Orthopedic & Manual Therapy Blog
 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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Anatomy:
When discussing thoracic spine anatomy, one of the first things to remember is that the thoracic spine is comprised of 12 vertebrae. These vertebrae have similar characteristics to the other vertebrae: a vertebral body (disk to vertebral body height ratio is 1:5), pedicles directed posterior from the body, lamina that connect to form a spinous process, and facets (Neumann, 2010). The transverse processes are directed posterolaterally and the spinous processes fall inferiorly (depending on the region). This orientation puts the transverse processes one segment below the corresponding spinous process. Clinically, this is an important consideration for palpation. T1-3 and T10-12 may actually have their spinous processes at the same level as the transverse processes (Egan et al, 2011). The spinous processes of T4-T6 fall half a level below the transverse processes, while T7-9 spinous processes fall a full level below the transverse processes (this is the “rule of 3’s” which has limited support at the time, so should be applied with caution). The pedicles actually sit directly posterior from the vertebral body, making the vertebral canal narrower here compared to other parts of the spine. T4-9 is known as the critical zone because the vertebral canal is narrowest here; it also has reduced blood supply (Egan et al, 2011). For this reasons, T6 is a tension point. At T6, motion of the spinal cord versus canal converge in different directions, meaning restriction in neural/spinal mobility can occur and may need to be addressed. The superior and inferior facets in the thoracic region are oriented about 60 degrees from the horizontal plane and 20 degrees from the frontal plane with the inferior facets facing anteriorly, inferiorly, and slightly medially; the superior facets face posteriorly, superiorly, and slightly lateral. Something to consider is that there is no immediate change between cervical to thoracic vertebrae and thoracic to lumbar vertebrae. The superior thoracic vertebrae bare qualities more similar to the cervical spine and the inferior thoracic vertebrae more so resemble the lumbar spine.
When discussing thoracic spine anatomy, one of the first things to remember is that the thoracic spine is comprised of 12 vertebrae. These vertebrae have similar characteristics to the other vertebrae: a vertebral body (disk to vertebral body height ratio is 1:5), pedicles directed posterior from the body, lamina that connect to form a spinous process, and facets (Neumann, 2010). The transverse processes are directed posterolaterally and the spinous processes fall inferiorly (depending on the region). This orientation puts the transverse processes one segment below the corresponding spinous process. Clinically, this is an important consideration for palpation. T1-3 and T10-12 may actually have their spinous processes at the same level as the transverse processes (Egan et al, 2011). The spinous processes of T4-T6 fall half a level below the transverse processes, while T7-9 spinous processes fall a full level below the transverse processes (this is the “rule of 3’s” which has limited support at the time, so should be applied with caution). The pedicles actually sit directly posterior from the vertebral body, making the vertebral canal narrower here compared to other parts of the spine. T4-9 is known as the critical zone because the vertebral canal is narrowest here; it also has reduced blood supply (Egan et al, 2011). For this reasons, T6 is a tension point. At T6, motion of the spinal cord versus canal converge in different directions, meaning restriction in neural/spinal mobility can occur and may need to be addressed. The superior and inferior facets in the thoracic region are oriented about 60 degrees from the horizontal plane and 20 degrees from the frontal plane with the inferior facets facing anteriorly, inferiorly, and slightly medially; the superior facets face posteriorly, superiorly, and slightly lateral. Something to consider is that there is no immediate change between cervical to thoracic vertebrae and thoracic to lumbar vertebrae. The superior thoracic vertebrae bare qualities more similar to the cervical spine and the inferior thoracic vertebrae more so resemble the lumbar spine.
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Ribs:
Additionally, when assessing the thoracic spine, one must consider the ribcage. There are 12 ribs (usually) in the body, just as there are 12 thoracic vertebrae. Ribs 1-7 are true ribs in that they attach directly to the sternum in the front of the body (Neumann, 2010). Ribs 8-12 are false ribs. Ribs 8-10 join in cartilage before attaching to the cartilage of the 7th rib. Ribs 11 and 12 are floating ribs and have no ventral attachments. Ribs 3-9 have demifacets on the thoracic vertebrae for attachment that span 2 vertebrae. Ribs 1, 11, and 12 have one facet on the corresponding vertebrae. The 2nd rib attaches to both T1 and T2 vertebrae. Additionally, ribs 1-10 have facet attachments at the costotransverse joints, while ribs 11-12 lack these as "floating ribs." Above T7, the rib portion of the costotransverse joints are concave, allowing for more rotation compared to the planar joints of the below T7 (Egan et al, 2011). The sympathetic chain lies on the anterior side of the rib heads next to the costovertebral joints.
Additionally, when assessing the thoracic spine, one must consider the ribcage. There are 12 ribs (usually) in the body, just as there are 12 thoracic vertebrae. Ribs 1-7 are true ribs in that they attach directly to the sternum in the front of the body (Neumann, 2010). Ribs 8-12 are false ribs. Ribs 8-10 join in cartilage before attaching to the cartilage of the 7th rib. Ribs 11 and 12 are floating ribs and have no ventral attachments. Ribs 3-9 have demifacets on the thoracic vertebrae for attachment that span 2 vertebrae. Ribs 1, 11, and 12 have one facet on the corresponding vertebrae. The 2nd rib attaches to both T1 and T2 vertebrae. Additionally, ribs 1-10 have facet attachments at the costotransverse joints, while ribs 11-12 lack these as "floating ribs." Above T7, the rib portion of the costotransverse joints are concave, allowing for more rotation compared to the planar joints of the below T7 (Egan et al, 2011). The sympathetic chain lies on the anterior side of the rib heads next to the costovertebral joints.
Clinical Implications:
As stated previously, the fact that the thoracic spine connects the cervical spine to the lumbar spine is reason alone that this anatomical area should be considered for treatment. Think about the impact of posture. In most patients that sit for prolonged periods with a forward head posture, the anterior shift of the center of gravity places an excessive flexion moment arm to the thoracic spine, furthering the already kyphotic nature of the thoracic spine. As with any tissue, prolonged stress and creep eventually leads to pain when the tensile stiffness is no longer sufficient and the patient experiences pain. Training postural muscles is key to encouraging a more neutral posture that does not stress the tissues excessively. This may include spinal stabilizers and scapular stabilizers and should be dosed appropriately (likely want some high repetition-based exercises to improve endurance).
Consider facet restrictions: Limited joint mobility in one location often leads to hypermobility and pain in other regions, either nearby or distant. A joint dysfunction can often lead to hypertonic/painful muscle tissue near the joint as well. We can treat these restrictions with manual therapy and exercise. Two conditions less commonly discussed but seen relatively often include rib dysfunction and neural tension. Rib impairments are typically considered after a blow to the side or pain with breathing, but that is not always the case (making it harder to identify). A partially subluxed or restricted rib can be quite painful and present as thoracic paraspinal pain or even abdominal pain as the tip of a floating rib presses against the anterior tissue.
As stated previously, the fact that the thoracic spine connects the cervical spine to the lumbar spine is reason alone that this anatomical area should be considered for treatment. Think about the impact of posture. In most patients that sit for prolonged periods with a forward head posture, the anterior shift of the center of gravity places an excessive flexion moment arm to the thoracic spine, furthering the already kyphotic nature of the thoracic spine. As with any tissue, prolonged stress and creep eventually leads to pain when the tensile stiffness is no longer sufficient and the patient experiences pain. Training postural muscles is key to encouraging a more neutral posture that does not stress the tissues excessively. This may include spinal stabilizers and scapular stabilizers and should be dosed appropriately (likely want some high repetition-based exercises to improve endurance).
Consider facet restrictions: Limited joint mobility in one location often leads to hypermobility and pain in other regions, either nearby or distant. A joint dysfunction can often lead to hypertonic/painful muscle tissue near the joint as well. We can treat these restrictions with manual therapy and exercise. Two conditions less commonly discussed but seen relatively often include rib dysfunction and neural tension. Rib impairments are typically considered after a blow to the side or pain with breathing, but that is not always the case (making it harder to identify). A partially subluxed or restricted rib can be quite painful and present as thoracic paraspinal pain or even abdominal pain as the tip of a floating rib presses against the anterior tissue.
A potential location for pathology and treatment of neural tension is the thoracic spine. Remember that the thoracic spine contains the critical zone where the vertebral canal is narrowest. The spinal cord can easily become compressed here, leading to pain/neural tension along the path of a nerve. A nerve can become irritated anywhere in the body. Additionally, sometimes neural tension in the thoracic spine may be related to the cervical spine. With cervical radiculopathy or Cloward’s Area, thoracic/scapular pain can be coming from the cervical spine. When the patient presents with thoracic restrictions, a manipulation to the mid-thoracic spine often improves pain and neural tension by improving mobility. This doesn’t only apply to thoracic pain. There is research showing that patients with shoulder or neck pain may benefit from thoracic manipulation. In fact, there is a clinical prediction rule recommending thoracic manipulation for neck pain (non-validated):
- Symptoms < 30 days
- No symptoms distal to shoulder
- Looking up does not aggravate symptoms
- FABQ Physical Activity Score < 12
- Diminished upper thoracic spine kyphosis
- Cervical extension ROM < 30 deg (Cleland et al, 2007)
For more information on topics like these, check out our FREE Cervical Spine Mini Course on how to treat Cervical Radiculopathy!
References:
1. Cleland JA, Childs JD, Fritz JM, Whitman JM, Eberhart SL. "Development of a clinical prediction rule for guiding treatment of a subgroup of patients with neck pain: use of thoracic spine manipulation, exercise, and patient education." Phys Ther. 2007 Jan.
2. Egan W, Burns S, Flynn T, and Ojha H. The Thoracic Spine and Rib Cage: Physical Therapy Patient Management Utilizing Current Evidence. Current Concepts of Orthopaedic Physical Therapy, 3rd Ed. La Crosse, WI. 2011.
3. Neumann, Donald. Kinesiology of the Musculoskeletal System: Foundations for Rehabilitation. 2nd edition. St. Louis, MO: Mosby Elsevier, 2010. 322-323. Print
1. Cleland JA, Childs JD, Fritz JM, Whitman JM, Eberhart SL. "Development of a clinical prediction rule for guiding treatment of a subgroup of patients with neck pain: use of thoracic spine manipulation, exercise, and patient education." Phys Ther. 2007 Jan.
2. Egan W, Burns S, Flynn T, and Ojha H. The Thoracic Spine and Rib Cage: Physical Therapy Patient Management Utilizing Current Evidence. Current Concepts of Orthopaedic Physical Therapy, 3rd Ed. La Crosse, WI. 2011.
3. Neumann, Donald. Kinesiology of the Musculoskeletal System: Foundations for Rehabilitation. 2nd edition. St. Louis, MO: Mosby Elsevier, 2010. 322-323. Print
 | No matter where you do your rotations or practice physical therapy, you are bound to work with both people who target the VMO with their interventions and people who think it's impossible to do so. Following trauma, knee surgery, or patellofemoral pain syndrome, many practitioners claim selective atrophy and weakness of the VMO relative to the rest of the quadriceps. |
This becomes a focus of several interventions in the patient's care plan. The goal of VMO isolation is to improve the tracking of the patella and medial "pull" of the quads. This would, theoretically, affect patellofemoral strain. Due to the controversial state of this case, we thought we would do a review on the isolation of the vastus medialis muscle. Let's start out with reviewing a little anatomy. The quadriceps is made up of four parts: rectus femoris, vastus lateralis, vastus medialis, and vastus intermedius
Quadricep Muscles Origin, Insertion, Innervation
| Rectus Femoris Origin: -Anteroinferior iliac spine (straight head), groove above rim of acetabulum (reflected head) Vastus Lateralis Origin: -Proximal part of intertrochanteric line, anterior and inferior to borders of greater trochanter, lateral lip of the gluteal tuberosity, proximal 1/2 of lateral lip of linea aspera and lateral intermuscular septum | Vastus Intermedius Origin: -Anterior and lateral surfaces of proximal 2/3 of the body of femur, distal 1/2 of linea aspera, and lateral intermuscular septum Vastus Medialis Origin: -Distal 1/2 of intertrochanteric line, medial lip of linea aspera, proximal part of medial supracondylar line, tendons of the adductor longus and adductor magnus and medial intermuscular septum |
Common Insertion:
-Tibial tubersoity (patella acts as sesamoid bone, but some call patella the insertion and then the attachment of patella to tibial tuberosity is known as the patellar ligament)
-Tibial tubersoity (patella acts as sesamoid bone, but some call patella the insertion and then the attachment of patella to tibial tuberosity is known as the patellar ligament)
Can You Isolate Part of a Muscle?
One way of analyzing this controversial issue is anatomically. Hubbard et al reviewed the anatomy of cadavers to enhance the interpretation of VMO isolation. The vastus medialis is commonly broken down into two components: vastus medialis longus (VML) and vastus medialis oblique (VMO). It is thought that the VMO is responsible for medial patellar tracking, due to its oblique fiber orientation. In the study, the VMO was unable to be found separated from the VML, meaning the VMO was not found to be a muscle independently. Any attempted separation required destruction of muscle fibers. Upon review of innervation, many studies in the past have come across independent innervation, leading to the hypothesis that the VMO was a separate muscle. However, these nerves have been found to be superficial separations from the femoral nerve leading to distal motor units, sensory contribution from the saphenous nerve, or penetrating innervation for the knee capsule. The authors argue that without isolated innervation, the VMO cannot be activated independently (the patella cannot solely be pulled medially); it is the activity of the femoral nerve the stimulates the entire vastus medialis to contract and extend the knee while pulling the patella medially.
Historically, many people were under the impression that the rectus femoris was the prime knee extensor. They thought the vastus medialis was responsible for the final 15 degrees of knee extension due to the inadequacies of the rectus femoris (Lieb & Perry, 1968). Boucher et al looked at the vastus medialis activity in patients with patellofemoral pain syndrome. They found that the vastus medialis and vastus lateralis were not more active in terminal extension. However, they did find that in patients with PFPS, there was a decreased VM:VL ratio compared to the control group. These differences were found to be attributable to a mechanical disadvantage (greater Q-angle); when the Q-angle was decreased, the ratio returned to normal. This same difference in VM and VL ratio was found in another study to be related to mechanical factors as well (Souza & Gross, 2001). Additionally, the authors discovered that isotonic quadriceps contractions elicited larger VM:VL EMG activity compared to isometric contractions. This may influence the treatment plan for patients with pathologies, such as patellofemoral pain syndrome. Ng et al. and Cowan et al. also came across this difference in VM and VL ratio with EMG activity. In fact, the authors were able to normalize the EMG activity with use of therapeutic exercise + biofeedback. Biofeedback has been found to be a useful component in motor retraining, especially regarding earlier activation of the VMO (Cowan et al., 2002). A delay of as little as 5 ms of the VMO relative to the VL can increase the compression forces on the lateral patellafemoral joint (Boling et al, 2006). Powers described a difference between VM and VL activity as well; however, it was attributed to patellar malalignment. Decreased VM activity was not found to be the cause of abnormal patellar tracking or patellar tilt.
Historically, many people were under the impression that the rectus femoris was the prime knee extensor. They thought the vastus medialis was responsible for the final 15 degrees of knee extension due to the inadequacies of the rectus femoris (Lieb & Perry, 1968). Boucher et al looked at the vastus medialis activity in patients with patellofemoral pain syndrome. They found that the vastus medialis and vastus lateralis were not more active in terminal extension. However, they did find that in patients with PFPS, there was a decreased VM:VL ratio compared to the control group. These differences were found to be attributable to a mechanical disadvantage (greater Q-angle); when the Q-angle was decreased, the ratio returned to normal. This same difference in VM and VL ratio was found in another study to be related to mechanical factors as well (Souza & Gross, 2001). Additionally, the authors discovered that isotonic quadriceps contractions elicited larger VM:VL EMG activity compared to isometric contractions. This may influence the treatment plan for patients with pathologies, such as patellofemoral pain syndrome. Ng et al. and Cowan et al. also came across this difference in VM and VL ratio with EMG activity. In fact, the authors were able to normalize the EMG activity with use of therapeutic exercise + biofeedback. Biofeedback has been found to be a useful component in motor retraining, especially regarding earlier activation of the VMO (Cowan et al., 2002). A delay of as little as 5 ms of the VMO relative to the VL can increase the compression forces on the lateral patellafemoral joint (Boling et al, 2006). Powers described a difference between VM and VL activity as well; however, it was attributed to patellar malalignment. Decreased VM activity was not found to be the cause of abnormal patellar tracking or patellar tilt.
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Some convincing evidence has been found that the vastus medialis cannot be isolated. One study discussed the fact that the decrease in knee extensor strength in the last 15 degrees is due to a loss in mechanical advantage (Lieb & Perry, 1968). Following surgery, many practitioners have noted increased atrophy at the vastus medialis. This decreased prominence has been found to be associated with the obliquity of fibers, lowness of insertion, and thinness of fascial covering compared to the rest of the quadriceps. The "atrophy" noted in the vastus medialis is actually representative of general quadriceps weakness. On the other hand, the vastus medialis was shown to have a selective role in patellar tracking. Another proposed component to PFPS is a difference in onset between the VM and VL. Gilleard et al and Powers et al were unable to reproduce any difference in timing of activation, cessation, or intensity between the VM and VL, while Smith et al. was able to show that the differences that were found in VM and VL activity were due to the effect pain has on EMG activity (this was noted in individuals with PFPS). One of the focal points of the study was to see the effect taping had on VMO activation. With taping, vastus medialis activation was shown to occur prior to vastus lateralis activation. The authors were unsure if the cause was through mechanical means or pain reduction.
A systematic review we looked at included 20 different studies. The authors concluded that the VMO cannot be preferentially activated and strengthened (Smith et al., 2009). Only 3 of the studies were able to display any preferential VMO activation. Each of the 3 were in different knee angles, however, and had several methodological issues, such as poor electrode placement, noise from other muscle activity, and more. Other studies, not included in the systematic review, have been prone to methodological inconsistencies when compared to each other as well. One such method involves measuring EMG activity between OKC and CKC. A lack of evidence has been shown in both OKC and CKC for delayed onset and decreased amplitude of the VM for individuals with PFPS (Stensdotter, 2007).
As it has probably become obvious, VMO isolation is a controversial issue with many conflicting studies. Thein Brody & Hall do an excellent job summarizing the research, while offering their own opinion. Regarding measuring EMG amplitude, they point out that EMG measures electrical activity, not force production. To truly assess the effects the VMO has on the patella, one must consider fiber orientation, and cross-sectional area. The authors then return back to an anatomical discussion, stating an isolated VMO contraction has never been displayed. This suggests training the VMO independently to improve timing may not be possible. In fact, VMO:VL timing has been shown to improve after training the quadriceps muscle as a whole.
In our opinion, the research shows pretty heavily that it is not possible to isolate the VMO. That being said, exercises that have a focus of "VMO isolation" may still serve a purpose, whether through focusing on improving end-range mobility into extension or general quad strengthening, both often are common goals in rehab. The only concern may lie in possibly training into a dysfunctional motion (some may try to improve VMO activity by working hip adduction - this may reinforce the impairment of femoral adduction/IR). Our advice, overall, is to focus on your impairments and movement pattern. Often, those with knee pain improve with quad and glute strengthening, but be sure to assess each case.
So what are your thoughts and what have your experiences been on this issue? Should we be spending so much time trying to isolate the VMO for rehabilitation or focus on a more general method? Let us know!
A systematic review we looked at included 20 different studies. The authors concluded that the VMO cannot be preferentially activated and strengthened (Smith et al., 2009). Only 3 of the studies were able to display any preferential VMO activation. Each of the 3 were in different knee angles, however, and had several methodological issues, such as poor electrode placement, noise from other muscle activity, and more. Other studies, not included in the systematic review, have been prone to methodological inconsistencies when compared to each other as well. One such method involves measuring EMG activity between OKC and CKC. A lack of evidence has been shown in both OKC and CKC for delayed onset and decreased amplitude of the VM for individuals with PFPS (Stensdotter, 2007).
As it has probably become obvious, VMO isolation is a controversial issue with many conflicting studies. Thein Brody & Hall do an excellent job summarizing the research, while offering their own opinion. Regarding measuring EMG amplitude, they point out that EMG measures electrical activity, not force production. To truly assess the effects the VMO has on the patella, one must consider fiber orientation, and cross-sectional area. The authors then return back to an anatomical discussion, stating an isolated VMO contraction has never been displayed. This suggests training the VMO independently to improve timing may not be possible. In fact, VMO:VL timing has been shown to improve after training the quadriceps muscle as a whole.
In our opinion, the research shows pretty heavily that it is not possible to isolate the VMO. That being said, exercises that have a focus of "VMO isolation" may still serve a purpose, whether through focusing on improving end-range mobility into extension or general quad strengthening, both often are common goals in rehab. The only concern may lie in possibly training into a dysfunctional motion (some may try to improve VMO activity by working hip adduction - this may reinforce the impairment of femoral adduction/IR). Our advice, overall, is to focus on your impairments and movement pattern. Often, those with knee pain improve with quad and glute strengthening, but be sure to assess each case.
So what are your thoughts and what have your experiences been on this issue? Should we be spending so much time trying to isolate the VMO for rehabilitation or focus on a more general method? Let us know!
References:
Boling MC, Bolgla LA, Mattacola CG, Uhl TL, Hosey RG. "Outcomes of a weight-bearing rehabilitation program for patients diagnosed with patellofemoral pain syndrome." Arch Phys Med Rehabil. 2006 Nov;87(11):1428-35.
Boucher JP, King MA, Lefebvre R, Pépin A. "Quadriceps femoris muscle activity in patellofemoral pain syndrome." Am J Sports Med. 1992 Sep-Oct;20(5):527-32. Web. 17 Nov 2012.
Brody LT & Hall CM. (2011). Therapeutic Exercise: Moving Toward Function. (3rd ed., pp. 530-531). Baltimore: Lippincott Williams & Wilkins.
Cowan SM, Bennell KL, Hodges PW, Crossley KM, McConnell J. "Delayed onset of electromyographic activity of vastus medialis obliquus relative to vastus lateralis in subjects with patellofemoral pain syndrome." Arch Phys Med Rehabil. 2001 Feb;82(2):183-9. Web. 26 Nov 2012.
Cowan SM, Bennell KL, Crossley KM, Hodges PW, McConnell J. "Physical therapy alters recruitment of the vasti in patellofemoral pain syndrome." Med Sci Sports Exerc. 2002 Dec;34(12):1879-85. Web. 26 Nov 2012.
Gilleard W, McConnell J, Parsons D. "The effect of patellar taping on the onset of vastus medialis obliquus and vastus lateralis muscle activity in persons with patellofemoral pain." Phys Ther. 1998 Jan;78(1):25-32. Web. 25 Nov 2012.
Hubbard JK, Sampson HW, Elledge JR. "Prevalence and morphology of the vastus medialis oblique muscle in human cadavers." Anat Rec. 1997 Sep;249(1):135-42. Web. 25 Nov 2012.
Kendall F, McCreary E, Provance P, Rodgers M, & Romani W. (2005). Muscles: Testing and Function with Posture and Pain. (5th ed., p. 420). Baltimore: Lippincott Williams & Wilkins.
Lieb FJ, Perry J. "Quadriceps function. An anatomical and mechanical study using amputated limbs." J Bone Joint Surg Am. 1968 Dec;50(8):1535-48. Web. 17 Nov 2012.
Ng GY, Zhang AQ, Li CK. "Biofeedback exercise improved the EMG activity ratio of the medial and lateral vasti muscles in subjects with patellofemoral pain syndrome." J Electromyogr Kinesiol. 2008 Feb;18(1):128-33. Web. 17 Nov 2012.
Powers CM, Landel R, Perry J. "Timing and intensity of vastus muscle activity during functional activities in subjects with and without patellofemoral pain." Phys Ther. 1996 Sep;76(9):946-55. Web. 25 Nov 2012.
Powers CM. "Patellar kinematics, part I: the influence of vastus muscle activity in subjects with and without patellofemoral pain." Phys Ther. 2000 Oct;80(10):956-64. Web. 25 Nov 2012.
Smith TO, Bowyer D, Dixon J, Stephenson R, Chester R, Donell ST. "Can vastus medialis oblique be preferentially activated? A systematic review of electromyographic studies." Physiother Theory Pract. 2009 Feb;25(2):69-98. Web. 25 Nov 2012.
Souza DR, Gross MT. "Comparison of vastus medialis obliquus: vastus lateralis muscle integrated electromyographic ratios between healthy subjects and patients with patellofemoral pain." Phys Ther. 1991 Apr;71(4):310-6. Web. 25 Nov 2012.
Stensdotter AK, Hodges P, Ohberg F, Häger-Ross C. "Quadriceps EMG in open and closed kinetic chain tasks in women with patellofemoral pain." J Mot Behav. 2007 May;39(3):194-202. Web. 26 Nov 2012
Boling MC, Bolgla LA, Mattacola CG, Uhl TL, Hosey RG. "Outcomes of a weight-bearing rehabilitation program for patients diagnosed with patellofemoral pain syndrome." Arch Phys Med Rehabil. 2006 Nov;87(11):1428-35.
Boucher JP, King MA, Lefebvre R, Pépin A. "Quadriceps femoris muscle activity in patellofemoral pain syndrome." Am J Sports Med. 1992 Sep-Oct;20(5):527-32. Web. 17 Nov 2012.
Brody LT & Hall CM. (2011). Therapeutic Exercise: Moving Toward Function. (3rd ed., pp. 530-531). Baltimore: Lippincott Williams & Wilkins.
Cowan SM, Bennell KL, Hodges PW, Crossley KM, McConnell J. "Delayed onset of electromyographic activity of vastus medialis obliquus relative to vastus lateralis in subjects with patellofemoral pain syndrome." Arch Phys Med Rehabil. 2001 Feb;82(2):183-9. Web. 26 Nov 2012.
Cowan SM, Bennell KL, Crossley KM, Hodges PW, McConnell J. "Physical therapy alters recruitment of the vasti in patellofemoral pain syndrome." Med Sci Sports Exerc. 2002 Dec;34(12):1879-85. Web. 26 Nov 2012.
Gilleard W, McConnell J, Parsons D. "The effect of patellar taping on the onset of vastus medialis obliquus and vastus lateralis muscle activity in persons with patellofemoral pain." Phys Ther. 1998 Jan;78(1):25-32. Web. 25 Nov 2012.
Hubbard JK, Sampson HW, Elledge JR. "Prevalence and morphology of the vastus medialis oblique muscle in human cadavers." Anat Rec. 1997 Sep;249(1):135-42. Web. 25 Nov 2012.
Kendall F, McCreary E, Provance P, Rodgers M, & Romani W. (2005). Muscles: Testing and Function with Posture and Pain. (5th ed., p. 420). Baltimore: Lippincott Williams & Wilkins.
Lieb FJ, Perry J. "Quadriceps function. An anatomical and mechanical study using amputated limbs." J Bone Joint Surg Am. 1968 Dec;50(8):1535-48. Web. 17 Nov 2012.
Ng GY, Zhang AQ, Li CK. "Biofeedback exercise improved the EMG activity ratio of the medial and lateral vasti muscles in subjects with patellofemoral pain syndrome." J Electromyogr Kinesiol. 2008 Feb;18(1):128-33. Web. 17 Nov 2012.
Powers CM, Landel R, Perry J. "Timing and intensity of vastus muscle activity during functional activities in subjects with and without patellofemoral pain." Phys Ther. 1996 Sep;76(9):946-55. Web. 25 Nov 2012.
Powers CM. "Patellar kinematics, part I: the influence of vastus muscle activity in subjects with and without patellofemoral pain." Phys Ther. 2000 Oct;80(10):956-64. Web. 25 Nov 2012.
Smith TO, Bowyer D, Dixon J, Stephenson R, Chester R, Donell ST. "Can vastus medialis oblique be preferentially activated? A systematic review of electromyographic studies." Physiother Theory Pract. 2009 Feb;25(2):69-98. Web. 25 Nov 2012.
Souza DR, Gross MT. "Comparison of vastus medialis obliquus: vastus lateralis muscle integrated electromyographic ratios between healthy subjects and patients with patellofemoral pain." Phys Ther. 1991 Apr;71(4):310-6. Web. 25 Nov 2012.
Stensdotter AK, Hodges P, Ohberg F, Häger-Ross C. "Quadriceps EMG in open and closed kinetic chain tasks in women with patellofemoral pain." J Mot Behav. 2007 May;39(3):194-202. Web. 26 Nov 2012
"How Long Will It Take to Get Better After My Surgery?"
Patients often have unrealistic expectations regarding their rehabilitation prognosis and expected symptoms throughout each stage of the healing process. I like to use the graph below to help educate patients regarding how long it takes to feel 'normal' post-surgery. While 12 months can seem daunting for many patients, this timeframe is an honest and realistic approach to surgical tissue healing.
Graph Overview
PHYSICAL THERAPY PHASE (0-3 months)
During the first 12 weeks following trauma or onset of symptoms, patients are generally improving. From a physiological perspective, collagen is maturing, remodeling, and getting stronger. In this stage patients are almost solely attending physical therapy and performing corrective exercises. At the end of 12 weeks, patients likely will feel 60-70% back to their prior level of function. Individuals who perform desk jobs should be back at full duty; more strenuous jobs are still on partial duty.
COMBO GYM + CONTINUED PHYSICAL THERAPY REHAB (3-6 months)
From 3-6 months the patient usually begins their normal gym routine (strength training and cardiovascular exercise) while performing rehabilitation concurrently. I generally think of this phase as someone attending PT 1x/week and performing their gym routine 3-4x/week. In this phase, the individual is starting to feel significantly better, but they have not reached full strength yet. They still have some discomfort (not necessarily pain), and transitional movements, such as getting out of bed and getting up from a chair are still not normal. Ultimately, they still need more work!
FULL RETURN TO NORMAL ACTIVITY/SPORT (6-12 months)
From 6-12 months, the patient has typically stopped their formal rehabilitation program. They are now performing their normal gym routine and daily activities. The individual continues to progress strength, mobility, flexibility, but now has all the tools needed to be independent. The occasional flare up may occur (especially if a novel training movement is incorporated), but is not anticipated. At the end of the 9-12 months, they should have reached life as usual.
During the first 12 weeks following trauma or onset of symptoms, patients are generally improving. From a physiological perspective, collagen is maturing, remodeling, and getting stronger. In this stage patients are almost solely attending physical therapy and performing corrective exercises. At the end of 12 weeks, patients likely will feel 60-70% back to their prior level of function. Individuals who perform desk jobs should be back at full duty; more strenuous jobs are still on partial duty.
COMBO GYM + CONTINUED PHYSICAL THERAPY REHAB (3-6 months)
From 3-6 months the patient usually begins their normal gym routine (strength training and cardiovascular exercise) while performing rehabilitation concurrently. I generally think of this phase as someone attending PT 1x/week and performing their gym routine 3-4x/week. In this phase, the individual is starting to feel significantly better, but they have not reached full strength yet. They still have some discomfort (not necessarily pain), and transitional movements, such as getting out of bed and getting up from a chair are still not normal. Ultimately, they still need more work!
FULL RETURN TO NORMAL ACTIVITY/SPORT (6-12 months)
From 6-12 months, the patient has typically stopped their formal rehabilitation program. They are now performing their normal gym routine and daily activities. The individual continues to progress strength, mobility, flexibility, but now has all the tools needed to be independent. The occasional flare up may occur (especially if a novel training movement is incorporated), but is not anticipated. At the end of the 9-12 months, they should have reached life as usual.
Closing Points
Many patients do NOT realize how long post-surgery rehabilitation takes. In my active cash-based population, many of my patient's have self proclaimed high pain tolerances and feel better relatively quickly. Despite subjectively feeling strong, practitioners must remember that scar tissue continues to mature and remodel for 2+ years! Strengthening and retraining movement patterns will take months (even after the patient feels better). Reaching 100% pain free and 'normal' activity generally takes longer than someone will anticipate. Being honest and giving appropriate education early on can change a patient's outlook on their condition. Use this graph when educating your patients!
-Jim Heafner PT, DPT, OCS
-Jim Heafner PT, DPT, OCS
In an earlier post, Jim went over how to differentiate between cervical myelopathy and radiculopathy, or an upper motor lesion and lower motor lesion. Once you have made that differentiation, you have to determine where that lesion is: peripheral nerve, plexus, or spinal nerve. In this post, we're going to go over specifically how to differentiate between peripheral neuropathy and radiculopathy. I am going to focus on the upper quarter region, but the same concept will apply to the lower quarter as well. Below are a couple pictures of the peripheral nerve layouts and dermatomal patterns that I will reference throughout this post
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For starters, remember that both peripheral nerve lesions and radiculopathy are lower motor neuron lesions, so they can both present with corresponding weakness and hyporeflexia. Additionally, they can sometimes present with pain (or numbness/tingling) in similar regions. Think of the ulnar nerve and C8. This is especially true due to the anatomical variation that occurs in the population. Just because a patient has radiculopathy doesn't mean they have to have symptoms centrally/proximally as well. They both can present with symptoms along the ulnar border of the hand. Other regions have more distinct differences, for example, C7 tends to refer down the middle finger and no peripheral nerve typically presents in just that region.
How Do We Differentiate Peripheral Nerve from Nerve Root?
There are several things to consider. An extremely useful assessment style is assessing muscle strength in muscles that have similar segmental input but different peripheral nerves. We'll go back to our C8 vs ulnar nerve example. Both are heavily innervated by the same segment and can present with symptoms in the same location. A key assessment feature is looking at the strength of Extensor Pollicis Longus. It is innervated by the radial nerve, but it's primary segmental input is C8. Should a patient have weakness here, we would be leaning more towards C8 radiculopathy. If it is strong, we would lean more towards ulnar neuropathy. The same concept can be applied to other areas. When trying to differentiate between L5-S1 radiculopathy and peroneal neuropathy, we look at strength of the gluteus medius and peroneals. While they share similar spinal nerve input, they have different peripheral nerve innervation (gluteus medius: superior gluteal nerve; peroneal longus/brevis: superficial peroneal nerve). Another useful assessment is neural tensioning. Should the patient's exact symptom be reproduced with it, we likely would consider the nerve involvement; however, often radiculopathy does have a neural tension component to it, so it is not as helpful as we would like. One of the best assessment techniques is using the cervical radiculopathy cluster developed by Wainner, et al:
This cluster has been shown to have high diagnostic accuracy for identifying those with cervical radiculopathy and is probably our best tool (3 positive: +LR = 6.1, 4 positive: +LR = 30.3). While one would think that pain with segmental mobility testing of the spine would be useful if pain is recreated, people can have symptoms in two locations as a result of Double Crush Syndrome or altered neurodynamics. Regardless, the most important thing is that we treat all impairments we are presented with. If the neck is stiff in someone with ulnar neuropathy, I'm still going to work on improving neck mobility. They key is that if there is research for a specific treatment for a specific diagnosis, it is important we try and identify these cases. Also, remember that there are other sources for symptoms other than peripheral nerves and radiculopathy. Patients can also present with symptoms in the exact same region due to trigger point referral patterns, local strains/sprains, a plexus, and more. Hopefully this will at least help with differentiating between two similar presentations. For a more in-depth review of examining patient's with neck pain with radiating pain, check out the lecture below:
| This lecture is part of a full course on the cervical spine. Learn more about the Orthopedic Management: Cervical Spine course by following the link! |
Reference:
Wainner RS, Fritz JM, Irrgang JJ, Boninger ML, Delitto A, Allison S. "Reliability and diagnostic accuracy of the clinical examination and patient self-report measures for cervical radiculopathy." Spine (Phila Pa 1976) 2003 Jan 1.
Wainner RS, Fritz JM, Irrgang JJ, Boninger ML, Delitto A, Allison S. "Reliability and diagnostic accuracy of the clinical examination and patient self-report measures for cervical radiculopathy." Spine (Phila Pa 1976) 2003 Jan 1.
Can you answer these questions? (Answers in post!)
- Is radiculopathy an upper motor neuron OR lower motor neuron problem?
- What is the plan of care for someone with cervical myelopathy (treat, refer out, both)?
- What are the 4 clinical criteria for a diagnosis of cervical radiculopathy?
Key Information to Know
Chronic cervical degeneration is the most common cause of progressive spinal cord and nerve root compression. These spondylotic (arthritic) changes can result in stenosis of the spinal canal, lateral recess, and/or foramina. Stenosis is defined as ANY narrowing of a canal leading to nerve compression. When stenosis occurs centrally, compressing the spinal cord, it is called myelopathy. When stenosis occurs laterally, compressing the nerve roots, it is called radiculopathy.
Cervical Myelopathy
Central spinal stenosis is known as myelopathy. An individual with myelopathy will present with Upper Motor Neuron signs and symptoms. These symptoms include gait ataxia, a positive Babinski test, a positive Inverted Supinator sign, a positive Hoffman's test, hyperreflexia, potential bowel and bladder changes, among other findings. Since the spinal cord is compressed, a referral for imaging is recommended to assess the amount of compression. Assuming the patient does not have severe compression with hard neurological findings, the patient will likely be appropriate to continue resume their Physical Therapy plan of care.
Cervical Radiculopathy
Cervical radiculopathy has many different symptoms than myelopathy. In radiculopathy, the nerve root (not the spinal cord) is the involved structure. When the nerve root is placed under compression or tension (or any additional stress), individuals will typically have a myotomal pattern of weakness, a dermatomal pattern of sensory loss, hyporeflexia, positive Spurlings Maneuver, positive Distraction Test, decreased cervical rotation to the involved side, and a positive median nerve tension test.
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Cervical Radiculopathy Case Study
See how Dr. Chris Fox PT, DPT, OCS treats Cervical Radiculopathy | |
For more information on treating cervical radiculopathy and myelopathy, please check out our new course on the Orthopedic Management of the Cervical Spine! In this course, we cover cervical anatomy, examination, differential diagnosis, advanced treatment strategies, case studies, and more!
References:
1. Kadanka Z, Bednarík J, Vohánka S, Vlach O, Stejskal L, Chaloupka R, Filipovicová D, Surelová D, Adamová B, Novotný O, Nemec M, Smrcka V, Urbánek I. Conservative treatment versus surgery in spondylotic cervical myelopathy: a prospective randomised study. Eur Spine J (2000) 9 :538–544
2. Cleland JA, Fritz JM, Whitman JM, et al. Predictors of short-term outcomes in people with a clinical diagnosis of cervical radiculopathy. Phys Ther. 2007;87(12):1619-1632
1. Kadanka Z, Bednarík J, Vohánka S, Vlach O, Stejskal L, Chaloupka R, Filipovicová D, Surelová D, Adamová B, Novotný O, Nemec M, Smrcka V, Urbánek I. Conservative treatment versus surgery in spondylotic cervical myelopathy: a prospective randomised study. Eur Spine J (2000) 9 :538–544
2. Cleland JA, Fritz JM, Whitman JM, et al. Predictors of short-term outcomes in people with a clinical diagnosis of cervical radiculopathy. Phys Ther. 2007;87(12):1619-1632
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Dr. Jim Heafner & Dr. Chris Fox write about their treatment philosophy.
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