Wondering about the idea that hEDS is fundamentally neurologic

Hey everyone,

I am a musculoskeletal/neurologic (PMR) physician who runs into many hEDS patients (genetically ruled out from other types) and I am starting to wonder if this is actually a neurologic disorder more than a connective tissue disease especially in those cases where we cannot find much wrong on testing. These are just my early thoughts, and I would be interested to see if anyone else is starting to think this way.

What I am seeing in almost all of my hEDS patients is the lack of a protective stretch reflex. That is that people do have a reflex to rapid stretching of a muscle, but when a joint is pushed beyond it's "normal range" more slowly, there is no muscle response to try to keep it from over extending. So instead it goes to the ligamentous/bony end range of motion as opposed to a neurologic/muscular end range of motion.

For most people their muscles with automatically contract to prevent a joint from locking out to it's full bony range. It's not actually ligaments/connective tissue that keep people from being flexible. Rather it's the muscles preventing hypermobility (especially in the shoulder). In medicine, sometimes we use this to our advantage to try to manipulate under anesthesia and most people are hypermobile when paralyzed. It also goes wrong with contractures.

All that is to say that what I see in patients with hEDS doesn't look like a connective tissue disorder, but rather a neurologic disorder in dysregulation of proprioceptive feedback and then joint damage.

In addition, what I notices is a significant increased sensitivity to painful stimuli. When I perform injections on hEDS patients, they often describe terrible pain to the point where I often recommend against interventions or at least proceed with caution. For most patients, the needle pokes aren't that painful, but for hEDS patients they often are.

These would both be explained by a common neurologic cause and neurologic genotyping isn't as well understood so it might explain why there is no genetic marker for hEDS.

Still just musings, but wonder if there is anyone else out there chasing this down.