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Front Neurosci. 2015 Feb 10;9:4. doi: 10.3389/fnins.2015.00004. eCollection 2015.

Neurovisceral phenotypes in the expression of psychiatric symptoms.

Author information

1
Psychiatry, Brighton and Sussex Medical School Brighton, UK ; Sussex Partnership National Health Service Foundation Trust Brighton, UK.
2
National Hospital Neurology and Neurosurgery, UCL National Health Service Trust London, UK ; Institute of Neurology, University College London London, UK.
3
National Hospital Neurology and Neurosurgery, UCL National Health Service Trust London, UK ; Department of Psychology, Keio University Tokyo, Japan.
4
Psychiatry, Brighton and Sussex Medical School Brighton, UK ; Sussex Partnership National Health Service Foundation Trust Brighton, UK ; Sackler Centre for Consciousness Science, University of Sussex Falmer, UK.

Abstract

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.

KEYWORDS:

anxiety; joint hypermobility; postural tachycardia syndrome; psychiatry; vasovagal syncope

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