Highlights
- The magnitude of the waterfall (the pressure difference Psv
– Pds) probably works as a buffer in the immediate
regulation of the intracranial pressure, and provides an explanation on why the brain is not drained of venous blood each time a person sits up. (View Highlight)
- Compared with ordinary arteries, the feeding arteries are usually dilated, tortuous, and elongated. Instead of a capillary network connecting arterial and venous circulations, in an AVM inflowing arteries supply a nidus consisting of a coiled tangle of primitive, malformed arterioles (50-200 micra in diameter), that branch off the feeding arteries and shunt directly into malformed venous loops (0.5-2 mm in diameter), which in their turn run into the main draining vein (s). The draining vein is as a rule particularly
dilated, sometimes aneurismal, and reversal
of blood flow direction may occur in tributaries of the draining vein (View Highlight)
- The draining
vein is subjected to intensive pressure‑ and flow‑related strains that may lead to structural fatigue, focal dilation, and varix formation. (View Highlight)
- Lack of a high‑resistance arteriolar bed and presence of a low‑resistance nidus generates high blood flow rate and hypotension in the feeding artery combined to intranidal and draining vein hypertension. (View Highlight)
- AVM feeder arteries are known to dilate with time. Studies on normal cerebral arteries[56]
and on arteries feeding cerebral AVMs[57]
seem to support the hypothesis that each segment of the cerebral arteries adapts the luminal diameter locally in response to sustained changes of blood flow so that wall shear stress (the force exerted along the endothelium by the viscous drag of flowing blood) on the long term is kept within optimum limits. (View Highlight)
- AVM patients who were asymptomatic
or had mild symptoms did not present any significant difference in wall shear stress in feeding vessels compared with normal contralateral vessels, whereas patients presenting with severe symptoms (hemorrhage, severe headache, intractable seizures, or focal neurologic deficits) had significantly higher wall shear stress in AVM feeding vessels compared with contralateral vessels. After removal of the AVM the feeder artery walls are known to remodel again, this time slowly reducing their caliber. (View Highlight)
- . On the long run, any effect of Pds on Pcsf probably depends on the magnitude of the shunt flow
and pressure transmission, and on whether the vascular waterfall at the entry of the subarachnoid veins into the dural sinus is present or is abolished, either intermittently or permanently. (View Highlight)
- In the extreme situation when Pds equals Pcsf
and a steady state is achieved, Pds and Pcsf
After removal of the AVM or clamping of the feeding artery, the pressure in the proximal stump of the feeding artery increased to approximately the level of the SAP, and the pressure in the draining vein decreased drastically. Pooling detailed data charts published in some of these studies[3,8,20,33,41,42,46,59]
and not considering methodological discrepancies (the zero pressure level may have been
calibrated using somewhat different reference sites), gives the following results: Before AVM excision the average feeding artery pressure was 49.3 mmHg (SD = 16.9; N = 75), corresponding to 64.1% (SD = 22.8; N = 75) of SAP, and the average draining vein pressure was 17.1 mmHg (SD = 6.1; N = 54). Draining vein pressure was in average 12.5 mmHg (SD = 6.6; N = 46) higher that the central venous pressure. After AVM excision the pressure in the artery stump was in average 72.2 mmHg (SD = 11; N = 19), or 84% (SD = 14.2; N = 18) of the SAP. Measurements of intravascular pressure done by microcatheterization of the feeders in transarterial embolization showed similar findings concerning feeder artery pressures, which in three representative studies[13,21,58] was in average 50%, 55%, and 68%, respectively, of the mean SAP before AVM embolization. A tendency for lower terminal feeder artery pressures to occur in longer feeding arteries was observed in one study,[46]
but it was not confirmed in another study.[20] Feeding artery
pressures were found to be significantly higher in AVMs with previous hemorrhage than in clinically unruptured AVMs.[24,41,59]
A tendency to higher feeder artery pressures
occurred in AVM feeders with brain‑nourishing branches distal to the nidus[58]
as well as in small AVMs (with nidus will
oscillate together over time, and general cerebral venous engorgement and CSF outflow obstruction will develop that may result in hydrocephalus development when other CFS outflow mechanisms (e.g., CSF bulk flow to the spinal canal) become exhausted. (View Highlight)