Increased pulsatile cerebral blood flow, cerebral vasodilation, and postsyncopal headache in adolescents.

Abstract

We hypothesize that, after a sudden decrease in cerebral blood flow velocity (CBFV) in adolescents, a faint, rapid hyperemic pulsatile CBFV occurs upon the patient's return to the supine position and is associated with postsyncopal headache. This case-control study involved 16 adolescent subjects with a history of fainting and headaches. We induced fainting during 70° tilt-table testing and measured mean arterial pressure, heart rate, end-tidal CO(2), and CBFV. Fifteen control subjects were similarly evaluated with a tilt but did not faint, and comparisons with fainters were made at equivalent defined time points. Baseline values were similar between the groups. Upon fainting, mean arterial pressure decreased 49% in the patients who fainted vs 6% in controls (P < .001). The heart rate decreased 15% in fainters and increased 35% in controls (P < .001). In patients who fainted, cerebrovascular critical closing pressure increased markedly, which resulted in reduced diastolic (-66%) and mean CBFV (-46%) at faint; systolic CBFV was similar to controls. Pulsatile CBFV (systolic-diastolic CBFV) increased 38% in fainters, which caused flow-mediated dilatation of cerebral vessels. When the fainters returned to the supine position, CBFV exhibited increased systolic and decreased diastolic flows compared with controls (P < .02). Increased pulsatile CBFV during and after faint may cause postsyncopal cerebral vasodilation and headache.