![]() Cervical spine pain is one of the more common complaints seen in outpatient orthopaedic physical therapy. With the relation to the rest of the upper quarter, the shoulder and thoracic spine, it is essential we be as proficient as possible when assessing and treating the region. While this may seem obvious, it is interesting to note how hesitant some clinicians are in treating the upper cervical spine. Why? Because it is different and there is risk for fatal injury. The upper cervical spine is made up of the Atlantooccipital (AO) Joint and the Atlantoaxis (AA) Joint. These joints have different anatomical and kinesiological considerations compared to the rest of the cervical spine. With the frequency with which the cervical spine is involved in upper quarter dysfunction, as well as temporomandibular dysfunction, it is imperative we have a solid understanding of the joints. Atlantooccipital (AO) JointThe Atlantooccipital Joint (AO) is made up of the atlas and occiput. The atlas has no body, pedicles, laminae, or spinous process, unlike typical vertebrae. There is an anterior arch with an anterior tubercle for attachment of the anterior atlanto-occipital membrane (Neumann, 2010). The posterior arch is larger and has a posterior tubercle. Additionally, there are two large transverse processes (one on each side) that are palpable between the mastoid process and mandibular ramus. There are two large concave facets that face medially and superiorly in order to accept the occipital convex condyles that face inferiorly and laterally (Abernethy, 2014). The atlanto-occipital membrane connects the anterior portion of the foramen magnum to the anterior arch of C1 for anterior-posterior stability. The posterior atlanto-occipital ligament connects the posterior ring of C1 to the occiput at the foramen magnum as well. This ligament is important for anterior translation of C1 and vertical translation of the occiput. Additionally, there are joint capsules surrounding the AO joints that limit movement in each direction. There are 2 degrees of freedom in the AO joint: flexion/extension and frontal sidebend (Abernethy, 2014). The OA joint is responsible for 10 degrees of flexion, 25 degrees of extension, 5 degrees of sidebend, and 4 degrees of conjugate rotation. To fully comprehend the arthrokinematics of the AO joint, we must know the plane of the joint. During flexion, there is a bilateral lateral, posterior, and superior (LPS) motion, while there is a bilateral medial, inferior, and anterior motion for extension (MIA). In order to determine which part and which side of the joint is restricted, we assess sidebend. Upper cervical sidebend to the left, results in left AO MIA and right AO LPS. In other words, if you sidebend the upper cervical spine to the left, you are essentially flexing on the right and extending on the left. To determine which side is at fault for the motion restrictions, sidebending should be reassessed in flexion and extension. For example, if sidebending to the left feels restricted in neutral, it is possible that either flexion (LPS) on the right or extension (MIA) on the left (or both) are limited. In a normal joint, sidbending should be smooth and through an axis that runs through the tip of the nose. When placed in flexion (of the same restricted motion), sidebend to the left now biases the right joint. By initially placing the AO joints in flexion, the condyles are moved lateral, posterior and superiorly (LPS). Thus, if there is a restriction on that right side, the condyle will meet its barrier sooner compared to neutral. By placing the AO joints in extension, the condyles are then moved medially, inferiorly, anteriorly (MIA). This forces the condyle on the left to meet its barrier sooner compared to neutral if there is a restriction. Typically, a flexion limitation is found due to the frequency with which we see forward head posture. If you find an extension limitation, I recommend re-checking the joints. Atlantoaxial (AA) JointThe Atlantoaxial Joint is made up of the atlas and axis, C1 and C2 respectively. The atlas has inferior and medially directed convex facets that are about 20 degrees inferior to the horizontal plane (Neumann, 2010). The axis has superior and laterally directed convex facets that match the 20 degrees of slope inferior to the horizontal plane of the atlas. The joint results in convex-on-convex surfaces (Abernethy, 2013). Due to the anatomy here, there is no sidebend possible at the AA joint. Instead, this joint is responsible for almost half of cervical rotation. Additionally, there is some flexion and extension possible here via bilateral C1 rolling anterior and gliding posteriorly for flexion; the opposite occurs for extension. The axis is different from typical vertebrae because of possession of the dens (odontoid process) (Neumann, 2010). It is theorized that the dens is the remnant of the body of the atlas. This base provides a rigid axis of rotation at the AA joint. The dens is held against the anterior tubercle of the atlas by the transverse ligament, forming a synovial joint between the dens and anterior arch. The axis of rotation is through the dens. When rotating to the left, the ipsilateral side of the atlas glides posteriorly (rotexion), while the contralateral side glides anteriorly (latexion) (Abernethy, 2014). The AA joint is responsible for 35 degrees of rotation bilaterally, 8 degrees of flexion, and 10 degrees of extension. There are several methods that are commonly used for assessing motion at the AA joint. One is the Flexion-Rotation Test, where the cervical spine is maximally flexed (and maintained there), while rotation is performed bilaterally. The issue with this test is that it tends to also include motion at the C2-3 joint, resulting in at least 45 degrees of rotation in a normal joint bilaterally. To truly assess AA rotation, maximally sidebend the cervical spine ipsilaterally and rotate contralaterally, while maintaining chin tuck (if chin tuck is lost, isolation to C1-2 is lost). This is also a position for manipulation. It should be noted that in those with moderate degeneration of the cervical spine (and presents of significant osteophytes), cervical sidebend may be limited, resulting in decreased ability to isolate the AA joint. Interested in more material like this? Check out our course Orthopedic Management of the Cervical Spine!References:
Abernethy, Jeff. "Upper Cervical." Upper Cervical Spine Orthopaedic Residency Lecture. Scottsdale Healthcare Osborn Campus, Scottsdale, AZ. 9 January 2014. Lecture. Neumann, Donald. Kinesiology of the Musculoskeletal System: Foundations for Rehabilitation. 2nd edition. St. Louis, MO: Mosby Elsevier, 2010. 315-322. Print.
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![]() When evaluating a patient with shoulder or neck pain, it is important to consider all of the structures that may contribute to their current symptoms. These structures include local muscles, peripheral or central nervous system dysfunction, soft tissue stabilizing structures, among others. Next, use this information in combination with other portions of the subjective history (mechanism of injury, description of symptoms, and pattern of symptoms) to identify the one or two primary causes of the problem. No recent injury, shoulder or neck pain, but still muscle atrophy...
Look Beyond the Local Muscle AtrophySince muscle atrophy was present (without signs of a single muscle trauma or strain), it is important to investigate other muscles with the same segmental and peripheral nerve contributions. This will determine if the weakness is localized or present in multiple muscle groups. Below I review the pectoralis muscle with a special emphasis on the sternocostal fibers. Later in the evaluation, the patient remembered that his biceps brachii and pectoral muscle strength had gradually decreased on his right (involved side) versus his left over the past few months while strength training. This statement is very important because it most likely ruled out a muscle strain, and ruled in nervous system dysfunction. Further physical examination helped rule out red flags for cervical myelopathy. Additionally, muscle strength testing found weakness in other C5, C6, and C7 muscles. At this point, I concluded that he was safe for treatment, but needed regular reassessment to ensure no further progression of neurological symptoms. To learn more about the outcome of this patient, watch the video below! |
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