In a sweat over the riddle of reflex syncope

Dijk, J. Gert van

doi:10.1007/s10286-004-0214-y

Cited by 2 publications

(2 citation statements)

References 8 publications

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“…Clinical cardiologists consider fear-triggered vasovagal fainting "puzzling" since it is "hemodynamically paradoxical" (Benditt et al, 2004;Van Dijk, 2004). However, as we have argued elsewhere (Bracha et al, 2005a;Bracha, 2004) based on the last decade of work on PTSD's proximal-neurobiology, it may be helpful for neurocardiologists to re-conceptualize the simultaneous bradycardia and vasodilatation which are the defining features of fainting during real or perceived inescapable threat as akin to a protective "self-administered propranolol-prazosin combination" or (more physiologically accurately) "self-administered clonidine."…”

Section: Fright-triggered Bradycardic Fainting As Protection For the mentioning

confidence: 99%

“…FIMS (efferent vasovagal syncope of malignant severity) is the most common indication for insertion of a pacemaker in young adults in the US. Malignant (lethal) vasovagal syncope has been perplexing to cardiologists who consider its etiology "puzzling" and a "riddle" (Benditt et al, 2004;Van Dijk, 2004), but as we have argued in two recent articles (Bracha et al, 2005a;Bracha, 2004), reflex vasovagal syncope of malignant severity may simply represent the extreme pathological tail of heart rate variability described above as a key component of fear-induced fainting. FIMS is arguably the best physiological explanation not only for karoshi and for Voodoo death, but also for the historical and ethnographic reports of healthy individuals being "stricken dead" by a verbal threat.…”

Section: Taijin-kyofushomentioning

confidence: 99%

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Human brain evolution and the “Neuroevolutionary Time-depth Principle:” Implications for the Reclassification of fear-circuitry-related traits in DSM-V and for studying resilience to warzone-related posttraumatic stress disorder

Bracha

2006

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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The DSM-III, DSM-IV, DSM-IV-TR and ICD-10 have judiciously minimized discussion of etiologies to distance clinical psychiatry from Freudian psychoanalysis. With this goal mostly achieved, discussion of etiological factors should be reintroduced into the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V). A research agenda for the DSM-V advocated the "development of a pathophysiologically based classification system". The author critically reviews the neuroevolutionary literature on stress-induced and fear circuitry disorders and related amygdala-driven, species-atypical fear behaviors of clinical severity in adult humans. Over 30 empirically testable/ falsifiable predictions are presented. It is noted that in DSM-IV-TR and ICD-10, the classification of stress and fear circuitry disorders is neither mode-of-acquisition-based nor brain-evolution-based. For example, snake phobia (innate) and dog phobia (overconsolidational) are clustered together. Similarly, research on blood-injection-injury-type-specific phobia clusters two fears different in their innateness: 1) an arguably ontogenetic memory-trace-overconsolidation-based fear (hospital phobia) and 2) a hardwired (innate) fear of the sight of one's blood or a sharp object penetrating one's skin. Genetic architecture-charting of fear-circuitry-related traits has been challenging. Various, non-phenotype-based architectures can serve as targets for research. In this article, the author will propose one such alternative genetic architecture. This article was inspired by the following: A) Nesse's "Smoke-Detector Principle", B) the increasing suspicion that the "smooth" rather than "lumpy" distribution of complex psychiatric phenotypes (including fear-circuitry disorders) may in some cases be accounted for by oligogenic (and not necessarily polygenic) transmission, and C) insights from the initial sequence of the chimpanzee genome and comparison with the human genome by the Chimpanzee Sequencing and Analysis Consortium published in late 2005. Neuroevolutionary insights relevant to fear circuitry symptoms that primarily emerge overconsolidationally (especially Combat related Posttraumatic Stress Disorder) are presented. Also introduced is a humanevolution-based principle for clustering innate fear traits. The "Neuroevolutionary Time-depth Principle" of innate fears proposed in this article may be useful in the development of a neuroevolution-based taxonomic re-clustering of stress-triggered and fear-circuitry disorders in DSM-V. Four broad clusters of evolved fear circuits are proposed based on their time-depths: 1) Mesozoic (mammalian-wide) circuits hardwired by wildtype alleles driven to fixation by Mesozoic selective sweeps; 2) Cenozoic (simian-wide) circuits relevant to many specific phobias; 3) mid Paleolithic and upper Paleolithic (Homo sapiens-specific) circuits (arguably resulting mostly from mate-choice-driven stabilizing selection); 4) Abbreviations: WR-PTSD, warzone-related posttraumatic stress disorder; FOXP2, forkhead box ...

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Section: Fright-triggered Bradycardic Fainting As Protection For the mentioning

confidence: 99%

Section: Taijin-kyofushomentioning

confidence: 99%

Human brain evolution and the “Neuroevolutionary Time-depth Principle:” Implications for the Reclassification of fear-circuitry-related traits in DSM-V and for studying resilience to warzone-related posttraumatic stress disorder

Bracha

2006

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Genetic aspects of vasovagal syncope: a systematic review of current evidence

et al. 2008

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Knowledge on the aetiology of vasovagal syncope (VVS) is of great importance to optimize its diagnostic and therapeutic options. To unravel the largely unknown pathophysiology, studies on genetic aspects of VVS can be of use. This systematic review on all available literature aims to provide an overview of the current knowledge of VVS genetics. The MEDLINE and EMBASE database were systematically searched for all studies discussing genetic factors as a cause of VVS. Hereditary aspects of VVS were studied in 19 studies. Six studies determined a positive family history in, respectively, 19-90% of the VVS patients. These numbers, however, are not higher than the cumulative incidence of VVS in the general population (35-39%). Four studies examined potential genetic polymorphisms associated with VVS. Only a Gly389 allele was more frequently present in VVS patients with a positive HUT test, although the significance level was set much higher than usual in genetic studies, and this result has not been replicated so far. Knowledge on genetic aspects of VVS could be very useful in clinical practice and research, but the current evidence that it has a genetic basis is not very strong.

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In a sweat over the riddle of reflex syncope

Cited by 2 publications

References 8 publications

Human brain evolution and the “Neuroevolutionary Time-depth Principle:” Implications for the Reclassification of fear-circuitry-related traits in DSM-V and for studying resilience to warzone-related posttraumatic stress disorder

Human brain evolution and the “Neuroevolutionary Time-depth Principle:” Implications for the Reclassification of fear-circuitry-related traits in DSM-V and for studying resilience to warzone-related posttraumatic stress disorder

Genetic aspects of vasovagal syncope: a systematic review of current evidence

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