A couple weeks ago I had to do a progress note on another PT's patient (something I don't enjoy). Typically I just re-take the measurements and continue with the treatment, but if a significant lack of progress has been noticed, I may adjust the plan of care. It is not an easy task or decision to make, changing a treatment plan, but we must look out for the patient, especially if we notice something is missing that is essential to the care. There are various ways you can accomplish this. You can speak with the regular PT about your findings with recommendations, include your findings and recommendations in the note (if you are unable to speak to the PT before the next treatment session), or sometimes adjust the plan right there...CONTINUE READING..
We recently had our second Fellowship class which focused on joint manipulation and adverse neural tissue tension. As you may have noticed with the recent increase in posts related to the neural system, the class had quite the impact on us. The obvious benefit the manipulation portion of the course was a dramatic improvement in our technique and clinical reasoning behind when and where to do a manipulation. As beneficial as that was, the part of the course focusing on neural tension had an even greater impact...CONTINUE READING
Recently, OPTIM Manual Therapy Fellowship wrote a response blog post to a Move Forward PT podcast entitled: "Could that Pain be Unhealthy Fascia." It appears that OPTIM was not the only group of individuals upset by this segment. The APTA removed that segment from the Move Forward PT website after backlash from a number of individuals. In short, the segment discusses fascia, how it is injured, and how the fascia can inhibit movement. This post is not to meant to criticize the podcast (that has been done by many others before me), but bring light to other issues and concepts surrounding the podcast.
First, I agree with the OPTIM PT response. When assessing patients with musculoskeletal dysfunction, one must go to the joint level first. This statement transcends fascia. It applies to muscles, nerves, and other connective tissues as well. For example, if the IT band is causing a friction syndrome, go to the levels that innervate the TFL. If an individual has a positive Thomas Test for two-joint shortness, assess L2-L4 for dysfunction. A novice clinician might only treat the tight rectus muscle with stretching or a tight IT band with a foam roller. Typically, this does not treat the cause of the dysfunction. In many instances, assessing the joint will lead you to the cause of the dysfunction. Go to the joint level before going to the tissue!
Second, in the podcast the interviewee, who is a PT, DPT, OCS, discusses using the foam roller as an initial line of treatment for patient's with IT band pain. If the foam roll does not correct the problem, the individual should then go see a physical therapist. Why is it not the other way around? The patient should first go see a PT who can properly diagnose the problem. As a profession we need to stop promoting passive modalities to take the place of our job. If we ever expect to advance in the medical world, we need to promote ourselves as the first line of defense in musculoskeletal dysfunction.
Finally, having a specialty certification does not automatically place your above and beyond your colleagues (sad to say since I am currently studying for my OCS). In the segment, the PT is also an OCS. Despite having these initials, she is still discussing the fascia as a cause of the problem and administering foam rollers for treatment for IT band pain. Simply having a specialty certification is not enough, we must stay on top of the literature and learn advanced treatments in order to practice with the highest quality care.
To check out OPTIM's response click HERE
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Recently a patient with low back pain also had complaints of UE symptoms. She had awakened that morning with burning in her L lateral 3 finger tips. Even though I was seeing her for her back, I quickly looked at her UE symptoms in order to give the patient some information about the impairments. Since she had neural complaints in her lateral 3 fingers, I thought it would be wise to assess neural tension of the median nerve. Upon placing the limb in a partially tensioned position, the patient exhibited clonus of elbow flexion. Questioning myself, I took the patient out of the tensioning position and immediately did rapid elbow extension without any resistance. Placing the limb back into the median nerve tensioned position slowly resulted in clonus again. This lead me to do a slightly more thorough neuromuscular screening. The patient had a history of decreased sensation on the R side and had seen a neurologist 5 years ago, which resulted in negative EMG studies. The patient denied any constitutional symptoms and had negative gait ataxia, Hoffman's, slump test and Inverted Supinator Sign. On the R side, she did present with some odd neuromuscular signs. With Babinski, she reacted with involuntary hip flexion on the R while L side was negative. With tensioning of the R median nerve, the patient rolled out of the tensioned position involuntarily. She was hyperreflexive on the R side as well. Due to this atypical presentation, I referred the patient to a neurologist. Afterwards I consulted with several physical therapist, including my mentor, all of whom had never heard of clonus with a neural tension test.
The reason I present this patient encounter is to review the essential components of a neuromuscular screening. Due to the fast pace of the clinic and the fact I was seeing her for her back, I was unable to do a thorough exam. Below I will include all things I should have looked at:
-Dermatomes: looking for altered sensation along different spinal levels
-Myotomes: looking for weakness along different spinal levels
-Reflexes: looking for either hyporeflexia (Lower Motor Neuron lesion) or hyperreflexia (Upper Motor Neuron lesion)
-Cluster for Cervical Myelopathy:
-Inverted Supinator Sign
-Slump Test and SLR: tensioning of the neural system from the LE
-ULNT's: tensioning of the neural system from the UE
-Clonus: looking for potential Upper Motor Neuron lesion
-S&S of Cauda Equina Syndrome
-Bowel &Bladder Changes
-Nausea & Vomiting
-Significant Changes in Weight in Last 6 Months
-Hx of Cancer
-Tolerance to Heat and Cold
The above list is many of the aspects one needs to consider in your neuromuscular examination. Our normal exams will also look for spinal and peripheral joint mobility and the joint's response to repeated loading. However, when concerned about a potential neuromuscular disease, we should be aware of the accumulation of these S&S. For example, with this patient's young age (20), history of decreased sensation on one side, difficulties with heat/cold, and odd reactions with neural tensioning diagnoses such as multiple sclerosis come to mind. It is for this reason that it is essential we screen our patients thoroughly for systemic conditions of all types.
What other exam measures do you include in your neuromuscular screening?
The ANS is comprised of the sympathetic and parasympathetic nervous systems. In physical therapy school, I was taught to look at the autonomic nervous system (ANS) as an up or down -regulator of homeostatic function. Its functions include pupil dilation, gut mobility, force of cardiac contractions, and much more. Early into my clinical practice as an Orthopedic Manual Physical Therapist, I did not perceive the connection between the sympathetic nervous system (SNS) and the musculoskeletal system. Entrapment of the sympathetic nervous system can be a contributing factor in anything from peripheral nerve pathology to chronic regional pain syndrome. Understanding the different components of the sympathetic chain can lead to better treatment strategies.
Anatomy & Function
The sympathetic nervous system lies just anterior to the costotransverse joints from T1-T12. Each region of the sympathetic nervous system corresponds with a region of the body. T3-T7 innervates the upper extremities, T7-T12 innervates the lower extremities, and the entire chain (T1-T12) innervates the trunk. In a healthy population, normal mobility exists in the SNS allowing information to flow uninterrupted. In the presence of chronic pain, the spinal inter-neurons may become more sensitive to stimuli. This phenomenon is known as central sensitization. The patient may develop hyperalgesia, allodynia, and have decreased pain thresholds. These symptoms are due to SNS dysfunction and can manifest in our musculoskeletal patients. No one understands the exact interaction between the sympathetic nervous system and pain, but we know there is a relationship. By altering the function of one, we can change the function of the other.
Patients who present with central sensitization can benefit from manual therapy. Since we know that each region of the SNS corresponds with a body region, manipulation or mobilization should be directed accordingly. A patient with hyperalgesia of the upper extremity will better benefit from a manipulation of the upper thoracic vertebrae. Contrarily, those with pain alterations of the lower extremity will benefit from a manipulation of the lower thoracic vertebrae. If the patient presents with CRPS, the patient may not tolerate the force of manipulation. Joint mobilizations of the respective area will suffice.
As therapists, people often need proper "validation" for performing a manipulation. Thoracic manipulations are very safe and mobilizing the SNS can help increase the pain threshold to provide a window of opportunity to maximize the effects of your treatment.
A couple months ago, we posted about the diagnosis and management of Lumbar Extension-Rotation Syndrome. The use of Shirley Sahrmann's Diagnosis and Treatment of Movement Impairment Syndromes text can be extremely useful in identifying the original fault in a patient's injury. Some of the more common shoulder pathologies, like shoulder impingement and rotator cuff tears, actually can result from a movement impairment syndrome. Recently, I have come across a couple patients that did not present like the typical subacromial impingement or rotator cuff tear. After looking at the patient's movement patterns, I recognized a link between the impairments and dysfunction of superior humeral glide syndrome, leading to the proper treatment.
-Arms in abduction relative to scapulae. Associated with downwardly rotated scapulae. When scapula position corrected, humerus is in abduction.
-During GH flexion or abduction, note excessive movement of head of humerus superiorly against acromion. More evident in abduction.
-Humeral superior glide more evident during active abduction versus passive.
-Decreased GH crease noted just distal to acromion with arm overhead.
-Decreased inferior glide and lateral distraction of GH joint.
-Short subscapularis and lateral rotators, supraspinatus, deltoid.
-Weak rotator cuff muscles.
-May find positive tests for rotator cuff tears and impingement.
-Often associated with scapular downward rotation syndrome.
So how does this happen? With elevation of the humerus, there tends to be over-activity of the deltoid muscle and decreased activity of the rotator cuff muscles responsible for inferior glide of the head of the humerus. If you are able to either increase deltoid activity or increase rotator cuff activity, a decrease in pain will be noted. While we should treat every patient based on the impairments they present with, I will list some of the important treatments I have found based on common impairments with this syndrome. Mobilization of the inferior capsule of the GH joint is necessary due to the excessive superior glide and lack of inferior glide. Exercises to restore the scapular fault are important as that provides the base for the shoulder. Since this syndrome is often associated with scapular downward rotation, I like to do standing wall shrugs to improve upper trap function. This must be coupled with decreasing the downward force the arms play on the humerus. It can be done by crossing arms against chest when unsupported or using well-positioned arm rests. Rotator cuff exercises are important as well. Sahrmann recommend using prone ER in 90 deg of abduction to improve infraspinatus and teres minor function. This helps to decrease posterior deltoid activity, unlike shoulder ER in adduction. Supine shoulder IR/ER can be used to regain shoulder mobility but I recommend it be done in 90 deg abduction again to limit deltoid activity. Finally, another exercise Sahrmann recommend is sliding ulnar borders of hands up on wall above head and then exerting a downward force to depress the head of the humerus. Hopefully this helps in identifying patients that you come across with this syndrome! For more information, check out Sahrmann's Diagnosis and Treatment of Movement Impairment Syndromes.
Sahrmann SA. Diagnosis and Treatment of Movement Impairment Syndromes. St. Louis, MO: Mosby. 2002. 234-236. Print.
Tension points are areas of the body with little or no movement between the nervous system and it's surrounding structures. Tension points can occur peripherally (at the carpal tunnel or superior tibiofibular joints for example) and centrally within the spinal column. The three main tension points of the spine are C6, T6, and L4. Clinically, it is important to investigate tension points whenever the patient reports radiating symptoms to an extremity.
Peripherally, tension points occur where the nervous system branches, at soft tissue or osseous tunnels, areas where the nervous system is relatively fixed, and areas where the nervous system passes closely to surrounding structures. Examples of each of these can be seen below.
EXAMPLES OF TENSION POINTS
I've been a fan of Erik Meira for some time now. He has great insight into the world of sports physical therapy as well as the science behind things. In addition, his journey into sports physical therapy is very interesting and uncommon.
However, he really did a good job with providing a foundation for those looking to stay more current with the latest research out there. It's so important to stay up to date with the research in your subspecialty area as well as attend conferences and CEU's. Being complacent in the field of physical therapy just won't work. You will get frustrated in the clinic and your patients will not get better. Check out his article and then check out our favorites page with other resources and names to follow. You won't be disappointed.
Sports Resources Page
Regular readers of the Sports Physio blog are well aware that there is definitely at least a dislike towards manual therapy (or what many claim to be manual therapy) with the author of the blog, Adam. He recently put up a post about his frustrations with certain theories of the mechanisms behind physical therapy. The post was well supported with various articles. While the tone of the article is somewhat extreme and definitely opinionated, Adam brings up some very important points, particularly about the lack of any evidence for biomechanical explanations behind manual therapy.
In our most recent fellowship class with the Manual Therapy Institute, we covered adverse neural tissue tension and manipulations. The instructors recognize that there is a lack of research to support a specific mechanism behind manual therapy, but do have a hard time factoring in studies as proposed by Adam in his blog post. They offer up both biomechanical and neurophysiological explanations for the techniques. To the casual reader, it would appear Adam's post argues against using manual therapy at all, when in reality, it is just arguing against a particular theory of it - the biomechanical one. Towards the end, he recognizes that most of the current research suggests that manual therapy works via the central nervous system. While this may be true, it is a difficult argument to fully support. According to Shirley Sahrmann, it is impossible to prove a neurophysiological mechanism behind the success of manual therapy. Even though some studies may suggest an existing mechanism behind the theory, we are incapable of actually proving it according to her.
Now the theme of the article would suggest that manual therapy has minimal applications. This may prove discouraging to those who have spent thousands of dollars trying to improve their manual skills. This is the point at which I disagree with the author. I have seen significant improvements in patients in which I use manual therapy. Measure a joint's mobility, perform some IASTM, reassess and find changes in ROM. Assess neural tension, perform a manipulation, reassess and find changes in neural tension. Of course this is not applicable to everyone, but it does affect a lot. There are quite a few studies that have shown improvements in patients after manual therapy has been applied (check out our previous post here). Even though we cannot prove why a technique works, should we stop using it if it is successful? That is the message I fear some will take away from Adam's article. Take IASTM for example. With my IASTM training (IASTM Technique), we learn the theory behind the changes are in activation of mechanoreceptors that allow the nervous system to have altered mobility. There is also some theory about cortical remodeling. Adam links to an article that he uses to defend his belief that IASTM has little effect. However, upon closer look, we do not know enough about the individuals selected in the study (possibly slow-responders) and the study's small sample size of 17 participants do not exactly qualify for normalizing to the population. Many that use IASTM, myself included, have seen immediate changes after the manual treatment alone. Now, of course we must reinforce any changes we acquire through manual therapy with some sore of exercise or education to make the patient more independent and lock in the changes. Manual therapy can be an extremely useful tool to accelerate your treatment plan. Be flexible as research continues to come out about manual therapy that might assist your decision making, but don't throw it away just yet.
From my clinical experiences thus far, I have found that many individuals with low back pain lack proper gluteus maximus strength. (This should not be a surprise to you unless you went to physical therapy school when dinosaurs were still roaming). I often find that the gluteals are weak due to a combination of disuse atrophy and muscle inhibition secondary to pain. In the case of disuse atrophy, the individual does not activate their gluts and therefore preferentially activates other muscles to perform the movement. For example, think about the individual who arches his/her back to pick up a box rather than perform a hip hinge and squat OR consider the individual who rests in lumbar extension, locking out the lumbar facets and resting on the anterior hip ligaments. They avoid the gluteals and activate their lumbar paraspinals and hamstrings to perform movements. With pain inhibition, the gluteals are not receiving proper neuromuscular facilitation because pain is overriding the movement. The muscles are temporarily unable to fire because pain is inhibiting the activation. In either situation, properly assessing hip strength and assessing the cause of weakness is a fundamental part of a low back evaluation.
In this post, I want to discuss hamstring dominance is relation to gluteus maximus testing. As I stated in the previous paragraph, poor movement patterns often lead to improper activation of the glut muscles. Since the gluts are not helping perform the movement, a different muscle overcompensates to perform the movement. Clinically, I often find that this other muscle is the hamstrings (or lumbar paraspinals). Individuals that preferentially activate their hamstrings prior to their gluts are called 'hamstring dominant.' This can be problematic because the gluteals are meant to act as a hip stabilizer and extensor. When they do not fire first, the gluteals do not stablize. The hamstrings attempt to act as both a prime mover and stabilizer.
The test for hamstring dominance is similar to the Kendall Glut Max testing position. Place the individual in prone with the tested knee bent to 90 degrees. Ask them to lift their leg off the table. In the normal healthy individual, the glut max engages prior to the hamstrings. Proper activation order: 1. TrA engages, 2. gluteus maximus activates, 3. hamstrings fire as the leg is lifted. If the hamstrings fire before the glut max, the individual drives that motion with the hamstrings.
Do not be fooled by strong gluts in the low back pain population. After assessing the glut max, retest for hamstring dominance to ensure they are not over-activating the hamstrings. Dominance patterns are extremely common. I highly recommend assessing for hamstring dominance in your lumbar patients.