Brain structure and joint hypermobility: relevance to the expression of psychiatric symptoms – Br J Psychiatry. 2012 Jun – free full text /PMC3365276/
This is not a new article, but a thorough scientific survey of the brain differences seen in people with hypermobility (which is usually undiagnosed EDS). This was the beginning of my understanding that EDS is not just a physical issue, but also affects our minds.
To me, it makes sense that the same instability (lack of balance, tendency to extremes) found in our bodies would also be represented in our brains/minds.
Joint hypermobility is overrepresented among people with anxiety and can be associated with abnormal autonomic reactivity.
We tested for associations between regional cerebral grey matter and hypermobility in 72 healthy volunteers using voxel-based morphometry of structural brain scans.
Strikingly, bilateral amygdala volume distinguished those with from those without hypermobility.
The hypermobility group scored higher for interoceptive sensitivity yet were not significantly more anxious.
Our findings specifically link hypermobility to the structural integrity of a brain centre implicated in normal and abnormal emotions and physiological responses.
Our observations endorse hypermobility as a multisystem phenotype and suggest potential mechanisms mediating clinical vulnerability to neuropsychiatric symptoms.
Joint hypermobility is a common but often poorly recognised connective tissue condition.
This article was written in 2012, before it became known that almost all people with “Benign Joint Hypermobility Syndrome” actually have EDS.
Individuals with hypermobility are (up to 16 times) overrepresented among those with panic or anxiety disorders.
Hypermobility is also linked to stress-sensitive psychosomatic disorders including irritable bowel syndrome, fibromyalgia and chronic fatigue and is associated with hypersensitivity to nociceptive stimuli.
Additionally, individuals with hypermobility often exhibit autonomic abnormalities, typically postural tachycardia syndrome, where there is enhanced cardiovascular reactivity and a phenomenological overlap with anxiety disorders.
Thus, direct and indirect evidence links hypermobility to anxiety and stress-sensitive medical disorders.
Within a programme of research motivated to detail the theoretical contribution of central autonomic control to emotion regulation and psychiatric disorders, we performed a voxel-based morphometry (VBM) study of brain magnetic resonance imaging (MRI) scans in participants with and without hypermobility, none of whom had an anxiety disorder.
High-resolution (0.9 mm isometric voxels) structural brain MRI scans (192 sagittal slices, repetition time 11.4 ms, echo time 4.4 ms, inversion time 300 ms) were acquired
We observed structural differences in key emotion-processing brain regions.
Notably, the effect size of this amygdala volume difference was comparable to, or greater than, observations from volumetric studies of clinical psychiatric populations.
The hypermobile group also displayed decreased volume within other regions implicated in emotional arousal and attention (anterior cingulate, parietal lobe).
Moreover, the degree of hypermobility correlated negatively with superior temporal volume, a region implicated in processing social and emotional signals.
Differences in brain structure were not due to overt psychopathology (the hypermobile group only trended toward higher anxiety scores) or basal physiology (no difference was observed in cardiovascular measures at rest).
Our data implicate the amygdala as a likely neural substrate mediating previously reported clinical associations between hyper-mobility, anxiety and psychosomatic conditions.
Speculatively, potential mechanisms include heightened susceptibility of individuals with hypermobility to (threat of) pain and/or a perturbation of autonomic control.
Differences in amygdala activity occur in pain disorders including fibromyalgia, irritable bowel syndrome and chronic regional pain syndrome.
Anxiety itself is also linked theoretically to the abnormal generation and mapping of bodily arousal through the engagement of amygdala and insula
It is also noteworthy that the hypermobility group showed structural differences within anterior cingulate cortex, a central driver of autonomic arousal and a region implicated in the cognitive control of pain and negative emotions
Enhanced interoceptive sensitivity also points to a more finely tuned sensory representation of internal bodily signals within the hypermobile group. Heightened interoceptive awareness is coupled to exaggerated cardiovascular arousal responses.
Moreover, in postural tachycardia syndrome, which commonly occurs with hypermobility (and may have a common basis in collagen variants), heart rate acceleration compensates for dysfunctional vasoconstriction giving rise to physiological symptoms (e.g. palpitations and light-headedness) that are shared with panic and anxiety states
Such deregulated responses are likely to affect neural processes supporting emotional feelings
Differences in the structural integrity of temporal and parietal cortices may underlie wider behavioural phenotypical expression of hypermobility: abnormalities in superior temporal cortex are also seen in autism
Inferior parietal cortex can affect proprioceptive awareness and hypermobility is itself linked to dyspraxia.
From Wikipedia: Dyspraxia [also known as Developmental coordination disorder(DCD) or developmental dyspraxia.] is a chronic neurological disorder beginning in childhood.
It is also known to affect planning of movements and coordination as a result of brain messages not being accurately transmitted to the body.
Our findings suggest that processes compromising function in neuro-developmental conditions may occur in individuals with hypermobility, putatively enhancing vulnerability to stress and anxiety.
Limitations to our study include the use of a non-clinical sample; interestingly, neuroimaging studies of clinical anxiety groups rarely report enlarged amygdala, suggesting that hypermobility is a distinct phenotype or that amygdala enlargement might be protective in our non-clinical group.
Additionally, we used an inclusive definition of hypermobility, although the categorisation of this condition remains debatable.
To conclude, we present the first neuroimaging study of hypermobility that also examines autonomic and interoceptive indices.
The observed differences in the structural integrity of specific emotional brain regions provide a starting point for future research into constitutional vulnerabilities to common psychiatric symptoms that have the potential to inform more individually tailored therapeutic approaches.
See also this newer post and study:
Neurovisceral phenotypes in the expression of psychiatric symptoms– free full-text /PMC4322642/ article |February 2015
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, [EDS]
- 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.