Preeclampsia (PE) is associated with endothelial dysfunction and impaired autonomic function, which is hypothesized to cause cerebral hemodynamic abnormalities. Our aim was to test this hypothesis by estimating the difference in the cerebrovascular response to breath holding (BH; known to cause sympathetic stimulation) between women with preeclampsia and a group of normotensive controls. In a prospective cohort analysis, cerebral blood flow velocity (CBFV) in the middle cerebral artery (transcranial Doppler), blood pressure (BP, noninvasive arterial volume clamping), and end-tidal carbon dioxide (EtCO2) were simultaneously recorded during a 20-s breath hold maneuver. CBFV changes were broken down into standardized subcomponents describing the relative contributions of BP, cerebrovascular resistance index (CVRi), critical closing pressure (CrCP), and resistance area product (RAP). The area under the curve (AUC) was calculated for changes in relation to baseline values. A total of 25 preeclamptic (before treatment) and 25 normotensive women in the second half of pregnancy were enrolled, and, 21 patients in each group were included in the analysis. The increase in CBFV and EtCO2 was similar in both groups. However, the AUC for CVRi and RAP during BH was significantly different between the groups (3.05 ± 2.97 vs. -0.82 ± 4.98, P = 0.006 and 2.01 ± 4.49 vs. -2.02 ± 7.20, P = 0.037), indicating an early, transient increase in CVRi and RAP in the control group, which was absent in PE. BP had an equal contribution in both groups. Women with preeclampsia have an altered initial CVRi response to the BH maneuver. We propose that this is due to blunted sympathetic or myogenic cerebrovascular response in women with preeclampsia.