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This article will explain in depth how to measure and correct the atlas joints, both at the much neglected atlanto-occipital junction, and the more popular atlantoaxial junction. It will reveal what I consider to be the main exacerbating factor behind atlas misalignment, why I believe that many approaches are missing crucial aspects and measurements of atlantal alignment, as well as essential factors that prevent correctives from sticking.
Once the muscles do not move nor hold the spine in proper position any more, excessive motion tends to develop between the A-A or A-O joints, over time leading to atlas joint hypermobility and misalignment. This is why normalizing and even optimizing craniocervical habits, as well as other factors, are key to resolve atlas misalignment in my experience.
The movement within the atlanto-occipital (A-O) joint, is the opposite. It yields about 30 degrees of total flexion-extension in the sagittal plane, but only about 15 degrees of lateral flexion and 5 degrees of rotation. Thus these two joints complete each other by providing more of the movements that its counterpart does not. The remaining movements come from the lower cervical spinal segments. Because the atlas bone holds the cranium, it craves stability. Compromisation of the A-O joint is common is long-standing neck injured patients, but lacking measurement criteria causes it to be neglected in most cases. Thus vital information on craniocervical alignment will remain hidden.
The outer layer of ligaments, roughly stabilizing and restricting excessive movements between the A-O and A-A joints, are the posterior and anterior atlanto-occipital and atlanoaxial ligaments. Connecting the atlas joints (articulate surfaces), we have the A-A and A-O capsular ligaments. These restrict greater joint movements in all vectors, making up the rougher atlas joint stability foundation. Running from the occiput and down to the C7 is a thick ligament called the nuchal ligament. It is the cervical version of the supraspinous ligament. Because the spinous processes between C2-7 are relatively short, the muscles of the neck that would normally attach to the spinous process, such as the trapezius muscle, instead attaches to the nuchal ligament.
Tightness of certain structures may also restrict optimal axial rotation of the cervical spine, and is also an important potentially exacerbating factor for misalignment and hypermobility. Let us have a closer look at the muscles that insert into the atlas, its functions and connections.
The suboccipital muscle group mainly attach between the atlas, axis and occiput, and are thus greatly involved in atlanto-occipital as well as atlantoaxial stabilization, both with regards to posture and craniocervical movement. The posterior suboccipital triangle consist of four main muscles, one set on both sides.
The levator scapulae is a contralateral rotator and lateral flexor of the cervical spine. It also elevates the shoulder blades and pull them into downward rotation and anterior tilt. The levator scapulae attaches between the scapulas superior angle and the C1-C4 transverse processes. Co-activation and balanced pull/tension from the levator scapulae will restrict anterior translation of the atlas joint and thus passively influence/restrict posterior gliding of the occiput, which are both commonly seen in these types of patients.
Because of its atlantocervical attachment sites, it has a great influence on atlas joint movement and stability. Tightness of the levator scapulae may restrict rotational range of motion in the cervical spine, often more on one side than the other. In such case it will cause continuous pulling forces to occur on the upper cervical transverse processes, often pulling these into a de-centrated position. Additionally the levator scapulae is a common cause of chronic headache, shoulder pain, and sometimes vertigo due to destabilization of the atlas joints.
This has been touched on already, but this section will address the various causes of atlas joint instability and misalignments. The most common precursor is forward head posture with cervical hinging, or cervical injuries such as whiplash. This will cause massive instability and may often pave the way for atlas misalignment down the lines. Furthermore the jaw will also affect posture and cervical stability, as will scapular positioning and resting habits.
Crooked atlas positioning is also often related to temporomandibular dysfunction (TMD). Many studies have shown significant associations between tooth occlusion (the bite) and posture. For example, people with tooth crowding have a significantly higher chance of getting forward head posture (Solow et al., 1998). Now, it is not the only cause of FHP, but I want to address this topic before addressing FHP and the corrective strategy I use for it.
As I see it, forward head posture and neck hinging is perhaps one of the most detrimental habitual factors with regards to cervical stability. Virtually every patient with atlas misalignments will have forward head posture and cervical hinging. Let me explain why I think this is such a big deal, and why it will affect atlantal stability and alignment.
Another common association with swayback posture, is scapular depression. I.e, improper resting position of the shoulder blades. When the scapula is resting too low in posture, the trapezius, levator scapulae and scaleni muscle groups will commonly inhibit and become very tight. The tighter they become, the greater they will restrict normal cervical posture and movement. This may once again lead to hypermobility of the upper cervical region, cervical hinging, and so on, which are all common denominators that pave the way toward atlas misalignment issues. Furthermore, It is almost impossible to resolve forward head posture, if the shoulderblades are situated too low, as it will pull the neck down and forward, often into a hinging pattern.
Extremely many conditions are associated with atlas misalignment, however I can not possibly include every single association, as there are so many, and I have mentioned several things already throughout this article, so I will try to stick to new information rather than reiterative rambling.
Many studies show the correlation between excess endolymphatic fluid and dizzness, but also hearing loss and migraines. The reason for this is mainly that compression of the internal jugular vein, which is a common problem patients who hinge at the neck and/or have atlas torsion, will cause impaired venous drainage from the inner ear and thus increase susceptibility to endolymphatic hydrops (excess endolymphatic volume and pressure). It may, of course, also cause generalized craniovascular hypertension in various degrees of severity, which may cause migarine.
On ultrasound you can also see, even in healthy patients with no anterior translation or rotation of the atlas, the neck-hinging may obstruct the internal jugular vein. A sensation of craniovascular hypertension may build up within seconds. Much more so if there is atlantal misalignment.
The diameter of IJV and distance between the styloid process and lateral mass of the atlas at IJV obstruction side in obstruction group were 1.6 1.0 mm and 4.1 2.1 mm respectively, which resulted in statistical significance (p
A common presentation is that dizziness occurs when looking in certain directions, whilst in certain cranial positions, or after loading the neck. When the atlas is (very) out of alignment, the suboccipital muscles attaching to the C1 and C2 will lose optimal tensegrity, and not be able to function properly. Some will be pulled too far and some become lax. Poor function of the suboccipitals may also migraine-like symptoms in and around the eyes.
Posterior occipital gliding may lead to cerebral herniation, i.e cerebral chiari, in severe cases. This is a condition where the cerebrum is herniated out of the foramen magnum and into the spinal canal. Statistical research have shown that neck injured population such as those who have gotten whiplash, are of much greater risk of cerebral herniation. I strongly believe that this is the case, because the distance between the posterior brain stem and the foramen magnum becomes greater as the occiput glides backwards on the atlas vertebrae, increasing risk of caudal cerebral herniation.
There are some radiologists measuring atlantal torsions, but as far as I know, they are measuring for torsions and subluxations between the axis and atlas, and not between the atlas and occiput. This is in my opinion a relatively big mistake, because a torsion between the C1 and occiput is much more serious than between the atlas and axis, because the atlantoaxial joint is supposed to have a lot of movement, where as the atlanto-occipital joint is supposed to be fixed. Now, this is not to imply that a loose A-A joint is optimal; of course it is not, as I have also made clear earlier i