Key result
The pathophysiology and treatment of neurally mediated syncope are complex and multifactorial, with various treatment options showing conflicting results.
Neurally mediated syncope (NMS) is the result of a critical cerebral hypoperfusion. The pathophysiology of this abnormality is multifactorial. Optimal cerebral perfusion depends on an adequate functioning of the control mechanisms maintaining cerebral oxygen delivery. This includes baroreflex-induced adjustments of the systemic vascular resistance, intravascular volume regulation, and also cerebral autoregulation.1 The tool to diagnose NMS has been the tilt table test. The complexity of the pathophysiology of NMS is illustrated by the different types of syncope as a response to a tilt table test: cardioinhibitory with or without asystole, vasodepressor, and mixed type.1 Furthermore, the type of syncope can vary in the same patient from one tilt test to another.2 The treatment of NMS has been shown to be difficult, with conflicting results. Treatment options vary from vagolytic drugs, β-blocking agents, fludrocortisone (to increase plasma … *Corresponding author. Tel: +32 16 342181; fax: +32 16 342184. E-mail address : tony.reybrouck{at}uz.kuleuven.ac.be
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Reybrouck et al. (2007) conducted an editorial in Neurally mediated syncope. Exercise training was evaluated. The pathophysiology and treatment of neurally mediated syncope are complex and multifactorial, with various treatment options showing conflicting results.
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