Dorsal Spinal Venous Occlusion in the Rat

Abstract

Occlusion of the major components of the spinal venous system is usually associated with spinal arteriovenous malformations or systemic thrombophlebitis. Although spinal venous system dysfunction has been implicated in compressive cord syndromes, myelopathies from decompression sickness, 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 dorsal spinal vein transdurally at the T7 and T10 vertebral levels. Following such occlusion, venous stasis, sludging and perivascular hemorrhages in the small venous branches were observed. By 1 week postocclusion, animals developed hindlimb paralysis from which they partially recovered over time. Histologic examination in the acute phase disclosed tissue necrosis, edema, and hemorrhages predominantly in the dorsal aspect of the spinal cord. This was gradually replaced by an intense macrophagic infiltration and the partial formation of a cystic cavity by 1 month. These findings indicate that dorsal spinal vein occlusion in the rat causes significant neurologic and pathologic alterations. We conclude that this procedure produces a relevant animal model for the study 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 disorders associated with spinal venous dysfunction.

Characterization of Blood Flow in the Mouse Dorsal Spinal Venous System before and after Dorsal Spinal Vein Occlusion

“…In line with our predictions of ischemic injury, longitudinal studies 42,43 of dSV occlusion in rats have shown atrophy of the posterior columns, reactive gliosis, macrophage infiltration, and onset of paraplegia. Interestingly, in a study examining the results of dSV ligation, 43 variability in the extent of pathologic SC 'softening' was attributed to unobserved venous anastomoses connecting to the dSV.…”

Syringomyelia: A review of the biomechanics

“…In parallel, there was speculation that swelling due to meningitis (Charcot and Joffroy, 1869;Joffroy and Achard, 1887) or just Chiari malformation (Lichtenstein, 1943;Tarlov et al, 1953;McGrath, 1965;Martinez-Arizala et al, 1995) could lead via venous obstruction and/or arterial clotting to ischaemic damage in the SC which became syringomyelia. However animal models of ischaemia tended to produce SC softening (myelomalacia) rather than cavitation.…”

Syringomyelia: Clinical Observations and Experimental Studies

“…This conjecture was not supported by a recent report of direct obstruction of the dorsal spinal vein in the rat documenting posterior column necrosis in the cord directly under the occluded segment. There was no evidence of a deep cavitary lesion in the parenchyma that even superficially resembled a traditional syringomyelic lesion (Martinez-Arizala et al, 1990). Further evidence disputing the ischémie hypothesis was reported by both Hall et al (1975) and Williams and Bentley (1980), who found no evidence for ischémie changes in their respective series of experimental animals prepared after the technique of McLaurin et al (1954).…”