Following a lateral ankle injury, a patient often presents with swelling, pain, decreased ROM, an acute joint dysfunction, and decreased proprioception in the foot and ankle. Depending on the severity of the injury, these symptoms usually begin to improve within a matter of weeks. However, occasionally symptoms persists despite doing all the proper things during your treatment sessions.
Most commonly, if a lateral ankle injury occurs the Anterior Talofibular Ligament (ATFL) will be stressed and injured. The mechanism of injury stressing the ligament typically includes adduction and traction of the talus on a plantarflexed and inverted foot. What many individuals fail to consider is the close interaction between the Intermediate Dorsal Cutaneous Nerve (a branch of the superficial peroneal nerve) and ATFL. The Intermediate Dorsal Cutaneous Nerve courses just superior to the ATFL and can also undergo a significant amount of stress during a lateral ankle inversion injury. The nerve is purely sensory and provides sensation to the dorsal aspect of the foot. When the nerve has been irritated, common clinical findings include pain, paresthesia, and a + Tinel's Sign.
To check for neural tension in the superficial peroneal nerve (you cannot solely tease out the Intermediate Dorsal Cutaneous Nerve), have the patient lie in supine. Bring the affected foot and ankle into plantar flexion and inversion. Next, perform a straight leg raise on the affected limb while maintaining the foot in PF and Inversion. If pain increases, this is positive neural tension. It is very important to perform the straight leg raise because if you only perform PF and Inversion, pain could be coming from either the ligamentous injury or neural tension. You must further tension the nerve proximally.
One should be quick to point out that neural tension may be present, but it is not always the cause of a person's symptoms. In order for the neural tension to be considered relevant adverse neutral tension it must fulfill 3 criteria:
1) Does the test reproduce their pain?
2) Is there a side to side difference?
3) Does the pain change by moving a distant component?
Assessing neural tension is one quality that differentiates the novice clinician from an expert. Next time you see a lateral ankle injury, consider the interaction between the Anterior Talofibular Ligament and the Superficial Peroneal Nerve.
The Upper Trapezius muscle (UT) is a muscle that is frequently accused of being responsible for dysfunction related to neck or shoulder impairments for being "too active" or "tight." We have even heard physical therapists exclaim how they hate seeing people try to strengthen their UT, because they feel people are overusing the muscle, and it is already too strong compared to the other muscles. While this is certainly possible, how frequently does this actually occur? Let's review the anatomy first (Kendall, 2005):
Origin: External occipital protuberance, medial 1/3 of superior nuchal line, ligamentum nuchae and spinous process of the 7th cervical vertebra.
Insertion: Lateral 1/3 of the clavicle and acromion process of the scapula.
Innervation: Spinal portion of cranial nerve XI (accessory) and ventral ramus, C2-4.
Action: (with origin fixed) adduction, upward rotation, and elevation of scapula; (with insertion fixed) extend, laterally flex ipsilaterally, and rotate the head contralaterally.
With the common perception that the UT is often short (especially with patient reports of the muscle feeling "tight" when put on stretch - of course), it is not surprising that stretching is frequently prescribed for the muscle in patients with neck and/or shoulder pain. That's not to say it is never warranted. If the muscle length is truly assessed and found to be adaptively shortened (and non-painful), of course we want to stretch the muscle. However, we must be certain that the muscle is indeed shortened first.
If the UT is truly shortened, you will find the entire shoulder heightened compared to normal, meaning both the superior angle and acromion of the scapula. Often patients are seen with an elevated superior angle but depressed acromion, suggesting a downwardly rotated scapula - components of an overactive/shortened levator scapula. An exercise commonly performed at the gym involved shoulder shrugs holding weights with the idea that the individual is strengthening the UT. However, in this position, the scapula is rotated downward and results in strengthening/reinforcing the levator scapula muscle (Sahrmann, 2002). An overactive UT is also frequently accused as the culprit in shoulder impingement. However, remember that about 1/3 of shoulder elevation is due to upward rotation of the scapula, an action of the UT. Frequently, the patient will display elevation of the scapula when trying to flex or abduct the humerus. Attention should be paid to whether or not the scapula is in upward or downward rotation with that elevation. If it appears to be downward rotation, it is essential that the UT undergoes retraining. In order to focus on the UT, the shoulders should be placed in at least 90 degrees of elevation in order to place the scapula in upward rotation and allow the shrugging aspect of the motion to come from the UT, not just the levator scapula.
An additional point that should be considered is the impact on the cervical spine. Sahrmann places a strong emphasis on relative stiffness and hypermobility vs. hypomobility in her teachings. As previously discussed, the UT attaches to the cervical spine and, in doing so, can be responsible for pain at the attachment site. There are at least two possible reasons for cervical pain resulting from UT impairment. One, the UT is overactive and stronger compared to the cervical intrinsic muscles. When the muscle contracts such as during upper extremity elevation, cervical extension or rotation is frequently seen (Sahrmann, 2002). You can even feel the individual cervical vertebrae rotating during shoulder flexion/abduction. This hypermobility (a precursor to hypomobility) provides the excess stress that can lead to degeneration and, in the long run, hypomobility. In this case, the UT needs to be retrained with an emphasis placed on maintaining cervical stability and neutral cervical positioning. Two, the UT is insufficient and lengthened, resulting in a pull on the proximal attachment (cervical vertebrae) due to the weight of the scapula and upper extremity, especially during movements. These patients, too, will report that "stretching feels good." Just as the previous example, however, we must strengthen the UT in these patients, with proper positioning as explained earlier.
The purpose of this post was to make us all more aware and pay specific attention to the scapulohumeral positioning both statically and dynamically in order to determine the true impairment that lies with the UT, or if there even is one at all. A starting point we like to use is assessing the medial side of the scapula at rest to determine if the resting position is upward or downward rotation. That should be followed up with a comparison of the superior angle of the scapula to the acromion as well to aid in confirmation. This positioning should then be tracked during flexion/abduction of the humerus. This is just one muscle's impact on the upper quarter, but as you can tell, it is a significant one. For more information on the topic, it is recommended you review the references listed below.
Kendall FP, McCreary EK, Provance PG, Rodgers MM, & Romani WA. Muscles Testing and Function with Posture and Pain. 5th edition. Baltimore, MD: Lippincott Williams & Wilkins, 2005. 326. Print.
Sahrmann, SA. Diagnosis and Treatment of Movement Impairment Syndromes. St. Louis, MO: Mosby, 2002. 206-208. Print.
I have had a few "higher level" patients in the past few weeks and one consistent trend I found in my practice is that I have been progressing them too quickly. I am not exactly sure why this in the case. Both groups of people present with the same impairments so why would I treat them differently? My assumptions are that I do not want them to become bored with a basic HEP or maybe because they are starting at a higher level they should require higher level exercises. Both of these are fallacies.
Despite starting from a higher functional baseline the higher level patients presented with similar impairments as the low level patient. A 3+/5 muscle grade is a 3+/5 no matter how you look at it. For example, with a low level patient, I gave the clamshell exercise to strengthen the posterior gluteus medius. For the higher level, I gave the clamshell exercise in a modified side plank position. Both exercises target similar muscle groups, but the higher level exercise is much more demanding across the entire system. I have given similar exercise prescriptions like this is the past and consistently found that the patient returns to the clinic performing the exercise improperly or having pain while performing it.
1. A weak muscle is a weak muscle regardless of what type of patient you find it on.
2. Start basic. In my example above, I added side planks to a clam exercise during the initial HEP. When prescribing this, I made sure the patient had adequate abdominal control, but it took away from the true target of my treatment. The primary impairment was gluteus medius weakness. I needed to start in the least aggressive position and isolate the glut medius.
3. Educate appropriately. My assumption is fairly true in that higher level patients get bored easily with low level exercises. This patient population is used to performing strenuous exercises. Generally, despite being in pain, they want to perform something hard. As a therapist, educating them on the importance of the low level exercises and discussing the exercise progression in future visits will allow for more patient buy-in to your treatment.
Do not be afraid to start at the most basic level. You are the expert and you no why they need to start at that level.
With our recent review
of management of Temporomandibular Dysfunction (TMD), we thought it would be interesting to see a case example of how to manage the care of patients with TMD. The Manual Therapist recently had a post
covering 5 cases that are somewhat unique, one of which involves TMD. What we hope you take away from the TMD write-up is the importance of a global treatment approach, addressing impairments aside from just those located in the TMJ, and the incorporation of behavioral modification. Our treatment techniques will only go so far if a patient continues to regularly assume abnormal posture and display parafunctional habits, such as nail biting. The other cases are pretty unique as well, seeing some treatment and assessment techniques that aren't regularly covered in physical therapy school.
I performed 3 evaluations yesterday morning. The first individual has been having cervical pain since a MVA in 1991, the second low back pain since her first child 7 years ago, and the last individual was having bilateral radicular symptoms for the past 6 months following a discharge from the military. All 3 can be defined as having chronic pain. Knowing their duration of symptoms alone, how does this change my plan of care? How does it change my prognosis? What sort of goals need to be set between the patient and I?
When a patient presents to you with pain for >6 months, they often are having pain in multiple joints. This makes sense from both a biomechanical and cortical reorganizing perspective. Biomechanically, if an individual is having pain, they will often start to move more from other body regions to avoid pain. These abnormal movements cause repetitive microstrains and result in pain as well. Additionally, individuals with chronic pain will posture themselves in non-painful positions throughout the day. You will often see them in a guarded, fearful posture. Looking at chronic pain from the cortical level, many changes begin occurring in the cortex in the presence of pain. Cortical smudging occurs and other areas of the brain become activated in the presence of pain. Some of these other areas are those associated with cognitive functioning and emotion so you can imagine how the pain completely envelopes their life.
As you can tell already, there is no magical solution to treating these patients. But good approaches include using graded exercises, addressing all barriers that will prevent them from succeeding, and creating realistic and specific goals to measure success. Graded exercise is essential because many of these people STOP exercising in the presence of pain. We see them completely deconditioned, making it difficult to distinguish between true tissue pain or simply the aches and soreness associated with starting a new exercise routine. Start small and start slow! For example, as part of their HEP, I gave one of these patients a home walking program (based off the results of their 6 minute walk test): Walk 4 minutes, 3x/day. Yes, it seems simple, but it is realistic! Barriers also need to be addressed. Typically if someone has been having pain for ~20 years, they have tried to seek care elsewhere but it has been unsuccessful. Why is it unsuccessful? Maybe the musculoskeletal pain is not the only factor. You need to determine if they have financial barriers, transportation issues, psychological issues, social barriers, and more (all of this is obtained during the subjective interview, but gathered much more throughout subsequent visits as you develop a relationship with the patient). Finally, realistic goals must be set. If someone believes they have 10/10 & have been having that pain for 7 years, completely eliminating their pain is not a realistic goal. You need to determine what the patient wants to achieve and set obtainable goals with a set time frame.
As you can imagine, adherence and compliance with therapy is another huge problem. Throughout these treatments, education is KEY. Sometimes it may feel that we turn into psychologists. This is partly true, but I say we have a little more power than them. Our research shows that graded exercise is beneficial for individuals with chronic pain. We can spend 1 hour listening to and educating the patient while having them exercise. Early in the treatment you may be taking on a "general exercising and conditioning" approach. This is fine! Stick with it and you will likely find you are often successful.
In recent years, Physical Therapy research has emerged that compares surgical interventions to placebo surgeries. For certain conditions, there is now fairly substantial evidence that surgical intervention is not always necessary despite what is considered standard societal practice. The most recent example of this is a December 2013 article written by Sihvonen et al, that investigated arthroscopic surgical menisectomy compared with placebo surgery
for individuals with degenerative meniscal tears. The results were pretty interesting! In a recent post
by Leonard van Gelder at Dynamic Principles, he discusses the reasons behind why this appears to continually be happening & gives several good examples of when conservative management is either more successful or equally successful as surgery. Questions you need to ask yourself
-If patients have similar results in surgery vs. placebo surgery, what is at fault in the patient? The mechanical system cannot solely be the answer. The answer lies in the patient's belief system regarding tissue healing and surgery.-How should this change the type of education you give a patient regarding certain conditions?
-How do you manage a patient that strongly believes surgery is the answer (after a disc herniation for example) despite knowing that surgery is not always the best course of action.
(As Leonard discusses in his post, we are well aware that certain conditions require surgical intervention. By no means are we saying surgery is a bad thing. We are simply bringing light to certain conditions that respond positively from conservative management.)
Dosage is one of the most important factors to consider when prescribing an exercise. This decision is often made based off level of acuity, tissue type, anatomical location, patient age, and more. In school, one learns the general principles of exercise prescription, but what is often neglected is WHY you prescribe in certain ranges. "Mechanotherapy: how physical therapists' prescription of exercise promotes tissue repair" is a 2009 article published in the Journal of Sports Medicine that elaborates on this topic.
Physiologically, what stimulates tissue repair of articular cartilage, muscles and tendons is a term called Mechanotransduction. In this article Mechanotransduction is defined as "the process by which the body converts mechanical loading into cellular responses." This can be thought of in clinical terms as what is occurring at the histological level to allow one to prescribe a certain exercise dosage without increasing the risk of injury.
Mechanotransduction can be broken down into 3 phases:
1) Mechanocoupling: This is the physical load cells undergo while in repair. The physical load is transferred into chemical signals which stimulate cellular changes.
2) Cell-Cell Communication: When one cell is stimulated, other cells in the area (whether directly stimulated by the initial mechanical stimulus or not) will undergo a cellular response.
3) Effector Response: When a cell is mechanically stimulated through compression, distraction, etc., several processes will occur intrinsically to allow change to occur.
Now knowing each of the 3 stages, you must think about them in relation to the Type of Tissue involved to understand how that tissue heals.
When a tendon is trying to heal, there is up-regulation of insulin-like growth factor, other growth factors, and cytokines which allows for cellular proliferation and tissue remodeling. Because healing is occur at the cellular level, too much stress OR too little stress on the tendon tissue could cause an alteration in the up-regulation, not allowing the tendon to rehabilitate optimally. The research up-to-date shows that tendons responds positively to "controlled loading." Research focusing on the type and intensity of controlled loading (eccentrics, assisted, resisted) is still ongoing.
The authors Khan and Scott state that "muscle offers one of the best opportunities to exploit and study the effects of mechanotherapy" because of how muscle tissue responds to loading. We know there is an overload of mechanogrowth factor (MGF) released when load is induced on the muscle force. This in turn causes muscle cell hypertrophy due to a cell-to-cell communication with nearby satellite cells. At this point, the research shows that early loading after a brief immobilization period is essential for minimizing atrophy and restoring normal cellular structure of the muscles.
Articular cartilage is comprised of a large population of mechanosensitive cells. It is hypothesized that by repetitively stimulating the articular cartilage with a low load/high repetition exercise dosage, better outcomes will result. One study assessing full thickness cartilage defects following periosteal transplantation demonstrated that individuals who used continuous passive motion (low load/high repetitions) had greater outcomes than those who did not receive this intervention. As with all things, research is ongoing.
When assessing bone healing, osteocytes are the primary mechanosensors. A recent study looking at individuals following a distal radius fracture had stronger bone growth if they received intermittent compression as an adjunct to the standard of care (compression & gripping exercises). The pneumatic compression allowed for extra stimulation of the bone cells and an increased healing rate.
We know parts of this article are dense, but understanding what is occurring at the cellular level can greatly change your viewpoint of how various tissues heal. Through each of these tissues we can see that Mechanotherapy plays a unique role in healing of different tissues types. The healing of osteocytes differs from that of chondrocytes which differs from myocytes. It is fundamental to understand these differences in order give appropriate doses during exercise - just as it is important to know the tissue type you should be treating following your examination.
As a general rule of thumb: Articular Cartilage: Low Load, High Repetition; ~15% 1 RM; Thousands of repetitions.
Tendon: Controlled Loading; consider eccentric exercises, but do not overload the tissue. Muscle: allow for a brief period of immobilization to restore homeostasis following injury. Bone: Based on location of the fracture, consider adding compression to your treatment to improve rate of bone growth and decrease healing time.
Khan and Scott. (2009) "Mechanotherapy: how physical therapists' prescription of exercise promotes tissue repair."
British Journal of Sports Medicine. 2009; 43: 247-251. Web. 5 Dec. 2013.
In the real world, not all of our patients will get 100% better on the first attempt. Sometimes patients stop progressing, which can be very discouraging for both us as clinicians and our patients. However, it is at this point that we must act. After about two to four weeks, we should see some significant changes in our patients' symptoms. When/If this does occur, there are three actions that you should consider as a clinician:
1. Reassess the Patient: Do another quick examination to check yourself (before you wreck yourself). We frequently are hurried in our initial evaluation and can occasionally get sloppy/lazy with our objective measures. Also, this allows you to expand your objective search. It's possible you missed an impairment that is a key contributor to the patient's symptoms but is located away from the symptomatic tissue (think regional interdependence). You may also want try consulting a more experienced or skilled practitioner if available.
2. Check Patient Compliance: This is a big one and a common culprit. It is our job to educate our patients on why it is essential that they are regularly performing their HEP. If you think how much time our patients spend working with us compared to being outside the clinic, any significant gains must be made (or maintained) independently. With regular performance of an HEP, we should expect to see a weak muscle get stronger, an adaptively shortened muscle lengthen, etc. If we are not seeing the expected improvements, it's time for another chat with the patient. Patients will often complain of not having time to do their HEP. It is here we must tell the patient that we cannot accomplish what we want to do in the clinic without the expected results from a regularly performed HEP. If they are too busy, maybe they need to reschedule their appointment once they have found time.
3. Refer Out: Physical therapy is sometimes used as a diagnostic tool for physicians. We are movement experts and often have a different perspective to offer when examining patients compared to medical doctors. This option actually has a couple different considerations. As you might have guessed, we all likely have impairments that would benefit from physical therapy. Whether or not these impairments are linked to the pathology is a separate issue. That explains why failure to respond to physical therapy after a month is a red flag. Another concern in this area is musculoskeletal pathology that sometimes benefits from skilled physical therapy. An example is meniscal tears. A study came out last year showing that conservative management of meniscal tears was just as successful as surgical outcomes. However, this does not mean that everyone will always respond to physical therapy. If after a few weeks the patient has not seen any significant improvements and is experiencing acute locking/catching in the joint, this patient may not be appropriate for conservative care. This applies to other pathologies as well.
Physical therapy school teaches you some of the fundamentals of the respiratory system: anatomy, physiology, breathing patterns, etc. While these are important, sometimes the assessment and treatment techniques are over-simplified. Not all breathing or respiration deficits can be managed by attempting to train diaphragmatic breathing. The Manual Therapist recently had a post
that reviewed some of the physiology and implications of managing breathing, along with the use of something called a Capnotrainer. What is really interesting about this post is how the physiology of the respiratory system impacts us as clinicians and what we can expect to see. This is something often lost upon us as we are scrambling to prepare an exam. With a true understanding, we can more appropriately select interventions for our patients.