Variable cerebral dysfunction during tilt induced vasovagal syncope.

Electroencephalographic (EEG) monitoring was performed during head-up tilt testing (HUT) in a group of 63 consecutive patients (27 males, 36 females, mean age 41.5 years) with a history of recurrent syncope of unknown origin despite extensive clinical and laboratory evaluation. Syncope occurred in 27/63 patients (42.8%) during HUT and was cardioinhibitory in 11/27 (40.7%) and vasodepressor in 16/27 (59.3%). All patients with a negative response to HUT had no significant EEG modifications. In patients with vasodepressor syncope a generalized high amplitude 4-5 Hz (theta range) slowing of EEG activity appeared at the onset of syncope, followed by an increase in brain wave amplitude with a reduction of frequency at 1.5-3 Hz (delta range). The return to the supine position was associated with brain wave amplitude reduction and frequency increase to 4-5 Hz, followed by restoration of a normal EEG pattern and arousal (mean total duration of syncope 23.2 s). In patients with cardioinhibitory syncope, a generalized high amplitude EEG slowing in the theta range was noted at the onset of syncope, followed by a brain wave amplitude increase and slowing in the delta range. A sudden reduction of brain wave amplitude ensued leading to the disappearance of electroencephalographic activity ("flat" EEG). The return to the supine position was not followed by immediate resolution of EEG abnormalities or consciousness recovery, both occurring after a longer time interval (mean total duration of syncope 41.4 s). EEG monitoring during HUT allowed the recording and systematic description of electroencephalographic abnormalities developing in the course of tilt induced vasovagal syncope.

Electroencephalographic correlates of vasovagal syncope induced by head-up tilt testing.

BACKGROUND AND PURPOSE: We sought to determine whether the introduction of EEG monitoring during head-up tilt testing could significantly improve the understanding of the cerebral events occurring during tilt-induced vasovagal syncope and the potential danger to the patient of this diagnostic procedure. METHODS: EEG monitoring was performed during head-up tilt testing in a group of 63 consecutive patients (27 males and 36 females; mean age, 41.5 years) with a history of recurrent syncope of unknown origin despite extensive clinical and laboratory assessment. RESULTS: Syncope occurred in 27 of 63 patients (42.8%) during head-up tilt testing and was found to be cardioinhibitory in 11 of 27 (40.7%) and vasodepressor in 16 of 27 (59.3%). All patients with a negative response to head-up tilt testing showed no significant EEG modifications. In patients with vasodepressor syncope, a generalized high-amplitude, 4- to 5-Hz (theta range) slowing of EEG activity appeared at the onset of syncope, followed by an increase of brain-wave amplitude with the reduction of frequency at 1.5 to 3 Hz (delta range). The return to the supine position was associated with brain-wave amplitude reduction and frequency increase to 4 to 5 Hz, followed by restoration of a normal EEG pattern and arousal (mean total duration of syncope, 23.2 seconds.). In patients with cardioinhibitory syncope, a generalized high-amplitude EEG slowing in the theta range was noted at the onset of syncope, followed by a brain-wave amplitude increase and slowing in the delta range. A sudden reduction of brain-wave amplitude then ensued, leading to the disappearance of electrocerebral activity ("flat" EEG). The return to the supine position did not allow either the immediate resolution of EEG abnormalities or consciousness recovery, both of which occurred after a further time interval (mean total duration of syncope, 41.4 seconds.). CONCLUSIONS: EEG monitoring during head-up tilt testing allowed recording and systematic description of electrocerebral abnormalities developing in the course of tilt-induced vasovagal syncope.