HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER
[Advanced]

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this link to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Add article to my folders
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mercader, M A
Right arrow Articles by Lee, S W
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mercader, M A
Right arrow Articles by Lee, S W
Heart 2002;88:217-221
© 2002 by Heart


CARDIOVASCULAR MEDICINE

New insights into the mechanism of neurally mediated syncope

M A Mercader1, P J Varghese1, S J Potolicchio2, G K Venkatraman2, S W Lee1

1 Division of Cardiology, Department of Medicine, The George Washington University, Washington DC, USA
2 Department of Neurology, The George Washington University

Correspondence to:
Correspondence to:
Dr P J Varghese, The George Washington University Medical Center, Department of Medicine, Division of Cardiology, 2150 Pennsylvania Avenue, NW, Suite 4–414, Washington DC 20037, USA;
domjxv{at}gwumc.edu

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° 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) µV2, p < 0.05), while none of the tilt negative patients exhibited lateralisation (24 (15) v 26 (19) µV2, 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.


Keywords: syncope; nervous system




This article has been cited by other articles:


Home page
HeartHome page
C T P Krediet, D L Jardine, P Cortelli, A G R Visman, and W Wieling
Vasovagal syncope interrupting sleep?
Heart, May 1, 2004; 90(5): e25 - e25.
[Abstract] [Full Text] [PDF]


Home page
CLIN PEDIATRHome page
S. O. Sapin
Autonomic Syncope in Pediatrics: A Practice-Oriented Approach to Classification, Pathophysiology, Diagnosis, and Management
Clinical Pediatrics, January 1, 2004; 43(1): 17 - 23.
[Abstract] [PDF]


Home page
Br J AnaesthHome page
N. N. Win, H. Kohase, T. Miyamoto, and M. Umino
Decreased bispectral index as an indicator of syncope before hypotension and bradycardia in two patients with needle phobia
Br. J. Anaesth., November 1, 2003; 91(5): 749 - 752.
[Abstract] [Full Text] [PDF]


Home page
HeartHome page
R Hainsworth
Syncope: what is the trigger?
Heart, February 1, 2003; 89(2): 123 - 124.
[Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS REGISTER
Terms and conditions relating to subscriptions purchased online  ¦  Website terms and conditions  ¦  Privacy policy
Copyright © 2002 BMJ Publishing Group Ltd & British Cardiovascular Society