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.
| Original language | English |
|---|---|
| Pages (from-to) | 199-208 |
| Number of pages | 10 |
| Journal | Journal of Neurotrauma |
| Volume | 12 |
| Issue number | 2 |
| State | Published - Jan 1 1995 |
Fingerprint
Keywords
- rat
- spinal cord disorders
- spinal cord injury
- spinal cord veins
- venous infarction
ASJC Scopus subject areas
- Clinical Neurology
- Neuroscience(all)
Cite this
Dorsal spinal venous occlusion in the rat. / Martinez-Arizala, Alberto; Mora, R. J.; Madsen, P. W.; Green, Barth A; Hayashi, N.
In: Journal of Neurotrauma, Vol. 12, No. 2, 01.01.1995, p. 199-208.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Dorsal spinal venous occlusion in the rat
AU - Martinez-Arizala, Alberto
AU - Mora, R. J.
AU - Madsen, P. W.
AU - Green, Barth A
AU - Hayashi, N.
PY - 1995/1/1
Y1 - 1995/1/1
N2 - 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.
AB - 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.
KW - rat
KW - spinal cord disorders
KW - spinal cord injury
KW - spinal cord veins
KW - venous infarction
UR - http://www.scopus.com/inward/record.url?scp=0028997419&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028997419&partnerID=8YFLogxK
M3 - Article
C2 - 7629866
AN - SCOPUS:0028997419
VL - 12
SP - 199
EP - 208
JO - Journal of Neurotrauma
JF - Journal of Neurotrauma
SN - 0897-7151
IS - 2
ER -