There are 4 types of spinal vascular malformations: Type I - dural arteriovenous fistula (DAVF); Type II - Intramedullary glomus type arteriovenous malformation (AVM); Type III - juvenile-type AVM; Type IV - intradural extra/perimedullary AVF. Type I is not a true AVM and represents 80% of all spinal vascular malformations. DAVF has no intervening small vessel network. The fistula drains directly into the venous outflow tract and is supplied by small tortuous arteries originating from the dura mater. Probably its origin is due to a thrombosis of the extradural venous system, and the venous hypertension derived causes reduced tissue perfusion and cord ischemia. Usually it is present in the 5th or 6th decade and 80% of patients are male. Most commonly it occurs at thoracolumbar level (T5-L3). Arterial supply arises from the dural branch of the radicular artery and the intadural vein drains directly into cord pial veins. Three pathophysiologic mechanisms underlying spinal AVMs may cause neurological injury: hemorrhage (rarely in DAVF), mass effect, or vascular steal.
Clinical presentation: progressive weakness in the lower limbs with involvement of both motor neurons. Other symptoms are back pain, sphincter disturbances, impotence, and rarely subarachnoid hemorrhage. The clinical course is slowly progressive and the time from symptom onset to diagnosis is often delayed. The surgical strategy for the treatment of DAVF involves posterior exposure at the appropriate spinal level (laminoplasty). High-powered magnification and illumination with the operating microscope are used to perform intradural dissection along the appropriate nerve root. An arterialized vein must be dissected sharply to its exit point at the margin of the dural root sleeve. Bipolar coagulation is used to interrupt the fistula. The advantage of surgical disruption is the relative ease of exposure and direct visualization of the vascular anatomy. The other form/method of treatment is endovascular. Finally, treatment should be individualized, depending on lesional angioarchitecture and the patient’s clinical status.
Clinical presentation: progressive weakness in the lower limbs with involvement of both motor neurons. Other symptoms are back pain, sphincter disturbances, impotence, and rarely subarachnoid hemorrhage. The clinical course is slowly progressive and the time from symptom onset to diagnosis is often delayed. The surgical strategy for the treatment of DAVF involves posterior exposure at the appropriate spinal level (laminoplasty). High-powered magnification and illumination with the operating microscope are used to perform intradural dissection along the appropriate nerve root. An arterialized vein must be dissected sharply to its exit point at the margin of the dural root sleeve. Bipolar coagulation is used to interrupt the fistula. The advantage of surgical disruption is the relative ease of exposure and direct visualization of the vascular anatomy. The other form/method of treatment is endovascular. Finally, treatment should be individualized, depending on lesional angioarchitecture and the patient’s clinical status.
References
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- Kim LJ, Spetzler RF. Classification and surgical management of spinal arteriovenous lesions: arteriovenous fistulae and arteriovenous malformations. Neurosurgery 59:S3-195 - S3-201, 2006.
