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Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Carotid Sinus Syndrome Fainting and fits occurring due to an overactive carotid sinus reflex, following minimal stimulation of the carotid sinus. Described by Jean Marie Charcot (1825–1893) in 1872. It was described again and explained by American physician, Soma Weiss (1898–1942) in 1929 and by James Porter Baker (b 1913) in 1933.
Neck Holds
Published in Darrell L. Ross, Gary M. Vilke, Guidelines for Investigating Officer-Involved Shootings, Arrest-Related Deaths, and Deaths in Custody, 2018
While reflex bradycardia has been noted in a number of studies, there have been no reported deaths or bradycardic events to the point of requiring cardiac resuscitation in any of these studies (Arnold, 1999; Berk, Shea, & Crevey, 1991; Kornblum 1986a). Moreover, the medical literature is replete with studies looking at the use of carotid sinus massage as a diagnostic and therapeutic examination tool. In studies of thousands of uses on elderly patients, there were no complications of death or bradycardic events requiring treatment or resuscitation, even though this age group is traditionally more likely to have carotid sinus syndrome and more likely to be symptomatic from carotid sinus stimulation (Pollanen et al., 1998; Reay & Mathers, 1983). In fact, the diagnosis of carotid sinus syndrome, although well written about, is essentially unheard of in patients under the age of 50 years (Brignole & Menozzi, 1992; Coplan & Schweitzer, 1984; Kenny & Richardson, 2001; Mallet, 2003).
Autonomic dysfunction in dementia with Lewy bodies
Published in John O'Brien, Ian McKeith, David Ames, Edmond Chiu, Dementia with Lewy Bodies and Parkinson's Disease Dementia, 2005
Rose Anne Kenny, Louise M Allan
Carotid sinus syndrome (CSS) is diagnosed in subjects with otherwise unexplained recurrent syncope who have CSH. The syndrome is an important but frequently overlooked cause of syncope and presyncope in older subjects. The symptoms are usually precipitated by mechanical stimulation of the carotid
The future of cardioneuroablation in cardiovascular medicine
Published in Expert Review of Cardiovascular Therapy, 2022
Tolga Aksu, Asad Khan, Henry Huang
In a retrospective case-control study, we assessed the long-term effect of CNA versus conservative therapy in patients with cardioinhibitory type VVS [50]. The 4-year Kaplan-Meier syncope free rate was 0.86 (95% CI, 0.63–1.00) for CNA group and 0.50 (95% CI, 0.30–0.82) for conservative therapy group. In the first and only randomized controlled trial, Piotrowski et al. [51] compared CNA versus optimal nonpharmacologic therapy in patients with cardioinhibitory type VVS. A total of 48 patients (24 in fragmented electrogram-guided bi-atrial CNA group, 24 in control group) entered the study. The primary endpoint occurred in 2 patients (8%) from the CNA group versus 13 control patients (54%) (P = 0.0004). Quality of life significantly improved in the CNA group (p = 0.0001), whereas it remained stable in control patients. Štiavnický et al. [52] recently presented the use of CNA for the treatment of recurrent swallow syncope. The patient remained asymptomatic after empirical ablation of RSGP via right atrium during the 3-year follow-up. In another case report, CNA was successfully used to treat ictal asystole in a patient with pharmacoresistant focal epilepsy [53]. Lastly, bi-atrial anatomical CNA was performed in a 77-year-old woman with carotid sinus syndrome [54]. The patient was discharged with an implantable loop recorder. After 6 months, she remained free of any symptoms, and no bradyarrhythmias have been registered in ILR.
Syncope in patients with transthyretin amyloid cardiomyopathy: clinical features and outcomes
Published in Postgraduate Medicine, 2022
Gonzalo Barge-Caballero, Eduardo Barge-Caballero, Manuel López-Pérez, Raquel Bilbao-Quesada, Eva González-Babarro, Inés Gómez-Otero, Andrea López-López, Mario Gutiérrez-Feijoo, Alfonso Varela-Román, Carlos González-Juanatey, Óscar Díaz-Castro, María G. Crespo-Leiro
In the absence of an underlying structural or arrhythmic cause of syncope, neurally mediated reflex syncope was suspected if the episode of transient loss of consciousness was precipitated by pain, fear, or standing and was associated with typical progressive prodromes like pallor, sweating, and/or nausea (vasovagal type); if it occurred during or immediately after typical triggers like micturition, gastrointestinal stimulation – swallow, defecation –, cough, sneeze, or post-exercise (situational type); or if it was triggered by cervical stimulation and carotid sinus massage was positive and reproduced symptoms (carotid sinus syndrome). Orthostatic hypotension was considered as the most likely cause of syncope when the transient loss of consciousness occurred shortly after standing from supine/sitting position and the active standing maneuver revealed significant orthostatic hypotension. Syncopal episodes that did not qualify for any of these clinical categories were classified as unexplained syncope.