A 34-year-old woman presented with abrupt onset headache and lethargy attributable to an acute SAH secondary to a ruptured P-1 aneurysm. She received standard therapy for SAH patients and had successful coiling of the aneurysm. On postbleeding day 4, while hemodynamically stable, she developed a new drift in the right upper extremity that progressed to grade 3/5 motor weakness with facial weakness within 30 minutes. A repeat plain CT showed no hydrocephalus. The CT perfusion showed no derangement of the cerebral blood volume (CBV) or the cerebral blood flow (CBF) with a slightly prolonged mean transit time (MTT) denoting intact brain tissue. The time-to-peak (TTP), on the other hand, was significantly prolonged in the left central Rolandic subcortical region, consistent with the clinical finding (Figure 1). A Bowman Perfusion Monitor (BPM, Hemedex, MA, USA) was inserted at the bedside, using free-hand technique aiming at the point of interest generated by the CT perfusion TTP scan. The cerebral blood flow (CBF) measured at this time was 14 cc/100 g/min, denoting severe hypoperfusion (normal level is above 25 cc/100 g/min). The patient was started on the MNH-milrinone protocol for the treatment of vasospasm. Within 1 hour, the patient did not improve, necessitating endovascular vasodilator therapy, during which she received 2 mcg of milrinone over 3 minutes with immediate vasodilation of the vasospastic segment. The CBF reading improved to the 50's with the maintenance of milrinone. On 2 occasions, weaning the milrinone infusion was associated with an asymptomatic but significant drop of the measured CBF to low 20's, which delayed the weaning for 24-48 hours each time, likely related to recoil of angioplastied vessel mitigated clinically by the milrinone effect. The total monitoring period was 9 days, after which milrinone was stopped and CBF measurement ranged from 40 to 50 and the patient did not have any residual motor deficits for an additional 48 hours.