Joint Hypermobility and Anxiety

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ekmf27050

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Hi All-

Sneaking in here as a premed to ask for some opinions. To be clear, I am NOT asking for medical advice for me! I came across these articles while researching some topics for orthopedic patient info sheets at work, and I wanted to know what the professional opinion was on them.

I started off by stumbling on this pared down Scientific American article:
People Who Are Double-Jointed Are More Likely to Be Anxious

Then, I was curious and looked at the Pubmed articles that they based it on:
Brain structure and joint hypermobility: relevance to the expression of psychiatric symptoms
Neurovisceral phenotypes in the expression of psychiatric symptoms

It's my basic understanding that people with joint hypermobility have collagen defects, which can lead to autonomic dysfunction, which can lower the "baseline" for triggering physical anxiety and panic symptoms.
I was wondering what the validity and applicability of these studies might be in practice-- do you see a lot of patients with autonomic causes for their anxiety? How would you separate "physically mediated" anxiety from situational anxiety or negative though patterns? It was all really interesting to me, but at certain points in the pubmed articles my contacts glazed over.

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wow. interesting stuff.

I have seen 2 marfanoid habitus patients with anxiety problems and wondered about this, but I thought of it in terms of cardiac problems. I hadn't considered brain architecture differences.

Now that i looked at the articles in more detail, I have seen, also syncope patients with anxiety problems.

It could help to formulate psychological vs physiological phenomenon as being more salient in the causes of anxiety.
 
Interesting, although it hadn't crossed my mind to consider it in this way.

Have seen one patient with hypermobile Ehlers-Danlos that presented with severe anxiety, but most of it was attributable to situational factors, chronic pain and other complications related to the syndrome - eg. if taking a bus somewhere and it stopped suddenly, they'd end up in a lot of pain with dislocated joints.
 
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wow. interesting stuff.

I have seen 2 marfanoid habitus patients with anxiety problems and wondered about this, but I thought of it in terms of cardiac problems. I hadn't considered brain architecture differences.

Now that i looked at the articles in more detail, I have seen, also syncope patients with anxiety problems.

It could help to formulate psychological vs physiological phenomenon as being more salient in the causes of anxiety.

I couldn't quite understand if it was only hypermobile patients who also had POTS who were more predisposed to "physiological anxiety", or if it was all patients with hypermobility

Interesting, although it hadn't crossed my mind to consider it in this way.

Have seen one patient with hypermobile Ehlers-Danlos that presented with severe anxiety, but most of it was attributable to situational factors, chronic pain and other complications related to the syndrome - eg. if taking a bus somewhere and it stopped suddenly, they'd end up in a lot of pain with dislocated joints.
If patients such as this don't improve with CBT/pain management psych, would you consider medicating the anxiety first or medicating for autonomic dysfunction first (I think one of the articles said beta blockers)?
 
CBT and medications might be great. Probing for signal anxiety for other unconscious phenomenon might not. Depends on the patient I guess. But understanding their own bodies and physiologic reasons for hyperarousal may be very helpful to them. Beta blockers might be just the right thing actually.
 
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If I’m remembering correctly though POTS patients become orthostatic right? Which may prohibit a beta blocker.
 
If I’m remembering correctly though POTS patients become orthostatic right? Which may prohibit a beta blocker.
Yeah, that part was admittedly beyond me. I understand why it may help with the autonomic triggering of panic and anxiety, but would think it would make the POTS worse?
 
If I’m remembering correctly though POTS patients become orthostatic right? Which may prohibit a beta blocker.
There's hyperadrenergic POTS in which case they have orthostatic hypertension and tachycardia.

Also people with POTS sometimes take very low doses of beta blockers which don't reduce blood pressure significantly, and they may also be taking medications at the same time that increase blood pressure or may be taking intravenous fluids, sodium, etc. Some also take ivabradine which lowers pulse but not blood pressure.

It's very complicated and not very well understood.
 
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Low dose beta blockers can relieve the hyperadrenergic state and improve symptoms without having much effect on the orthostasis if they are already doing other things to improve it. It can be pretty helpful to refer for autonomic testing -- this is a subject than many doctors, even neurologists and cardiologists, don't understand well.

In my neck of the woods, I see lots of people self-diagnosing with Ehlers-Danlos and POTS who seem to me to mostly be anxious and somatically preoccupied. It seems to be the trending diagnosis these days. So I like to try to verify this. Patients with actual hypermobilitiy syndormes also have increased rates of chronic pain and fibromyalgia as well.
 
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In my neck of the woods, I see lots of people self-diagnosing with Ehlers-Danlos and POTS who seem to me to mostly be anxious and somatically preoccupied. It seems to be the trending diagnosis these days.

I've definitely noticed an upswing myself as well, and the typical profile for self diagnosed ED or POTS does seem to be those who are more prone to anxiety, hyperarousal, and emotional dysregulation.
And if I have one more well meaning friend tell me I have Ehlers-Danlos, simply because I score as hypermobile on the Beighton scale, I just might be tempted to punch them in their well meaning faces.
 
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If patients such as this don't improve with CBT/pain management psych, would you consider medicating the anxiety first or medicating for autonomic dysfunction first (I think one of the articles said beta blockers)?

Depends on the patient. I'd probably try and manage the anxiety using therapies and medication strategies like I normally do, and look towards alternatives only if these prove to be unsuccessful. As a personal rule of thumb if patients have medical co-morbidities I need to be sure that these issues are being managed adequately by the other doctors involved in their care. In most cases things are usually already optimised by the time they come to me.
 
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CBT and medications might be great. Probing for signal anxiety for other unconscious phenomenon might not. Depends on the patient I guess. But understanding their own bodies and physiologic reasons for hyperarousal may be very helpful to them. Beta blockers might be just the right thing actually.

I definitely found CBT, MB-CBT, and ACT based therapies to be very helpful in managing chronic pain. It always puzzles me a bit when I see other people with legitimate chronic pain issues talking about how they won't go to a Psychiatrist or Psychologist, because the pain isn't in their head damnit!, in the one breath, and in the next breath turn around and complain about how stressed, and anxious, and depressed they feel because of their pain issues. Well, yeah, hello, that's where the psychiatric/psychological part comes into play.
 
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Depends on the patient. I'd probably try and manage the anxiety using therapies and medication strategies like I normally do, and look towards alternatives only if these prove to be unsuccessful. As a personal rule of thumb if patients have medical co-morbidities I need to be sure that these issues are being managed adequately by the other doctors involved in their care. In most cases things are usually already optimised by the time they come to me.
Definitely makes sense. If this link hadn't been made by a PCP or other specialist, who would you prefer to refer to for something like this? Cardiology even if they don't have POTS?
 
I definitely found CBT, MB-CBT, and ACT based therapies to be very helpful in managing chronic pain. It always puzzles me a bit when I see other people with legitimate chronic pain issues talking about how they won't go to a Psychiatrist or Psychologist, because the pain isn't in their head damnit!, in the one breath, and in the next breath turn around and complain about how stressed, and anxious, and depressed they feel because of their pain issues. Well, yeah, hello, that's where the psychiatric/psychological part comes into play.
I can kind of understand the knee jerk reaction, where a patient assumes the worst- their doctor thinks it's all in their head, and wants to shuttle them off to psych. That's the unfortunate thing, because your point about the benefits is spot on-- pain psychology (almost) certainly won't make things worse, and might help. I don't know the best way to avoid the immediate negative reaction to the suggestion though. :(
 
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Low dose beta blockers can relieve the hyperadrenergic state and improve symptoms without having much effect on the orthostasis if they are already doing other things to improve it. It can be pretty helpful to refer for autonomic testing -- this is a subject than many doctors, even neurologists and cardiologists, don't understand well.

In my neck of the woods, I see lots of people self-diagnosing with Ehlers-Danlos and POTS who seem to me to mostly be anxious and somatically preoccupied. It seems to be the trending diagnosis these days. So I like to try to verify this. Patients with actual hypermobilitiy syndormes also have increased rates of chronic pain and fibromyalgia as well.
This was reminded me of something and I realized it was one of the articles (first pubmed one):
"Within the hypermobile group, degree of hypermobility correlated positively with the volume of left lateral occipital cortex and negatively with right superior temporal cortex and bilateral inferior parietal cortices (online Fig. DS1, Table DS2). Interestingly, this group scored significantly higher for interoceptive sensitivity (mean PBPQ scores: non-hypermobile 88.4, s.d. = 31.0; hypermobile 104.3, s.d. = 32.2; t(1,70) = 2.13, P = 0.018) and showed a trend towards higher anxiety (non-hypermobile 6.47, s.d. = 7.0; hypermobile 9.31, s.d. = 9.7; t(1,70) =1.42, P = 0.08). The relationship between hypermobility and interoceptive sensitivity persisted after controlling for anxiety differences (P = 0.041)."

So, if I'm reading that correctly, hypermobile people have significantly higher interoceptive sensitivity and they can see changes in brain activity signifying this. Is interoceptive sensitivity the same as somatic preoccupation?
 
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This was reminded me of something and I realized it was one of the articles (first pubmed one):
"Within the hypermobile group, degree of hypermobility correlated positively with the volume of left lateral occipital cortex and negatively with right superior temporal cortex and bilateral inferior parietal cortices (online Fig. DS1, Table DS2). Interestingly, this group scored significantly higher for interoceptive sensitivity (mean PBPQ scores: non-hypermobile 88.4, s.d. = 31.0; hypermobile 104.3, s.d. = 32.2; t(1,70) = 2.13, P = 0.018) and showed a trend towards higher anxiety (non-hypermobile 6.47, s.d. = 7.0; hypermobile 9.31, s.d. = 9.7; t(1,70) =1.42, P = 0.08). The relationship between hypermobility and interoceptive sensitivity persisted after controlling for anxiety differences (P = 0.041)."

So, if I'm reading that correctly, hypermobile people have significantly higher interoceptive sensitivity and they can see changes in brain activity signifying this. Is interoceptive sensitivity the same as somatic preoccupation?


Fascinating question. I also wonder how all of these map on trait neuroticism in the Big 5 model. sensitivity to negative emotions aka higher rates of anxiety and depression seem from my clinical experience to be very positively correlated with pain phenomenon. These seem also to be the same people who experience fulminant PTSD with lower traumatic exposures.

Maybe the connective tissue problems effect the same neural tracts that regulate negative emotion and pain perception.
 
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Fascinating question. I also wonder how all of these map on trait neuroticism in the Big 5 model. sensitivity to negative emotions aka higher rates of anxiety and depression seem from my clinical experience to be very positively correlated with pain phenomenon. These seem also to be the same people who experience fulminant PTSD with lower traumatic exposures.

Maybe the connective tissue problems effect the same neural tracts that regulate negative emotion and pain perception.
I think one of the studies mentioned amygdala differences, and if so would definitely point to negative emotion problems
 
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