Tilt table testing in the diagnosis of unexplained syncope.

While the investigation of the physiological and vasovagal syncope. The pathophysiology of the vasopathophysiological effects of orthostatic stress vagal response is thus central to an understanding induced by head-up tilt table testing in humans of the role of tilting in its diagnosis. began more than 50 years ago,1 it was not until 1986 Although central, higher cortical provocation of that the utility of tilt testing in the diagnosis of vasovagal syncope through emotional stress6 and unexplained syncope was demonstrated.2 In the pain7 is a clinical commonplace, the neuronal conabsence of a ‘gold-standard’ diagnostic test for vasovnections mediating the response are far from certain. agal syncope, an appropriate clinical history in Animal models implicate the limbic system as the association with a positive head-up tilt test currently relay region for stress-related neuronal activity,7,8 provides the cornerstone for the diagnosis of vasovawith the ultimate control mechanisms residing in gal syncope.3 This article will provide an overview hypothalamic and brain-stem autonomic nuclei.9 of the rationale for the head-up tilt test in relation to Human vasovagal syncope tends to present more its main diagnostic use, vasovagal syncope, a discusprosaically, with many episodes following periods of sion of the methodological issues surrounding the prolonged standing, for example in church or in test and the uses of tilt table testing in the further shopping queues. This observation led to the hypodifferential diagnosis of unexplained syncope. thesis that defective neurocardiovascular compensatory mechanisms during orthostatic stress were responsible for the initiation of the vasovagal casVasovagal syncope and the cade through an inappropriate Bezold-Jarisch-type reflex.10,11 Exaggerated venous pooling in capacipathophysiological rationale for tance vessels in the lower part of the body12 is head-up tilt testing thought to provoke relative central hypovolaemia7 with compensatory vigorous left ventricular contracMore than 60 years after the introduction of the term tion and sympathetic stimulation, resulting in inap‘vasovagal syncope’ by Lewis,4 the exact mechanisms propriate mechanoreceptor activation.13–15 The responsible for loss of consciousness associated with resultant afferent traffic is then relayed via unmyprofound hypotension and/or bradycardia, and medielinated vagal C-fibres to the nucleus tractus solitarius ated by vagal excess and sympathetic withdrawal, of the medulla16 which orchestrates the efferent limb remain uncertain. The main trigger factors for the of the vasovagal response by undetermined mechanvasovagal cascade can be divided into central and isms. Further support for this hypothesis is derived peripheral provocateurs,5 with the latter providing from the echocardiographic demonstration of vigorthe substrate for the diagnostic use of the tilt table. ous left ventricular contractions15 and relatively low Head-up tilt table testing provides a powerful, conventricular volumes17 in patients with tilt-induced trolled orthostatic stimulus simulating under laboratory conditions the peripheral provocation of syncope, but the demonstration of classic vasovagal