higher than in a group of age-matched controls (Schreiber et al. 2003b). Using the echo contrast bolus-tracking tech­nique, we found a significant shortened gCCT (2.9 s) within the range that is also seen in patients with a classic AVM (1.4–5.1 s) (Schreiber et al.2002). A gCBV calculation in our patient revealed an increased blood volume (126 mL) com­pared with healthy subjects (approximately 80 mL) (Doepp et al. 2003), which matched well with PET findings in classic AVM patients (Tyler et al.1989). The latter result, however, has to be interpreted cautiously because a prox­imally located arteriovenous shunt between a mainstem artery and a main draining vein would lead to a short gCCT and a possible underestimation of the real gCBV, interdict­ing gCBV calculations in classic AVM patients. However, our patient’s unique malformation comprises a distal and leptomeningeal shunt location. The gCCT shortening might therefore result not just from the arteriovenous shunting alone, but also from the generally increased flow velocities in all cerebral vessels, reducing the effective error of the approach. The calculated high gCBV argues in favor of this hypothesis, although the value is probably still an underestimation. Considering the clinical symptoms of continuing headache, nausea, and vomiting in our patient as possible signs of raised intracranial pressure, a high gCBV might be a plausible explanation, in particular as cerebral MRI excluded hydrocephalus or cerebrospinal fluid (CSF) circulation disturbances.