Neurally mediated syncope may occur in patients whose hemodynamic picture d
oes not fit the characteristics of orthostatic intolerance as decribed else
where in this issue. Nonetheless, patients who suffer from neurocardiogenic
or vasovagal syncope may be seriously incapacitated by their episodes of s
yncope or presyncope. Although it has been assumed that vagal activation as
a result of stimulation of ventricular mechanoreceptors is essential to th
e production of these episodes, several critical observations are presented
that suggest that other mechanisms may also be operative in some patient s
ubsets. In addition, evidence is presented that the sympathetic responses o
f many of these patients may be reduced rather than increased and that abno
rmal baroreflex responsiveness may also play an causative role. These findi
ngs suggest new avenues for therapy in this field in which carefully contro
lled, randomized, double-blind trials are scarce.