EXPLAIN PAIN!! THE WHY & HOW.

First of all, I would like to apologize to everyone who is reading this article. I apologize for the fact that you have pain, whether chronic or acute, that may be as a result of unfortunate circumstances or the result of an inadequate health care system.  Pain is very misunderstood even in the medical community. Chronic pain sufferers can be stigmatized because of this lack of understanding. Currently, one in four Americans have chronic pain. That’s 75 million people! I want to reassure you that there is an answer. There is a physiological reason WHY you have pain. I want to convince you that the pain you feel may not be coming from where you think and feel it is. You WILL get better. Let me explain your pain!

 

Anatomically, we are essentially all the same. Each of us has approximately 206 bones, 640 muscles, and 400 nerves in our bodies. Our spine consists of 24 vertebra which are attached via ligaments and muscles to our head at the top and to our sacrum and pelvis at the bottom. Each vertebra is separated from the next via our discs. At each vertebral level, there is a spinal nerve that exits a small hole called a foramen. This nerve is the connection between your spinal cord and the rest of your body. Each spinal nerve sends branches to specific locations in your body. They connect the muscles adjacent to your spine to the small nerves at the ends of your fingers and toes. Think about your spine as the tree and the nerves as all of the branches.

 

Your nerves respond to any and all types of stimulation such as touch, temperature, pressure, pain and relay a message thru the spinal nerve to your spinal cord and then up to your brain. Impulses and/or commands from your brain are then transmitted back down the spinal cord to the spinal nerve and out to the targeted area. This communication system is active ALL the time. Our brain determines whether we are consciously aware of it or not. For example, if you are running from a lion attack and step on a tack do you think your brain will tell you “Ouch! Stop. You stepped on a tack?” Hopefully not or else “Dinner is Served!” So what happens if something goes wrong with this system? What happens if this system becomes over-sensitive?

As mentioned above, we have 400 nerves in our bodies. That amounts to 45 MILES of nerves! So how does a nerve “talk” to the brain? At rest, a nerve is always “listening”. Every nerve has a certain threshold that, once surpassed, will generate an electrical signal (called an action potential) that will be sent thru the spinal nerve to the spinal cord and up to the brain. If the threshold isn’t reached, then the nerve just continues to “listen”. For example, how long does it take for you to shift your weight while sitting in the movie theater?  The threshold of your “buttock nerves” has been surpassed when your brain tells you to shift your weight. This threshold is different for everyone. In the diagram below, you can see that that the resting state of the nerve is at a certain level while it is “listening”. After the action potential occurs, the nerve returns to its previous resting state. However, in certain circumstances, the nerve does NOT return to the previous resting state and the nerve remains in a heightened state. It is essentially MORE sensitive, or hypersensitive, and will fire an impulse much more easily.

After an injury, 1 in 4 people experience this heightened nerve state. Why? The answer has a lot to do with the individual’s response to stress. For example, people that get injured in a stressful environment such as a car accident, playing competitive sports, or a stressful job are 7-8x more likely to develop a chronic pain syndrome. In addition, emotional responses to the injury such as worry, fear, and anxiety perpetuates this stress cycle. To use the lion example above, this fear is like an ongoing emotional lion attack to the nerves of a chronic pain sufferer. The Kendall study found that the biggest predictor of developing chronic pain is FEAR! Fear that your pain will not go away. Fear that your life will never return to normal. All of these responses have one thing in common physiologically, they release both inflammatory chemicals and several stress hormones including one that I am sure you have heard of called ADRENALINE.

 

Throughout the length of our nerves, there are channels or pores that open or close in response to physical or chemical stimulation. They are called ion channels. The amount and type of ion channels are based on our genetic coding as well as what our brain THINKS we need to survive. Ion channels live for only 48 hours so the amount and type is always changing. When the channel is closed the nerve is “listening”. When it is open the nerve is “reacting”. During cold weather we produce more temperature sensitive channels. During times of stress or fear we produce more adrenaline sensitive channels. The more that we focus on the pain, the more that our brains perceive a threat and continue to send inflammatory chemicals and adrenaline into the area. This response is like a constant “knock on the door” of the ion channels. Regular ion channels stay open for milliseconds. Certain adrenaline channels can stay open for up to 5 minutes! As a result, the nervous system up-regulates and becomes much more sensitive. Can you see the physiological link now between your emotions and your nerves? The initial trauma or injury caused your pain, but it is your BRAIN that perpetuates the pain.

 

Logically, your next question would be “Is that what’s wrong with me” and “How do we know this?” The explanations are based on what we know about nerve science. We know that you have a pain syndrome based on your physical examination and what you have told us about your pain.

 

Your next question may be “Why did this happen to ME?” As I mentioned earlier, 1 in 4 people after a traumatic event develop chronic pain. The greatest predictor of chronic pain is uncontrolled acute pain from the injury. Medications, icing, rest, bracing are important strategies in the beginning. Our brain determines our pain tolerance and everyone is different in this regard. Having high levels of stress chemicals in our system not only perpetuates the pain cycle, it also leads to chronic fatigue, depression, mood swings, and sleep disorders to name a few.

 

So then, “What can we do to treat it?” Our objective is to determine what we can physically as well as mentally do to control your pain. The more that you understand your pain, the more control you have over your brain. Studies have been done that demonstrate a significant reduction in perceived pain just by understanding the physiological process. So re-read this article several times until you REALLY get it. Doing this means you are already moving in the right direction! Choosing the right medications is an important part of the healing process as well. Non-steroidal anti-inflammatories (NSAID’s) such as ibuprofen and Aleve may help. Medications such as Cymbalta, Lyrica, and Neurontin(Gabapentin) function by plugging the openings in your ion channels. Narcotics such as morphine can actually make nerve pain worse! As a side note, your brain can produce pain relieving chemicals that are 50x more powerful than any drug that your doctor can prescribe.

 

So how do we turn on our brains? As I mentioned earlier, education is the key. The more you know, the more you control. Secondly, choose your foods wisely. Tryptophan is an  amino acid that cannot be produced by our bodies. It is a powerful precursor to the “happy” hormone our bodies produce called serotonin. High levels of serotonin can also aid in plugging holes in ion channels. Serotonin is also a precursor to melatonin which plays an important role in mood and sleep disorders. Foods with high levels of tryptophan are turkey, bananas, soy products, tofu, almonds, sesame seeds and walnuts. Lastly, the right type of physical activity is key to controlling your pain and normalizing your nervous system. “Move it or lose it!” certainly applies in this case. There is Gold Level evidence in the literature that aerobic activity performed daily for 10 minutes at 50% max effort can reduce chronic pain. Aerobic exercise cleanses our system of inflammatory chemicals and stress hormones. The most important things that our nerves need to heal are proper movement, adequate space to move, and lots of blood! Our nerves constitute 2-3% of our body weight and use 25% of our blood. The circulation to a nerve will be cut off if the nerve is stretched more than 7-8%. It is very important to determine what kind of movement and/or irritability is occurring in the nervous system. We call this nerve movement “neural dynamics”. Stretching a nerve is NOT something that you want to do. A qualified physical therapist will perform a thorough assessment of your neural dynamics and establish an appropriate plan of care to restore proper and painfree nerve mobility. Manual techniques such as soft tissue and joint mobilizations, Primal Reflex Release Techniques and spinal manual traction can also be beneficial. Hands-on techniques can help to retrain your brain and to desensitize the system. Proper diaphragmatic breathing is also key. If you don’t get enough oxygen, how will you feed your healing nerves?

 

Once again, I apologize to everyone who has read this article. I know that having pain every day must be very difficult and challenging. I want you to know that there is HOPE. Reading my article is only the beginning. Please let me know if we can help you further.

Plantar Fasciitis & Foot Orthotics

Yes. We treat a lot of plantar fasciitis. There is a lot of foot pain out there. While performing a literature review of heel pain in 2005 (follow this link to READ MORE), I made reference to several articles about the prevalence of heel pain. One United States study estimated that one million patient visits each year are for the diagnosis and treatment of plantar heel pain. This disorder appears in the sedentary and geriatric population, it makes up one quarter of all foot injuries in runners, and is the reason for 8% of all injuries to people participating in sports. As many of you know, all that we do regarding foot orthotic fabrication and physical therapy is with good, evidence-based reason. I fabricate custom foot orthotics based on sound biomechanical principles and evidence-based research. Patients are always asking me “so how will foot orthotics help my plantar fasciitis?” Here is the answer! I have included both a clinical description as well as a more basic description in the video. This will allow you to refer your doctor and/or PT as well as a relative who may ask WHY or HOW we made your foot orthotics. I have included references for several articles that have had a profound influence on my treatment and fabrication philosophy regarding plantar fasciitis.  I would like to share my insights with you.

It has been my experience that positive results can be achieved much more quickly for cases of plantar fasciitis using the combination of softer materials to cushion the foot in combination with stiffer, denser materials to redistribute pressures on the foot. My direct molding techniques produce a total contact orthotic which reduces weight bearing pressure on both the heel and forefoot.  These findings for total contact orthoses have been confirmed by both Mueller et al10,11 and Ki et al12. As you can see from my samples on the video, I utilize softer materials as a top layer with the addition of a heel pad on the bottom.  I reinforce the arch in order to redistribute pressures up against the talonavicular joint (or midfoot).  I utilize a forefoot valgus post (higher on the outside of the forefoot) with a slight reverse Morton extension (ledge under toes 2-5) in order to plantar flex the first ray (big toe lower than the other four toes) and unload both the fascia and 1st MTP joint (big toe joint)  As I tell my patients, the foot orthotic is only as good as the shoe you put around it. Our best results with the over-pronating foot are achieved via the combination of motion control shoes and custom orthoses.

In regards to prefabricated orthotics such as ALine, it is one-shape-fits-all and only utilizes rearfoot posting “to help align the leg from foot to hip” per the website. The concept of rearfoot posting for biomechanical control is a much debated topic in the literature. Forefoot modifications are not an option. It is also a very rigid material against a painful heel.  It has been my experience that prefabs such as ALine or Powerstep are a good option for the younger, athletic patient.

Don’t forget, our custom foot orthotics range in price from $120 to $165. I direct mold, fabricate, educate and issue in one hour!  All adjustments included. Our WalkWell guarantee since 1997!!

Research findings continued……

Research done by Kogler1,2,3 et al has been instrumental in determining the appropriate type of rearfoot and/or forefoot posting for foot orthotics for plantar fasciitis. Kogler showed that rearfoot posting had little effect on plantar fascia strain, forefoot varus posting increased the stress, and forefoot valgus posting actually decreased the strain.  Kogler concluded that foot orthotics which raised the talonavicular joint and prevented dorsiflexion of the first ray were most effective in reducing the strain on the central band of the plantar fascia. I recently made orthotics for a patient who said her doctor issued bilateral heel lifts “to take the stress off of the fascia”.  Kogler actually showed no change in plantar fascia strain using heel lifts.  However, heel lifts have been shown by Trepman et al4 in 2000 to decrease the compressive forces in the tarsal tunnel.  Benno Nigg5, a researcher in Canada, has also published over 200 articles on biomechanics.  He has stated that based on his results, custom foot orthotics, on average, control only 2-3 degrees of motion.  This would be his kinematic results, however, he has done a lot of enlightening research on the kinetic effects of foot orthotics. A little bedtime reading for you!

Paul Scherer6,7,DPM has published several articles on the effects of custom orthotics on the 1st MTP joint. The concept of maintaining the first ray in a plantar flexed position unloads both the 1st MTP joint as well as the plantar fascia. Howard Dananberg8,DPM has also written several articles on this topic. Doug Richie9,DPM has been a great resource for the evidence behind the treatment of plantar fasciitis as well as posterior tibialis dysfunction.  You may have heard of the Richie brace.  Dr Richie states that the “most effective foot orthotic for plantar fasciitis is one that hugs against the navicular and flares away from (or plantar flexes) the first ray.”

1.Kogler, G. F.; Solomonidis, S. E.; and Paul, J. P.: Biomechanics of longitudinal arch support mechanisms in foot orthoses and their effect on plantar aponeurosis strain. Clin. Biomech., 11: 243-252, 1996.

2.Kogler GF, Veer FB, Solomonidis SE, et al. The influence of medial and lateral placement of   wedges on loading the plantar aponeurosis, An in vitro study. J Bone and Joint Surg Am. 81:1403-1413, 1999

3.Kogler GF, Veer FB, Verhulst SJ, Solomonidis SE, Paul JP.

The effect of heel elevation on strain within the plantar aponeurosis: in vitro study.

Foot Ankle Int. 2001 May;22(5):433-9.

4.Trepman E, Kadel NJ: Effect of foot and ankle position on tarsal tunnel compartment pressure. Foot Ankle Int 20(11):721, 2000

5.Nigg, B. Biomechanics of Sport Shoes. 2011

6.Scherer PR, Sanders J, Eldredge, DE, et al. Effect of functional foot orthoses on first metatarsophalangeal joint dorsiflexion in stance and gait. J Am Podiatr Med Assoc 2006;96(6):474-481.

7.Scherer,P. Recent Advances in Orthotic Therapy. 2011

8.Dananberg HJ. Functional hallux limitus and its relationship to gait efficiency. J Am Podiatr Med Assoc. 1986; 76(11):648-52

9.Richie,D. Offloading the plantar fascia: What you should know. Podiatry Today, Vol 18. Issue 11, Nov 2005.

10.Mueller MJ, Hastings M, Commean PK, et al. Forefoot structural predictors of plantar pressures during walking in people with diabetes and peripheral neuropathy. J Biomech 2003;36(7):1009-1017.

11.Mueller MJ, Lott DJ, Hastings MK, et al. Efficacy and mechanism of orthotic devices to unload metatarsal heads in people with diabetes and a history of plantar ulcers. Phys Ther 2006;86(6):833-842.

12.Ki SW, Leung AK, Li AN. Comparison of plantar pressure distribution patterns between foot orthoses provided by the CAD-CAM and foam impression methods. Prosthet Orthot Int 2008;32(3):356-362.

Literature Review – Heel Pain

Plantar heel pain is a very common and painful condition.  One United States study estimates that one million patient visits each year are for the diagnosis and treatment of plantar heel pain. (1 in Radford, 07)  This disorder appears in the sedentary and geriatric population (2-4 in Radford), it makes up one quarter of all foot injuries in runners (5 in Radford), and is the reason for 8% of all injuries to people participating in sports. (6-8 in Radford, 07)  The exact nature of the disorder as well as the most appropriate treatment, however, remains unclear. (Martin 98, Radford 07, Wolgin 94, Crawford 02, Gill 97, Gill 96, Davis 94, Lynch 98)  A study of 364 painful heels could find no causal relationship. (Lapidus in Wolgin 94)  Few random, controlled studies document the efficacy of conservative care, (Barrett 11/06, Atkins in Barrett article, Radford 07, Crawford 02, Davis 94) ,yet success rates for conservative treatment of plantar heel pain vary from 46% to 100% in the literature. (Wolgin 94, Martin 98, Lynch 98,)   It becomes clear from a review of the literature that the etiology of plantar heel pain is multi-factorial i.e. “multiple etiology heel pain syndrome”.  There is not one specific cause, nor is there a panacea for conservative treatment.  In 1972, Snook and Chrisman (36 in Wolgin) wrote “ it is reasonably certain that a condition which has so many different theories of etiology and treatment does not have valid proof of any one cause”.  Are we any better off today?

The management of plantar heel pain begins with the correct differential diagnosis. (Gill 97, Shapiro 97, Meyer 02)  Plantar fasciitis is the most common diagnosis for plantar heel pain. (1-Aldredge in Barrett 06)  Clinical findings include medial heel pain which is often worse in the morning, worse after periods of rest, worse after prolonged weight bearing activity, and pain to palpation at the medial/plantar heel. (Perelman 95, 10-Scherer in Richie, Gill 97)  Most researchers agree that the pain is caused by microtrauma to the origin of the plantar fascia at the medial tubercle of the calcaneus. (Perelman 95, Richie 05, 7-Grasel in Richie 05, 10-Scherer in Richie, 7-Schon in Gill 97).  Subsequently, this microtrauma causes marked thickening and fibrosis at the origin of the plantar fascia. (Grasel in Richie, Schepsis, Martin 98) Many practitioners believe that the pain of plantar fasciitis is caused by inflammation. (Barrett, Khan’s work, Almekinder)  However, researchers have shown through histological examination that there is an absence of inflammatory cells in chronic overuse tendinopathies. (Khan’s, Almekinder, Huijregts 99, Puddu 76)  Animal studies conclusively demonstrate that, within 2-3 wks of insult to tendon tissue, inflammatory cells are not present. (Khan BMJ 02)  Histologic findings from plantar fasciotomies have been presented to support the thesis that plantar fasciitis is a degenerative fasciosis without inflammation, not a fasciitis. (Lemont, Schepsis 91).  In addition to the absence of inflammatory cells, tendinosis is characterized by a degeneration of tenocytes and collagen fibers with a subsequent increase in non-collagenous matrix. (Khan)   The collagen tissue of tendons, for example, have only 13% of the oxygen uptake of muscle and require >100 days to synthesize collagen. (Khan, 94-95 in Khan)  Thus, tissue repair in tendinosis may take 3 to 6 months. (Khan)  With this increasing body of evidence suggesting fasciosis, not fasciitis, the practitioner needs to shift his/her treatment perspective.

As payers demand practitioners to maximize outcomes and minimize costs, the need for evidence-based interventions becomes clear.  As stated above, however, there are few studies that have tested the efficacy of treatment protocols. (Khan, plus above)  The first treatment goal for plantar fasciosis should be to protect the healing tissue. (Khan, Chandler 93, Cornwall 99, McPoil 95, Ross 02, Crosby 01))  How can damaged tissue heal if environmental stresses are not controlled? (McPoil 95)  The second goal should be to restore the normal mechanical behavior of the tissue and to positively influence the structural reorientation of damaged collagen fibers. (Graston)  Physical therapists have proposed that the treatment of plantar heel pain should be impairment based. (Young 04)  A detailed examination would identify these impairments and an appropriate plan of care would utilize manual therapy, exercise, and modalitites. (Young 04)  There is no standard physical therapy protocol for plantar fasciosis, however, upon review of the literature by this author, a framework of evidence is available to establish an appropriate protocol.

Iontophoresis and corticosteroid injections have been used to treat the proposed presence of inflammation at the origin of the plantar fascia.  Iontophoresis is a process that uses bipolar electric fields to propel molecules of a drug such as dexamethasone across intact skin and into underlying tissue. (Anderson 03)  The depth of drug penetration averages 8-12 mm with deeper penetration occurring through a slower process of passive diffusion. (Anderson 03, Li 95, Costello 95)  Two articles have documented an improvement of plantar heel pain using iontophoresis with dexamethasone, yet long term relief was questionable. (Gudeman 97, Page 99)  Steroids have been shown to inhibit the early stages as well as the later manifestations of the inflammatory process. (Fredberg 96)  Corticosteroid injections for relief of plantar heel pain have had mixed results. (Martin 98, Wolgin 94, Crawford 02, Acevedo 98, Davis, Gill)  However, ultrasound guided peritendinous injections of achilles and patella tendonitis have shown a significant reduction in the average diameter of the affected tendons (Fredberg 04) as well as a disappearance of neovascularization. (Koenig in response)  Improper injection technique may be the reason for unfavorable results. (Wolgin 94)

Tissue protection can occur through rest, activity modification, taping techniques, and foot orthoses.  Low-dye taping and various plantar strapping techniques have been shown to be effective in relieving plantar heel pain as well as altering foot kinematics and plantar pressures. (Lange 04, Hyland 06, Keenan 01, Holmes 02, Vicenzino 00)  Although limited evidence exists  (Gross 02, Kogler 99, Kogler 96, Scherer&Waters 07, Mundermann 03,Razeghi 00, Pfefer, Lynch), no conclusive evidence has been found to demonstrate the effectiveness of foot orthoses on plantar heel pain. ( Young 04, Lynch, Gill, Davis, Gross 02, Brown 95, Landorf in Pod Tod)

Manual therapy procedures used by medical practitioners can include soft tissue mobilization, massage, manual traction, joint mobilization, and joint manipulation. (DiFabio 92)  Clinical interventions involving joint mobilizations and manipulations have been developed or refined by many authors. (Difabio 92, In DiFabio Maitland Periph/Spine, Grieve, Kaltenborn Periph/Spine, Cyriax, McKenzie)  Although there is clear evidence to justify the use of manual therapy on spinal disorders, there is an absence of controlled trials in peripheral joints. (DiFabio 92)  We can only speculate that a relationship exists between the identified joint impairment and the patient’s plantar heel pain. (Young)  There is, however, a body of work that attempts to demonstrate the effect of mobilizations and/or manipulations of the talus and fibula on ankle dorsiflexion range of motion, yet with varied results. (Dananberg 00, Pellow 01, Denegar 02, Soavi 00, Nield 93, Dimou 04, Green 01)

Dorsiflexion range of motion restrictions have been identified as a significant impairment associated with plantar heel pain. (Young 04)  One study reported a 5 degree or more dorsiflexion restriction in 78% of his patient population with unilateral plantar fasciitis. (Amis 88)  Numerous studies have shown that heel cord stretching is one of the most effective treatments for resolving plantar heel pain. (Richie, Wolgin, Gill, Davis, Pfeffer)  Plantar fascia-specific stretches have been shown to be even more effective than calf stretches in alleviating plantar heel pain (DiGiovanni 03,06)   Due to the viscoelastic properties of muscle-tendon units, the duration of the stretch, active warm-up, and the concept of reciprocal inhibition can influence the outcome of stretching. ( Shrier 00, Taylor 90)  Dorsiflexor and plantarflexor muscle weakness via isokinetic testing has  also been identified as impairments in chronic plantar fasciitis. (Chandler 93, Kibler 91)

Collagen production is probably the key cellular phenomenon that determines recovery from tendinosis. (Khan 00)  Animal experiments have revealed that loading the tissue improves collagen alignment and stimulates cross-linkage formation, both of which improve tensile strength. (Khan 00, Villarta #34 in Khan 00)  Interventions such as friction massage (DeLuccio, Loghmani 05, Davidson, Gehlsen 98, Chamberlain 82),  ultrasound (Enwemeka 89, Ramirez 97, Young 89, Crawford/Snaith 96,Gum 97,Speed 01, DeDeyne 95,Dyson 68, Noble 06,Cunha 01,Draper 95,Doan 99Jackson 90,Ng 03,Harvey 75), and eccentric exercise (Stanish 85,Cannell 00,Ohberg 02,Alfredson 98, Khan 99,00,00 have been shown to stimulate collagen production and, thus, help to reverse the tendinosis cycle.

The purpose of this outcome study is to determine the effect of a standardized treatment protocol on a group of subjects that present with the diagnosis of plantar fasciosis or fasciitis.  The subjects are required to have at least 3 of the 4 criteria listed above for the diagnosis of plantar fasciitis and to have a >4 week history of plantar heel pain.  The specific goals of this outcome study are the following: 1) to evaluate how the subject population responds to the treatment protocol in terms of pain reduction and functional outcome measures, 2) to determine improvements in ankle dorsiflexion range of motion utilizing the protocol, 3) to assess changes of thickness at the origin of the plantar fascia via diagnostic ultrasound after utilizing the protocol, 4) to investigate the duration of time between start of treatment and maximal improvement in symptoms,  5) to investigate the time relationship between onset of symptoms and start of treatment to clinical outcome, 6)  to investigate and document any reoccurrences of symptoms while performing a maintenance home program over a 6 month period, and 7) to assess patient compliance with the home program.

IT HURTS!! HEAT or ICE?

As your therapist, one of my most important roles in your recovery is teaching you the fundamentals of proper healing.  Healing of injured tissue is a physiological process that can be inhibited by many factors.  Pain management strategies, activity modification, and proper exercise are three such factors that need to be examined.

PAIN MANAGEMENT

All new injuries or aggravation of old injuries need to be addressed with the acronym P.R.I.C.E.  –  Protect, Rest, Ice, Compress, Elevate.  We will talk about the protection aspect in the next section on activity modification.  After an acute injury, there is resulting tissue trauma and inflammation.  Inflammation is part of the healing process as the body attempts to bathe the injured tissue with protein rich fluid as well as cells that cleanse and repair the injured tissue.  Inflammatory cells can be present up to 21 days after an injury, but are the most prevalent during the acute inflammatory stage i.e. first 7-10 days.  Uncontrolled inflammation is what delays healing and it is what we attempt to control with R.I.C.E.  Ice should be applied for 10-15 minutes only in order to prevent frostbite.  You can use soft, gel cold packs, bags of frozen peas or ice, or submerge the injured part into an ice water bath.  You can ice every hour if you wish, but at a minimum of 2-3 times per day, for at least the first 7-10 days.  Remember that the inflammatory process (in the controlled environment) can last 21 days.  The adage “ice for the first 48 hours only” does not make physiological sense.  Icing is not only anti-inflammatory, but it is also a great pain reliever.  You should also consult with your physician regarding an anti-inflammatory medicine.  Examples would be medicines such as Aleve 2x/day or 600-800mg of ibuprofen i.e. Advil or Motrin 3x/day for at least 7-10 days.  Compression and elevation of the injury helps to prevent uncontrolled inflammation as well.  Athletic taping, neoprene or Acewrap sleeves for ankles or knees, and back braces are examples of compression as well stabilization of an injury.  Heating tissue can be relaxing and pain relieving, but it also causes the blood vessels to dilate, hence, increasing the flow of fluids to the area.  If you wish, heating for 15-20 minutes can be added after the first 7-10 days as long it does not increase the swelling.

ACTIVITY MODIFICATION

Protecting the injury will prevent uncontrolled inflammation, thus encouraging proper healing.  Pain is a warning sign.  It is your body’s attempt to remind you that something is wrong.  Pushing “through the pain” is NEVER a good idea.  When a lower extremity joint is injured and walking becomes painful or limited, we advise and instruct patients in using crutches or canes.  This is a temporary modification of activity in order to prevent reoccurrences of pain as the body is healing.   Our patients use an assistive device as long as is needed, but most typically for the first 7-10 days.  Proper posture and body mechanics are also very important in removing the stresses to an injured back or spinal condition.  Remember that causing pain during activity is like taking a hammer and “banging” on the injured tissue.  Take frequent breaks and pace your activity as to not provoke your pain.  It is important to wean slowly back into walking or running.  We will help to guide you in that process.

PROPER EXERCISE

Proper exercise can be initiated after the acute inflammatory stage.  Movement of joints and tissues during exercise causes a mechanical “pumping”.  This “pumping” can help to “push in the good and push out the bad”, prevent post-traumatic stiffness, and encourage a quicker return to function.  Proper technique in these early stages would entail pain free, high rep, and low weight exercises.  We will guide you in that process.  Creating a global circulatory effect via pain free cardiovascular exercise is also beneficial to healing as it helps to cleanse and nourish the injured area.

I hope that helps!!

Chris Dukarski, PT

Shoulder Impingement Syndrome

Shoulder pain is the third most common musculoskeletal disorder, following low back and neck pain (Donatelli).   Because of the mechanical demands placed on the shoulder, it is susceptible to numerous soft-tissue injuries.   One of these injuries is called shoulder impingement syndrome.  It is the result of compression of the soft tissues i.e. most typically, the rotator cuff tendon, within the sub-acromial space.  Impingement results from the cumulative stresses of repetitive shoulder motion such as pitching or sustained overhead activity such as painting.  This repetitive stress can lead to tendonitis, rotator cuff tears, bone spurs, or bursitis.

Impingement syndrome can be classified in two ways – external vs. internal and primary vs. secondary.  An external impingement affects the superior surface of the humeral soft tissues in the sub-acromial or coraco-acromial region.  Applicable clinical tests include the Neer and Hawkin’s/Kennedy tests.   An internal impingement may affect the undersurface of the rotator cuff, the posterior labrum, and is, more specifically, a post/sup impingement.  Clinical exam may produce post/sup shoulder pain with passive ER which can be alleviated with a passive posterior humeral glide.  A primary impingement is caused by the structural anatomy of the sub-acromial region.  X-Rays can determine an abnormal variation in the shape of the acromion process.  A type 3 “hooked” acromion may require surgical intervention to correct.  On the other hand, a secondary impingement is the result of dysfunctional biomechanics of the shoulder joint.  It may be due to weakness of the rotator cuff muscles, poor posture, gleno-humeral joint stiffness, thoracic hypomobility, and/or in-coordination/weakness of the scapular stabilizing muscles. And that is what WE treat at OrthoWell?

“I play tennis and developed pain in my shoulder so strong that I could not even sleep, let alone play!  After the very first treatment (ART combined with joint mobilization) 80% of my pain was gone!  I am practically pain free now after 4 visits.  Thank-you Chris!  Great job!” – DK

What are the BEST shoulder exercises?

Everything we do at OrthoWell is evidence-based!  Maximizing results in minimal time depends on the expertise of the clinician. As our knowledge of biomechanics and muscle function improves, more of an emphasis is placed on scientifically based rehabilitation protocols.  This is particularly true regarding the shoulder and scapulothoracic complex.  In the February 2009 volume of JOSPT, Mike Reinold, the Boston Red Sox team physical therapist, presented a thorough analysis of the shoulder and scapular stabilization exercise literature.  One of the most effective exercises for each muscle will be presented.


Supraspinatus
*Full Can Exercise
*Enhances scapular position>
*Decreased deltoid compared to empty can
*Minimizes superior humeral translation

Infraspinatus/Teres Minor
*Side-lying ER
*Minimal capsular strain
*25% increased EMG using towel roll
*Highest EMG for infraspinatus

Subscapularis
*IR at 90 deg abd
*Position of shoulder stability
*Enhanced scapular postion
*Less pectoralis activity than 0 deg abd

Serratus Anterior
*Push-up with plus
*Easy position to resist protraction
*High EMG activity
*Also activates subscapularis

Lower Trapezius
*Prone full can at 135 deg abd
*Full can = horiz abd with ER(thumbs up)
*High EMG activity
*Also activates infraspinatus, teres minor, Mid traps, supraspinatus

Middle Trapezius
*Prone Full Can at 90 deg abd
*High EMG activity
*Also activates infraspinatus, teres minor, Mid traps, supraspinatus

Rhomboids
*Prone Row
*Below 90 deg abduction
*High EMG activity
*Good ratio of upper, mid, low traps

Combo Exercise
*Bilateral T-band ER
*25% increased EMG ER’s with towel roll
*Good ratio upper:lower traps per McCabe
*Emphasize scapula retraction and post tilting

In addition, it is clinically imperative to ensure proper technique during all therapeutic exercises especially as you progress to other exercises such as plyometrics, closed chain UE exercises, and sport- specific exercise training. Proper exercise TECHNIQUE and proper exercise CHOICE is required to effectively treat the muscular imbalances seen in most shoulder pathologies.

OUCH!!…My shoulder hurts!!

Shoulder pain is the third most common musculoskeletal disorder, following low back and neck pain (Donatelli). Because of the mechanical demands placed on the shoulder, it is susceptible to numerous soft-tissue injuries. One of these injuries is called shoulder impingement syndrome. It is the result of compression of the soft tissues i.e. most typically, the rotator cuff tendon, within the sub-acromial space. Impingement results from the cumulative stresses of repetitive shoulder motion such as pitching or sustained overhead activity such as painting. This repetitive stress can lead to tendonitis, rotator cuff tears, bone spurs, or bursitis.

Impingement syndrome can be classified in two ways – external vs. internal and primary vs. secondary. An external impingement affects the superior surface of the humeral soft tissues in the sub-acromial or coraco-acromial region. Applicable clinical tests include the Neer and Hawkin’s/Kennedy tests. An internal impingement may affect the undersurface of the rotator cuff, the posterior labrum, and is, more specifically, a post/sup impingement. Clinical exam may produce post/sup shoulder pain with passive ER which can be alleviated with a passive posterior humeral glide. A primary impingement is caused by the structural anatomy of the sub-acromial region. X-Rays can determine an abnormal variation in the shape of the acromion process. A type 3 “hooked” acromion may require surgical intervention to correct. On the other hand, a secondary impingement is the result of dysfunctional biomechanics of the shoulder joint. It may be due to weakness of the rotator cuff muscles, poor posture, gleno-humeral joint stiffness, thoracic hypomobility, and/or in-coordination/weakness of the scapular stabilizing muscles. And that is what WE treat at OrthoWell?

“I play tennis and developed pain in my shoulder so strong that I could not even sleep, let alone play! After the very first treatment (ART combined with joint mobilization) 80% of my pain was gone! I am practically pain free now after 4 visits. Thank-you Chris! Great job!” – DK

Heel Pain – The scientific facts!!

Plantar heel pain is a very common and painful condition. One United States study estimates that one million patient visits each year are for the diagnosis and treatment of plantar heel pain. (1 in Radford, 07) This disorder appears in the sedentary and geriatric population (2-4 in Radford), it makes up one quarter of all foot injuries in runners (5 in Radford), and is the reason for 8% of all injuries to people participating in sports. (6-8 in Radford, 07) The exact nature of the disorder as well as the most appropriate treatment, however, remains unclear. (Martin 98, Radford 07, Wolgin 94, Crawford 02, Gill 97, Gill 96, Davis 94, Lynch 98) A study of 364 painful heels could find no causal relationship. (Lapidus in Wolgin 94) Few random, controlled studies document the efficacy of conservative care, (Barrett 11/06, Atkins in Barrett article, Radford 07, Crawford 02, Davis 94) ,yet success rates for conservative treatment of plantar heel pain vary from 46% to 100% in the literature. (Wolgin 94, Martin 98, Lynch 98,) It becomes clear from a review of the literature that the etiology of plantar heel pain is multi-factorial i.e. “multiple etiology heel pain syndrome”. There is not one specific cause, nor is there a panacea for conservative treatment. In 1972, Snook and Chrisman (36 in Wolgin) wrote “ it is reasonably certain that a condition which has so many different theories of etiology and treatment does not have valid proof of any one cause”. Are we any better off today?

The management of plantar heel pain begins with the correct differential diagnosis. (Gill 97, Shapiro 97, Meyer 02) Plantar fasciitis is the most common diagnosis for plantar heel pain. (1-Aldredge in Barrett 06) Clinical findings include medial heel pain which is often worse in the morning, worse after periods of rest, worse after prolonged weight bearing activity, and pain to palpation at the medial/plantar heel. (Perelman 95, 10-Scherer in Richie, Gill 97) Most researchers agree that the pain is caused by microtrauma to the origin of the plantar fascia at the medial tubercle of the calcaneus. (Perelman 95, Richie 05, 7-Grasel in Richie 05, 10-Scherer in Richie, 7-Schon in Gill 97). Subsequently, this microtrauma causes marked thickening and fibrosis at the origin of the plantar fascia. (Grasel in Richie, Schepsis, Martin 98) Many practitioners believe that the pain of plantar fasciitis is caused by inflammation. (Barrett, Khan’s work, Almekinder) However, researchers have shown through histological examination that there is an absence of inflammatory cells in chronic overuse tendinopathies. (Khan’s, Almekinder, Huijregts 99, Puddu 76) Animal studies conclusively demonstrate that, within 2-3 wks of insult to tendon tissue, inflammatory cells are not present. (Khan BMJ 02) Histologic findings from plantar fasciotomies have been presented to support the thesis that plantar fasciitis is a degenerative fasciosis without inflammation, not a fasciitis. (Lemont, Schepsis 91). In addition to the absence of inflammatory cells, tendinosis is characterized by a degeneration of tenocytes and collagen fibers with a subsequent increase in non-collagenous matrix. (Khan) The collagen tissue of tendons, for example, have only 13% of the oxygen uptake of muscle and require >100 days to synthesize collagen. (Khan, 94-95 in Khan) Thus, tissue repair in tendinosis may take 3 to 6 months. (Khan) With this increasing body of evidence suggesting fasciosis, not fasciitis, the practitioner needs to shift his/her treatment perspective.

As payers demand practitioners to maximize outcomes and minimize costs, the need for evidence-based interventions becomes clear. As stated above, however, there are few studies that have tested the efficacy of treatment protocols. (Khan, plus above) The first treatment goal for plantar fasciosis should be to protect the healing tissue. (Khan, Chandler 93, Cornwall 99, McPoil 95, Ross 02, Crosby 01)) How can damaged tissue heal if environmental stresses are not controlled? (McPoil 95) The second goal should be to restore the normal mechanical behavior of the tissue and to positively influence the structural reorientation of damaged collagen fibers. (Graston) Physical therapists have proposed that the treatment of plantar heel pain should be impairment based. (Young 04) A detailed examination would identify these impairments and an appropriate plan of care would utilize manual therapy, exercise, and modalitites. (Young 04) There is no standard physical therapy protocol for plantar fasciosis, however, upon review of the literature by this author, a framework of evidence is available to establish an appropriate protocol.

Iontophoresis and corticosteroid injections have been used to treat the proposed presence of inflammation at the origin of the plantar fascia. Iontophoresis is a process that uses bipolar electric fields to propel molecules of a drug such as dexamethasone across intact skin and into underlying tissue. (Anderson 03) The depth of drug penetration averages 8-12 mm with deeper penetration occurring through a slower process of passive diffusion. (Anderson 03, Li 95, Costello 95) Two articles have documented an improvement of plantar heel pain using iontophoresis with dexamethasone, yet long term relief was questionable. (Gudeman 97, Page 99) Steroids have been shown to inhibit the early stages as well as the later manifestations of the inflammatory process. (Fredberg 96) Corticosteroid injections for relief of plantar heel pain have had mixed results. (Martin 98, Wolgin 94, Crawford 02, Acevedo 98, Davis, Gill) However, ultrasound guided peritendinous injections of achilles and patella tendonitis have shown a significant reduction in the average diameter of the affected tendons (Fredberg 04) as well as a disappearance of neovascularization. (Koenig in response) Improper injection technique may be the reason for unfavorable results. (Wolgin 94)

Tissue protection can occur through rest, activity modification, taping techniques, and foot orthoses. Low-dye taping and various plantar strapping techniques have been shown to be effective in relieving plantar heel pain as well as altering foot kinematics and plantar pressures. (Lange 04, Hyland 06, Keenan 01, Holmes 02, Vicenzino 00) Although limited evidence exists (Gross 02, Kogler 99, Kogler 96, Scherer&Waters 07, Mundermann 03,Razeghi 00, Pfefer, Lynch), no conclusive evidence has been found to demonstrate the effectiveness of foot orthoses on plantar heel pain. ( Young 04, Lynch, Gill, Davis, Gross 02, Brown 95, Landorf in Pod Tod)

Manual therapy procedures used by medical practitioners can include soft tissue mobilization, massage, manual traction, joint mobilization, and joint manipulation. (DiFabio 92) Clinical interventions involving joint mobilizations and manipulations have been developed or refined by many authors. (Difabio 92, In DiFabio Maitland Periph/Spine, Grieve, Kaltenborn Periph/Spine, Cyriax, McKenzie) Although there is clear evidence to justify the use of manual therapy on spinal disorders, there is an absence of controlled trials in peripheral joints. (DiFabio 92) We can only speculate that a relationship exists between the identified joint impairment and the patient’s plantar heel pain. (Young) There is, however, a body of work that attempts to demonstrate the effect of mobilizations and/or manipulations of the talus and fibula on ankle dorsiflexion range of motion, yet with varied results. (Dananberg 00, Pellow 01, Denegar 02, Soavi 00, Nield 93, Dimou 04, Green 01)

Dorsiflexion range of motion restrictions have been identified as a significant impairment associated with plantar heel pain. (Young 04) One study reported a 5 degree or more dorsiflexion restriction in 78% of his patient population with unilateral plantar fasciitis. (Amis 88) Numerous studies have shown that heel cord stretching is one of the most effective treatments for resolving plantar heel pain. (Richie, Wolgin, Gill, Davis, Pfeffer) Plantar fascia-specific stretches have been shown to be even more effective than calf stretches in alleviating plantar heel pain (DiGiovanni 03,06) Due to the viscoelastic properties of muscle-tendon units, the duration of the stretch, active warm-up, and the concept of reciprocal inhibition can influence the outcome of stretching. ( Shrier 00, Taylor 90) Dorsiflexor and plantarflexor muscle weakness via isokinetic testing has also been identified as impairments in chronic plantar fasciitis. (Chandler 93, Kibler 91)

Collagen production is probably the key cellular phenomenon that determines recovery from tendinosis. (Khan 00) Animal experiments have revealed that loading the tissue improves collagen alignment and stimulates cross-linkage formation, both of which improve tensile strength. (Khan 00, Villarta #34 in Khan 00) Interventions such as friction massage (DeLuccio, Loghmani 05, Davidson, Gehlsen 98, Chamberlain 82), ultrasound (Enwemeka 89, Ramirez 97, Young 89, Crawford/Snaith 96,Gum 97,Speed 01, DeDeyne 95,Dyson 68, Noble 06,Cunha 01,Draper 95,Doan 99Jackson 90,Ng 03,Harvey 75), and eccentric exercise (Stanish 85,Cannell 00,Ohberg 02,Alfredson 98, Khan 99,00,00 have been shown to stimulate collagen production and, thus, help to reverse the tendinosis cycle.

The purpose of this outcome study is to determine the effect of a standardized treatment protocol on a group of subjects that present with the diagnosis of plantar fasciosis or fasciitis. The subjects are required to have at least 3 of the 4 criteria listed above for the diagnosis of plantar fasciitis and to have a >4 week history of plantar heel pain. The specific goals of this outcome study are the following: 1) to evaluate how the subject population responds to the treatment protocol in terms of pain reduction and functional outcome measures, 2) to determine improvements in ankle dorsiflexion range of motion utilizing the protocol, 3) to assess changes of thickness at the origin of the plantar fascia via diagnostic ultrasound after utilizing the protocol, 4) to investigate the duration of time between start of treatment and maximal improvement in symptoms, 5) to investigate the time relationship between onset of symptoms and start of treatment to clinical outcome, 6) to investigate and document any reoccurrences of symptoms while performing a maintenance home program over a 6 month period, and 7) to assess patient compliance with the home program.

Patellar Tendinopathy – The role of Eccentrics.

Patellar tendinopathy can be a resistant and recurrent condition in running and jumping sports. An important part of your patient’s physical therapy program should include eccentric exercise. What are eccentrics? Eccentric contractions occur when the muscle-tendon unit LENGTHENS during exercise, producing so-called “negative work”. Squatting down is an example of a quad eccentric. Eccentric force production may exceed concentric (shortening contraction) and isometric (tensing without motion) forces 2-3 times. (Stanish et al) Eccentric training drills stimulate mechanoreceptors in tenocytes to produce collagen. (Khan et al) This effect helps to reverse the tendinopathy cycle.

The eccentric exercise commonly recommended for the patellar tendon is the squat. What kind of squat is best? A mechanism that may decrease the eccentric load on the quad is active or passive calf tension. This tension may limit the forward movement of the tibia over the ankle while performing a squat. This effect can be minimized, and load on the patellar tendon maximized, by performing a squat on a 25 degree decline. (Purdam et al) In a small group of patients with patellar tendinopathy, eccentric squats on a decline board produced good clinical results in terms of pain reduction and return to function. (Purdam et al) In the flat-footed squat group, the results were poor.

The eccentric training protocol for patellar tendinopathy should include 3 sets of 15 reps, 2 times per day, for up to 12 weeks.

“I started therapy at a rehab close to home but was not getting results after 12 visits. I then came to Chris and within 2 weeks (4 visits) the results have been substantial. What a difference!” — Kristin M.