Abstracts

Rationale: Transient loss of consciousness (TLOC) may be developed by much other causes. We must consider syncope as differential causes. In syncope, transient global cerebral hypoperfusion result in TLOC. Therefore, in all types of syncope, global cerebral hypoperfusion must be present with or without systemic hypotension. Grubb first demonstrated that cerebral vasoconstriction in the absence of systemic hypotension occurs concomitant with or precedes TLOC by use of transcranial doppler (TCD) ultrasonography done during head-up right tilt table test (HUTT) at 1998. This type of syncope was defined as cerebral syncope and isolated paradoxical cerebrovasoconstriction. We performed HUTT associated with TCD in patients with TLOC for analyzing incidence of cerebral syncope.Methods: We included 296 patients (164 females, 132 males, mean age 44.03 years) who experienced TLOC at least one episode from January, 2009 to March, 2012. We performed HUTT associated with TCD by Italian protocol (nitroglycerin challenge). The middle cerebral artery systolic velocity (Vs), diastolic velocity (Vd), mean velocity (Vm), and pulsatility index (PI=Vs-Vd/Vm) were continuously measured and assessed by TCD. We classified syncopes as mixed, cardioinhibitory, vasodepressor, paroxysmal orthostatic tachycardia syndrome (POTS), cerebral type according to changes of heart rate, arterial pressure, cerebral blood flow velocity (CBFV) and then analyzed cerebral cases.Results: In total 296 patients (164 females, 132 males, mean age 44.03 years), positive response group was 224 (75.7%) patients (129 females, 95 males, mean age 40.3years). Of the syncopal events during tilt testing, 46 (20.5%) patients as cerebral type, each 19 (42.2%) and 27 (15.1%) patients in baseline and provocation stage. The change of CBFV in TCD was that Vd and Vm decreased but PI increased. This CBFV decreased before change of arterial pressure during HUTT with TCD in all patients with syncope. Conclusions: CBFV begins to change before arterial pressure begins to fall. These results suggest that altered cerebrovascular autoregulation contributes to physiologic changes leading to syncope. Especially in patients with syncope who have not synchronized systemic hypotension, we must consider cerebral syncope as differential cause of TLOC due to incidence of cerebral case is not infrequent.