Many of the primary symptoms of orthostatic intolerance (fatigue, diminished concentration) as well as some of the premonitory symptoms of neurally mediated syncope (NMS) are thought to be due to cerebral hypoperfusion. Transcranial Doppler measurements of middle cerebral artery blood velocity (CBV) is at present the only technique for assessing rapid changes in cerebral blood flow, and hence for evaluating dynamic cerebral autoregulation. However, controversies exist regarding data interpretation. At syncope, during the collapse of blood pressure (BP), diastolic CBV diminishes, whereas systolic CBV is maintained. Some consider this increase in CBV pulsatility to be indicative of a paradoxical increase in cerebrovascular resistance (CVR) prior to syncope. Others note that mean CBV decreases much less than does mean BP, implying that cerebral autoregulatory mechanisms are intact and functioning at syncope. Similarly, there is no evidence of impaired dynamic cerebral autoregulation, as measured by standard linear transfer-function analysis, in patients with NMS. Some patients with exaggerated postural tachycardia (POTS) have been found to have an excessive decrease in CBV during head-up tilt. Controversy exists as to whether this decrease results from an excessive sympathetic outflow to the cerebral vasculature or from hyperventilation. However, many other equally symptomatic patients with a similar hemodynamic profile of exaggerated tachycardia during head-up tilt have normal CBV changes during this maneuver and have normal dynamic cerebral autoregulation as determined by transfer-function analysis. Whether these discrepancies reflect different pathologies in patients with POTS is currently unknown.