Neural processes linking joint hypermobility and anxiety: Key roles for the amygdala and insular cortex

Read the full article See related articles

Listed in

This article is not in any list yet, why not save it to one of your lists.
Log in to save this article

Abstract

Background and Aims

Anxiety symptoms are elevated among people with joint hypermobility. The underlying neural mechanisms are attributed theoretically to effects of variant connective tissue on the precision of interoceptive representations contributing to emotions.

Methods

We used functional magnetic resonance neuroimaging (fMRI) to quantify regional brain responses to emotional stimuli (facial expressions) in patients with generalised anxiety disorder (N=30) and a non-anxious comparison group (N=33). All participants were assessed for joint laxity and were classified (using Brighton Criteria) for the presence and absence of Hypermobility Syndrome (HMS: now considered Hypermobility Spectrum Disorder).

Results

HMS participants showed attenuated neural reactivity to emotional faces in specific frontal (inferior frontal gyrus, pre-supplementary motor area), midline (anterior mid and posterior cingulate cortices), and parietal (precuneus and supramarginal gyrus) regions. Notably, interaction between HMS and anxiety was expressed in reactivity of left amygdala (a region implicated in threat processing) and mid insula (primary interoceptive cortex) where activity was amplified in HMS patients with generalised anxiety disorder. Severity of hypermobility in anxious, compared to non-anxious, individuals correlated with activity within anterior insula (implicated as the neural substrate linking anxious feelings to physiological state). Amygdala-precuneus functional connectivity was stronger in HMS, compared to non-HMS, participants.

Conclusions

The predisposition to anxiety in people with variant connective tissue reflects dynamic interactions between neural centres processing threat (amygdala) and representing bodily state (insular and parietal cortices). Correspondingly, interventions to regulate of amygdala reactivity while enhancing interoceptive precision may have therapeutic benefit for symptomatic hypermobile individuals.

Article activity feed