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Neurovisceral phenotypes in the expression of psychiatric symptoms
This review explores the proposal that vulnerability to psychological symptoms, particularly anxiety, originates in constitutional differences in the control of bodily state, exemplified by a set of conditions that include Joint Hypermobility, Postural Tachycardia Syndrome and Vasovagal Syncope. Res...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4322642/ https://www.ncbi.nlm.nih.gov/pubmed/25713509 http://dx.doi.org/10.3389/fnins.2015.00004 |
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author | Eccles, Jessica A. Owens, Andrew P. Mathias, Christopher J. Umeda, Satoshi Critchley, Hugo D. |
author_facet | Eccles, Jessica A. Owens, Andrew P. Mathias, Christopher J. Umeda, Satoshi Critchley, Hugo D. |
author_sort | Eccles, Jessica A. |
collection | PubMed |
description | This review explores the proposal that vulnerability to psychological symptoms, particularly anxiety, originates in constitutional differences in the control of bodily state, exemplified by a set of conditions that include Joint Hypermobility, Postural Tachycardia Syndrome and Vasovagal Syncope. Research is revealing how brain-body mechanisms underlie individual differences in psychophysiological reactivity that can be important for predicting, stratifying and treating individuals with anxiety disorders and related conditions. One common constitutional difference is Joint Hypermobility, in which there is an increased range of joint movement as a result of a variant of collagen. Joint hypermobility is over-represented in people with anxiety, mood and neurodevelopmental disorders. It is also linked to stress-sensitive medical conditions such as irritable bowel syndrome, chronic fatigue syndrome and fibromyalgia. Structural differences in “emotional” brain regions are reported in hypermobile individuals, and many people with joint hypermobility manifest autonomic abnormalities, typically Postural Tachycardia Syndrome. Enhanced heart rate reactivity during postural change and as recently recognized factors causing vasodilatation (as noted post-prandially, post-exertion and with heat) is characteristic of Postural Tachycardia Syndrome, and there is a phenomenological overlap with anxiety disorders, which may be partially accounted for by exaggerated neural reactivity within ventromedial prefrontal cortex. People who experience Vasovagal Syncope, a heritable tendency to fainting induced by emotional challenges (and needle/blood phobia), are also more vulnerable to anxiety disorders. Neuroimaging implicates brainstem differences in vulnerability to faints, yet the structural integrity of the caudate nucleus appears important for the control of fainting frequency in relation to parasympathetic tone and anxiety. Together there is clinical and neuroanatomical evidence to show that common constitutional differences affecting autonomic responsivity are linked to psychiatric symptoms, notably anxiety. |
format | Online Article Text |
id | pubmed-4322642 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-43226422015-02-24 Neurovisceral phenotypes in the expression of psychiatric symptoms Eccles, Jessica A. Owens, Andrew P. Mathias, Christopher J. Umeda, Satoshi Critchley, Hugo D. Front Neurosci Neurology This review explores the proposal that vulnerability to psychological symptoms, particularly anxiety, originates in constitutional differences in the control of bodily state, exemplified by a set of conditions that include Joint Hypermobility, Postural Tachycardia Syndrome and Vasovagal Syncope. Research is revealing how brain-body mechanisms underlie individual differences in psychophysiological reactivity that can be important for predicting, stratifying and treating individuals with anxiety disorders and related conditions. One common constitutional difference is Joint Hypermobility, in which there is an increased range of joint movement as a result of a variant of collagen. Joint hypermobility is over-represented in people with anxiety, mood and neurodevelopmental disorders. It is also linked to stress-sensitive medical conditions such as irritable bowel syndrome, chronic fatigue syndrome and fibromyalgia. Structural differences in “emotional” brain regions are reported in hypermobile individuals, and many people with joint hypermobility manifest autonomic abnormalities, typically Postural Tachycardia Syndrome. Enhanced heart rate reactivity during postural change and as recently recognized factors causing vasodilatation (as noted post-prandially, post-exertion and with heat) is characteristic of Postural Tachycardia Syndrome, and there is a phenomenological overlap with anxiety disorders, which may be partially accounted for by exaggerated neural reactivity within ventromedial prefrontal cortex. People who experience Vasovagal Syncope, a heritable tendency to fainting induced by emotional challenges (and needle/blood phobia), are also more vulnerable to anxiety disorders. Neuroimaging implicates brainstem differences in vulnerability to faints, yet the structural integrity of the caudate nucleus appears important for the control of fainting frequency in relation to parasympathetic tone and anxiety. Together there is clinical and neuroanatomical evidence to show that common constitutional differences affecting autonomic responsivity are linked to psychiatric symptoms, notably anxiety. Frontiers Media S.A. 2015-02-10 /pmc/articles/PMC4322642/ /pubmed/25713509 http://dx.doi.org/10.3389/fnins.2015.00004 Text en Copyright © 2015 Eccles, Owens, Mathias, Umeda and Critchley. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neurology Eccles, Jessica A. Owens, Andrew P. Mathias, Christopher J. Umeda, Satoshi Critchley, Hugo D. Neurovisceral phenotypes in the expression of psychiatric symptoms |
title | Neurovisceral phenotypes in the expression of psychiatric symptoms |
title_full | Neurovisceral phenotypes in the expression of psychiatric symptoms |
title_fullStr | Neurovisceral phenotypes in the expression of psychiatric symptoms |
title_full_unstemmed | Neurovisceral phenotypes in the expression of psychiatric symptoms |
title_short | Neurovisceral phenotypes in the expression of psychiatric symptoms |
title_sort | neurovisceral phenotypes in the expression of psychiatric symptoms |
topic | Neurology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4322642/ https://www.ncbi.nlm.nih.gov/pubmed/25713509 http://dx.doi.org/10.3389/fnins.2015.00004 |
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