Autonomic Reflex Laboratory, Department of Neurology, McGill University, Sir Mortimer B. Davis Jewish General Hospital, Montreal, Quebec, Canada H3T 1E2
Address for correspondence: Ronald Schondorf, Ph.D., M.D., Department of Neurology, Sir Mortimer B. Davis Jewish General Hospital, 3755 chemin de la Côte St. Catherine, Montreal, Quebec, Canada H3T 1E2. Voice: 514-340-8222, ext. 4767 or 3525; fax: 514-340-7567.
ronald.schondorf{at}mcgill.ca
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.
