During my residency, I had the pleasure of hearing Dr. Cohen, D.D.S. speak on the TMJ. Dr. Cohen is an Orofacial Pain Specialist that works out of the Phoenix area. As you may have noticed, we have not exactly covered the TMJ significantly before on this website due to what we thought was a low prevalence. However, as you'll soon see, it couldn't be further from the truth. For example, did you know that the American Dental Association does not require Dental schools to teach the temporomandibular joint? In fact, treatment techniques for TMJ issues by dentists (distraction, surgery to alter the bone/joint structure, etc.) often actually cause a greater TMJ issue or sometimes a TMJ issue that otherwise did not previously exist. As physical therapists, we are in an excellent position to screen for dysfunction at this joint and direct the patient to proper clinicians if appropriate.
Anatomy & Kinesiology
The Temporomandibular Joint is made up of a posterior concave mandibular fossa and anterior convex articular eminence of the temporal bone that is combined with the convex condyle of the mandible. These surfaces are separated by an articular disc that is made primarily of fibrocartilage (this is important because this disc exhibits incredible self-healing abilities!). The disc reciprocally fits the TMJ in that the superior side is convex to match the concavity of the mandibular fossa and the inferior side is concave to match the mandibular condyle convexity (Neumann, 2010). The blood supply and innervation of the articular disc is somewhat debatable in that some say the entire disc is aneural (incapable of signaling pain), while others say only the middle third is aneural, leaving the anterior and posterior thirds with some innervation. With the joint being synovial, there obviously is a fibrous capsule that surrounds it as well. There are also several key ligaments involved with the joint, but that goes beyond the purpose of this review.
There are two basic components of jaw opening and closing: rotation and translation. Basically, the first half of the motion occurs as a result of joint mechanics in the inferior side of the articular disc - the convex condyle rolls posteriorly and slides anteriorly (convex-concave rules!). During the second half, the superior part of the disc slides anteriorly on the articular eminence (Neumann, 2010).
In general, the primary muscles of mastication include the temporalis, medial pterygoid, lateral pterygoid, and masster. The masseter is responsible for elevation of the mandible, slight protrusion, and, if unilateral, slight ipsilateral excursion. The temporalis elevates, retrudes, and, if unilateral, pulls the mandible ipsilaterally. The medial pterygoid is responsible for elevation and protrusion, while the lateral pterygoid is the only primary muscle that depresses the mandible (along with protrusion). Both muscles contralaterally deviate the jaw if acting unilaterally. It is worth noting that the superior head of the lateral pterygoid has fibers that attach to the capsule, suggesting an involvement with eccentric control of disc translation; however, the evidence is lacking on this. In addition, there are more than a few other muscles that are involved with TMJ function, the suprahyoid and infrahyoid muscles, but the reader is directed to other resources for further information in this area.
Signs & Symptoms
Some common symptoms of TMD include jaw/ear pain, headaches, ear stuffiness, dizziness, tinnitus, hearing loss, and jaw clicking. True TMJ pain can be identified by asking if the patient has pain with chewing. Remember, the disc is aneural, so the pain is not coming from the disc, but potentially the capsule, ligaments, or muscles involved. How can the ear be involved? The TMJ is connected to the ear's eustachian tube by the "Pinto's ligament." Any abnormal mechanics or pathology in the TMJ can stress the ligament causing ear pain, stuffiness, or even loss of hearing. Another potential cause for ear symptoms is the trigeminocervical nucleus and auriculotemporal nerve. (Fun Fact: Amoxicillin is often used for screening for ear infections. The problem with this is that Amoxicillin also contains an analgesic component. Antibiotics typically take 2-3 days to have effect. If a patient's ear pain subsides a couple hours after taking Amoxicillin, it's possible the TMJ was responsible for the ear pain). Headaches are often associated with TMD patients as a result of hypermobility in either the upper cervical spine or TMJ. Due to the lack of stability, the larger muscles are overused trying to hold the head up, thus causing a headache. This muscle tightness may instead exert excessive pressure over the trigeminal nerve or greater occipital nerve. When dizziness is involved, suboccipital tightness may result in compression of the greater occipital nerve or vertebrobasilar blood flow. Jaw clicking is a result of disc displacement in the TMJ typically. A history of jaw clicking can lead to the patient experiencing either an open or closed locked jaw. The closed locked jaw is related to an anteriorly displaced disc that does not reduce or a muscle spasm. Do not try and stretch these individuals open as you are likely to displace the disc even further forward. An open locked jaw is a result of a posteriorly displaced disc.
The symptoms listed above are some of the more common symptoms related to Temporomandibular Dysfunction. Another important finding to consider is that of trigger points. Dr. Cohen spent extensive time discussing the relation of trigger points to headaches, TMD, and head/neck pain in general. If you have ever reviewed some of the trigger point referral patterns by Travell and Simons, you might realize that quite a few muscles have referral patterns to the head and neck that may mimic or contribute to TMD, headaches, etc. In fact, muscles like the temporalis can even refer to teeth, simulating a toothache (dentists may proceed to inappropriately pull a tooth out as a result). Trigger point injections often alleviate these symptoms immediately. While this is useful, remember this just treats the symptoms. We must treat the cause (often abnormal posture and the associated impairments). So be sure to assess trigger point contributions in your examination. Some treatment techniques by physical therapists may also be useful for this i.e. trigger point release, dry needling.
When you are assessing an individual referred for TMD and cervicalgia, your examination should include both (along with the rest of the upper quarter). Some obvious thing to include are ROM, resisted isometrics, segmental mobility, palpation, listening for joint sounds (disc displacement), cotton roll test, and posture. ROM of the TMJ can reveal potential limitations of the capsule. Normal ROM is: 45 mm for depression, lateral excursion is 1/4 of depression, protrusion is 6-9 mm and retrusion is 3 mm (Ho, 2011). Lateral deviation to one side may signify capsular restrictions ipsilaterally, potential muscle dysfunction, or an anteriorly displaced disc without reduction ipsilaterally. This may be represented as a "C-curve" when opening (an "S-curve" is associated with hypermobility). Resisted isometrics can help you to identify a particular muscle that is not functioning properly. Segmental mobility of both the TMJ and upper cervical spine can potentially assist in identifying hyper- or hypomobility in a segment related to the abnormal mechanics. Palpation can be useful for assessing trigger points or tenderness in a capsule. The cotton roll test can help differentiate between muscular and joint involvement. If a patient complains of pain when chewing on one side of the mouth, have the patient bite down on a cotton roll. By doing so, this gaps the ipsilateral TMJ. Thus, if pain is decreased, it would appear the pain is joint related, but if it doesn't change or increases, the pain is muscular (it is still possible that the pain is related to the cervical spine as well). And of course, it all comes back to posture. Knowing the resting position of the teeth is important to understand the individual's TMJ mechanics and we have already discussed the impact cervical posture can have on the TMJ. Also, be sure to check for any poor habits such as bruxism, chewing on ice, grinding teeth, etc. that impact the TMJ
Treatment of TMD contains many of the methods that are regularly used for other joints and vary based on the impairments found and underlying condition. We must educate the patient on the pathology, postural correction, relaxation training for hyperactive muscles, and adjusting the patient's oral habits. Aerobic exercise can be useful in allowing relaxation of TMJ musculature and managing stress (Ho, 2011). The resting position of the mouth includes having the tongue on the palate of the mouth with the mouth closed and teeth not touching in a relaxed manner. Additionally, patients should be reminded to not bite nails, chew on pens, or continue other habits that affect the TMJ. In more acute cases, the patient should consume a softer diet and transition from chewing on the unaffected side to the affected side. Modalities may be used as indicated and joint/soft tissue mobilization can be used based on findings. As discussed before, trigger points can be treated with trigger point injections, dry needling, manual release, botox, etc. The home exercise program should involve retraining the patient on proper opening of the mouth. This is done by keeping the tongue on the roof of the mouth and slowly opening the mouth. This is useful because it prevents the anterior translation phase, thus preventing additional damage to the disc. The technique should be done regularly throughout the day. Isometrics to TMJ muscles are important for improving control of the joint, enhancing stability. Something that needs to be considered in TMD cases is splint therapy. The purposes include relaxing hyperactive muscles, reducing bruxing, altering clenching behavior, redistributing occlusal forces, preventing wear of enamel, and repositioning of a condyle (Ho, 2011). These splints are worn anywhere from constantly to just at night and may last up to 3 months or more. Due to the malleable effects splints have on the mouth, they need to be regularly adjusted. This brings up the important point of how modifiable the TMJ is. Dr. Cohen states that surgery and joint manipulation are the last options. The TMJ has the ability to adapt to changes and maintain full function for affected ligaments and muscles and sometimes even in cases like fractures.
As stated several times before, we must include treatment of the cervical spine and entire upper quarter. Remember regional interdependence! This typically includes mobilization, manipulation, METs, etc. to restricted joints and cervical stabilization training. Anterior cervical muscles like the longus colli and longus capitis are often insufficient in patients with abnormal posture and require retraining. This strengthening/stretching/motor control training approach to postural muscles needs to be used down to the lumbar spine even, because poor core stability often leads to forward head displacement.
This description of treatment techniques is a brief overview of how to manage patients with TMD. It is in no way all-inclusive. Each specific pathology may have a specific technique or exercise plan that has been shown to be especially beneficial. For example, there are specific exercise plans for displaced discs that are designed to retrain the muscles and recapture the disc in order to produce increased stability and motor control. The reader is advised to seek out other sources or the references for further information on these pathologies. Additionally, the outcome of patients with TMD can be improved with proper coordination with other health care practitioners like Orofacial Pain Specialists. The earlier these patients begin the conservative route, the more likely they will be able to avoid surgery.
Cohen, Richard. "Temporomandibular Dysfunction." Scottsdale Healthcare Orthopedic Residency Lecture. Scottsdale Healthcare Osborn Campus, Scottsdale, AZ. 21 Jan 2014. Lecture.
Ho S. The Temporomandibular Joint: Physical Therapy Patient Management Utilizing Current Evidence. Current Concepts of Orthopaedic Physical Therapy, 3rd Ed. La Crosse, WI. 2011.
Neumann, Donald. Kinesiology of the Musculoskeletal System: Foundations for Rehabilitation. 2nd edition. St. Louis, MO: Mosby Elsevier, 2010. 427-438. Print.
Young PA, Young PH, Tolbert DL. Clinical Neuroscience. 2nd edition. Philadelphia PA: Lippincott Williams & Witkins, 2008. 145-149. Print.
Just a week into my residency and I probably had already learned enough to give me an entirely new perspective on physical therapy. Anatomy and physiology are probably two of the first courses you take in the PT track. Obviously, they are not only important, but we utilize the information with each patient when evaluating patient and designing plans of care. Origins and insertions of muscles probably get one of the biggest emphases in school due to their implication on muscle function, but should we be considering more? On day 1, my mentor, the other resident, and I had about a 30 minute discussion on the impact of an adaptively shortened iliopsoas and how to treat it. I started off by saying we could obviously stretch it. Our mentor countered by saying we could also perform bridges or perform a lumbar manipulation. Bridging would increase mobility in the hip through reciprocal inhibition, while a manipulation would work through neurogenic inhibition. This may or may not have been common sense to some people, but it lead to a further discussion about the path of the muscle and its implications.
The iliopsoas is commonly regarded as a hip flexor, but it has two additional major functions: spinal compression and hip lateral rotation. The path of the muscle from origin to insertion begins on the lateral sides of the lumbar vertebral bodies, passes posterior to the vertebral column and then wraps posteriorly around the femur to the lesser trochanter. Acting as a spinal compressor, this muscle can be responsible for low back pain if short or stiff. Its role in lateral rotation can have a large impact on gait and jump mechanics as well. An individual that displays valgus knee positioning with squats often has weak hip abductors and lateral rotators. With the muscle wrapping around the femur posteriorly and acting as a lateral rotator, the iliopsoas is a muscle we definitely should consider in our intervention planning. This discussion lead me to realize the necessity of a 3-Dimensional understanding of our anatomy to further my knowledge in orthopaedics.
An example of anatomy's impact hit me with a patient in week 1. This patient presented with pretty clear signs/symptoms of a herniated disc. This patient described excruciating pain in her low back and hips after "trying to stretch her back and hamstrings out (this patient indicated she was doing so in a long-sitting method using primarily lumbar flexion)." She stated her pain is worsened by sitting and improved by standing/walking around. Pain increased and peripheralized with repeated lumbar flexion and centralized with extension. (+) SLR, Crossed SLR, and Slump Test. Following the evaluation, I prescribed prone press-ups, some core stabilization training exercises, and modification of lifting techniques. Stretching was deferred at this time as the patient was too acute and sensitive. At the follow-up visit a week later, the pain was mainly localized to the central spinal column, however her pain had switched from her posterior RLE to her L lateral thigh and inguinal area. This was somewhat an abnormal presentation to me, so I consulted my mentor. It turns out her distribution of her new symptoms were along the lateral cutaneous nerve at the lateral thigh, but also along the path of the nerve as it passes just inferior to the ASIS. The reason for the irritation lies in its lumbar innervation. This just happened to be an odd presentation as the pain switched extremities. So as you can see, it's not good enough to simply know what areas peripheral nerves and dermatomes contribute to and where the origins/insertions of muscles lie, but we must also strive to understand the path of the structures throughout the body. This will lead to improved clinical reasoning in both our examinations and interventions.
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Core strengthening appears to be a very abstract term in the world of physical therapy. To some, it means very specific motor control training. To others, it means planks. Several years ago, a proposed core stabilization clinical prediction rule was shown to lack validity. Regardless, due to the lack of established guidelines for core stability training, there will continue to be a variety of techniques, based on the clinician's preference.
When it comes to lumbar manipulation, there has been a significant amount of research to show our inability to manipulation a specific segment. Even when we try to "isolate" an area, movement can occur several segments above and below. It would appear the lack of specificity with manipulation is rather insignificant, so certain patients may just respond to manipulation in general. Can the same theory apply to stabilization? I recently read a study that compared specific motor control training in the lumbar spine to high-load deadlift training. The results showed that there was no difference in strength, pain intensity or muscle endurance between the two groups. The motor control group did have better motor control and activity, but the fact that pain, strength, and endurance were similar can help us in not needing to be so specific with our exercises. Sometimes, the particular instructions we give to our patients can actually cause a fear of movement, which is something we want to avoid.
Now, I am not necessarily saying there is no point to motor control training. I would simply argue that it's not as important as we used to think. If there is a subtle pelvic motion when reaching overhead, we don't necessarily need to be stopping the exercise altogether. It may still be beneficial to establish some general patterns of motion during earlier stages of rehab in order to prevent re-aggravation during high load training. Personally, following my manual treatment (if indicated), I will start with a couple mobility exercises to help get the spine moving. I then follow that up with some motor control training to prep for whatever movement I am going to have the patient perform. For example, if my patient will be doing a deadlift, I will prime them with a quad rock back and/or hip hinge, in order to help dissociate lumbar and hip motion with heavy lifting. My end-goal however, is to get my patient strengthening with heavier weight.
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The diagnosis of disc herniation as the source of back pain is a controversial issue. There is a large proportion of the population that is asymptomatic and shows disc herniation in MRIs, which leads to the issue of the disc often being incorrectly labeled as the source of the patient's complaints. With the appearance of a herniating disc, some surgeons, patients, and other medical providers jump to the conclusion that a surgical procedure is necessary for correction without considering conservative treatment. While surgery can be effective for some individuals, it may represent an expensive overreaction to the patient's symptoms
The study we looked at this week was a systematic review of conservative treatment for lumbar disc herniation with radiculopathy. Studies were only included if the patients were over 18 years old and referred with leg pain (with or without low back pain). 75% of the patients had to have a confirmed lumbar disc herniation through MRI or CT as well. Participants with discs that were only "bulging" were not included. Studies were also excluded if surgery was performed or an injection was used; acupuncture, along with other physical therapy interventions, was labeled as conservative therapy
The review found that advice had poorer short and intermediate outcomes for back pain and leg pain compared to surgical microdiscectomy, but there was no difference in the long term. Those who pursued surgery had better function compared to the advice group at short-term follow-up, but no difference was noted at intermediate and long-term outcomes. Manipulation was found to be effective as long as the annulus was still intact. No difference was found between traction, Low Level Laser Therapy, and ultrasound, but traction had good results when combined with electrotherapy and medications in the short term. The review found moderately strong evidence that stabilization exercises were better than no treatment at all. It should also be noted that there are possible adverse effects linked between ibuprofen use and traction
While this article offers some information on the effectiveness of various conservative treatment methods in treating lumbar disc herniation radiculopathy, it does not sufficiently examine the entire scope of physical therapy interventions, such as repeated motions, extension based exercises, neuromuscular education of the core, etc. While there are plenty of studies out there that look at the effectiveness of interventions like repeated motions, neuromuscular education, and core stabilization, there weren't many studies looking at those treatment methods that fit the specific inclusion criteria of this systematic review. It does not mean they are not effective, but it points out an excellent research opportunity for anyone interested. Be sure to keep an eye out for some posts coming out in the near future for treating low back pain
Hahne AJ, Ford JJ, McMeeken JM. "Conservative management of lumbar disc herniation with associated radiculopathy: a systematic review." Spine (Phila Pa 1976). 2010 May 15;35(11):E488-504. Web. 09/15/2012
Whether you are studying for a PT school practicum, the OCS examination, or simply brushing up on your cervical spine knowledge, these infographics can help!
Cervical Radiculopathy Infographics
Cervical Facet Dysfunction Infographics
Cervical Clinical Guidelines Infographics
Serratus Anterior Infographics
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In many cases, the patient's subjective history alone should be enough to diagnose the musculoskeletal issue. Whether it's the mechanism of injury, location of pain, and/or pattern of pain, we are often able to formulate our treatment plan from the patient's subjective report. That being said, there are cases where the subjective report doesn't match the typical presentation and is, therefore, insufficient in evaluating the patient. It is for this reason that we must be thorough with our examination.
Recently I had a patient that presented with a subjective history of Lumbar Extension Movement Impairment Syndrome (MIS). However, when I got to the objective examination, all the findings matched with a Lumbar Flexion Movement Impairment Syndrome. Cases like this can be challenging due to the conflicting presentation. This is where implementation of an asterisk sign or a system that utilizes asterisk signs can be useful.
The two systems I typically use are repeated motions and Sahrmann's Movement Impairment Syndromes. In both methods, first an asterisk sign is measured, followed by the assessment. The asterisk sign is then re-measured. With repeated motions, we want to see an improvement in pain, mobility, strength, reflexes, or other measurement with our asterisk sign after performing sets of 10-20 repetitions. The more repetitions, the more the asterisk sign should improve. With Movement Impairment Syndromes, the painful/abnormal movement pattern is observed, then corrected. If the corrected form eliminates or significantly improves the pain, that increases the likelihood of that direction of preference. Another way of thinking about it is stabilizing the region from excessive movement into a specific direction that it is susceptible to.
In most cases, the subjective report and objective findings match a pattern or presentation. However, what do we do when the pattern doesn't match? What I recommend is to focus on the direction that the objective findings match with. Sometimes the patient doesn't give the most accurate subjective history and the objective examination is reproducible and can show immediate change. That being said, be prepared to re-examine the patient and switch directions following the first couple visits if the patient is not responding (or worsening). Check out the lecture below on how Examination of the Cervical Spine works utilizing Movement Impairment Syndromes!
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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) Joint
The 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) Joint
The 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.
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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.
Depending on your patient population, you may treat acromioclavicular joint (ACJ) injuries on a daily basis or only on a rare occasion. While the ACJ is often involved in shoulder dysfunction, it may or may not be directly injured. A specific ACJ injury occurs with either a fall (or similar trauma) to the lateral shoulder with the arm adducted or with a FOOSH (fall on outstretched hand) injury. Pain is anatomically localized with this joint as it is primarily located directly over the ACJ.
To test for ACJ injury, first start with observation. ACJ injuries are sometimes palpable/visible with a step-off. The amount of step-off will depend on the severity of injury. As far as our clinical tests go, the Horizontal Adduction Test (the shoulder is adducted and may be elevated simultaneously as well) is preferred as it stresses the ACJ directly. Additionally, an x-ray series of the shoulder is often ordered to assess alignment and rule-out clavicular fractures.
How Do We Classify the Severity of Injury?
If there is no visual deformity (meaning if it is Type I or II), it will most likely be managed conservatively. This incorporates a period of rest and relative immobilization for up to a week before transitioning to protective ROM and isometric exercises. During the initial stages, we will limit end-range elevation with strength training as this position strains the ACJ. After the acute phase, isotonics, closed kinetic chain, end range of motion exercises, and higher level strengthening can be initiated. Below are several higher level exercises that the patient can progress to during later stage therapy.
Type IV-VI ACJ injuries will almost always be managed surgically, so these patients are rarely seen in the PT clinic prior to surgery. The type of injury and procedure will dictate the rehab. As always, use the physician's protocol and EBP to guide the program. As you may have noticed, we have not talked about type III ACJ injuries. These are the most difficult type manage as they can be treated either surgically or conservatively. The decision is based off the patient's occupation, hand dominance and activities he/she likes to perform. Typically, conservative management is tried first for a few months. Should the patient have a difficult time getting back to their desired level of function, surgery may be performed, however, this delay may impact the prognosis.
As we have highlighted, the staging of the injury is essential to dictating how to proceed with rehab. At times, surgical consultation is recommended and/or necessary for proper recovery. My recommendation is to start with conservative management if no step-off deformity is present; however, be ready to reach out for a second opinion as needed.
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 Atrophy
Since 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!