CEREBRAL SYNCOPE - LOSS OF CONSCIOUSNESS ASSOCIATED WITH CEREBRAL VASOCONSTRICTION IN THE ABSENCE OF SYSTEMIC HYPOTENSION

Citation
Bp. Grubb et al., CEREBRAL SYNCOPE - LOSS OF CONSCIOUSNESS ASSOCIATED WITH CEREBRAL VASOCONSTRICTION IN THE ABSENCE OF SYSTEMIC HYPOTENSION, PACE, 21(4), 1998, pp. 652-658
Citations number
33
Categorie Soggetti
Cardiac & Cardiovascular System","Engineering, Biomedical
Journal title
PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY
ISSN journal
01478389 → ACNP
Volume
21
Issue
4
Year of publication
1998
Part
1
Pages
652 - 658
Database
ISI
SICI code
0147-8389(1998)21:4<652:CS-LOC>2.0.ZU;2-Y
Abstract
Transcranial Doppler (TCD) ultrasonography done during head-upright ti lt induced neurocardiogenic syncope has demonstrated that cerebral vas oconstriction occurs concomitant with (or precedes) loss of consciousn ess. This article demonstrates evidence that cerebral blood flow chang es alone (vasoconstriction), in the absence of systemic hypotension, m ay result in syncope. Five patients (4 men, 1 woman; mean age 41 +/- 1 7 years) with recurrent unexplained syncope were evaluated by use of a n upright tilt table test for 45 minutes with or without an infusion o f low dose isoproterenol. TCDoppler ultrasonography was used to assess middle cerebral artery systolic velocity (Vs); diastolic velocity (Vd ); mean velocity (Vm); and pulsatility index (PI = Vs = Vd/Vmean). Syn cope occurred in five patients during the baseline tilt and in one pat ient during isoproterenol infusion. During tilt induced syncope, at an average mean arterial pressure of 89 +/- 16 mmHg, TCD sonography show ed a 2% +/- 10% increase in systolic velocity; a 51% +/- 27% decrease in diastolic velocity and a 131% +/- 87% increase in pulsatility index . One patient underwent continuous electroencephalographic recording d uring tilt, which demonstrated diffuse slow wave activity (indicating cerebral hypoxia) at the time of syncope concomitant with the aforemen tioned TCD changes in the absence of systemic hypotension. These findi ngs reflect an increase in cerebrovascular resistance secondary to art eriolar vasoconstriction distal to the insonation point of the middle cerebral artery that occurred concomitant with loss of consciousness a nd in the absence of systemic hypotension. We conclude that in some in dividuals abnormal baroreceptor responses triggered during orthostatic stress may result in a derangement of cerebral autoregulation leading to cerebral vasoconstriction with resultant cerebral hypoxia in the a bsence of systemic hypotension.