Central and cardiovascular responses to emotional stimuli are normal in non-phobic subjects with Reflex Syncope
Abstract Objective Reflex Syncope (RS) is a self-limited loss of consciousness due to systemic arterial hypotension resulting from widespread vasodilatation and/or bradycardia. Higher neural centres have been implicated in the pathophysiology of RS, particularly in blood/injury phobic patients. We i...
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Veröffentlicht in: | Clinical neurophysiology 2008-09, Vol.119 (9), p.1966-1972 |
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Zusammenfassung: | Abstract Objective Reflex Syncope (RS) is a self-limited loss of consciousness due to systemic arterial hypotension resulting from widespread vasodilatation and/or bradycardia. Higher neural centres have been implicated in the pathophysiology of RS, particularly in blood/injury phobic patients. We investigated interictal central autonomic functions in non-phobic RS subjects compared to non-phobic controls evaluating their central and cardiovascular responses to emotional stimuli. Methods Cardiovascular responses to Valsalva Manoeuvre (VM), Deep Breathing (DB) and during presentation of 108 slides selected from the International Affective Picture System were assessed in 20 non-phobic RS subjects and 20 controls. Slide onset visual event-related potentials (ERPs) were also computed. Results No significant difference in cardiovascular responses and ERP amplitude were found in non-phobic RS subjects and controls at rest, in response to VM and DB or during picture presentation. Conclusions Non-phobic patients with RS not only have a normal interictal autonomic control of the cardiovascular system but also a normal modulation and adaptation of central and cardiovascular response to emotional processing, in our experimental setting. Significance Non-phobic patients with RS present normal interictal central and cardiovascular responses. Autonomic dysfunction observed in phobic RS patients could be related to mechanisms underlying the phobia itself rather than the mechanisms causing RS. |
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ISSN: | 1388-2457 1872-8952 |
DOI: | 10.1016/j.clinph.2008.03.033 |