Angiographic signs of venous hypertension and clinical findings of increased intracranial pressure in dural arteriovenous fistulas: evolution after endovascular treatment

Dural arteriovenous fistulas (dAVFs) can cause cerebral venous hypertension (VHT). The most common mechanism is dire to the fact that some dAVFs can d rain retrogradelly in cortical (better defined as leptomeningeal) veins (di rectly or after drainage in a dural sinus) causing venous engorgement and c onsequently an impairment of the cerebral venous drainage. However, more ra rely, dAVFs without a cortical venous drainage can also be responsible for VHT probably due to dAVF shunts causing insufficient antegrade cerebral ven ous drainage. In addition, dAVFs are often associated with stenosis and/or thrombosis of dural sinus(es) which can worsen the VHT. Raised pressure wit hin the superior sagittal sinus causes impeded cerebrospinal reabsorption i n the arachnoid villi allowing increased intracranial pressure. The venous engorgement in the cortical veins can cause a venous congestive encephalopa thy analogous to the venous congestive myelopathy of the spinal dural AVFs. Clinically VHT can cause, not only symptoms related to increased intracran ial pressure but also seizures, neurological deficits, impairment of the co gnitive functions and dementia. An important aspect is the risk of hemorrha ge in dAVFs with a leptomeningeal venous drainage leading to VHT. Although the term VHT sensu strictu should be used if venous pressure measurements a re performed, angiographic criteria for VHT such as delayed circulation rb, lc, venous engorgement and abnormal visualization of the cerebral veins are well established The purpose of our study was to evaluate the angiographic signs of VHT in patients with dAVF and to study the course of the VHT and of the clinical signs of increased intracranial pressure before and after d AVF endovascular treatment. A retrospective chart analysis of 22 patients (13 males, 9 females) ranging in age from 20 to 87 years (mean : 53 ys.) with a dAVF associated with ang iographic signs of VHT was performed. Ten dAVFs were located on the transve rse/sigmoid, sinus(es), 6 on the superior sagittal sinus, 3 on the petro-te ntorial incisura, 1 on the inferior petrosal sinus, 1 on the anterior ethmo idal region and 1 on the Galen vein region. All dAVFs had a retrograde lept omeningeal venous drainage. Stenosis or thrombosis of the dural AVF sinus w as observed in 17 cases and stenosis or thrombosis of another sinus(es) and /or of the jugular vein in 8 cases. In 11 patients, the angiographic signs of VHT were global affecting the entire cerebral venous drainage and, in th e other 11 patients, the VHT was focal. The VHT caused clinical symptoms of increased intracranial pressure in 18 patients. Other clinical findings in cluded : bruit (11 cases), seizures (3 cases), vertigo 13 cases), visual de ficits (2 cares and impairment of cognitive functions (4 cases). Three pati ents presented hemorrhage (one parenchymal hematoma, one hemorrhagic infarc tion and one subarachnoid hemorrhage). The 4 patients without clinical symp toms of increased intracranial pressure presented only bruit in 2 cases, br uit and vertigo in 1 case, bruit and hemorrhagic infarction in another one. The dAVFs were treated by endovascular therapy (arterial approach : 3 case s, venous approach : 6 cases and both arterial and venous approach : 13 cas es). Endovascular sessions ranged from 1 to 7 (mean : 2.8) for Each patient . After die endovascular treatment, in 12 patients with complete occlusion of the dAVF, the disappearance of angiographic signs of VHT and clinical cu re were observed. Oz 8 patients with partial occlusion of the dAVF, the dis appearance of angiographic signs of VHT anti clinical dire were observed in 4 cases (almost complete dAVF occlusion in 2 cases); in the other 3 cases, only reduction the angiographic signs of VHT and clinical improvement were obtained. In all 16 patients who were clinically cured angiographic signs of VHT disappeared despite the persistence of dAVF shunts as observed in 4 cases. In 2 patients, who presented a very serious clinical status and died a few days after embolization, a slight reduction of the dAVF shunts cause d no modifications of the angiographic signs of VHT; the patients were clin ically unchanged. Complete recovery or dramatic improvement of cognitive fu nctions was observed in the 4 patients with impaired mental status. In conc lusion, VHT is an important consequence of dural AVFs. It must be kept in m ind that, despite serious clinical and angiographic findings, these patient s may dramatically improve if treated. Evolution of the angiographic signs of VHT seems to be a predictive factor of the endovascular treatment effica city. In most of the cases endovascular treatment, el era if partial, can o btain the disappearance of angiographic signs of VHT with cure of the clini cal symptoms of increased intracranial pressure.