Pathophysiological basis of syncope and neurological conditions that mimic syncope

Abstract

The definition of syncope has clinical and pathophysiological parts. The clinical part is that syncope is a form of transient loss of consciousness (TLOC), while the pathophysiological element is that syncope differs from other forms of TLOC by virtue of the basis of true syncope - specifically cerebral hypoperfusion. As such, the signs and symptoms of syncope rely on three steps, starting with the cause of syncope and including the response of the systemic circulation and neurological effects. The causes of syncope all result in low blood pressure through low peripheral resistance and/or low cardiac output. The next step is the cerebral circulation, which is a large-volume and low-resistance system, characterized by relatively high diastolic flow. The cerebral circulation is usually protected against swings in arterial pressure by cerebral autoregulation, but in abrupt syncope, autoregulation acts too slowly to have much effect. In syncope, diastolic flow velocity is more impaired than systolic flow velocity, probably because closing vascular forces then opposes flow. The third step concerns neurological signs and symptoms; the cerebral cortex first responds by disruption of normal activity, followed by a complete cessation of activity when hypoperfusion deepens. The latter is likely when there is asystole or marked bradycardia. The neurological signs and symptoms suggest different principles: a loss of normal cortical activity, abnormal cortical activity and activity due to disinhibition of brainstem activity.