New insights into the mechanism of neurally mediated syncope

Abstract

Objective: To determine the role of the cerebral cortex in neurally mediated syncope, the electroencephalograms (EEG) of patients recorded during head up tilt table test were analysed.

Design: Retrospective study.

Setting: University hospital.

Patients: 18 patients with syncope or near syncope underwent head up tilt table test with simultaneous ECG and EEG monitoring.

Methods: Standard 70 degrees tilt table test was done with simultaneous ECG and EEG monitoring. EEG waveforms were analysed by both visual inspection and spectral analysis.

Results: 6 of 18 patients (33%) had a positive tilt table test. Before syncope slow waves increased in patients with a positive test. In addition, five of six tilt positive patients (83%) had slow wave activity that lateralised to the left side of the brain (mean (SD) 822 (724) v 172 (215) micro V(2), p < 0.05), while none of the tilt negative patients exhibited lateralisation (24 (15) v 26 (19) micro V(2), NS). Spectral analysis showed that the lateralisation occurred in the delta frequency. The lateralisation preceded the event by 5-56 seconds (18 (21) seconds).

Conclusions: EEG activity lateralises to the left hemisphere of the brain before syncope. The lateralisation precedes syncope and is associated with the onset of bradycardia, hypotension, and clinical symptoms. These findings suggest that the central nervous system may have a role in neurally mediated syncope.

Figure 1

Typical electroencephalographic (EEG) findings in patients with neurocardiogenic syncope. Top: 15 selected EEG channels. A channels: left central temporal region; B channels, right central temporal region (B); C channels: left frontotemporal region; D channels: right frontotemporal area. Bottom: topographs of the δ frequency band. The front of the head is on top on each topograph. The amplitude of the δ wave is represented by a colour gradient with black being the lowest and white the highest. Increased δ activity appears first over the left hemisphere as denoted by the rectangle and the corresponding topograph (open arrow). The amplitude of the δ activity increases but remains lateralised to the left hemisphere as shown on the third topograph (solid arrow).

Figure 2

Peak δ activities of left and right cerebral cortex in patients with tilt positive and negative results. Tilt positive patients have significant lateralisation of δ activity before syncope. The difference between left and right peak δ activity in tilt positive patients was significant (p < 0.05).

Figure 3

Topographic views of δ activity in tilt positive patients before syncope are shown. Peak δ activity is lateralised and localised to the left hemisphere (solid arrows). The areas of high amplitude seen in the frontal region and the occipital region are caused by artefacts from lead dislodgment and eye movements (open arrow).

Figure 4

The δ activity (Delta) in the left temporal lobe and heart rate changes (HR) over 30 seconds before syncope in a patient with typical cardioinhibitory response. Peak δ activity precedes the drop in heart rate.