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A fall in cerebral perfusion is the final common pathway leading to syncope. While we commonly investigate syncope as though the only cause of loss of perfusion is loss of arterial pressure, there is another possible contributing factor: failure of cerebral autoregulation.1
IS CEREBRAL AUTOREGULATION AT FAULT IN SYNCOPAL PATIENTS?
Cerebral autoregulation is the intrinsic ability of cerebral vasculature to maintain constant cerebral blood flow over a wide range of cerebral perfusion pressures.2–4 If this autoregulation is deranged, cerebral perfusion is less able to resist a decline when arterial blood pressure falls.
Clinical studies into cerebral autoregulation around the time of syncope can be carried out using provocation by head-up tilt or by lower-body negative pressure. Transcranial Doppler can be used to measure middle cerebral artery flow velocity. This can then be compared with arterial blood pressure to give an index of cerebrovascular resistance. Because both flow and pressure are fluctuating dynamically, it is useful to apply transfer function analysis to determine how the oscillatory components of the two are related.
Previous studies have provided conflicting data. It would be predicted that during vasovagal syncope, reduced cerebral perfusion should induce cerebral vasodilatation. However, it has been noted that head-up tilt leads to a decrease in diastolic velocity in the middle cerebral artery but preservation of systolic velocity in syncopal patients. Therefore there was a paradoxical rise in cerebral resistance, presumed to be secondary to arteriolar constriction.5
On the other hand, a comparison of controls with neurogenic syncope patients while undergoing head-up tilt, found no significant differences between the two groups with regards to transfer gain, coherence and phase …