I was asked by a member of this forum to comment on the concept of atlantoaxial instability (AAI) and how it might relate to symptoms of ON. This is an interesting question, but one that is important as it has relevance for patients with a number of clinical conditions such as Ehlers-Danlos Syndrome (EDS – which is not known to be associated with AAI) or those with rheumatoid arthritis (RA – which has been associated with AAI). I also promise to try to minimize the alphabet soup of abbreviations in an effort to avoid confusion.
First of all, what is AAI? Briefly, AAI results from osseous or ligamentous pathology between the two cranial-most vertebrae (spinal column bones) – the atlas (i.e. C1) and the axis (i.e. C2). This instability can result in too much or abnormal movement between the bones and soft tissues surrounding these two structures. AAI can happen secondary to a traumatic event, degeneration due to an infectious or inflammatory insult (e.g. rheumatoid arthritis) and/or a congenital abnormality such as Down Syndrome. When there is excessive or unusual movement of the atlas on the axis a number of problems can occur. The vertebrae can impinge directly on the spinal cord thereby resulting in neurologic manifestations. Compression of the nerve roots as they emerge from the spinal column in also a possibility as is neural pathology more peripherally as will be mentioned below. The good news is that AAI is quite uncommon in patients without any pre-disposing factors.
While the most common presenting symptom is non-descript neck discomfort and/or headache, these symptoms are quite non-specific. Appropriate imaging along with neurosurgical evaluation if pathology is discovered in patients, especially those who have predisposing risk factors are therefore warranted. Fortunately, almost all of the patients I see in my practice have already these evaluations and have come up without a diagnosis of AAI and remain unclear as to the cause of their pain. So how does any of this information relate to ON?
Well, as you can imagine, if you have abnormal or excessive motion at the bony level, it may result in undue traction on the overlying soft tissues which can certainly include the peripheral nerves. As I’ve mentioned in a previous blog post about whiplash and occipital neuralgia about two years ago, (http://peledmigrainesurgery.com/blog/entry/whiplash-and-occipital-neuralgia-what-s-the-connection.html) traction on peripheral nerves can lead to microscopic and in some cases macroscopic tears of the nerve itself which, in turn, can result in outright neuroma formation or cause scarring around the nerve. This scarring that can result in mechanical neural compression or limitation of motion and further traction injury. Similarly, in EDS, the same excessive motion can result from overall laxity in ligamentous structures. Please keep in mind that I am not a neurosurgeon or an orthopedic spine surgeon and this blog post should not take the place of a trained neurology, ortho spine or neurosurgical evaluation. That being said, from what little I’ve read and do know, the take home message is that when you have neck pain and/or headaches, it is unlikely to be AAI in most patients. As always, a good work up and exclusion of other causative factors is important, but if despite that, everyone is left scratching their heads, ON may just be the culprit.