EEG-recordings during syncope
J.G van Dijk* and W. Wieling§ Department of Neurology * , Leiden University Medical Centre Department of Medicine § , Academic Medical Centre, University of Amsterdam, Amsterdam (The Netherlands)
These are tilt table results from a 14-years old girl with recurrent vasovagal syncope. The period shown lasted 30 seconds and occurred 5 minutes after tilting. Blood pressure had already gradually dropped to 70/50 mm Hg and heart rate had slowed to 51 beats per minute, when asystole set in, lasting for 11 seconds. After about 7 seconds of asystole the EEG changed from a normal alpha rhythm to slow large delta waves, which lasted for about 4 seconds. Consciousness was lost. Then the EEG was flat for 7 seconds. The tilt table returned to the horizontal position in this period. The resumption of cortical activity started 9 seconds after the first heart beat following asystole. The EEG then changed in the reverse order. Some myoclonic jerks were observed, and can be recognised in the ECG channel. Only four EEG channels are shown (right frontal and occipital, left frontal and occipital). The ECG shows some movement artifacts. Blood pressure was measured with a Finapress device.
During syncope the EEG in our patient showed a progressive slowing with an increase in amplitude, followed by a sudden reduction of brain-wave amplitude, resulting in a “flat” EEG. The end of syncope was accompanied by changes in the reverse order, giving rise to a typical ‘slow-flat-slow’ pattern. Myoclonic jerks occurred during the slow and flat stages of the EEG. These findings are in concordance with observations following eyeball pressure and carotid sinus massage to induce abrupt onset asystolic syncope , for review see . Asystole lasting 3-6 seconds produces no EEG abnormalities and almost no clinical symptoms, except possibly unclear thinking. However, after 7-13 seconds of asystole slow waves (theta and delta) appear, followed by abrupt flattening. This change is accompanied by rapid clouding and then complete loss of consciousness. With asystole longer than 10-14 seconds myoclonic jerks can be observed, sometimes followed by a generalized tonic spasm in extension and even opisthotonus, while on the EEG there is cortical silence . EEG findings during presyncope and syncope induced by tilt-table testing  show similar, but more variable patterns than syncope induced by the fainting lark and eyeball pressure. The slower fall in systemic blood pressure during vasovagal syncope may be involved.
The myoclonic activity during a prolonged syncopal episode is postulated to originate from the reticular formation; a release phenomenon of the lower brainstem neurons no longer suppressed by higher centres is postulated . It is, however, unknown why sometimes they do and sometimes they do not appear. Cerebral hypoxia has potent epileptogenic effects, therefore hyperventilation (causing cerebral vasoconstriction) is routinely used during EEG recordings to activate epileptic discharges . Nevertheless, only a few EEG documented epileptic seizures evolving from syncope have been reported. Almost all of the cases involve young children. Only one adult case has been reported .
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