Tilt table testing in neurology and clinical neurophysiology

Paroxysmal Cerebral Disorder

Temporal Relationship of Asystole to Onset of Transient Loss of Consciousness in Tilt-Induced Reflex Syncope

ObjectivesThe purpose of this study was to investigate the relationship between the onset of asystole and transient loss of consciousness (TLOC) in tilt-induced reflex syncope and estimate how often asystole was the principal cause of TLOC.BackgroundThe presence of asystole in vasovagal syncope (VVS) may prompt physicians to consider pacemaker therapy for syncope prevention, but the benefit of pacing is limited in VVS.MethodsWe evaluated electrocardiography, electroencephalography, blood pressure, and clinical findings during tilt-table tests. Inclusion required TLOC (video), electroencephalographic slowing, accelerating blood pressure decrease, and an RR interval ≥3 s. We excluded cases with nitroglycerin provocation. Asystole after onset of TLOC (group A) or within 3 seconds before TLOC (group B) was unlikely to cause TLOC, but an earlier start of asystole (group C) could be the cause of TLOC.ResultsIn one-third of 35 cases (groups A [n = 9] and B [n = 3]), asystole was unlikely to be the primary cause of TLOC. The median of the mean arterial pressure at the onset of asystole was higher when asystole occurred early (45.5 mm Hg, group C) than when it occurred late (32.0 mm Hg, groups A and B), which suggests that vasodepression was not prominent at the start of asystole in early asystole, further suggesting that early asystole was the prime mechanism of syncope.ConclusionsIn one-third of cases of tilt-induced asystolic reflex syncope, asystole occurred too late to have been the primary cause of TLOC. Reliance on electrocardiography data only is likely to overestimate the importance of asystole.</div

long-term follow-up of psychogenic pseudosyncope

Objective: To determine the outcome of patients with psychogenic pseudosyncope (PPS) aftercommunication of the diagnosis.Methods: This was a retrospective cohort study of patients with PPS referred in 2007 to 2015 toa tertiary referral center for syncope. We reviewed patient records and studied attack frequency,factors affecting attack frequency, health care use, and quality of life using a questionnaire. Weexplored influences on attack freedom and attack frequency in the 6 months before follow-up forage, sex, education level, duration until diagnosis, probability of diagnosis, additional syncope,and acceptance of diagnosis.Results: Forty-seven of 57 patients with PPS could be traced, of whom 35 (74%) participated.Twelve (34%) were attack-free for at least 6 months. The median time from diagnosis tofollow-up was 50 months (range 6–103 months). Communicating and explaining the diagnosisresulted in immediate reduction of attack frequency (p 5 0.007) from the month before diagnosis(median one attack, range 0–156) to the month after (median one attack, range 0–16). In the6 months before follow-up, the number of admissions decreased from 19 of 35 to 0 of 35 (p 50.002). The use of somatic and mental health care shifted toward the latter (p , 0.0001). Qualityof life at follow-up (Short Form Health Survey 36) showed lower scores for 7 of 8 domainscompared to matched Dutch control values; quality of life was not influenced by attack freedom.Conclusions: After communication of the diagnosis in PPS, attack frequency decreased andhealth care use shifted toward mental care. Low quality of life underlines that PPS is a serious condition. Paroxysmal Cerebral Disorder

Five cases of complete atrioventricular block induced by bending forward: unusual but not unique

Aims We describe five patients with syncope caused by a complete atrioventricular block (AVB) while they were bending forward, not rising after bending, and aim to describe the occurrence and the association between bending forward and AVB.Methods and results In two patients, bending forward was the exclusive trigger for syncope, while in the remaining three, other postural changes (sitting down, standing up, and exertion) could also provoke syncope. Complete AVB as the cause of syncope was documented using ECG monitoring in two cases and an implantable loop recorder in the other three. Ectopic beats without preceding sinus slowing occurred before syncope in four cases. Two cases had a left bundle branch block. All patients responded favourably to cardiac pacing.Conclusion This is the first case series on complete AVB provoked by bending forward. Syncope during bending forward should suggest a search for an AVB. Arguments in favour of a vagal mechanism were syncope triggered by bending forward, and that other triggers could also evoke syncope. However, the absence of sinus slowing before syncope in some cases and the fact that bending forward did not seem to provoke reflex syncope without AVB, cast doubts on a reflex mechanism. There were also arguments favouring conduction disorder: i.e. ectopic beats before syncope and pre-existing conduction disturbances in two cases. The cases are reminiscent of paroxysmal AVB. Discrimination between paroxysmal AVB and vagal AVB is important because a pacemaker is warranted in arrhythmic complete AVB, while the benefit is limited or absent in reflex AVB.Paroxysmal Cerebral Disorder

Abnormal cardiovascular response to nitroglycerin in migraine

Paroxysmal Cerebral Disorder

Influence of Age on Magnitude and Timing of Vasodepression and Cardioinhibition in Tilt-Induced Vasovagal Syncope

BACKGROUND Cardioinhibition may diminish with age, but the changing balance of cardioinhibition and vasodepression with age has not been quantified, leaving the mechanism of vasovagal syncope (VVS) in old age unclear.OBJECTIVES This study sought to quantify age-related changes of vasodepression and cardioinhibition in tilt-induced VVS.METHODS We studied 163 cases of tilt-induced WS, evoked using the Italian protocol with blood pressure, heart rate, and video-etectroencephalographic monitoring. Presyncope was excluded. Cardioinhibition was defined as the heart rate decrease before syncope; asystotic pauses (>= 3 seconds) were divided into early and late asystole, ie, beginning early enough to or too late to be the major cause of toss of consciousness. The log-ratio method was used to quantify contributions of cardioinhibition and vasodepression, assessed in 2 10-second periods before the onset of cardioinhibition and before syncope.RESULTS With increasing age, cardioinhibition decreased, ie, heart rate decreased less and more slowly near syncope (P < 0.0001), white vasodepression increased. Asystotic pauses were less frequent in the older one-half of the group than the younger one-half (26% vs 57%; P < 0.00001), but when it did, late asystole occurred more often (58% vs 15%; P < 0.001).CONCLUSIONS The shift toward less cardioinhibition and more vasodepression with increased age probably reflects a physiological shift in circulatory control. The weakening of cardioinhibition with age may detract from the efficacy of pacing in older patients with VVS. Cardioinhibition-vasodepression balance should be considered in pacing decisions in older subjects with VVS. (C) 2022 by the American College of Cardiology Foundation.Neurological Motor Disorder