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.
The atlas is the first and top cervical vertebrae (C1), holding the head (occiput) and thus forms the atlanto-occipital joint (A-O). The second cervical vertebrae, is the axis, or C2. The atlas (C1) pivots on the axis of the dens, making it a unique type of joint compared to the other vertebral joints. It’s called the atlantoaxial joint or A-A (C1-C2).
Thick ligaments hold these joints in place, but patients with atlas misalignment often have ligament laxity after e.g whiplash injuries and/or years of improper cervical posture and movement patterns. Most of the time, despite some level of ligamentous laxity, great and lasting results can be achieved by re-establishing proper postural and cervical movement habits, as well as significantly strengthening the muscles that stabilize and syncronize the movements of the atlas joints. The key lies in changing the patient’s habits.
What do I mean by that? What does our habits have to do with atlas misalignment?
Certain factors either ‘make you or break you’. For instance, certain muscles stabilize and syncronize the atlas joints’ movements and position, as I mentioned above. These muscles are greatly reliant on proper cervical posture and movement patterns to function properly. If these structural dependencies are compromised, the muscles will be as well. A downward spiral with loss of tensegrity (i.e loss of muscle tension and stability), muscle dysfunction and imbalances, compensatory patterns, tightness and pain tend to develop.
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.
Let’s move on and have a look at the most important anatomical aspects of the atlas joints.
This article is written for educational purposes only. It does NOT promote self-treatment for patients. Playing around with the craniocervical junction is NOT risk free!
Anatomy of the atlas joints
As mentioned already, the atlas joints are made up of the A-A and A-O joints. The atlantoaxial (A-A) joint is a special cervical level, as it yields more rotation than the other cervical vertebrae. According to some medial literature, it makes up 50% of total cervical rotation. It is however relatively limited with regards to flexion and extension (10 degrees) and side flexion (5 degrees – Magee, D. Orthopedic Physical Assessment)
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.
Laxity of the above mentioned ligaments would cause inappropriate increase in A-A and A-O joint articulation, such as increased rotation, side flexion etc. This could cause the occiput to improperly glide forward, backward or to the side on the atlas bone. Additionally, it may predispose the axial (odontoid peg’s attachments) ligaments to injury, due to the abnormal movement ranges or joint positioning.
Between the axis (C2) and the C3 vertebrae and further down the spine, runs the flaval ligament. In similar fashion it will restrict movement between the axis and C3, C3/C4 and so on. The first spinal disc is located between the axis and C3 vertebrae, and this is also where the zygapophysial (45° facet joints) first appear.
The integrity of rotational symmetry and positioning between the A-A and A-O joints is maintained by ligaments that ensure a proper axis of rotation within the region. Some of the most relevant ones, are the apical ligament (anterior to the longitudinal part of the cruciate ligament), alar ligament and transverse (cruciate) ligament that connect the odontoid process to the C1 and occiput, and also maintain axis of rotation (see fig. 2). Behind these, are the tectorial (proximal part of posterior longitudinal) ligament.
The odontoid process, C1 and occiput are tightly held in position of optimal axial rotation by the above-mentioned ligaments. If they get stretched, the axis (spine) and occiput will no longer move in proper symmetry, as the external ligaments do not uphold axis of rotation in the same manner. This may thus result in improper gliding and rotation between the A-A and A-O joints, leading to many potential problems which will be addressed later on in this article. Considerable injuries to these ligaments will usually require surgery. This article is primarily focused on treating chronic injury and not acute injury.
Thankfully, the ligaments are not left to handle all the strain by themselves. Several muscles stabilize the atlas joints, both proximally (shorter muscles) and regionally (longer muscles). When these muscles activate properly, movement of the head and neck will pull the A-A and A-O joints symmetrically, so that the ligaments do not overburden due to improper vertebral movements. There are many muscles in the neck, but I’ll elaborate on those whose functions are more often compromised and causing imbalances.
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.
- Rectus capitis posterior minor & major (RCP min/maj)
- Obliquus capitis superior & inferior (OCS / OCI)
All of these muscles, except the OCI contribute to occipital extension and prevent posterior glide of the occiput on the atlas joint. Additionally the RCP major will cause ipsilateral rotation of the occiput, and OCS contralateral rotation of the occiput. It’s useful to understand these pulling vectors in order to know which muscles are imbalanced when the atlas joints are not positioned or moving symmetrically, but not paramount. Generally they all require significant strengthening in the typical atlas patient. The seemingly contradictory muscle fiber orientation of the muscles within the suboccipital triangles will ensure that the atlas joints move symmetrically together with the occiput. Their coactivation will thus also contribute to joint centration.
The suboccipital muscles will also level the head in the sagittal and coronal planes, ensuring levelled eye sight. These muscles are in fact intrinsically connected to the eyes to such a degree, that if you palpate them while moving the eyes, you’ll feel the suboccipitals respond directly to your eyes’ movement. Research has shown that the suboccipitals have a tremendously high spindle cell density. The spindle cells are (amongst other things) responsible for proprioception, which simplified means control and awareness of the respective limbs. Not a surprise, as these muscles hold the head itself.
The distribution and arrangement of spindles within the muscle and their arrangement was studied. The spindle density of superior oblique muscle was found to be 190, that of inferior oblique was 242 and the rectus capitis posterior contained 98 spindles per gram of muscle. – Kulkarni et al., 2001
Muscle spindle density is extremely high in the deep muscles of the human neck. – Liu et al., 2003
Scientists have found that the cervical muscles muscles and especially suboccipitals, are often atrophied in patients with whiplash, neck pain and vertigo (Kristjansson 2004, Andary et al. 1998, McPartland et al. 1997, Elliott et al. 2015). It has also been shown that saline and procaine injections into the suboccipitals significantly relieved symptoms of vertigo, disequilibrium (lack of balance), and pain levels (Campbell, 1944; Hinoki, 1972; Gimse, 1996).
Based on the above, it’s clear that the suboccipitals have tremendously important functions in the body. Stabilizing and symmetrically pulling the A-A and A-O joints, intrinsic relations to our vision, balance and posture. It therefore makes me cringe when I see therapists and patients release (needle, massage, stretch) the suboccipitals; I consider it iatrogenic treatment. These muscles are unique and should be handled with the utmost care. Rarely (never!) is it appropriate to release the muscles; they should be strengthened to ensure proper function.
Asymmetrical A-A or A-O articulation, vertigo, headaches, whiplash, etc are all indicators of potential suboccipital compromisation, and means that they should be assessed. The best way to assess their functions is by strengthening them, or by MMT. The MMT for the suboccipitals are too complex to detail in this article, but if the exercise is heavy then they will often need significant strengthening. Palpative examination is also useful. They are often atrophied and very tight, and squeezing into them may cause great pain, headaches and migraines for the patient. I reiterate; this is NOT an indicator that they need release, but rather means that they are in need of strengthening.
The cruveilhier’s plexus
The cruveilhier’s plexus, also called the posterior cervical plexus, is a bundle of posterior rami nerves stemming from the upper three cervical levels, C1 to C3. Through the suboccipitals and more superficial neck extensors (such as the trapezius and splenius capitis) emerge the suboccipital & occipital nerves. When these muscles are severely inhibited and can not function properly, the nerves may get entrapped within their fibers, leading to occipital neuralgia.
Occipital neuralgia can be devastatingly painful, in similar fashion to trigeminal neuralgia (which you can read more about in my TMD article), and may cause severe neuralgic pain, radiating into the posterior neck and head. It is sometimes described as an electric shock, a sharp and stabbing pain.
The solution to this issue is to exercise the suboccipitals along with the more superficial cervical and occipital extensors. Exercising these muscles may lead to significant exacerbation of the patient’s symptoms initially. This phase may last between 1-6 months. Symptom exacerbation is usually a confirmation that the exercises are done properly, but degree of exacerbation can be controlled by starting ‘slow and easy’, not doing too high intensity training of these muscles until they are capable of doing so. In other words, gradually increasing load and volume as the muscles improve.
The rectus capitis lateralis
The rectus capitis lateralis muscles control and restrict lateral gliding as well as excessive rotation of the occiput on the C1, and it attaches from the skull’s jugular process to the C1 transverse process. If exercised unilaterally, they may also cause lateral translation of the C1 (or contralateral translation of the occiput), especially if the atlanto-occipital ligaments are lax.
Having strong rectus capitis lateralis muscles is beneficial, because it restricts excessive movements within the A-O joint, however one must be somewhat cautious when working these special muscles, so that no unwarranted translation will occur between the C1 and occiput. Using equal intensity on both sides, and of course measuring the distance between the edge of the C1 transverse process and the lateral edge of the mastoid process both before and after the strengthening, to ensure that no unwanted lateral translation has occurred.
The measurement for lateral translation of the occiput, is measuring the distance between the lateral edge of the C1 transverse process and the lateral edge of the mastoid process. Estimate based on palpation whether or not the distance is greater on one side.
It may sound absurd that these small muscles can shift the whole head’s position on the atlas bone, but I assure you that this is the case if the patient has ligamentous laxity, and you will be able to detect this for yourself with the protocol outlined in this article.
Rectus capitis lateralis exercise
The scalenes are very important muscles as well, because of their relation to the brachial plexus, subclavian artery and subclavian veins. The scalenes are lateral flexors, lateral translators, and ipsilateral rotators of the cervical spine. They also elevate the ribs during inspiration.
There are three portions of the scalene muscle; the anterior, middle and posterior heads. The anterior scalene attaches from the first rib, to the transverse processes of C3-C6. The (largest) middle scalene, between first rib, and (some illustrations show that it also connects to the C1-TVP) C2-C7. And, lastly, the posterior scalene between the second rib and C5-C7.
The scalenes are often very weak, due to postural abnormalities such as slouching shoulders and forward head posture. In turn, they may greatly restrict the movement of the cervical spine, especially with regards to rotation and extension. When there’s severe restriction in rotation, this may cause excessive movement to occur between the A-A (C1/C2) or axiocervical (C2/C3) joints, ultimately leading to ligament laxity and instability of the upper cervical spine, as I touched upon earlier.
Additionally, their tightness may entrap the nervous and vascular bundles of the thoracic outlet, causing thoracic outlet syndrome. An especially relevant point to note is that the vertebral artery that supplies the brain, is a branch of the subclavian artery. When the scalenes compress this artery, it may compromise the brain’s blood flow, and lead to many different problems such as vertigo, fatigue, migraines, and similar symptoms of vertebrobasilar insufficiency. So far I have yet to see a patient with noteworthy atlas misalignment who didn’t also have TOS, but fairly I have indeed seen many patients with TOS who did not have atlas misalignment.
The scalenes are usually weak, and it’s a huge mistake to release them, in my opinion. Strengthening is the key, but the exercise can cause tremendous pain if done too intensively in patients whose thoracic outlet is compromised within the interscalene triangle. Start with 5-10 repetitions every day or every-other-day. I’ve seen dramatic symptoms occur in relation to these exercises many times. If they’re worked too hard, too fast, inflammation will occur and symptoms may greatly exacerbate. This will, of course, subside, but it’s better to start carefully and then gradually increase over time.
The levator scapulae
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.
The main cause of levator scapulae dysfunction is faulty posture, and especially faulty resting position of the shoulder blades. I’ve written a detailed explanation about this in my TOS article that’s mentioned earlier, and thus won’t repeat that here. I’ve already written about it in my scapular dyskinesis article.
In short, though, continuous slouching of the shoulder girdles will cause inhibition and severe tightening of the scapular elevators such as the levator scapulae. The only long-lasting way to deal with this is through postural correctives. It is however also beneficial to strengthen the LS and trapezius muscles in a parallel manner, to support the postural re-education and speed up the the muscles’ healing. It is almost always injured and require strengthening in whiplash injury victims.
The levator scapulae may also be used in order to force symmetry upon the atlas joints. I’ll come back to this muscle in later parts of this article.
The longus colli and longus capitis
The longus colli and capitis muscles prevent anterior gliding of the atlas in relation to the occiput, as well as preventing hyperextension (“hinging”) on the cervical spine. They are therefore very important structures to be aware of when treating atlas and neck dysfunction. The longus capitis extends from the skull and down to C6, while the longus colli spans from the C1 and to the T3 vertebrae. Because they control cervical hyperextension, habitual (postural) hyperextension and hinging on the cervical spine will cause them to inhibit. Therefore they are usually weak and need to be strengthened significantly.
The alar fascia of the neck ties together the longi muscles and the sympathetic chain, i.e the cervical ganglia, in the anterior cervical column. Dysfunction of these muscles may cause irritation of these sympathetic nerves structures, causing diffuse issues. More about this later.
They longus capitis can be trained seated by pulling the chin down while maintaining a long neck (no hinging), and resisting downward movement of the chin with your hands. The longus colli can be trained supine, by tucking the chin down to the sternum and then flexing the neck. The suprahyoid muscles must be controlled and shouldn’t contract excessively.
The infamous sternocleidomastoid, or SCM in short. Often blamed for virtually any occipito-cervical pathology, ranging from neck pain, headaches, tinnitus, etc – You name it. In reality the SCM is a very important muscle, and very misunderstood. a neck flexor and occipital extensor, attaching from the mastoid process and splitting into two heads that attach into the clavicle and sternum. It also functions as a contralateral occipital rotator, raises the clavicle and sternum during inspiration, and prevents posterior A-O gliding of the occiput.
Contrary to popular belief, the SCM is often weak and requires strengthening, not releasing. Because the SCM is a neck flexor, and when a patient is hanging forward with their heads, this function is inhibited as the head is just hanging forward. It is absolutely NOT pulling the head forwarda nd down, as many mistakenly believe. Muscle test it and see for yourself, by having the patient pull their ear towards their sternum, while you resist at the back of the head. It will be weak!
Between the SCM and the anterior scalene, lies the phrenic and vagus nerves. These autonomic nerves control an array of functions in the body, such as hiccups, coughing, heart rates, etc. The vagus nerve is also referred to as “the wandering nerve” because it is unique in innervating almost all of the organs in the abdomen, controlling many autonomic tasks. In addition to these nerves, the carotid sheath containing the internal jugular vein and internal carotid artery also resides, as the main blood suppliants for the brain.
Fig. 11 – 1: SCM, 2: anterior scalene, 9: vagus nerve, 10: phrenic nerve, 14, carotid sheath
When the clavicular portion of the SCM and the anterior scalene becomes very tight (often when severely weak), this may cause entrapment of the above-mentioned nerves and vascular structures. Chronic cough, headaches, migraines, cervicogenic headaches and all kinds of different symptoms may be experienced as a result. I’ve treated several patients for chronic cough caused by vagal compression within the SCM / scalene interval.
Below is an exercise demonstration for the sternocleidomastoid.
The splenius cervicis and longissimus cervicis
The splenicus cervicis is a cervical spinal erector, and spans between the transverse process of the C1 & C2, and down unto the T6 vertebrae. It also contributes to some ipsilateral flexion and rotation of the cervical spine.
Because it attaches to the atlantoaxial joints, it may restrict the motion between these vertebrae and thus promote excessive movement at the atlanto-occipital junction, if there is significant tightness, perhaps due to forward head posture or similar factors.
The longissimus cervicis does not attach to the atlas, but rather spans between the C2-C6’s transverse processes, and down unto the T1-T5. Similar to the splenius cervicis, it will contribute to cervical extension, as well as some ipsilateral rotation and lateral flexion.
Although it does not restrict atlantal movement, it will restrict mid- and lower cervical movement if there is severe tightness. Restricted axial rotation of the cervical spine may, as mentioned several times already, lead to excessive atlantoaxial movement, compromised joint integrity (laxity, subluxations), and so on. The main factor for this is once again forward head posture. As you know, there’s much greater movement at the A-A junction than the A-O junction, so the margin of error is much greater here than at the above level. Even minor laxity at the A-O junction, which may occur if the atlantoaxial joints are both restricted, can be quite detrimental. More on this throughout this article.
Here is an exercise demonstration for the cranio-cervico-thoracic extensors.
Common causes of misalignment
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.
The head weighs between eight and 14 pounds. It must remain in perfect alignment in order to prevent interference in every brain-to-body function. Misalignment can result from automobile accidents, poor posture, falls and countless other causes. When the head becomes misaligned, it reacts adversely with pain and poor health. – Dr. Peter Gott M.D.
The jaw’s effect on posture and the upper neck
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.
Many dentists agree that the most common trait of people who have dental crowding and improper development of the upper jaw, is that they are walking around with the mouth open, breathing through it instead of through the nose, and that their tongue is not properly situated in the roof of their mouths in posture. When the jaw remains open and the tongue is lying down, not only will the face and cranial bones develop asymmetrically, together with the occlusion, but cervical tensegrity is lost along with it. When tensegrity is lost, the neck becomes unstable, and over time this may cause atlantal misalignment. Furthermore, underdevelopment of the maxilla may cause TMD in many circumstances.
If we look at Thomas Myer’s ‘deep front line’, we can perhaps understand why the jaw is so intimately connected with cervical stability. The longus colli and longus capitis, whose functional integrity are absolutely essential for neck posture and stability, are directly connected to the tongue and muscles of mastication through fascial bonds. Research has shown that a staggering 30 to 40% of muscle force transmission actually occurs through these bonds, and not the muscle itself (Huijing et al., 2003; Stecco et al.,). These bonds continue all the way down, through the core and unto the foot. Then, when [especially] the tongue is not properly positioned, and the muscles of mastication are not stimulated properly, the subsequent loss of tensegrity may cause a spiral effect through all of the deep front line, affecting our posture.
I do have some more hypothetical thoughts with regards to why malocclusion may directly affect posture through changing the alignment of the sphenoid bone (through whom all of the ocular nerves pass), as I’ve found that stimulating the pterygoid muscles in certain ways, will contribute to relatively predictable craniocervical movements. For instance I’ve found that the medial pterygoid will promote contralateral cranial tilt, and the lateral pterygoid, contralateral cranial rotation. However, this topic is too esoteric and will probably end up in an article on its own, rather than being elaborated upon here in this one.
I must elaborate on an important topic with regards to the occlusion vs. posture phenomenon. It has become a popular notion within dentistry and related communities, that posture is impossibly altered without addressing dental occlusion. While I agree that dental occlusion will help, it is without a single doubt NOT necessary to balance occlusion to improve posture with permanent gains. It is a false claim.
Dental occlusion does guide posture to some degree, I think this is well proven in much literature as well as clinically, however it is paramount to understand that we can override this guided dysfunction by being aware of our habits, and incorporating good habits. Poor occlusion can not override our efforts. For instance, poor dental occlusion may increase the patient’s tendency to hang forward with the head, due to reduced cervical tensegrity. However, being aware of this, we can easily change it.I know that many claim otherwise, but I can assure you that I’ve resolved a lot of patients postures who had significant malocclusion. It is absolutely doable with some work and discipline. Here’s some interesting research on the topic of occlusion and posture. I’ll address this in the next section.
A clear pattern of associations between crowding and craniocervical posture was found. – Solow et al., 1998
According to the literature reviewed, we believe that there are real correlations between posture and the SS (stomatognathic system). In this way, an increase in postural swaying may indicate a general malaise caused by problems in the SS. – Cuccia et al., 2009
The individual’s postural position can suffer biomechanical alterations due to stomatognathic alterations, causing clinically visible changes in dysfunctional individuals and affecting the performance of the involved structures. – Strini et al., 2009
Significant correlations could be obtained with respect to the facial axis and the lordotic angle, the facial axis and the pelvic inclination, the inner gonial angle and the lordotic angle, the inner gonial angle and the pelvic inclination, the mandibular plane angle and the lordotic angle, the mandibular plane angle and the pelvic inclination, as well as the facial depth and the pelvic inclination. – Lippold et al., 2006
Five animals received no alteration on their bite. Bite was increased on 10 animals and molar teeth were extracted on 10 other animals. Frontal and lateral radiographs were taken on days 0, 7, 14 and 21. Distances from landmarks to a true vertical line were measured on both radiographs. Results: Repeated measures analysis showed statistically significant differences between the amount of the curvature at the cervical and thoracic spines on frontal and lateral radiographs over time Ramirez-Yanez et al., 2014
The data that is available points to the existence of a correlation between posture and occlusion and also asserts the prevalence of associations between cranio-facial anomalies and idiopathic scoliosis in adolescents. – Amat et al., 2009
The data confirmed a beneficial effect of balancing the occlusion with an acrylic wafer on the following paired postural muscles: sternocleidomostoid, erector spinae, and soleus. – bergamini et al., 2008
Based on these findings, it was concluded that changing mandibular position affected body posture. Conversely, changing body posture affected mandibular position. – Sakaguchi et al., 2007
The findings indicate that eye dominance and direction of head rotation are strongly associated in both TMJ and control subjects. Further, in TMJ subjects mandibular deviation occurred in greater frequency than in controls and tends to occur in the contra lateral direction of head rotation. – Pradham et al., 2001
Postural problems were significantly more common among children in the group with mouth breathing syndrome, highlighting the need for early interdisciplinary treatment of this syndrome. – Conti et al., 20111
High mouth breathing prevalence without significant statistical difference between genders,age and type of mouth breathing. There was no association between behavior characteristics and type of breathing. There were significant differences between physical traits and breathing pattern. – Braz, 2006
It was observed that mouth breathers do maintain an extended head posture, which was evident from a decrease in distance between the occiput and dorsal arch of atlas vertebra. – Kumar et al., 1995
The mouth breathing group exhibited reduced cervical lordosis, increased thoracic kyphosis, increased lumbar lordosis and the position of the pelvis was tilted forward. The distance traveled outwards by the diaphragm muscles of mouth breathing children was shorter than that traveled by the muscles of nose breathing children. – Yi et al., 2008
Mouth breathing children presented pathologic adaptations in the postural and morphological characteristics of the stomatognathic system. This suggests the importance of early diagnosis in order to avoid orofacial alterations. – Cattoni et al., 2007
TMD exacerbated by cervical instability
When the neck is unstable, many patients may start to habitually clench the suprahyoid muscles in order to create some cervical stability. The suprahyoid muscle complex can mimic the functions of the longus colli and longus capitis, by pulling the head into flexion and may thus somewhat restrict forward head posture (although not effective in preventing cervical hinging).
One massive problem with this strategy is that the suprahyoid pulls the mandible backward, and when the mandible is pulled back, TMJ shear forces greatly increase, over time causing disc ruptures and TMD symptoms. This is why many people also get jaw pain after first acquiring cervical issues (e.g after a neck injury), but the opposite may of course also occur, as TMD exacerbates cervical instability as well, as shown above.
TMD is mainly caused by underdevelopment of the maxilla, resulting in a dental occlusion that is established too far back. This will cause the mandibular condyle to rest too far back, and thus jam too hard into the TMJ, and wear the joint down over time.
This can be relatively easily resolved by getting the mandible forward in posture, strengthening the pterygoid muscles, and establishing proper tongue posture, as all of these factors contribute to decompression of the TMJ. However, if cervical stability is not regained, and the patient keeps clenching their suprahyoid muscles, this will most likely make it impossible for the patient to alter their mandibular posture, and thus also very difficult to cure TMD. Once again, a multifactorial approach is required to resolve this issue.
Read my TMD-article for more detailed information on this topic. I can not possibly include it all in this article; it’ll become so long that no one will read it!
Forward head posture and ‘the dreaded cervical hinge’
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.
The first rule that we need to know about, is that if the patient is in swayback posture, it is almost impossible to correct forward head posture in solitude. If the pelvis is anterior to the thorax in posture, the nervous system will attempt to maintain equilibrium by pulling the head and shoulders down and forward. Thus it is close to impossible to get lasting results with regards to craniocervical positioning if swayback posture is not addressed first. I’ll talk more about this in the treatment section as well as demonstrate it in a video.
In continuation; if the cervical spine is too kyphotic (forward head posture) and especially if there’s a hinge at one of the cervical levels, this may cause severe movement impairment of most of the cervical spinal segments, as axial rotation is compromised. In turn, this will cause abnormal increase of movement to occur within the upper vertebral segments, especially the atlas joints, in order to uphold normal daily life cervical mobility. Over time, the protective ligaments of the upper cervical spine will loosen up and will thus no longer be able to withstand excessive motion between the A-A and A-O joints. Atlanto-occipital, and perhaps more commonly noted, atlantoaxial laxity and hypermobility will often occur as a result.
In the image below we see patient whose lower cervical spine is hinging, and over time this has caused a buildup of connective tissue at the region of dysfunction (Langevin et al., 2009 has a good paper talking about this phenomenon, in the lumbar spine). The hump that occurs is called dowager’s hump aka buffalo hump. In addition to being a common cause of disc injuries at the given spinal segment as well the proximate levels, ‘the hinge’ will cause regional muscular dysfunction. This is indeed serious if it’s not getting noticed nor addressed. The reason for this is that muscular structures need to have a solid holding point in able to pull origin toward insertion or vice versa. When the muscular origin, such as the transverse or spinous processes of the neck are ‘loose’ due to an unstable foundation (the level of the hinge), most of the muscles that attach in the region will become inhibited by the nervous system, as the nervous system do not allow pulling on unstable structures.
When muscle testing cervical structures of patients who have this dysfunction, global cervical inhibition is often present. And, of course, the patient is usually in pain. Headaches, migraines (hinging may occlude the vertebral artery and vein, more in my migraine article), muscle pain, stiffness, disc herniations, spondylotic injuries and so on. Again, global cervical loss of tensegrity will often occur, which is why it is of paramount importance to identify and treat the cervical hinge.
To identify the hinging pattern, first have a look at the patient’s posture. The neck will usually be visibly hyperextended at one level of the cervical spine, usually at the lower or middle levels. Additionally, and also as a double check if there’s no obvious hinge, run your fingers down the spinous processes and feel for an asymmetrical indent (divot) between these spinous processes. For example, when palpating the spinous processes at the C6-7, which is where most patients hinge on their neck, you’ll feel an obvious decreased prominence of the C5-6 spinous process, which should be just slightly anterior to the C7 spinous process.
If the hinge is identified, this means that the patient’s habits are poor, and that the longus colli and longus capitis (i.e the deep neck flexors) are inevitably weak and inhibited by this nasty habit. Yes, their dental occlusion is probably also poor, but changing habits is free where as fixing occlusion is a very slow and expensive project, and finding a truly skilled dentist (such as Michael Mew or Anthony Sims) is very difficult. And, a more or less unnecessary project if one knows how to treat posture and the TMJ conservatively. I know that this challenges the current paradigm, i.e the unwritten law of therapy for chronic jaw and neck pain sufferers. Much because dentists are some of the only professionals that are able to help these patients.
This is not, though, because dental approach is the only approach. It is because current conservative postural and corrective means are simply of poor value. Common practices for postural and muscular correctives often lack important nuances and tend to be wrong, and even downright detrimental. I know this is tough to swallow for some of you, especially if you are a therapist yourself, but let’s face it; these patients are rarely being helped by conservative measures. If the current therapeutic means were effective, they would be better. Let’s not fool ourselves – And let’s keep an open mind. With proper TMJ and cervical postural correctives, no occlusive work is needed in my experience.
To get the patient out of the hinge, it is not sufficient to simply strengthen the deep neck flexors. We need to consciously change the patient’s habits (the cause), and strengthen the deep neck flexors (the symptoms). When we address both the cause and the symptoms, the patient will get better, faster. If we address just the cause, it’ll take forever to get well. If we address the symptoms, most often it won’t be an effective treatment, and other times it simply won’t give lasting results. It depends.
So, back to the point; once the hinge has been identified, the patient needs to learn to be ‘long in the neck’ by pulling the back of their head up toward the roof, and gently pull the chin down (cue courtesy of Evan Osar’s book from 2012) . Re-palpate the spinous process after the correction, and if done properly, the spinous processes will now be of natural symmetry, indicative of proper alignment. This will restore tensegrity (i.e muscle function and tension) and proper alignment in the cervical spine and pave the way for healing. This is not a mere exercise, it’s a permanent postural change. The patient must learn to stay there forever, and it’ll be hard in the beginning but they’ll get used to it, and then it will feel tremendously better.
As already mentioned, forward head posture and cervical hinging will often lead to hypermobility of the upper cervical junction, as the spine’s movement is impaired and is thus not able to rotate axially as one unit any more. It will also often cause hypermobility in regards to extension, and ability to properly extend the occiput is often lost.
If you recall, the sternocleidomastoid and suboccipital muscles are the ones that mainly extend the head, and of course these muscles will become inhibited and atrophied as the years go by without them being properly utilized. Sadly these muscles have gotten an infamous reputation for being “over-active and tight”, but this could not be further from the truth. Seeing therapists needle and massage these muscles, only to, potentially exacerbate the patient’s dysfunction down the line (many get this ‘treatment’ for years on end).
Muscles should be thick and and have a decent amount of tone, if they are strong and working properly. It’s a great misconception that muscles should be sloppy and soft; they should NOT. Rather, soft and hypotonic muscles are most often inhibited, and thus weak, tight and painful (both to touch and otherwise). Using muscle tests and exercise strength tests as well as evaluating tonus and thickness of muscles, will help to get a true status of the given muscle’s function and ability, rather than ‘tightness’ alone, which means absolutely nothing when interpreted in solitude.
Back to the point; after years of cervical hinging, many clients thus lose their ability to extend the occiput properly. This will exacerbate spinal hyperextension and promote dysfunctional movement- and muscle activation patterns, which in turn causes a worsening of atlas joint instability. It is of utmost importance to not only re-establish proper cervical alignment, but to also teach the client how to rotate and extend the neck and head without falling back into the hinging pattern. In addition to this, of course, we will exercise the suboccipital, longus colli and longus capitis muscles, which I refer to as the ‘trio of success’, as they both stabilize the atlas joints, syncronize their movements and maintain a ‘long neck’ position during craniocervical movements.
Palpation of these muscles, especially the suboccipitals in patients with severe cervical dyskinesia and misalignment, will commonly reveal significant hypotrophy and lack of tone. When the suboccipitals aren’t firing properly, they’re not able to syncronize the cranium with the eyes’ motions, and thus vertigo, sea sickness, car sickness and similar symptoms of seemingly vestibular origin will occur. In reality, it is craniocervical instability.
It is of paramount importance to identify and treat the cervical hinge, and restore proper cervical kinematics. This is a topic not widely discussed; rather, it is like the beast of cervical dysfunction that no one are talking about nor treating. Therefore, as I touched upon already, most symptomatic treatment will not prove very fruitful, especially in the long run. The hinge MUST be corrected if supplementary therapy is to be successful, in my experience. It is definitely not enough to normalize dental occlusion, in my experience.
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.
The scapula should be resting between the T2 and T7 vertebrae height wise, which means that the superior scapular angle should be in level with the T2, and the inferior angle in level with the T7. Lower than this, and the trapezius will inhibit. Higher than this, and it usually indicates a dysfunction of the levator scapulae, which is also not beneficial. The trapezius should be mildly active in posture, NOT relaxed as many mistakenly, and iatrogenically claim. The trapezius muscle is the main stabilizer and load bearer of the scapula, and is thus an extremely important muscle. When the trapezius inhibits in posture, bad things tend to happen, both to the neck and to the shoulders!
Below you can see two images of improper, and proper scapular resting position. On the right we see significant depression and some scapular winging, a very common appearance for people with neck and shoulder pain. On the left, however, we see proper upward rotation and height in resting position, caused by a healthy and functioning trapezius muscle. Do not pay attention to the muscle mass, that’s not at all the point here. The point is the scapular positioning.
In addition to normalizing scapular resting positioning, I recommend strengthening the trapezius. The levator scapulae can also be strengthened, but I’ll get back to exactly how and why a little further down, as this muscle greatly affects the atlas joints. If you want to learn more detailed information about scapular posture and movement, you’ll have to review my scapular dyskinesis article.
Other contributing factors
Other factors could be work with extremely monotonous movement patterns, especially on one side or toward a certain direction. I could impossibly list all such examples, but just make sure that you balance out whatever the patient is doing at work, with the correctives that are prescribed.
As a therapist, for example, I look down a lot. Looking down in large portions of the day will inhibit the suboccipitals (this is quite common for many professions who look down a lot, such as hair dressers), and it will therefore be necessary to do maintenance work on these muscles in order to keep them adequately functioning. Certain machinery may require the operator to continuously look toward a certain direction, or continuously load and use the arms very differently.
The hairdresser below, for example, would be required, first of all to use a better general posture, but because looking down a lot every day is more or less inevitable, it would be beneficial to strengthen the neck flexors and suboccipitals.
Monotonous cervical and occipital movement is perhaps a greater precursor to dysfunction than imbalanced shoulder loading, but all of these kinds of factors should be considered. If the person has a job or hobby that promotes monotonous movement patterns, it’s a good idea to balance this out with regular maintenance work for the muscles that aren’t being stimulated. I generally do not recommend much stretching when it comes to dysfunction, but dry needling or massaging of certain muscles may prove beneficial in these exceptional circumstances.
The sideways forklift seen below is another example, and is a pretty horrible piece of machinery. It promotes extremely monotonous and downright detrimental cervical habits. Yes, so does the hairdressing, but continuously looking to one side (rotation) is genereally worse than flexion/extension patterns. Problems that would arise at the below situation is that not only will be left levator scapulae become stretched, and pull the atlas into leftward rotation, but it’ll also become weak. The right levator will shorten and is unlikely to get tense enough to balance the atlantal pull and encouraged torsion that is coming from the left side.
In cases like this, extremely good posture while working, as well as cervical flexibility will required. Furthermore, maintenance correctives to the atlas, although not optimal, is probably inevitable. Moreover the suboccipitals, left levator scapulae, right SCM, right scalenes, as well as the deep neck flexors would all most likely require maintenance strengthening. If you drive a lift like this, however, and I’m talking about those who do so for large portions of the day; the best option is probably to demand another machine, or to find another job!
These are of course just examples. A thorough examination is key, together with good questions, to reveal any potential cause of dysfunction. An evaluation will have to be made with regards to whether or not the monotonous work or hobby is or is not a burden too great for the patient’s condition.
Potential consequences of misalignment
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.
If you search for it on the internet, you will find that many claim it to be the cause and solution to virtually anything. I agree that many things are associated with atlas misalignment, but I do not necessarily agree that they’re all caused by atlas misalignment. In my experience, however, the same causes of atlas misalignment may also cause issues such as thoracic outlet syndrome, severe muscle imbalances, headaches, postural abnormalities, and so on. In this section I will try to address the symptoms that I think are more or less directly related to atlas misalignment.
What came first, the hen or the egg?
Potential direct symptoms caused by atlas misalignment are: upper neck pain, vertigo, intracranial vasal hypertension, vertebrobasilar insufficiency (from atlantal torsion), imbalanced posture, cerebellar herniation (chiari). Even stroke and death can occur in extremely rare & severe cases (don’t get scared; people also die driving cars, so take a deep breath and relax. I must mention these things if I am to get all the necessary information into the article.) Thankfully though, in extreme cases, any conventional ERs will more than likely identify such an issue, e.g vertebral artery dissection or brain stem compression.
Usually though, the underlying cause and exacerbative factor of the atlantal instability, will carry many symptoms on its own. Such underlying causes may often be whiplash injuries or extremely poor postural habits and/or dental occlusion, over time leading to forward head & generally poor posture with neck “hinging”, thoracic outlet syndrome, cervical disc herniations, vertebrobasilar insufficiency (from TOS), headaches, muscle imbalances and muscle pain.
Vertigo / dizziness
Atlantal misalignment is a common cause of symptoms that may appear to be of sole vestibular origin, but rather originate from upper cervical dysfunction. The three most common causes for this are 1: thoracic outlet syndrome, causing symptoms of vertebrobasilar insufficiency (by occluding the vertebral artery), 2: dysfunction of the suboccipital muscle complex, and 3: Compression of the internal jugular vein. There is also a fourth and more rare cause, called bow hunter’s syndrome, where the A-A or A-O joints have become very lax, and therefore compromised.
Compression of the internal jugular vein is probably the factor most relevant to the vestibular system, as it may prevent drainage of endolymphatic fluid from the cochlea and vestibular chambers.
The inner ear senses both balance and hearing based on movement of hair cells within the vestibular chamber and scala media of the cochlea. These hair cells are moved by a fluid called endolymph. For hearing and balance to be normal, endolymphatic fluid must be in homeostasis (balance). Increase of endolymphatic fluid will cause hearing loss and excessive movement of the hair sensory organs within the semicircular canals, causing vertigo, which is often the case with Meniere’s disease patients, vestibular migraines and similar.
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.
The CT scan below shows that the left IJV is compressed by the atlas vertebrae’s transverse process in a migraine patient, as it has torsioned toward the right. Symptoms were only present on the compressed side (left). Note the difference between the transverse process and the mandibular ramus on the left and right sides. Arrow shows compression of internal jugular vein.
Fig. x – Gweon et al., 2011
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.
In the image below, where there is good cervical posture, there is a decent margin between the IJV and atlas.
When the neck hinges backward, however, the atlas drives forward into the IJV and occludes it, causing craniovascular hypertension. Seen in realtime in this video.
It has been demonstrated that internal jugular vein (IJV) compression aggravates headache intensity in patients of migraine. In the result, the venodilatation of IJV in response to each level of Valsalva pressure in patients with migraine was significantly less than that in normal individuals. – Chung et al., 2010
We aimed to assess whether migraine is associated with changes in the distribution of the venous drainage through primary and secondary pathways by using phase-contrast magnetic resonance imaging (MRI). Cine-phase contrast scans with high-velocity encoding were employed to quantify arterial inflow and flow in the primary venous channels (right and left jugular veins), whereas scans with low-velocity encoding were employed to quantify flow in the secondary venous channels (epidural, vertebral, and deep cervical veins). CONCLUSION: Migraine patients showed a significantly larger percentage of venous outflow through secondary channels. The mechanism of this alteration remains to be elucidated. Potential mechanisms include repeated release of vasoactive substances or growth factors. – Koerte et al., 2011
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<0.01). The maximum area of lateral mass of the atlas at IJV obstruction side in obstruction group was 103.4 ± 25.3 mm2 which is significantly larger than in control group (p<0.05). – Gweon et al., 2011
Episodic vertigo is usually due to endolymphatic hydrops, distension of the inner ear membranes, and may be primary (Ménière’s disease) or secondary (otic syphilis, delayed endolymphatic hydrops, Cogan’s disease, recurrent vestibulopathy). Patients with typical Ménière’s disease have recurring attacks of vertigo, sensorineural hearing loss, tinnitus, and, sometimes, a fluctuating fullness in the ear. – Smouha & Wanna, 2009
The symptoms of progressive endolymphatic hydrops can be correlated with two principal types of pathologic change: (1) distentions and ruptures of the endolymphatic system,2,3 and (2) alterations in the cytoarchitecture of the auditory and vestibular sense organs, sometimes accompanied by atrophic changes. Coincident with rupture, there is sudden contamination of the perilymphatic fluid with neurotoxic endolymph (140 mEq/L of potassium) that causes paralysis of the sensory and neural structures and is expressed clinically as episodic vertigo, fluctuating hearing loss, or both. – Schuknecht, 2010
In animals with surgically induced hydrops, similar anatomical changes are found to those in patients, including degeneration of fibrocytes in the lateral wall, loss of spiral ganglion cells, disruption of hair cell stereocilia, and eventual loss of hair cells (Nadol, J. B., Jr. et al., 1995) – Harris & Salt, 2008
Micromechanical indentation of the horizontal canal (HC) duct and utricular vestibule was used to simulate sinusoidal head rotation and fluid volume injection. Single-unit neural spike trains and endolymph pressure within the ampulla, on both sides of the cupula, were recorded simultaneously. ΔP averaged 0.013 Pa per 1°/s of sinusoidal angular head velocity and P0 averaged 0.2 Pa per 1 nL of endolymph volume injection. The most responsive afferents had a threshold sensitivity to ΔP of 10-3 Pa and to P0 of 5 × 10-2 Pa based on a discharge modulation criterion of 1 impulse/s per cycle for 2 Hz pressure stimuli. Neural sensitivity to ΔP was expected on the basis of transverse cupular and hair bundle deflections. Analysis of mechanics of the end organ, neuronal projections into the crista, and individual neural firing patterns indicates that P0 sensitivity resulted from pressure-induced distension of the ampulla that led to a nonuniform cupular deformation pattern and hair bundle deflections. – Konrádsson et al., 1994
The pathogenesis of isolated headache in cerebral venous thrombosis (CVT) in the absence of intracranial hypertension, SAH, meningitis or intracerebral lesion is unknown but may involve changes in the walls of the occluded sinus. Hence MRI/MRV should be used to look for signs of CVT in all patients with recent headache (progressive or thunderclap) even when the CT scan and CSF examination are normal. – Cumurciuc et al., 2005
Normal venous drainage of the vestibular organs through the vein of the paravestibular canaliculus (PVC) may be crucial to inner ear fluid mechanics. It is proposed that increased venous pressure, with resultant venous insufficiency of the vestibular organs, may result in endolymphatic hydrops unless collateral venous circulation develops. Certain variations in pattern of venous drainage where the vestibular organs drain predominantly through the PVC vein may be a predisposing factor. In patients with Meniere’s disease, different mechanisms can cause venous insufficiency. One suggested mechanism is morphologic change in the microcirculation of the intermediate portion of the endolymphatic sac. Microcirculation changes may be associated with fibrosis of the perisac tissues or shortening of the intermediate sac region or might be physiologically determined. Venous insufficiency may also result from anomalies of the PVC vein – Gussen, 1983
Entrapment of the cervical ganglia and sympathetic chain
Neck hinging will cause dysfunction of the longus colli and longus capitis muscles, as explained earlier. Between these muscles and the alar fascia, resides the sympathetic chain and its cervical ganglia. Studies have shown that dysfunctional musculature cause increased density, thickness and rigidity of connective tissue. This is why we so often see nerve entrapment syndromes nearby dysfunctional musculature (more on this in my lumbar plexus entrapment article). Thus, fascial restrictions may develop subsequent to dysfunction of the longi muscles, causing friction and reduced neural tissue gliding, leading to irritation of the cervical ganglia and sympathetic chain.
The cervical ganglia controls a lot of processes in the body, and the symptoms may therefore be quite diffuse. Knowledge of this phenomenon and its associated potential symptoms is required in order to detect and treat the issue.
For example, the superior cervical ganglion innervates the vestibular system, the eyes, carotid bodies, pineal gland and so on. Not surprisingly, Ménière’s disease, which is a vestibular disorder of supposed idiopathic origin, has been associated with dysfunction of the superior cervical ganglion. Tinnitus has been associated with the cervical ganglia as well. I’ve also found irritation of these nerves to cause itchy ear syndrome, which is a problem often reported by Ménière’s sufferers.
With regards to the eyes, they control dilation and constriction of the pupils, and may thus affect vision, concentration and so on. Moreover, it has been documented that both tinnitus and ocular impairment may occur post whiplash injury. It may even explain why the term “book worm” came into play; meaning, the child’s maladaptive vision may be caused by improper cervical postures, which in turn cause irritation of the cervical ganglia. The latter, though, is hypothetical, but not so far fetched in my opinion. I cited a somewhat relevant study below, where kids with myopia (near-sightedness) and hearing loss (hearing loss has also been somewhat associated with sympathetic disturbances (Bielefeld & Henderson, 2007)) had a tendency to have poor craniocervical postures. It is, however, unsure whether or not the poor postures occurred first.
Complex regional pain syndrome pain syndrome has also been correlated with disruption of the cervical sympathetic chain (Yucel et al., 2009; Meredith C.B. Adams, Robert W. Hurley, in Practical Management of Pain (Fifth Edition), 2014), along with Reynaud’s diease (Shreeve & La Rose, 2011) and probably many other diffuse topics.
Myofascial entrapment of the cervical sympathetic chain and ganglia may be relieved by optimizing cervical posture, atlantal alignment and strengthening the longus colli and longus capitis muscles. All of these measures are detailed throughout this article.
Note: Because of the great amount of possible references, I have had to limit the quote quantity below. More research definitely exists, and may be found by searching for it.
The sympathetic chain is enclosed within the alar fascia, a thin fascia that separates the cervical sympathetic chain from the retropharyngeal space. The carotid sheath is connected to the alar fascia by a mesothelium-like fascia. The fascial plane that encloses the sympathetic chain may be in direct communication with several spaces and structures, including the brachial plexus, vertebral artery, endothoracic fascia, and the thoracic wall muscle at T1-T2. At the C6 level, the cervical sympathetic trunk is located posterolaterally to the prevertebral fascia on the surface of the longus colli muscle. – Adams et al., 2014
The cervical sympathetic chain lies anterior to the longus colli and longus capitis muscles and deep to the prevertebral fascia – Civelek et al., 2008
The effect of novocain block on vertigo of Menie’re’s disease.-I have had the satisfaction of abruptly terminating two cases of Meniere’s disease during acute severe attacks by means of a procaine block. One case occurred at the Wembley Hospital. The patient was wheeled into the theatre lying curled up vomiting, with nystagmus, pallor and sweating. 5 ml. of procaine were injected in the stellate ganglion and within three minutes the patient had recovered sufficiently as to walk back unaided to the ward. – Garnett Passe, Sympathectomy in Relation to Meniere’s Disease, Nerve Deafness and Tinnitus
Superior cervical ganglion neurons project to the dilator pupillae muscle of the iris to control pupil dilation. Ocular blood flow is controlled both via direct autonomic influences on the vasculature of the optic nerve, choroid, ciliary body, and iris, as well as via indirect influences on retinal blood flow. – McDougal & Gamlin, 2015
It is generally believed that the cause of Meniere’s disease is related to autonomic dysfunction (Hilger’, 1950; Beickert’, 1953; Watanabe10, 1955; Hisaki’, 1960; Williams”, 1965). The positive rate showing a response of either the sympathetic hyperreactor or sympathetic hyporeactor type in the cases with Meniere’s disease and aural vertigo was 79% and 87% respectively in the acute stage when nystagmus was present. – Uemura et al., 1972
After local anesthetic was applied to the facet joints, patients reported within 10 minutes that their tinnitus had diminished significantly. Simultaneously, mydriasis disappeared. In one patient, tinnitus was controlled completely. Tinnitus can temporarily be reduced by the application of local anesthetic to Cl-C2 facet joints and buprenorphine analgesia of the superior cervical ganglion in patients with Cl-C2 facet joint disorders. – Franz et al., 1998
Whiplash or indirect injuries to the neck as a consequence of motor vehicle collisions are a common occurrence in which the frequency of ocular complications is largely unknown. Ophthalmic and oculomotor function was investigated in a longitudinal study of 39 cases who had their initial ophthalmological assessment within one week of the whiplash injury. Ten of 39 cases had ocular symptoms and signs which developed shortly after the accident. – Burke et al., 1992
Frequently, patients report the development of tinnitus after traumatic injuries. However, to which extent this specific etiologic factor plays a role for the phenomenology of tinnitus is still incompletely understood. – Kreuzer et al., 2012
Symptoms of cervical spine disorders, such as head and neck/shoulder pain, were all significantly more frequent in the patient group than in the control group. Most of the patients (75%) reported a strong association between head neck movements in the atlanto-occipital and atlanto-axial joints and triggered attacks of vertigo. Also, 29% of the patients could influence their tinnitus by mandibular movements. Signs of cervical spine disorders, such as limitations in side-bending and rotation movements, were significantly more frequent in the patient group than in the control group. Tenderness to palpation of the transverse processes of the atlas and the axis, the upper and middle trapezius, and the levator scapulae muscle were also significantly more frequent in the patient group. The study shows a much higher prevalence of signs and symptoms of cervical spine disorders in patients diagnosed with Meniere’s disease compared with control subjects from the general population. – Bjorne et al., 1998
The results of this study indicate that visual and hearing impairments can affect the head and neck alignment of children and this alignment has a significant relation with some of the anthropometrical dimensions. – Daneshmandi et al., 2014
Thoracic outlet syndrome
Thoracic outlet syndrome can lead to symptoms of vertebrobasilar insufficiency, such as vertigo, confusion, and blurred vision, especially during cervical rotation and/or extension. It may also cause migraines, thunderclap headaches and more. And, as mentioned, although this may seem to be a vestibular dysfunction, it may turn out to be of vascular origin. It may also cause entrapment of the vagus and phrenic nerves, as well as the whole brachial plexus, affecting the autonomic nervous system and causing many diffuse issues, such as coughing, tinnitus, clogged ear syndrome, chest pain, heart pain, dry throat, hiccups, difficulty breathing and even atrial fibrillation. Read more in my thoracic outlet syndrome article.
The easiest way to diagnose whether or not there is TOS, is to squeeze into the interscalene triangle. If it reproduces severe neuralgic symptoms (patient will jump in pain on the treatment table), it’s likely TOS. The vertebral artery dissection test (VAD) may also be positive if the patient has TOS, reproducing the symptoms that are described above. I’ll quote some interesting research below the illustration.
Thoracic Outlet Syndrome (TOS) causes dizziness because of positional compression of the vertebral artery with resultant symptoms of vertebrobasilary insufficiency. Compression of 7,C8,and T1 nerves fibers is responsible for the neck pain. – Selmonosky, 2007
Chest pain or pseudoangina can be caused by TOS. Dorsal sympathectomy is helpful for patients with sympathetic maintained pain syndrome or causalgia and patients with recurrent TOS symptoms who need a second procedure.
Compression of the sympathetic nerves in the thoracic outlet may occur alone or in combination with peripheral nerve and blood vessels. The sympathetics are intimately attached to the artery as well as adjacent to the bone. They may be compressed or irritated in primary or recurrent TOS. Atypical chest pain (pseudoangina) simulates cardiac pain (48). Major indications for dorsal sympathectomy include hyperhidrosis, Raynaud’s phenomenon or disease, causalgia, SMPS, reflex sympathetic dystrophy, and vascular insufficiency of the upper extremity.
Cough attacks elicited by movement of the neck and right arm are reported in a patient who had sustained several shoulder injuries and who had an anterior scalenectomy. The coughing was accompanied by weakness in the right upper limb. At exploration, the phrenic nerve was found adhered to the brachial plexus. The cough attacks disappeared, and the weakness of the right upper limb improved somewhat after lysis of the adhesions between the phrenic nerve and the plexus and after external neurolysis of the upper, middle, and lower trunks. Postoperatively, the patient could elevate his right arm without coughing. – Yamagami et al., 1994
Symathetically mediated atrial fibrillation is observed in the presence of any heart disease, the first effect of which is to provoke a vagal withdrawal. The role of the autonomic influences should be taken into consideration every time conventional antiarrhythmic treatment is insufficient. – Coumel, 1994
A 44-year-old female presented with severe right posterior neck pain and vertigo followed closely by thunderclap headache that was confirmed as right VAD (V4 segment) with delayed right dorsal medullary infarction two days later. Her headache, vertigo, and truncal ataxia were completely improved one week later. – Hsu & Sung, 2014
Dysfunction of the suboccipital muscles
As I mentioned earlier, the suboccipitals syncronize the head with the eyes’ movements. If this function is compromised, vertigo may occur, especially during certain eye- or cranial movements. These patients will virtually always be hinging on their necks, as this promote inhibition of the suboccipitals. Because neck hinging also contributes to TOS, it’s important to distinguish where the symptoms are coming from. Especially IF the patient has TOS as well, which they often do.
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.
Bow hunter syndrome
Through the transverse foramen of the (C6-) C2 and C1 vertebrae, through the posterior atlanto-occipital membrane and into the foramen magnum, passes the vertebral artery. The V.A supplies the brain with blood. If there’s instability such as severe hypermobility with regards to rotation, this may strain or occlude the vertebral artery (Bow hunter’s syndrome), leading to symptoms such as confusion, migraine, headaches, blurred vision, lack of concentration, etc. In extreme and rare cases, this may rupture the vertebral artery, causing stroke and even death. Occlusion of the vertebral artery, be it from TOS or the atlas joints, may also cause migraines.
A pathognomonic finding of BHS is the improvement of symptoms when the patient is in a neutral position, even after he claims to have dizziness or blackout when he turns his head to one side. When BHS is suspicious, considerable authors used digital subtraction angiography as the diagnostic modality1). In our cases, clinical symptoms were aggravated when patients turned their head to one side; symptoms were improved when the patients’ heads returned to a neutral position. Prior otolaryngological evaluations were unremarkable. – Go et al., 2013
Leftward head rotations in a patient with a rotational vertebral artery occlusion syndrome elicited recurrent uniform attacks of severe rotatory vertigo and tinnitus in the right ear. These attacks were accompanied by a mixed clockwise torsional downbeat nystagmus with a horizontal component toward the right. – Strupp et al., 2000
In our series, symptoms of vertebrobasilar insufficiency were reproducible with rotational head movement. Compression of the vertebral artery was demonstrated angiographically. The correct site of occlusion of the vertebral artery was apparent only by dynamic angiography with progressive head rotation. All of the patients presented in the illustrative cases had occlusion at the C2 level; however, one patient had been previously misdiagnosed and another had an additional site of occlusion. The anatomic course of the vertebral artery is described in addition to the sites of rotational occlusion. Rotational vertebral occlusion is an important cause of vertebrobasilar symptoms, which may lead to permanent neurological deficit if left undiagnosed. Dynamic angiography is the established method of diagnosis. Great care must be taken to avoid misdiagnosing the site of occlusion or missing a second occlusive site. For this reason, it is crucial to have a thorough understanding of the anatomic course of the vertebral artery and the muscular and tendinous insertions, which may cause rotational occlusion. – Kuether et al., 1997
A 41-year-old male developed dizziness and light-headedness during chiropractic manipulation when his head was turned to the extreme right position. Computed tomography angiography (CTA) of the neck and selective digital subtraction angiography (DSA) of the vertebral arteries revealed that when the patient turned his head to the extreme right position the dominant right vertebral artery was compressed between the posterior aspect of the thyroid cartilage and anterior aspect of the right transverse process of C6 resulting in focal stenosis, while the left vertebral artery is severely compressed with significant flow limitation at the level of C1-2. – Dabus et al., 2008
What is known is that the greatest mechanical stress affecting the contralateral artery occurs at a position of cervical rotation and extension. Furthermore, if this position is sustained, the arterial flow takes longer to return to normal.32 In addition to the C1–2 portion, the VA is vulnerable to compression in the portion that courses through the transverse foramen from C6 to C1. Because of its fixation to the spine in this segment, subluxations of one vertebral body on another may exert undue tension and traction on the artery. Positions of the cervical spine can cause compression of the VA.19,33 Rotation–extension–traction appears to be the most stressful, followed by rotation–extension, rotation alone, side flexion alone, extension alone, and then flexion.19,33,34 – Dutton’s orthopaedic examination evaluation & intervention, 4e, 2016
There are three, perhaps four major ways that altas misalignment can contribute to migraines.
- Compressing the internal jugular vein
- Pulling on the vertebral artery
- Pseudomigraines caused by weakness of the suboccipitals
- Theoretically, extreme atlantal torsions may also compress the internal carotid artery
Read more about migraines in my migraine article. The above points are also connected to other dysfunctions that are described more in detail both above and below.
The jugular foramen and carotid canal
Right in front of the atlas vertebrae’s transverse process emerges the neurovascular bundle coming out of the jugular foramen, carotid canal and hypoglossal canal. As seen in the illustration below, these are the internal jugular vein, internal carotid artery, hypoglossal nerve, vagus nerve, accessory nerve and glossopharyngeal nerve. These nerves are all controlling many autonomic processes, and these may be disturbed if they become compressed, causing varying degrees of dysautonomia. They may of course also cause pain, tingling and similar common indications of somatic nervous irritation. If the transverse process of the atlas vertebrae comes forward, it may compress these structures to varying degrees between itself and. the styloid process. The CN 9-12 transmit between the TP and SP in about 66% of the population (Kim et al., 2014).
Anything related to autonomic nerve dysfunction is a massive rabbit hole. I’ve written about this in my TOS and lumbar plexus compression syndrome (LPCS) articles as well. It is almost impossible to list or even estimate all of the potential consequences in some of these circumstances, especially if a whole plexus is affected as with TOS and LPCS. Although there’s no plexus entrapment with regards to compression of the emerging structures from the jugular foramen, the vagus nerve does innervate most of the body’s organs, and it is therefore difficult to realistically estimate the level of possible dysfunction.
The vagus nerve controls the cough reflex. It also opens and closes the eustachian tube by controlling the salpingopharyngeus and levator veli palatini muscles. It is not uncommon that irritation of the vagus nerve can lead to ‘clogged’ ears, tinnitus, and chronic cough. Many of these patients also have bowel issues, and considering the fact that the vagus nerve stimulates secretion of hydrochloric acid and digestive enzymes, a lack of such will likely cause maldigestion and gut issues.
Moreover it is commonly known that the vagus nerve slows the heart rate. Now, I am not saying that this is always an issue, but it is definitely an association that I’ve noticed in several patients with vagus nerve entrapment. I truly do not know how many problems this *could* *realistically* cause, but I am discovering new and interesting things all the time. I have seen some unthinkable things happen with regards to lumbar plexus compression syndrome, such as atrial fibrillation both caused and resolved, prostate dysfunction (involuntary seminal discharge), urinary inconsistency and so on. Autonomic entrapment issues caused by muscles and/or atlas misalignment is more or less an uncharted area, but I prefer to tell you what I have discovered, not because I have all the answers, but to create awareness and interest in these somewhat mysterious and generally rarely spoken of topics.
The accessory nerve originates from the C1-6 levels of the spinal cord. It then separates into two divisions, the spinal and cranial divisions. The spinal division exit via the jugular foramen, pierces the sternocleidomastoid muscle before it ventures into the dorsum, between the levator scapulae and trapezius muscles. Posterior to the sternocleidomastoid muscle, it also anastomosis (connect) with the cervical plexus. Accessory nerve pain may be generated along its path if there is entrapment within the myofascial structures, or at the craniocervical level.
Further, it controls the sternocleidomastoid and trapezius muscles. These are often affected in dystonia patients. Could the atlas be the cause? I don’t know, but it’s plausible. For your information, Dr. Anthony Sims DDS (et al., 2007, 2009) claims that continuous noxious input into a nerve may cause such symptoms, especially with regards to TMD and the trigeminal nerve. I have also talked to patients whose pulling sensation have ceased temporarily after getting certain atlas adjustments (not my treatment).
The hypoglossal nerve controls the movements of the tongue. Additionally, it supplies movements including clearing the mouth of saliva and other autonomic activities. The hypoglossal nucleus also interacts with the reticular formation, which amongst other things suboconsciouly affect speech and articulation. There could be a relation between this nerve’s dysfunction and tourette’s syndrome (Sims & Stack, 2007).
The glossopharyngeal nerve interacts with several structures as well, such as the tongue, tonsils, parotid gland and the trigeminothalamic tract. It is also forms a part of the pharyngeal plexus along with the vagus nerve. Disturbances within all of these regions may thus potentially occur if the glossophargyneal nerve is irritated, such as salivary production, taste, tonsilar hypersensitivity. Perhaps most interestingly, interaction and dysregulation via the trigeminothalamic tract may cause disturbances in perceived touch, temperature, and pain, which are relatively common symptoms in many chronic sufferers.
If you have a look at the illustration below, it is obvious that these important structures are lying very close to the atlas and its transverse process. Now, in a perfect world, the atlas should not move significantly on the occiput, and thus it would never get a chance to jam into either of the neurovascular bundles. Sadly, though, this may definitely occur. Furthermore, they emerge between the rectus capitis anterior & longus capitis muscles posteriorly, and the alar fascia anteriorly, the first-mentioned both of which prevent prevent posterior occipital gliding, A-O torsions, and also protect the neurovascular bundle from rubbing against the atlas’ transverse process and anterior vertebral body.
This is also why it is important to at least evaluate the atlas joint when treating patients with migraines for instance, as the jugular venous outlet or even carotid inlet may be occluded by the atlas vertebrae. This is a scary thought indeed, and some may claim it to be impossible, but I have seen some scary cases with tremendous A-O misalignments in my clinic. We should both consider and understand, that years upon years of faulty movement patterns (such as severe cervical hinging) will cause laxity and lead to joint movements that were never supposed to happen. Of course, to varying degrees once again. I have seen patients who have been whiplash injured whose atlas was lax, but A-O joint relatively well positioned, and I have seen the dead opposite. Don’t assume anything until a proper examination has been conducted.
Fig. 27 – 3: Vagus nerve, 4: IJV, 5: ICA
Temporomandibular joint compression
Atlas misalignment can [mildly] contribute to TMD. It’s not a large factor. I do consider the opposite relationship, i.e jaw influencing the atlas joint as a more important factor, but when the head tilts to one side, be it due to occlusal issues or atlas misalignment (e.g due to whiplash injury or longstanding cervical dysfunction), the mandible tends to shift to that side.
When the mandible shifts to one side, the shearing forces within the ipsilateral TMJ will be greater. 1-2 millimeters of lessened space between the mandibular condyle and the TMJ’s glenoid fossa may be enough to trigger shearing within the joint and eventually wear it down over time. This may also compress the trigeminal nerve, and cause a lot of difficulties.
The actor in the picture above has probably had malocclusion since a young age and thus the cranial bones have not developed symmetrically. It’s not expected to see such a great cranial dysmorphia if the atlas alone is the underlying factor, unless, perhaps, it happened at a very young age. Either way it does nicely illustrate how the jaw follows cranial tilt, which is why many get more symptoms on one side. A droopy eyelid will usually also occur on the higher eye, i.e the opposite eye of cranial tilt’s direction.
Another factor that I also mentioned above, is that many patients clench their suprahyoidal muscles in a subconscious attempt to force neck stability. The suprahyoid muscle complex promotes posterior translation of the mandible, and may thus increase shearing forces in the temporomandibular joints.
Trigeminal nerve dysfunction
I have covered this in my TMD article, but I’ll briefly address the trigeminal nerve. The trigeminal nerve is the largest cranial nerve, also known as cranial nerve V, or 5. It has three main branches, the ophthalamic (V1), maxillary (V2) and mandibular (V3) branches.
The trigeminal nerve is often affected in patients who have TMD and underdeveloped upper jaws. Its auriculotemporal branch can be compressed between the mandibular condyle when it’s resting too far back, which is, as I mentioned earlier, a very typical occurrence for TMD sufferers. Furthermore, some of its branches, such as the buccal and and lingual nerves, pass through the lateral pterygoid muscles which are also commonly found to be extremely weak in TMD population.
Because it has both autonomic as well as motor and sensory nervous functions, and connects to most cranial ganglia, a lot of diffuse problems may arise when it is affected. Involuntary tear secretions, facial, palatal and tooth numbness, toothaches, tremendous stabbing headaches in the temple and facial region (trigeminal neuralgia), eye pain, salivary gland pain and even swelling, tinnitus (as it controls the tensor tympani and tensor veli palatini muscles, which again control sound modulation and the eustachian tube within the ear), and so on. It also has sensory innervation of the cranial vessels, and research has shown an association between it, and migraines.
Once again, read more about this topic and its respective treatment strategy in my temporomandibular joint disorder (TMD) article. However, in short, we want to get the mandible forward in posture as well as retrain the pattern in which the mouth opens and closes. The mouth should open with protraction, not retraction, as this is very detrimental and increases shear forces within the joint and thus also the degree of compression and noxous input imposed on the auriculotemporal nerve. Furthermore, it is beneficial to strengthen the pterygoids, as they both help to bring the jaw forward, in opening it properly (without retraction), and relieve tension on the buccal and lingual nerves.
When the head moves, the body will move. It is a well known anecdotal ‘fact’ that when the head either rotates or tilts in one direction, the whole body will zig-zag in compensation in order to get the cranium back into equilibrium and the eyes levelled.
Commonly, if the head tilts to one side, the neck will rotate contralaterally. The body zig-zags all the way down, where one shoulder is up and one down, similarly with the pelvis, and one femur will be externally rotated where the other internally rotated. These are not rules, but common occurrences and observations I have made.
Now, this is where I somewhat disagree with many others. I disagree that minor discrepancies should be always considered as pathology. I also disagree that atlas correctives will resolve all of the body’s compensatory patterns; they will usually require to be addressed individually, especially if the issue has been long standing.
It is common to have some asymmetry. Sometimes the perceived “misalignment” may even be bone (osseous) anomalies, and not at all misalignment! Thus, use discernment and common sense while evaluating and treating asymmetries. It is also my impression that many chase extreme detail with regards to minor issues, such as a minor hip height difference, leg length, or femoral rotation. Although sometimes important, it seems to me that more important principles are often neglected in this process, especially in the sagittal plane, such as ignoring proper pelvic extension, removing the cervical hinge and so on; things that are of much greater importance. Working on minor issues while neglecting or being oblivious to more major problems, will not yield optimal results, in my experience.
Moreover, my experience is that when the neck is not hinging, the pelvis is extending and the patient isn’t slouching with their shoulders, the body will be able to handle quite a bit of asymmetry just fine. You don’t need perfect symmetry to be healthy (does perfect symmetry even exist?). That said, a top athlete may have a much greater requirement for symmetry and ‘flawless’ function than someone that goes to the gym twice per week, for instance. Honestly, I rarely treat minor discrepancies in patients who aren’t high level athletes, unless they specifically want me to (i.e because it’s important to them to fix it).
And, when we correct the atlas, these compensations have often been present for so long that they will not resolve by mere cervical correction, without also being targeted with specific individual exercises. A weak hip for example, won’t miraculously resolve by aligning the atlas. It will require rehabilitation just like the atlas, shoulders and neck will. Any significant weak point will cause compensation and thus alter structural alignment. It is important to address both the symptoms (e.g significant hip weakness) and the main causes (habits, atlas, jaw, etc).
I have seen a lot of patients that have received so-called postural corrective “cures”, both by dentists and atlas correction practitioners. Yet when I examine them, their posture is still way off, they’re still in pain, and muscles have not adapted to any corrective what so ever. I do think that most of these practitioners believe in their approaches and that they genuinely want to help their patients, but I also think it’s very naive to believe that a single correction to one joint (be it the jaw or the atlas) will resolve all of the body’s problems. I hope I have made it clear in this article how deep these problems really go, and that they must be, in my opinion, individually addressed for optimal results.
Chiari malformation (tonsillar descent)
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.
Chiari malformation is defined as herniation of the cerebellar tonsils through the foramen magnum, also known as cerebellar tonsillar ectopia (CTE). CTE may become symptomatic following whiplash trauma. The purpose of the present study was to assess the frequency of CTE in traumatic vs non-traumatic populations.
Cervical MRI scans for 1200 neck pain patients were reviewed; 600 trauma (cases) and 600 non-trauma (controls). Half of the groups were scanned in a recumbent position and half were scanned in an upright position. Two radiologists interpreted the scans for the level of the cerebellar tonsils.
A total of 1195 of 1200 scans were read. CTE was found in 5.7% and 5.3% in the recumbent and upright non-trauma groups vs 9.8% and 23.3% in the recumbent and upright trauma groups (p = 0.0001). – Freeman et al., 2010
Atlanto-occipital misplacement also causes jugular vein compression, which in turn causes brain swelling. This swelling, usually subtle volume increase of the brain, results in narrowing of the ventricles, the CSF cisterns, and may also push the cerebellar tonsils downward into the foramen magnum. The renowned neurosurgeon Atul Goel found that reestablishing craniocervical stability in this patient group may reverse the cerebellar descent. Because his technique also frees the jugular vein, I think that reduction in brain swelling is also a large contributing factor to this phenomenon.
Proper atlantal measurements & identification
There are many techniques today claiming to measure atlantal misalignment, but the problem is that most of these measurements look for serious pathology, and not for chronic misalignments which are more common. Therefore many will have an MRI, but be deemed ‘healthy’ although they feel that something is unmistakenly wrong.
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 in this article. The point, however, is that the margin of error is a lot slimmer at the A-O joint than the A-A joint due to a potentially altered position of the foramen magnum in relation to the spinal canal, as well as potential compression of the neurovascular bundle emerging from the jugular foramen and carotid canal.
I have seen quite dramatic atlantoaxial torsions as well as atlanto-occipital torsions in long-standing neck pain sufferers. The torsions are sometimes so great that I dare not to touch these clients until I have a radiologist assess their cranial vessels and confirm their integrity. This is also why I am generally opposed to performing regular upper cervical manipulative techniques, as the patients who ask for this often already have upper cervical laxity, and the manipulative treatment may cause rupture of the vertebral artery, which may lead to stroke or death in worst case scenario (very, very rare, but not a chance we’d like to take if the patient’s atlas is in obvious torsion, now is it?).
Vertebral artery (VA) occlusion by rotation of the head is uncommon, but can result from mechanical compression of the artery, trauma, or atlantoaxial instability. – Tominaga et al., 2002
One of the reasons this occur, is that the measurements for the atlas joint that many practitioners use, do not account for atlanto-occipital torsion. Thus, a practitioner may find himself “correcting” the A-A joints, unaware that the A-O joint is extremely misaligned. This can be EXTREMELY DANGEROUS and is why I do not recommend upper cervical manipulation for anyone with possible A-O torsion.
To address this safely, one must first know how to properly measure the atlas joint. We then need to know how to palpate the landmarks, as well as some rules for positioning.
The patient must be lying flat, supine, without a hinge at the neck. Put the bench pillow at the occiput rather than mid-cervical, to prevent hinging. Improper position can and will skew the measurements.
- Measure C2 spinous process in relation to C3-4 spinous process
- Measure cranial mastoid process in relation to C1 transverse process (TVP)
- Lateral gliding can be measured by comparing the lateral edge of the mastoid process and the tip of the C1 transverse process. You are then looking for lateral occipital translation and not torsion.
- Estimate A-A alignment based on step A-O and axiocervical measurements
Fig. x – Good atlantooccipital alignment
The spinous processes should be lined up, naturally. But to measure the occiput and C1, one needs to be aware that the C1’s transverse processes should be situated directly below the mastoid processes. Not behind, not in front. Sometimes I will find one transverse process far anterior to the mastoid process, and the opposite side properly lined up. This means that a facet joint subluxation has likely occurred. Other times one transverse process will be anterior to the mastoid process while the opposite side will be posterior to it. This usually implies ‘mere’ rotation.
Lateral occipital translation may be measured by comparing the distance between the lateral edge of the C1 transverse process, and the lateral edge of the mastoid process. If it’s greater on one side, the occiput may have shifted slightly to one side. We are talking millimeters here, and it’s difficult to know whether or not an osseous anomaly rather than true gliding is the cause of such a discrepancy, when the margines are so small. Use healthy judgement when assessing and treating lateral gliding.
The whole C1 may also translate forward in relation to the cranium when there’s ligamentous laxity, in which the transverse processes will be anterior to the mastoid processes on both sides, unless one is further back due to co-occurring C1 rotation. This will increase the opening of the foramen magnum posterior to the brainstem, and may in extreme circumstances it cause the cerebrum to herniate down into the spinal canal.
If the C1 transverse process is thought to be anterior to the mastoid process, make absolutely sure that you are not indeed palpating the styloid process of the skull. They may seem similar, but the difference is that the styoid process is thinner and longer, and can be tracked toward the skull, where as the transverse process is thicker and will not track superiorly. In some patients, the styloid process may be abnormally long. DO NOT mistake the styloid process for the transverse process of the atlas. If you are unsure, do not correct anything.
Manual palpation of the C1 TVP can be very accurate and likely to direct a manual therapist or other health professional to the intended diagnostic or therapeutic target. As another potentially confounding issue, craniocervical anomalies are found in 1–4% of the population. Possible anomalies include elongated mastoid processes, lateral ponticles, and ossification of the stylohyoid ligament.19–22 – Cooperstein et al., 2015
Officially, non-severe atlanto-occipital misalignments is a topic of diffusivity, as far as I am aware, as valid landmarks of measurement are not established. Therefore its milder (mild as in not a complete subluxation or dissociation, i.e serious trauma) degrees of subluxation and interpretation is an uncharted waters. I do hope, though, that this article will contribute to stopping that, and help practitioners to evaluate the A-O joints with greater accuracy and confidence. The below illustration shows degrees of atlantoaxial subluxations, especially post trauma. They are not 100% fitting what I am talking about here, but it still gets the point of mechanical behaviour and of course also the potential severity of these issues across.
I received a patient with long standing neck pain, which occurred after a car accident years ago. She had been to visit a specialty clinic, whose radiologist was an expert of assessing atlas misalignment. She also underwent a special atlas adjustment at another clinic (I won’t mention any names, but it was done with a device and not manually) right after having the MRI, and this was all just two months prior to visiting my clinic.
I read the report before seeing this patient. The MRI report said that the A-O junction was indeed nicely aligned, but the A-A was not. Since I didn’t know how to measure the MRI by myself at the time, I trusted the expert’s measurement. It was a radiological measurement after all, so why wouldn’t I?
Let me quote the report:
At the craniocervical junction, there is good symmetry between the right and left occipito-atlantal joints.
Now, when I assessed the client in person, I was shocked. The left C1 transverse process was far anterior to the mastoid process on the left side. So far forward that I had to make the patient protract the jaw in order to find it! This, despite having both an MRI claiming its symmetry and receiving a special atlas correction, which was even followed up with an x-ray that was said to demonstrate the corrective’s success.
I went back to the MRI images to identify the landmarks and make my own measurements. Something was obviously not right. What I discovered, was that the MRI showed exactly what I observed in clinic; a significantly anterior left C1 transverse process demonstrating rightward rotation of the atlas (i.e leftward occipital rotation on the atlas, if you will).
Let’s look at the MRI. The yellow line (not drawn by me) shows A-A subluxations, which were also noted in the report. The mastoid process’ alignment is shown by the green line, where as the C1 transverse processes are indicated by the red line. The C1 has translated extremely far forward, and rotated toward the right.
How could this have been missed? …Unless it was never looked for?
Fig. 34 – Partial obstruction. of the right and complete occlusion of the left internal jugular veins
Here is another patient of mine who became disabled after severe neck trauma. As you can see, the atlas has translated forward and rotated to the left. Upon examination the patient was severely ‘hinging’ at the neck, has TOS, and many other problems.
Another patient with chronic migraine and dizziness after whiplash injury. Large forward translation of the C1; 11 mm anterior to the mastoid process.
Fig. x – 6,4 mm forward subluxation of the AO facet in a patient with intracranial hypertension
I am writing this, not to mock or bash anyone, (I sincerely believe that most health professionals do try their best to help their patients), but rather to shed light on what I perceive to be obvious lack of knowledge and measurement criteria with regards to “moderate” (i.e non-acute) torsions of the atlanto-occipital joints. If such criteria existed per this date, it is unlikely that I would be able to point out an obvious torsion that was missed by several atlas specialists.
Furthermore, and as I already mentioned, this patient was [mistakenly] assured that her atlas had been aligned, and was even showed demonstrable ‘proof’ of this in a follow-up x-ray. This, although she still had a significant, elusive atlanto-occipital torsion. So, based on the above case study and many similar cases, it is my impression that there does not exist a protocol per this date that properly measures and corrects the atlanto-occipital joint. For the very same reason I am making this article’s information available, for free.
Now that we have learned how to evaluate atlas misalignment by using certain landmarks, let us move on to the treatment section.
As implied several times by now, the approach to resolve misalignment of the atlas joint must consist of more than just the correction itself, or a mere occlusal appliance for that matter. An atlas correction will not last if the underlying cause is not addressed; hinge neck and muscular dysfunction. It is absolutely necessary to rehabilitate the muscles that stabilize the atlas joints, as well as reestablish proper craniocervical habits, i.e movement and postural patterns.
If the ligaments of the atlas have become excessively lax, i.e to the degree that vigorous rehabilitation of muscles and posture do not cause adequate stability, prolotherapy injections of the ligaments may be necessary. Of course, if there’s a full blown rupture of the ligaments holding the A-O and A-A joints together, surgery will likely be required. In circumstances like the latter, though, the patient will usually be diagnosed and get the necessary surgical intervention at any conventional ER room.
Once again, this article is focused on assessing and resolving chronic dysfunction and not acute trauma. I usually setup the corrective sequence in the following manner:
- Postural corrective
- Muscular corrective
- Movement corrective
- Hobby/work corrective
The reason posture comes first is that it’s the simpler thing to change, and is also the most detrimental and exacerbative factor when it’s dysfunctional. To support the postural changes and lay the foundation for proper movement, the muscles that stabilize the cranium and cervical spine (i.e the trio of success) will be strengthened as a daily or every-other-day routine homework. Once posture and the muscles are greatly improved, I will address the patient’s cervical movement pattern by teaching them to extend, flex and rotate the neck without compromising alignment, which more or less means to avoid cervical hinging. Cervical hinging MUST vanish if the patient is to get lasting results.
If there’s no risk of serious injury, or massive misalignment of the A-A or A-O joints, I’ll correct the atlas first by using the protocol outlined further down. If there is severe atlas misalignment, especially at the A-O junction, I may not dare to touch ut until a radiologist has cleared the vertebral artery. Even then, sometimes it’s better to let the body sort it out on its own and just starting with the postural and muscular correctives. That is, if the patient has really bad atlas misalignment. In most cases, slowly but surely things will get back to normal once important underlying factors are addressed. Either way, it will prevent things from getting worse, should there be a rare case where the atlas will not accommodate the improved structural habits and muscular functions.
After all this work I will evaluate the patient’s progress. If everything is looking good, but misalignments keep occurring (this is relatively rare), their hobby or work routines may need to be altered, or more specific homework to balance out certain structures may be necessary.
I have touched upon most of the these elements already, but it is crucial to understand that our postural habits greatly contribute to the atlas joint’s integrity. If the posture and habits are poor, it may compromise the atlas joints in several ways, as I’ve shown several times throughout this article. Without changing these, it will be close to impossible to resolve the cervical issues, in my experience.
Swayback posture must be addressed and corrected first, as it promotes forward head posture and shoulder slouching, which again promotes atlas misalignment and thoracic outlet syndrome, headaches, migraines, disc herniations and much more. If the patient keeps hanging backward with their chest, it will be close to impossible to correct forward head posture and scapular depression in the long term, because the body wants to regain an optimal center of gravity.
The woman in the picture below presents with a pretty common postural type in modern society. The pelvis is in posterior tilt with swayback posture, causing the low back to round (butt pointing down), and the thoracolumbar junction to hyperextend. Furthermore the hip joint hyperextends, the shoulders protract and depress, and the neck comes forward, often along with a nasty cervical hinge. Sadly many will mistake this posture for anterior pelvic tilt, and malcorrect the patient into a posture that exacerbates her symptoms. Please read my article on the myth of anterior pelvic tilt, to read some – in my opinion – damning evidence against this common malpractice and dogmatic belief.
Moreover, to correct these patterns, it is ABSOLUTELY NOT enough to train the weak antagonists. Posture is a result of habits, not strength. Weakness is also a result of habits, which is why strengthening them is mere symptom-work. Symptom work is important too, don’t get me wrong, but it will not address nor correct the underlying cause(s). Treat both the cause and the symptoms, for quicker and long lasting results.
The patient has to correct his or her habits. We pull the pelvis back and up, get the chest gently forward, pull the shoulders gently up and remain long in the neck. Stay there, forever! This takes a lot of effort from the client and it’ll take a few months before it sits well, but it’s completely doable; I do it every day in clinic. In the beginning, the patient will feel tired and even like they’re in pain, and this may of course seem very contraintuitive. Keep on fighting, it’ll get better in a week or two, and as I said, normal in 2-3 months. You CAN do it, don’t let your excuses stand in the way of your healing.
Watch my video demonstration on this below.
Once the posture is good, and the ‘trio of success’ has been worked on and improved significantly, the patient will need to learn how to extend and rotate the head without falling back into the old cervical hinging pattern. I did explain this in detail as well as attach a video demonstration in the forward head posture section, and thus won’t do it again here. Review that section if you need to.
Posture, movement patterns, and muscles will need to be rehabilitated. It is hard work, but you will be repaid greatly if you do a good job. I have seen it happen time and time again, on cases deemed to be “impossible to treat”! I have resolved whiplash injured patients with more than 20 years of pain using this protocol. That’s not to brag, just to show that it can be done if the patient gets the [correct] job done. There is almost always a solution!
Now, I know that I also wrote extensively above about the relationship between dental occlusal factors and posture & muscular functions. However, it is important to emphasize, and I repeat the following FACT; we can override a guided dysfunction caused by occlusal factors by being conscious of our habits, as well as incorporating the proper corrective exercises for one’s individual dysfunction. Try and see for yourself. You are not damned to poor posture nor to having TMD just because you have malocclusion, but you will need to work a little harder to maintain a decent posture.
The muscle trio of success; re-stabilizing the atlas joints
In addition to re-establishing proper craniocervical posture and movement habits, and of course as well as correcting atlantal torsion, it is important to understand what needs to be done in order for the corrections to stick permanently. This is where the ‘trio of success’ comes in, namely the suboccipitals, longus colli and longus capitis muscles. I have explained the functions of these muscles already, in the initial sections of this article, so review those sections if you do not remember.
Most of the time, the atlas joints are ‘savable’ in terms of reestablishing stability, with very conservative measures, such as muscle and postural rehabilitation, even if it started out very misaligned. If the atlantoaxial, atlanto-occipital, and cranioaxial (such as the transverse, cruciate and alar ligaments) ligaments have become lax, a much greater responsibility will be put on the muscles to keep the joints syncronized and moving orderly. We therefore need to make sure that these muscles are working in an exceptional manner.
The longus colli and longus capitis will prevent posterior occipital gliding on the atlas, which is a very common form of misalignment in atlas misalignment sufferers, along with torsions, of course. The suboccipitals will also restrict anterior gliding of the upper cervical below the occiput, and it will syncronize and align cranial motion with atlantoaxial motion. These are key functions, and is why I refer to these muscles as the trio of success!
In addition to strengthening the ‘trio of success’, it is a good idea to strengthen the muscles that may restrict normal atlantoaxial and craniocervical motion. Tight muscles are virtually always weak muscles in my experience, and I’ve made many errors before coming to this conclusion, which is why I recommend strengthening rather than stretching and massaging for most of the circumstances. The scalenes, trapezius, levator scapulae (more on this one soon) are perhaps the most important ones here, but the splenius cervicis and longissimus may also be considered. The latter muscles may be strengthened by performing neck extension (no hinging!) while simultanously mildly rotating the neck ipsilaterally.
The trapezius may be strengthened by elevating the shoulders vertically. I did post exercise videos for the scalenes further up, but please be careful when starting these exercises as they may trigger tremendous symptoms initially, if performed too intensively, too early.
How manually correct atlas misalignments
We can correct torsions of the A-O joint by tractioning the levator scapulae muscle. Lateral gliding can be resolved by tractioning the rectus capitis lateralis muscle. Forward gliding is theoretically possible by pushing the patient’s head forward while they maintain an anteriorly rotated scapular position, to engage the levator scapulae bilaterally, but I’ve never tried it.
With regards to correcting and tractioning the A-O joint, one needs to understand that we do not play around with the bones that hold the cranium. Maltreatment of this region can, in utterly worst case scenarios, cause serious injury such as stroke and death. It is not a simple “pop” and we’re back in action. Such a pop could potentially dissect the vertebral artery and be fatal. Patients must NEVER play around with atlas corrections, and qualified practitioners must use a high level of caution.
Vertebral artery dissection in a patient practicing self-manipulation of the neck
A 42-year-old female patient sought care for left shoulder pain with a secondary complaint of left lower neck pain. Twelve days prior, she had had “the worst headache of her life,” which began in her left lower cervical spine and extended to her left temporal region. The pain was sudden and severe, was described as sharp and burning, and lasted 3 hours. She reported nausea, vomiting, and blurred vision.
Initial history and examination suggested that the patient’s head and neck pain was not musculoskeletal in origin, but vascular. She repeatedly requested that an adjustment be performed, but instead was referred to the local emergency department for further evaluation. Magnetic resonance angiogram revealed a dissection of the left vertebral artery from C6 to the C2-C3 interspace and a 3-mm dissecting pseudoaneurysm at the C3 level. She underwent stent-assisted percutaneous transluminal angioplasty combined with antiplatelet therapy (clopidogrel) and experienced a good outcome. – Mosby & Duray, 2011
Thus also a qualified practitioner must use the absolute fullest caution when attempting to treat these joints. It can be corrected relatively safely by pulling on the levator scapulae muscle, as it attaches to the C1 transverse process and may thus pull it posteriorly, as a sort of muscle energy technique, rather than twisting on the head, which pulls on the [unstable] joint itself, as it is done conventionally.
Lateral movements may be controlled by pulling on, or strengthening the rectus capitis lateralis. The rectus capitis lateralis will pull the C1 ipsilaterally, and the occiput contralaterally. So if you find the distance between the edge of the C1 transverse process and the edge of the mastoid process to be greater on the left side, that means that you may need to work the rectus capitis lateralis on that same side. As I said though, I consider NOTHING completely safe if the patient has massive torsion of the A-O joint. If manipulation is out of the question, strengthening the levator scapulae on the side that has an anterior transverse process, as well as the deep neck flexors and suboccipitals, will promote adjustment and realignment between the occiput, atlas and axis. The recuts capitis lateralis may also be strengthened bilaterally, just make sure to recheck coronal alignment afterwards.
Now to be fair and reasonable, I have seen some really banged up patients (with severe A-O torsion) who have been receiving conventional upper cervical ‘adjustment’ (therapist was of course oblivious to the massive A-O torsion, it was not identified and not treated) for up to four years, and is still alive. The body can handle a lot of beating. But, do you really want to test those limits? Take those chances? Of course not. I think that if the therapist in question knew how misaligned the in question A-O was, he would wet his pants. Ignorance can indeed be very dangerous. There are reports of patients dying from stroke after routine adjustments, but thankfully these are very rare and few.
I am, and I reiterate, not writing this to bash anyone. I really do believe that we all do the best that we can. Knowledge is key, however, and the current protocols for atlas measurement as well as corrections are not adequate. I hope that this has been made reasonably clear so far – A paradigm shift is needed so that awareness and knowledge related to both measurement and correction of the atlanto-occipital joint can spread out to the [qualified] masses.
Using the levator scapulae as a lever of traction
The side that the transverse process is identified to be anterior to the mastoid process on, is also the side you’ll also want to exercise the levator scapulae on. You can also traction it to immediately alter atlantal alignment, by having the patient gently raising and protracting their shoulder (to engage the L.S.), and then the practitioner simultaneously pushes the head diagonally forward to the opposite site while twisting it contralaterally. It is a static pull and no significant movement should occur, hence you’re just “pulling” the levator scapulae and using it to twist the atlas back.
So, if the C1 transverse process is forward on the right side for example, the right shoulder is slightly elevated and protracted (by the patient), the head is pushed forward to the left while simultaneously rotating it toward the left (by the practitioner). The patient, of course, tries to resist your pulling (it should be a static hold, NOT a movement, and excessive force is NOT used). Repalpate the transverse process after correction and see whether or not it has come backward. Also palpate the opposite side; it should have come forward, unless there is a facet joint subluxation.
If there is a torsion between the atlas and axis, e.g atlas rotated to the left and axis to the right, it may be necessary to traction both of the levators in order to pull both back into position, but always correct the A-O joint first. Needless to say, you do not attempt the above if you don’t understand what you are reading, and also, naturally, if you are not qualified. Only perform this traction if you understand the protocol, you’re qualified, and are absolutely certain of what you’re doing.
Be aware though, that this should only be done if there is a light misalignment. If there is severe misalignment, ALWAYS refer the patient out to a radiologist first to take ultrasound of the cervical vessels, to ensure that you absolutely do not risk injuring the patient. You do NOT KNOW whether or not any of those vessels are compromised before you start working on their neck. The outlined protocol for correction in this article is quite safe, as it’s a muscular traction and not a pull on the joint’s ligaments. However, the vertebral artery can rupture upon mere sneezing, in patients who are greatly predisposed to injury (“the last drop”), and you really do not want your treatment to be that last drop. Get the patient checked out first, if it looks bad.
What about the vertebral artery dissection test, you may ask? The vertebral artery dissection test has been shown not be specific enough to reliably detect wearing of the vessel. It is a relatively reliable test once the damage is already done, but not to test general integrity of the vertebral artery. This is why a negative VAD test is simply not a sufficient confirmation of vertebral artery integrity, to go on with corrective procedures. Once again, this only applies if there are obvious severe misalignments of the atlas; not to minor ones. Or, of course, if symptoms of VAD are present. Beware though that TOS and VAD may both share some symptoms of vertebrobasilar insufficiency, and because the scalenes stretch during the VAD test, it may possible also cause similar symptoms and thus mimic a positive test.
Levator scapulae exercise
Most of the time, great results can be achieved with musculoskeletal rehabilitation, when it’s done right. And surgical or prolotherapeutic internventions will only address a specific injury, but not the whole system. Therefore it’s paramount to understand that these latter interventions, although sometimes mandated, do not substitute proper musculoskeletal rehabilitation. As I said, though, there may be times where the cervical ligaments are extremely stretched, so stretched that muscular and postural rehabilitation alone won’t be enough to adequately normalize jointal articulation and stability. In such cases, prolotherapy may be a relatively conservative and low-risk supplemental treatment option.
Some consider prolotherapy to be conservative treatment (it definitely is compared to surgery), others do not. I guess the truth lies somewhere in between, but who cares about formalities anyway. Prolotherapy has been shown to be an effective intervention against ligamentous laxity. It involves injecting a serum of dextrose into the ligaments, which will cause the ligament to inflame and then contract, restoring it to a better (shorter) length and thus increasing its stabilizing potential and function.
Especially post trauma, but also in relation to long standing cervical dysfunction, the transverse (a part of the cruciform) and alar ligaments of the atlas joints may lengthen or even rupture. Laxity of the atlantoaxial and atlanto-occipital capsules may also occur over time, if there is movement dysfunction.
Because most prolo-practitioners are afraid of hurting neck injured patients, they dare not to inject their neck, even when it’s ultrasound guided. I think a “the last drop” mentality is the cause of this, as they perceive such clients as fragile, which I can understand to some degree, because they often are fragile. In Europe it’s hard to find therapists who will inject the upper cervical. I do know that several American clinics do so, though.
Moreover, there is a clinic in the states that injects the deep alar and transverse atlantal ligaments. The prolotherapeutic injection is inserted through the articular gap located between the odontoid process and the articular facet joints. Very cool and pioneering work, in my opinion! The clinic is called Regenexx, and you can watch a video of this procedure in the link below the underlying pictures.
In patients with symptomatic anterior cruciate ligament laxity, intermittent dextrose injection resulted in clinically and statistically significant improvement in ACL laxity, pain, swelling, and knee range of motion. – Reeves et al., 2003
Prolotherapy injection with 10% dextrose resulted in clinically and statistically significant improvements in knee osteoarthritis. Preliminary blinded radiographic readings (1-year films, with 3-year total follow-up period planned) demonstrated improvement in several measures of osteoarthritis severity. ACL laxity, when present in these osteoarthritic patients, improved. – Reeves et al., 2000
Use of dextrose prolotherapy is supported for treatment of tendinopathies, knee and finger joint OA, and spinal/pelvic pain due to ligament dysfunction. – Hauser et al., 2016
Relaxation of ligaments and tendons occurs when fibers do not regain their normal tensile strength after having been sprained or torn. This condition causes more chronic whiplash and low back pain, more referred pain and more sciatica than does any other entity. Diagnosis may be confirmed by intraligamentous injection of a local anesthetic solution. An incompetent structure may be rehabilitated by intraligamentous injection of a proliferating solution which stimulates the production both of new bone and of fibrous tissue cells. Hacket et al., 1960
My goal for this article was to include all of the necessary material needed to assess and addresss the atlas joints. It is a truly a multifactorial problem, mandating a mutlifactorial approach in order to resolve the problem for good. Forward head posture and neck hinging is perhaps the most common denominator that contributes to and exacerbates atlas misalignments, as it will cause utter loss of tensegrity within the whole cervical complex.
I have yet to see a single whiplash or long-standing neck pain patient whose neck is not massively hinging. Neck hinging will, in addition to causing loss of tensegrity and massive muscular dysfunction, also restrict normal axial movement of the upper cervical, and may thus cause hypermobility and improper vertebral gliding within the joints.
Atlas joint misalignment is often associated with thoracic outlet syndrome, disc herniations, headaches, migraines, vertigo, TMD, and so on. Some of these are direct causes of atlas misalignment, others are not. The treatment approaches suggested in this article will, however, address both direct and most of the indirect associations of atlas misalignment.
I reiterate; the underlying causes of atlas misalignment must be addressed if one wishes to have lasting results. Cervical posture need to be optimized and hinging must be vanquished. The ‘trio of success’, namely the longus capitis, longus colli and suboccipitals will all require significant strengthening, as they are perhaps the most important stabilizers of the atlas joints. They prevent neck hinging, forward atlantal gliding, posterior occipital gliding, and syncronizes A-A and A-O joint movements. It is absolutely not a sufficient therapeutic measure to merely manipulate the atlantoaxial joint; it won’t deal with the real problem what so ever.
The atlanto-occipital joint is one poorly understood and vastly neglected. Many claim to address and correct the atlas joints, yet do not measure this joint at all, because no official measurement criteria exists. Most atlas joint ‘correctives’ today focus on the atlantoaxial joint. In this article, I propose a very easily palpable approach to measure these joints, by using the following rules and landmarks:
- C1 transverse process situated beneath mastoid process
- C2 spinous process in line with C3-5 spinous processes
By measuring the atlanto-occipital junction we can detect A-O torsions and improper glidings, both anterior/posterior and lateral. The A-A junction is estimated, not measured. The C2 is measured in relation to the cervical spinous processes. Once you have measured both the A-O and axiocervical landmarks, it’s easy to estimate whether or not there is also an A-A torsion.
Both atlanto-occipital and atlantoaxial torsion may be corrected by a traction maneuver with the levator scapulae muscle, whose muscle fibers attach to the C1-C4 transverse processes. But, if the correction is to last, the trio of success must be worked out, and posture as well as movement habits must be optimized. A non-qualified practitioner or even patient should and must never attempt to traction the levator scapulae.
A torsion at the A-O joint is much more serious than an A-A torsion, and because it’s virtually always missed (unless there’s severe trauma and subluxation), many will be oblivious to such factors. The main reason the A-O is more important, is that this joint is not supposed to move much with regards to rotation nor gliding, where as the A-A joint has great innate rotational capabilities, and is thus less critical to be out of alignment. It is of course not optimal, especially with regards to the vertebral artery, but less critical.
And, I feel the need to repeat, once again, that it is not my intention to bash on anyone. But because proper information on this topic is so tremendously important, I feel the urgency to reveal these things. This is all, of course, in my opinion and in my experience. My word is of course not God’s word, and I am not expecting everyone to agree with me either. Use your own discernment and make of it what you will.
I do hope that this article has shed light on this greatly important, yet controversial topic, and that many will read it and incorporate these measurements into their clinical practice.
- Kulkarni V, Chandy MJ, Babu KS. Quantitative study of muscle spindles in suboccipital muscles of human foetuses. Neurol India. 2001 Dec;49(4):355-9. PMID: 11799407.
- Liu JX, Thornell LE, Pedrosa-Domellöf F. Muscle spindles in the deep muscles of the human neck: a morphological and immunocytochemical study. J Histochem Cytochem. 2003 Feb;51(2):175-86. doi: 10.1177/002215540305100206. PMID: 12533526.
- Kristjansson E. Reliability of ultrasonography for the cervical multifidus muscle in asymptomatic and symptomatic subjects. Man Ther. 2004 May;9(2):83-8. doi: 10.1016/S1356-689X(03)00059-6. PMID: 15040967.
- Andary MT, Hallgren R, Greenman PF, et al. Neurogenic atrophy of suboccipital muscles after a cervical injury: a case study. Am J Phys Med Rehabil. 1998;77:545–549. doi: 10.1097/00002060-199811000-00019
- McPartland JM, Brodeur RR, Hallgren RC. Chronic neck pain, standing balance, and suboccipital muscle atrophy—a pilot study. J Manip Physiol Ther. 1997;20:24–29.Elliott JM, Courtney DM, Rademaker A, Pinto D, Sterling MM, Parrish TB. The Rapid and Progressive Degeneration of the Cervical Multifidus in Whiplash: An MRI Study of Fatty Infiltration. Spine (Phila Pa 1976). 2015;40(12):E694-E700. doi:10.1097/BRS.0000000000000891
- Campbell DG, and Parsons CM. 1944. J. nerv. ment. Dis., 99, 544.
- Hinoki M, Hine, Kada Y. Neurological studies on vertigo due to whiplash injury. Equilibrium Research 1971;(suppl 1):5–29.
- Gimse R, Tjell C, Bjorgen IA, Saunte C. 1996. Disturbed eye movements after whiplash due to injuries to the posture control system. J Clin Exp Neuropsychol 18:178-186.
- Solow B, Sonnesen L. Head posture and malocclusions. Eur J Orthod. 1998 Dec;20(6):685-93. doi: 10.1093/ejo/20.6.685. PMID: 9926635.
- Huijing PA, Maas H, Baan GC. Compartmental fasciotomy and isolating a muscle from neighboring muscles interfere with myofascial force transmission within the rat anterior crural compartment. J Morphol. 2003;256:306–321.
- Stecco C, Gagey O, Macchi V, et al. Tendinous muscular insertions onto the deep fascia of the upper limb. First part: anatomical study. Morphologie. 2007b;91:29–37.
- Cuccia A, Caradonna C. The relationship between the stomatognathic system and body posture. Clinics vol.64 no.1 São Paulo Jan. 2009 http://dx.doi.org/10.1590/S1807-59322009000100011
- Strini PJ, Machado NA, Gorreri MC, Ferreira Ade F, Sousa Gda C, Fernandes Neto AJ. Postural evaluation of patients with temporomandibular disorders under use of occlusal splints. J Appl Oral Sci. 2009 Sep-Oct;17(5):539-43. doi: 10.1590/s1678-77572009000500033. PMID: 19936539; PMCID: PMC4327687.
- Lippold C, Danesh G, Schilgen M, Drerup B, Hackenberg L. Relationship between thoracic, lordotic, and pelvic inclination and craniofacial morphology in adults. Angle Orthod. 2006 Sep;76(5):779-85. doi: 10.1043/0003-3219(2006)076[0779:RBTLAP]2.0.CO;2. PMID: 17029510.
- Ramirez-Yanez G, Mehta L, Mehta NR. The effect of dental occlusal disturbances on the curvature of the vertebral spine in rats. July 2014Cranio: the Journal of Craniomandibular Practice 33(3):2151090314Y0000000017
- Amat P. Occlusion, orthodontics and posture: are there evidences? The example of scoliosis. J. Stomat. Occ. Med. (2009) 2: 2–10 DOI 10.1007/s12548-009-0001-4
- Bergamini M, Pierleoni F, Gizdulich A, Bergamini C. Dental occlusion and body posture: a surface EMG study. Cranio. 2008 Jan;26(1):25-32. doi: 10.1179/crn.2008.041. PMID: 18290522.
- Sakaguchi K, Mehta NR, Abdallah EF, Forgione AG, Hirayama H, Kawasaki T, Yokoyama A. Examination of the relationship between mandibular position and body posture. Cranio. 2007 Oct;25(4):237-49. doi: 10.1179/crn.2007.037. PMID: 17983123.
- Pradham NS, White GE, Mehta N, Forgione A. Mandibular deviations in TMD and non-TMD groups related to eye dominance and head posture. J Clin Pediatr Dent. 2001 Winter;25(2):147-55. doi: 10.17796/jcpd.25.2.j7171238p2413611. PMID: 11314215.
- Conti PB, Sakano E, Ribeiro MA, Schivinski CI, Ribeiro JD. Assessment of the body posture of mouth-breathing children and adolescents. J Pediatr (Rio J). 2011 Jul-Aug;87(4):357-63. doi: 10.2223/JPED.2102. Epub 2011 Jul 18. PMID: 21769416.
- De Menezes VA, Leal RB, Pessoa RS, Pontes RM. Prevalence and factors related to mouth breathing in school children at the Santo Amaro project-Recife, 2005. Braz J Otorhinolaryngol. 2006 May-Jun;72(3):394-9. doi: 10.1016/s1808-8694(15)30975-7. PMID: 17119778.
- Kumar R, Sidhu SS, Kharbanda OP, Tandon DA. Hyoid bone and atlas vertebra in established mouth breathers: a cephalometric study. J Clin Pediatr Dent. 1995 Spring;19(3):191-4. PMID: 8611488.
- Yi LC, Jardim JR, Inoue DP, Pignatari SS. The relationship between excursion of the diaphragm and curvatures of the spinal column in mouth breathing children. J Pediatr (Rio J). 2008 Mar-Apr;84(2):171-7. doi: 10.2223/JPED.1771. PMID: 18372937.
- Cattoni DM, Fernandes FD, Di Francesco RC, Latorre Mdo R. Características do sistema estomatognático de crianças respiradoras orais: enfoque antroposcópico [Characteristics of the stomatognathic system of mouth breathing children: anthroposcopic approach]. Pro Fono. 2007 Oct-Dec;19(4):347-51. Portuguese. doi: 10.1590/s0104-56872007000400004. PMID: 18200382.
- Langevin HM, Stevens-Tuttle D, Fox JR, et al. Ultrasound evidence of altered lumbar connective tissue structure in human subjects with chronic low back pain. BMC Musculoskelet Disord. 2009;10:151. Published 2009 Dec 3. doi:10.1186/1471-2474-10-151
- Osar E. Corrective exercise solution to common hip and shoulder dysfunction. Lotus Publishers; 2012
- Gweon HM, Chung TS, Suh SH. Evaluation of the Cause of Internal Jugular Vein Obstruction on Head and Neck Contrast Enhanced 3D MR Angiography Using Contrast Enhanced Computed Tomography. January 2011. Journal of the Korean Society of Magnetic Resonance in Medicine 15(1):41
- Chung CP, Chao AC, Hsu HY, Lin SJ, Hu HH. Decreased jugular venous distensibility in migraine. Ultrasound Med Biol. 2010 Jan;36(1):11-6. doi: 10.1016/j.ultrasmedbio.2009.08.007. PMID: 19900748.
- Koerte IK, Schankin CJ, Immler S, Lee S, Laubender RP, Grosse C, Eftimov L, Milde-Busch A, Reiser M, Straube A, Heinen F, Alperin N, Ertl-Wagner B. Altered cerebrovenous drainage in patients with migraine as assessed by phase-contrast magnetic resonance imaging. Invest Radiol. 2011 Jul;46(7):434-40. doi: 10.1097/RLI.0b013e318210ecf5. PMID: 21317790.
- Smouha E, Wanna G. Vertigo Lasting Minutes to Hours. Encyclopedia of Neuroscience, 2009
- Schuknecht HF, Boyev KP. Cochleosacculotomy. Otologic Surgery (Third Edition), 2010
- Harris JP, Salt AN. Audition. The Senses: A Comprehensive Reference, 2008
- Yamauchi A, Rabbitt RD, Boyle R, Highstein SM. Relationship between inner-ear fluid pressure and semicircular canal afferent nerve discharge. J Assoc Res Otolaryngol. 2002;3(1):26-44. doi:10.1007/s101620010088
- Cumurciuc R, Crassard I, Sarov M, Valade D, Bousser MG. Headache as the only neurological sign of cerebral venous thrombosis: a series of 17 cases. J Neurol Neurosurg Psychiatry. 2005 Aug;76(8):1084-7. doi: 10.1136/jnnp.2004.056275. PMID: 16024884; PMCID: PMC1739763.
- Gussen R. Vascular mechanisms in Meniere’s disease. Otolaryngol Head Neck Surg. 1983 Feb;91(1):68-71. doi: 10.1177/019459988309100112. PMID: 6405352.
- Benzon HT, Wu CL, Argoff CE, et al. Practical Management of Pain Book, Fifth Edition 2014
- Shreeve MW, La Rose JR. Chiropractic care of a patient with thoracic outlet syndrome and arrhythmia. J Chiropr Med. 2011;10(2):130-134. doi:10.1016/j.jcm.2010.09.002
- Meredith C.B. Adams, Hurley RW. Chemical Neurolytic Blocks. Practical Management of Pain (Fifth Edition), 2014
- Civelek E, Karasu A, Cansever T, Hepgul K, Kiris T, Sabanci A, Canbolat A. Surgical anatomy of the cervical sympathetic trunk during anterolateral approach to cervical spine. Eur Spine J. 2008 Aug;17(8):991-5. doi: 10.1007/s00586-008-0696-8. Epub 2008 Jun 12. PMID: 18548289; PMCID: PMC2518767.
- McDougal DH, Gamlin PD. Autonomic control of the eye. Compr Physiol. 2015;5(1):439-473. doi:10.1002/cphy.c140014
- Uemura T, Katsura M, Iwashima E. Repeated mecholyl tests on patients with vertigo. Equilibrium res. suppl. 3, 1972
- Franz B, Collis-Brown G, Altidis P, et al. Cervical Trauma and Tinnitus. International Tinnitus Journal, Vol. 4, No.1, 3/-33 (1998)
- Burke JP, Orton HP, West J, Strachan IM, Hockey MS, Ferguson DG. Whiplash and its effect on the visual system. Graefes Arch Clin Exp Ophthalmol. 1992;230(4):335-9. doi: 10.1007/BF00165941. PMID: 1505764.
- Kreuzer PM, Landgrebe M, Schecklmann M, Staudinger S, Langguth B; TRI Database Study Group. Trauma-associated tinnitus: audiological, demographic and clinical characteristics. PLoS One. 2012;7(9):e45599. doi: 10.1371/journal.pone.0045599. Epub 2012 Sep 26. PMID: 23049821; PMCID: PMC3458888.
- Bjorne A, Berven A, Agerberg G. Cervical signs and symptoms in patients with Meniere’s disease: a controlled study. Cranio. 1998 Jul;16(3):194-202. doi: 10.1080/08869634.1998.11746057. PMID: 9852812.
- Daneshmandi H, Majalan AS, Babakhani M, Karanian F. The Comparison of head and neck alignment in children with visual and hearing impairments and its relation with anthropometrical dimensions, Phys. Treat. : Specif. Phys. Ther. J. 2014; 4 (2): 69-76
- Yamagami T, Handa H, Higashi K, Kaji R. Brachial plexus injury with cough attack: case report. Neurosurgery. 1994 Jun;34(6):1084-6; discussion 1086. doi: 10.1227/00006123-199406000-00023. PMID: 8084397.
- Coumel P. Autonomic influences in atrial tachyarrhythmias. J Cardiovasc Electrophysiol. 1996 Oct;7(10):999-1007. doi: 10.1111/j.1540-8167.1996.tb00474.x. PMID: 8894942.
- Hsu YC, Sung SF. Spontaneous vertebral artery dissection with thunderclap headache: a case report and review of the literature. Acta Neurol Taiwan. 2014 Mar;23(1):24-8. PMID: 24833212.
- Go G, Hwang SH, Park IS, Park H. Rotational Vertebral Artery Compression : Bow Hunter’s Syndrome. J Korean Neurosurg Soc. 2013;54(3):243-245. doi:10.3340/jkns.2013.54.3.243
- Strupp M, Planck JH, Arbusow V, Steiger HJ, Brückmann H, Brandt T. Rotational vertebral artery occlusion syndrome with vertigo due to “labyrinthine excitation”. Neurology. 2000 Mar 28;54(6):1376-9. doi: 10.1212/wnl.54.6.1376. PMID: 10746615.
- Kuether TA, Nesbit GM, Clark WM, Barnwell SL. Rotational vertebral artery occlusion: a mechanism of vertebrobasilar insufficiency. Neurosurgery. 1997 Aug;41(2):427-32; discussion 432-3. doi: 10.1097/00006123-199708000-00019. PMID: 9257311.
- Dabus G, Gerstle RJ, Parsons M, Cross DT 3rd, Moran CJ, Thompson R, Derdeyn CP. Rotational vertebrobasilar insufficiency due to dynamic compression of the dominant vertebral artery by the thyroid cartilage and occlusion of the contralateral vertebral artery at C1-2 level. J Neuroimaging. 2008 Apr;18(2):184-7. doi: 10.1111/j.1552-6569.2007.00177.x. Epub 2007 Oct 22. PMID: 18298678.
- Dutton M. Dutton’s orthopaedic examination evaluation & intervention, 4e, 2016
- Kim SM, Seo MH, Myoung H, Choi JY, Kim YS, Lee SK. Osteogenetic changes in elongated styloid processes of Eagle syndrome patients. J Craniomaxillofac Surg. 2014 Jul;42(5):661-7. doi: 10.1016/j.jcms.2013.09.012. Epub 2013 Sep 28. PMID: 24161467.
- Sims AB, Stack BC, Demerjian GG. Spasmodic Torticollis: The Dental Connection. The Journal of Craniomandibular & Sleep Practice Volume 30, 2012 – Issue 3. Pages 188-193
- Sims A, Stack B: Tourette’s syndrome: a pilot study for the discontinuance of a movement disorder. J Craniomandib Pract 2009; 27(1):11–18.
- Freeman MD, Rosa S, Harshfield D, Smith F, Bennett R, Centeno CJ, Kornel E, Nystrom A, Heffez D, Kohles SS. A case-control study of cerebellar tonsillar ectopia (Chiari) and head/neck trauma (whiplash). Brain Inj. 2010;24(7-8):988-94. doi: 10.3109/02699052.2010.490512. PMID: 20545453.
- Tominaga T, Takahashi T, Shimizu H, & Yoshimoto, T. (2002). Rotational vertebral artery occlusion from occipital bone anomaly: a rare cause of embolic stroke, Journal of Neurosurgery, 97(6), 1456-1459. Retrieved Jan 22, 2021
- Cooperstein R, Young M, Lew M. Validity of palpation of the C1 transverse process: comparison with a radiographic reference standard. J Can Chiropr Assoc. 2015;59(2):91-100.
- Mosby JS, Duray SM. Vertebral artery dissection in a patient practicing self-manipulation of the neck. J Chiropr Med. 2011 Dec;10(4):283-7. doi: 10.1016/j.jcm.2011.01.007. PMID: 22654686; PMCID: PMC3315865.
- Reeves KD, Hassanein KM. Long-term effects of dextrose prolotherapy for anterior cruciate ligament laxity. Altern Ther Health Med. 2003 May-Jun;9(3):58-62. PMID: 12776476.
- Reeves KD, Hassanein K. Randomized prospective double-blind placebo-controlled study of dextrose prolotherapy for knee osteoarthritis with or without ACL laxity. Altern Ther Health Med. 2000 Mar;6(2):68-74, 77-80. PMID: 10710805.
- Hauser RA, Lackner JB, Steilen-Matias D, Harris DK. A Systematic Review of Dextrose Prolotherapy for Chronic Musculoskeletal Pain. Clin Med Insights Arthritis Musculoskelet Disord. 2016;9:139-159. Published 2016 Jul 7. doi:10.4137/CMAMD.S39160
- George S. Hackett (1960) Prolotherapy in Whiplash and Low Back Pain, Postgraduate Medicine, 27:2, 214-219, DOI: 10.1080/00325481.1960.11712804