procedure produces a relevant animal model for the stud
y of the pathophysiology of spinal venous occlusion, and it allows the
characterization of its effects on spinal cord blood flow, the blood-
spinal cord barrier, and the development of edema independent of cord
compression, Our findings in this model provide an insight into one of
the mechanisms of injury extension in spinal cord trauma and other di
sorders associated with spinal venous dysfunction.