Biologic hypotheses that have been proposed to explain the link between anxiety and JHS/hEDS are described in the Box6,16-28.
What underlying mechanisms link anxiety and joint hypermobility?
Interestingly, both anxiety and joint hypermobility syndrome/Ehlers-Danlos type 3-hypermobile type (JHS/hEDS) are often underdiagnosed and undertreated, and have similar prevalence in the general population. While it is possible that some psychiatric symptoms can be a consequence of adaptation and difficulties in dealing with chronic illnesses, biologic hypotheses have been considered to explain the association between JHS/hEDS and anxiety. The most accepted biologic hypotheses include:
- genetic risks
- interoceptive sensitivity
- somatosensory amplification
- emotion processing variances
- autonomic nervous system dysfunction.
A duplication of chromosome 15 (DUP-25) was found in patients with both JHS/hEDS and an anxiety disorder,16 but to date, this finding has not been replicated.17,18 The fact that both conditions are highly heritable suggests high likelihood of a genetic linkage. Other theories about the neural connections between mind and body have been proposed. Brain and body are intrinsically and dynamically coupled; perceptions, emotions, and cognitions respond to and change the state of the body.19 In this sense, body perception and dysautonomia have gained recognition.
Patients with JHS/hEDS have higher interoception,20 meaning greater signaling and perception of internal bodily sensations. This is in line with Critchley's hypothesis, in which he describes the influence of visceral inputs over thoughts, feelings, and behavior.21 Consistent with Critchley's views, Porges described the Polyvagal Theory,22 which is phylogenetic approach relating the autonomic nervous system to behavior. Atypical body awareness is a feature of multiple disorders, including anxiety, depression, and JHS/hEDS.19,23-25 Interestingly, a recent neuroimaging study found that interception sensitivity mediated the relationship between anxiety and hypermobility.20
JHS/hEDS patients have greater exteroception (perception of environment), nocioception (pain perception), and somatosensory amplification.6,26 At the same time, they also have decreased proprioception,27 which could explain the coordination difficulties they experience. Neuroimaging studies have confirmed that individuals with JHS/hEDS have structural differences in key emotion processing regions, notably affecting the amygdala bilaterally.28
Together, these findings increase our understanding about the mechanisms through which vulnerability to anxiety disorders and somatic symptoms arises in certain patients.
Continue to: How JHS/hEDS is diagnosed