Syncope is a common clinical problem in a general population that is responsible for a significant number of emergency department visits (3%) and hospitalizations (1%) each year. The clinical spectrum of etiologies of syncope includes disorders classified as cardiovascular, noncardiovascular and unexplained. A majority of syncopal events are believed to be caused by vasovagally mediated episodes by hypotension and bradycardia. Although vasovagal syncope is essentially equivalent to simple fainting, the physiologic events that lends to this phenomena are complex. Although not completely understood, the most commonly held theory explaining vasovagal syncope involves a series of reflexive interactions between cardiac mechanoreceptors and the autonomic nervous system. Until the advent of head upright tilt table testing, diagnosis of vasovagal syncope has been an assumption, made when all other causes have been eliminated. Frequently an accurate history, a physical examination and a standard ECG are enough to formulate a correct diagnosis. Head-up tilt test must be considered in patients with an unknown diagnosis, before starting invasive investigation. Tilt table testing, either alone or with a graded-dose infusion of isoproterenol, allows reproduction of the syncopal event in susceptible individuals and monitoring of the patients physiologic responses during the episode. Direct observation and documentation of symptoms permit accurate diagnosis and yield information vital to treatment and symptom control. This article reviews our current understanding of the mechanisms involved in the development of neurally mediated syncope.