Objective: To examine the incidence and possible determinants of impaired vascular reserve in arteriovenous malformation (AVM)-affected brain, before and after surgery.
Methods: In a prospective study of 30 patients, the regional cerebrovascular reserve capacity (rCRC) and the vasodilated regional cerebral blood flow (rCBF) were assessed during an acetazolamide challenge, using xenon-enhanced computed tomography, before and after complete AVM resection. Single brain slices at the level of the basal ganglia were examined, and scanning through the AVMs was avoided. Five regions of interest in the AVM-bearing hemisphere were compared with their counterparts in the unaffected hemisphere. Vasodilated rCBF reductions of at least 20% in one or more regions of interest and rCRC values of less than 10 ml/100 g/min were considered to be significant.
Results: Ipsilateral vasodilated rCBF was significantly reduced in 17 patients before surgery and 15 patients after surgery. Ipsilateral rCRC was impaired in 14 patients before surgery and 12 patients after surgery. Large AVM size, venous congestion, and AVM-related vascular territories were correlated with impaired vascular reserve in AVM-nonadjacent brain tissue before surgery. Similar correlations were observed after surgery, except that not AVM size but a large number of AVM-supplying vascular territories was correlated. Moreover, the smallest AVMs and those supplied by a single vascular territory, as well as hemorrhage and nonhemorrhagic neurological deficits as presenting symptoms, were correlated with reduced ipsilateral vasodilated rCBF before surgery. Among patients with AVMs and nonhemorrhagic epilepsy, a trend of impaired cerebrovascular reserve was observed. In the only case of postresectional "breakthrough," the preoperative rCRC was not impaired but abnormally high.
Conclusion: Among the determinants of impaired cerebrovascular reserve, AVM size is already a constituent of current grading scales and decision-making paradigms, whereas factors such as venous congestion have been less closely considered or less obvious but may deserve increased attention in the future. Nonhemorrhagic epilepsy in patients with AVMs may constitute the clinical equivalent of chronic cerebral ischemia in a murine model. Postresectional breakthrough may be partly attributable to individual predisposition to excessive vasoreactivity in the whole brain.