Monthly Archives: July 2016

Let’s Talk About Stress: A Reason Why Your Patients May Not Be Healing Faster

Think of the last time you were under aSl_StressBrain lot of stress, whether it be work/school related, financially driven, relationship troubles, or some other component of your life not going exactly as you intended.  How did it make you feel? Were you having trouble eating, sleeping, or concentrating? It’s amazing how this emotional response can have such an impact on us physically.

Now think of the last time you had a patient say that they WERE NOT under a lot of stress (I know personally these individuals are few stress boomand far between). In addition to the previously mentioned stressors, our patients may have a few more on their mind (duration of symptoms, unable to return to work, previously failed treatments, increased pain, etc). In addition to all of these things, they now need to find the time in their already stressful day to do their home exercises, which may make them feel like they’re about to explode.

But why should we, as physical therapists, care about our patients’ stress levels? Well, it may play a huge reason behind why your patient is not getting better as fast as you thought they would. Now if your next thought is that “it’s all in their head,” first of all you should be ashamed of yourself, and secondly, please check out my recent post about how to talk to patients regarding their pain. So if it’s not “all in their head,” how do you talk to your patients about the role of stress in their recovery?

That’s where research comes into play. Back in 1998, Marucha et al examined the effects of stress on wound healing. Who were the lucky subjects? Dental students of course, because learning how to put your hands in other people’s mouths without getting your finger bitten off wasn’t stressful enough. The researchers created punch biopsy wounds on the hard palate of the students during two different scenarios; one during summer vacation (couldn’t think of any better way to spend your summer), and the other three days before their first huge exam. scumbag-dentist_o_656833 Now if I remember back to the first exams of the semester during PT school, I’d say that tensions were high and my classmates were just a little bit more stressed out than usual, so I can imagine how happy these dental students must have been. The researchers then tracked to see how long it took each of the wounds to heal, and compared them between the two scenarios.

What did they find? The wounds that were made days before the big exam took nearly 40% longer to heal. Once again in case you missed it, it took FORTY PERCENT LONGER TO HEAL. Same type of wound, same person, all that changed were the situational stressors. Now why is that important? Remember all of those potential stressful events going on in our patients’ lives; how do you think they will help their tissue healing rates? As I have said before, pain does not always equal tissue damage. There are a variety of reasons which can exacerbate someone’s symptoms, and stress can be one of those many factors. Helping the patient make the realization that their stress can impact their tissue healing may actually be a huge breakthrough in your ability to treat the patient.

But think back to the specific scenario in the study; the wound was made BEFORE the actual stressful event occurred. Now granted the students were most likely starting to get test anxiety several days in advance of the actual exam, but this concept can be a game changer in regards to your subjective history taking. When a patient comes in for an evaluation reporting some insidious flare up or onset of symptoms, I often ask them what else was going on around that time in their life. Now this can be a touchy subject, so do not pry if they do not want to share, but often I’ve had patients tell me about a loved one passing away, a recent change in their job situation, or that they were moving into a new home around the same time that their symptoms increased. For them, this may be their “first big exam,” and this stressful situation could play a role in their persistent symptoms.

So what’s the take home message? Well, there are several. First of all, realize that your patient’s pain does not always have to be due to some type of pathological tissue issue. There are a variety of factors that can exacerbate an individual’s symptoms, and stress is one of them. By helping your patient identify these potential stressors, it may allow for them to take the appropriate steps to start managing their stress. Secondly, patient education is crucial. Tell them about the study with the dental students, and let them know that research shows changes in your immune system functioning during stressful periods of times which can impact your tissue healing rates. While you’re at it, maybe tell them about the Red Light/Blue Light study, and use that as an avenue to talk about pain sciences. Finally, and most importantly, remember to stay within your skill set. Like I said earlier, some of these topics can be very difficult to discuss with a patient, and you need to be comfortable enough with your pain science education techniques to not make the patient think you are telling them “it’s all in their head.” Remember, pain is in your brain, not in your head. You also need to recognize when a situation may be outside our scope of practice, and be willing to refer a patient to the appropriate professional if need be. So long story short, by identifying the potential stressors in your patients’ lives they may heal as fast as if they were hurt during summer vacation. Trust me, that’s a good thing.

The Pain Game: Changing the Perception of Pain

painLet’s play a word association game. When you hear the word “pain,” what do you think? Are they positive or negative thoughts? Since birth, pain has been associated with being injured, damaging tissue, danger…the list goes on and on. So when a patient comes into your clinic complaining of pain, odds are they are associating these symptoms with some of these previous thoughts. But what if there was a way to change how your patients perceive pain? I don’t mean adopting the “no pain, no gain” philosophy on treating, just maybe reinforcing the concept that, “pain does not equal tissue damage.”

shin bruiseHow many of you have found a bruise on your leg, but cannot remember how it got there? Did you damage tissue? Of course you did, you can see the reminisce of ruptured blood vessels, so obviously something has been damaged. But the bigger question is the following: did you experience pain? Or what about a paper cut? How much tissue damage occurs? Not a lot, yet it can hurt like crazy. Being able to talk through examples like this may help your patients make the connection that although there may be “pathological” findings on imaging, it does not mean that those “issues in their tissues” are the source of the pain.

Now let’s go back to that bruise on your shin. What if you got the bruise scoring the game winning goal to win the championship; would it change your perception of the tissue damage? The pain typically associated with the injury may not have such a negative connotation anymore, because every time you look at it you are reminded of that game winning goal. And what if the role was reversed…what happens if you got that bruise while losing the championship game, think your perception of the injury may change?

A recent study by Benedetti et al dove a little deeper into this concept of changing our perception of pain. What if you were rewarded for your pain? That’s right, what if the negative emotional experiences you have when you feel pain were actually encouraged? Well the researchers in this study did just that. The source of the pain? A blood pressure cuff, inflated to the point in which it would create an ischemic pain. blood pressure cuffThe lucky participants? Two different groups of subjects were used, both instructed to try and endure the pain as long as possible. The game changer? One group was told that cutting off the blood supply would be beneficial to the muscles and help them get stronger, whereas the other group was simply told to try and withstand the pain. The findings? The group who was told that they’d get stronger was able to keep the blood pressure cuff on nearly 50% longer than the control group. That’s a pretty significant difference!

Now the researchers go into talking about, “a positive approach to pain reduces the global pain experience through the co-activation of the opioid and cannabinoid systems.” Instead of getting into the neurophysiological significance of these systems, let’s talk about how we can use this study  in a clinical setting. What if you have a patient who just had a total knee replacement, and is afraid to bend it. Instead of just telling them that they need to work through the pain, maybe you set small milestones for each week (ex: our goal is to reach 90 degrees of flexion at the end of the week), and praise them for all of their hard work once they accomplish these goals. Maybe you acknowledge how difficult it is right now, but reinforce the fact that better motion will allow for them to do things they’ve been wanting to do. Besides, motion is lotion after all.

So what’s the big take home message? The way our patients perceive their pain can significantly impact their lives, and as physical therapists, we play a huge role in educating our patients about their pain. Take the time during your next treatment session to talk a little pain science with your patients, whether they are a high school athlete with an ankle sprain or an elderly woman with chronic back pain, because everyone can benefit from knowing more about why they may be in pain. Remember, knowledge is power.knowledge-is-power-41

 

The Perfect Storm: A Case Report on a Deep Vein Thrombosis in a Collegiate Female Soccer Player

Did you ever see the movie (or better yet, read the book), The Perfect Storm? You know, the one where this commercial fishing boat gets caught in the middle of two huge weather fronts…and a hurricane. Talk about being stuck between a rock and a hard place. Well the following case is similar in that a multitude of factors contributed to the development of a deep vein thrombosis (DVTs) in a collegiate female athlete (note: this is word for word from the actual report, and you can access the PDF online). Along with providing some beneficial information regarding DVTs, I hope this case opens your eyes to the importance of a differential diagnosis (see the following blog post about another interesting case). Hope you enjoy the read!

Introduction
A deep vein thrombosis (DVT) or venous thromboembolism (VTE) is a blood clot that develops within the deep venous structures of the body, typically affecting the thigh or calf but is not limited to the lower extremity [1,2]. Epidemiological studies indicate that a correlation exists between age and incidence, with a 0.005% (<5/100,00 persons/year) occurrence in individuals under the age of 15, and an estimated 0.5% (450-600/100,000/year) occurrence for those over the age of 80 [3]. Sixty years seems to be the critical age threshold as the incidence has been found to increase dramatically once the 7th decade begins. Furthermore, only about 30 first time cases of DVT occur for every 100,000 persons in the 25-35 age year range, and despite the concern for the increased risk that oral contraceptives offer, females and males actually suffer from the same rate of occurrence. Regarding race and ethnicity, Caucasians and African Americans suffer similar rates, while Asian-Pacific Islanders and Hispanics have a 2.5-4 fold lower risk [3]. It is estimated that 600,000 new DVT cases are diagnosed each year, with one percent of those cases resulting in death [4]. The cause of death is primarily due to a pulmonary embolism (PE), in which the thrombus dislodges from the vascular wall and becomes trapped within the lungs. The resulting hypoxia causes cardiac failure, which can be fatal if the condition is not diagnosed and treated early. Up to 70 percent of patients diagnosed with PE had an existing lower extremity DVT, emphasizing the significance of accurately diagnosing DVTs in patients and securing early intervention [5].

Case Review
An otherwise healthy, 20-year-old, collegiate female soccer athlete presented in our athletic training room complaining of deep and diffuse knee pain after a non-contact, weight bearing and torque producing mechanism while playing indoor soccer. Her past medical history revealed a successfully reconstructed anterior cruciate ligament following an ACL tear in the right lower extremity status post three years. Upon physical exam, she presented with diffuse swelling and subjective pain as a 3 out of 10 that was aggravated with weight bearing and palpation over the lateral joint line and lateral tibial plateau. Passive range of motion was limited to 90 degrees of flexion, and a 5-degree terminal extension lag was obvious. McMurray’s test was negative, and Lachman’s test proved to be equivocal. Based on the mechanism of injury and her history, meniscal and ACL pathologies were suspected. Initial treatment involved the PRICE (protection, rest, ice, compression, and elevation) protocol, including the use a compression wrap and of crutches to protect the injured joint and to allow pain free partial weight bearing (PWB) ambulation.

Upon referral to the team physician, magnetic resonance imaging (MRI) was ordered and findings indicated a small osteochondral defect along the lateral femoral condyle, and a subjacent cartilage defect along the lateral tibial plateau. Subchondral bone marrow edema was present in the distal femur and proximal tibia, and a moderate sized suprapatellar joint effusion was noted. MRI indicated that the anterior cruciate ligament and menisci were normal. Based on the physician’s final diagnosis, low level quadriceps contractions and electrotherapy for pain management were added to her initial treatment plan.

Early conservative care resulted in significant improvement with considerable pain relief within one week. The team physician instructed the athlete to continue this treatment plan and to maintain PWB status until a follow-up appointment in ten days. Based on the significant improvements on physical exam, the athlete was cleared by the team physician to travel with her team for an overseas training trip. The athlete traveled with her team on a five-hour bus ride and an additional five-hour flight to the final training destination. Four days after her departure date, she complained of increasing pain in the posterior aspect of the right calf, redness and marked edema in the lower leg. As pain increased, her ambulatory ability deteriorated from weight bearing as tolerated, to non-weight bearing.

Upon return to campus three days after the reported increase in symptoms, a follow up evaluation noted a fairly unremarkable physical exam:

  • Diffuse edema in the popliteal fossa extending distally into the calf
  • Calf pain recorded as 4+/10 (during gait)
  • Knee pain decreased to 0/10
  • (-) Homan’s Sign
  • Normal distal pulses (posterior tibialis, dorsal pedis)
  • Discolored skin on the anterior and posterior aspects of the lower leg
  • Unable to perform toe raises on the affected extremity (secondary to pain)

At this point, concern was raised over the possibility of a DVT, but the patient’s overall health and age rendered the suggestion unlikely. Concerned with our mixed findings (negative Homan’s Sign in particular), we consulted the literature and found support for our suspicions. According to Well’s Clinical Prediction Rule (CPR) for DVT, the presence of 3 or more major, and 2 or more minor criteria indicate with 98% specificity that a DVT may be present [6]. For Well’s major criteria, this athlete experienced 1) prolonged immobilization (10 hours of travel), 2) complained of localized tenderness and 3) presented with calf and lower leg swelling. For Well’s minor criteria, she had 1) a history of recent trauma and 2) presented with pronounced erythema in her affected calf and lower leg. According to Wells CPR, the presence of these 5 key features indicates a positive likelihood ratio of 39, and a diagnostic odds ratio of 124. In other words, our clinical findings meant that our young soccer player was extremely likely to be suffering (124 times more likely) from a DVT, and the (-) Homan’s Sign was a false negative result (supporting the low evidence for this test). Given such strong evidence, this athlete was referred to the local hematology department for a diagnostic ultrasound to confirm our suspicions. Imaging results indicated an extensive occlusive deep vein thrombosis present within the distal femoral, popliteal, posterior tibial and peroneal veins.

Treatment
Following confirmation of a DVT, the attending hematologist immediately initiated a treatment plan. Anticoagulation therapy consisted of 60 mg dosages of Lovenox (an enoxaparin injection administered subcutaneously adjacent to the naval), twice a day for two weeks, and a daily dosage of 5 mg of Coumadin administered orally. Weekly blood tests were performed to monitor the athlete’s International Normalized Ratio (INR) to ensure levels were within a therapeutic range (between 2-3 INR). The athlete was experiencing severe back pain one month after beginning anticoagulation therapy, and follow up blood tests revealed high INR levels. Based on these findings, subsequent modifications were made to the Coumadin dosage, which lowered the INR and resolved the back pain. Coumadin treatments continued for four months until the clot was completely dissolved as determined by Doppler ultrasound. The athlete also maintained a PWB status for four weeks to provide adequate recovery time for the osteochondral pathology.

To decrease the likelihood of developing post thrombotic symptoms (PTS), a 40 mmHg thigh-length compression stocking was prescribed for continuous use. Compression stockings can help reduce blood from pooling, or remaining stagnant in the lower leg. In a study involving the duration of compression stocking use, it was noted that prolonging the compression therapy (therapy lasting longer than six months post diagnosis) had significantly better results than those who had shorter treatments [7]. Limb elevation while sleeping was also prescribed to avoid PTS.

Additionally, the team physician prescribed therapeutic exercises including isometric quadriceps contractions (3 sets of 10 repetitions with 3 second hold) and straight leg raises (2 sets of 20 repetitions) to address the osteochondral trauma and subsequent decreased lower extremity function. One month after diagnosis of the DVT, the athlete was cleared to begin light exercise by the hematologist and team physician. This exercise included the use of an upright stationary bicycle and elliptical machine. Stationary bike was first utilized for 5 minutes during the initial session with subsequent sessions adding 5 minutes per session until 30 minutes was reached. This same progression was utilized for the elliptical machine once 30 minutes of pain free activity was reached with the stationary bike. In addition, the athlete added various closed chain exercises (including leg press, body weight squats) to her rehabilitation during the next couple of months to address her overall lower extremity strength and function. Four months after the initial trauma, the athlete was cleared to begin a pain free return to running.

To decrease the likelihood of future clot formation, the medical team recommended the athlete take several actions. A compression stocking was prescribed for any travel-induced immobilization lasting longer than two hours, as well as air travel of any duration. Also, oral contraceptive use was discontinued due to the increased risk of clot development [8]. At five months following the DVT diagnosis, anticoagulant medication was discontinued and no additional follow up appointments were indicated.

Discussion
It is well accepted that recent trauma and/or surgery, followed by prolonged immobilization in certain, higher risk individuals should raise suspicion for the development of DVTs, especially in the lower extremities. However, there are few documented cases of young and otherwise healthy athletes developing DVTs, but due to the serious and significantly hazardous outcomes, it’s essential for clinicians to carefully identify potential risk factors that may predispose certain patients to clot formation, regardless of their demographics. Chiefly, it’s prudent for a thorough medical history to be taken in order to recognize those situations in which a DVT might not be suspected, and as demonstrated here, to regard the results of the Homan’s Sign with suspicion (Cranley, et al reported a sensitivity of 48%, a specificity of 41% and a DOR of only 0.64, demonstrating its poor diagnostic utility) [9].

In reflecting on the particulars of this specific case, our athlete’s risk factors were:

  • Osteochondral defect along lateral femoral condyle and sub adjacent tibia, as well as subchondral bone marrow edema
  • Combined twenty hours of immobilization during the travel period
  • Four separate plane flights totaling over ten hours at significant altitude
  • Athlete was currently taking Tri-Lo Sprintec, an oral contraceptive
  • Blood tests revealed the genetic mutation for Factor V Leiden

These risk factors are explained and reviewed to ensure a better understanding of the etiology specific to this case.

Limb trauma
The torsion forces caused by the mechanism of trauma in this case proved capable of damaging the osteochondral surfaces of both the femur and tibia. This resulted in focal cartilaginous edema about the tibial and femoral articular cartilage of the lateral joint space with a small amount of reactive edema about the lateral femoral condyle. Traumatic events can cause disruption of the endothelium lining of the vein wall, causing platelets to begin to adhere to the venous wall and results in the deposition of leukocytes, erythrocytes, and fibrin [10]. This accumulation of cells and proteins result in a thrombus formation.

Immobility
The combined twenty hours of immobilization from the initial and return trips resulted in decreased muscle pump from the lower extremity, and increased venous stasis. Venous stasis increases the risk of thrombosis by inhibiting activated coagulation factors from being removed through normal blood flow [11]. The higher concentration of coagulation factors facilitates the continued development of the thrombus. Also, the endothelial protein thrombomodulin that is responsible for converting thrombin into an anticoagulant enzyme requires blood flow to travel from the capillaries into the veins to take effect [11].

Air travel
Of the twenty hours of travel immobilization, ten hours were spent via air travel at significant altitude (greater than 3000 kilometers). A previous case report indicated that air travel lasting at least four hours resulted in an increased risk of venous thromboembolic disease [12]. Reasons behind this increased risk have been accredited to the pressure being placed upon the legs while seated cross legged [13]. The popliteal vein has been known to develop “transverse rippling” while seated, which not only facilitates venous stasis, but may cause damage to the endothelial wall [14]. With the increase in altitude the concentration of ambient air decreases, resulting in a decrease in fibrinolysis and increases the risk of clot formation [15]. The literature suggests that deep vein thrombosis development is four times more likely to develop within a given “hazard period,” which is two to four weeks following a flight [16]. Interestingly, the DVT in this case developed 3-4 days post travel, which occurred much more rapidly than the typical “hazard period” of air travel.

Oral contraceptives
The athlete had been taking oral contraceptives for over a year prior to the injury. One case report indicated that the risk of DVT increased by a magnitude of four when women were using oral contraceptives (OCs) [8]. The oral contraceptive specific to this case, Tri-Lo Sprintec, is known as third generation progesterone which has a higher associated risk than some OCs [17]. The hormonal effect of both increasing coagulation and decreasing fibrinolysis can explain the genesis of the DVT. Most relevant to our case, a study found that the risk of developing a DVT was increased by a factor of fourteen when combining OCs use and air travel [8].

Genetic factors
After the diagnosis of a DVT was formulated, the hematologist pursued further testing to determine if there were any underlying genetic components contributing to the pathogenesis. Testing consisted of a blood test with DNA analysis, which confirmed a genetic mutation of Factor V. Factor V is a protein found in the blood that is required for normal clotting to occur in the body. The genetic mutation of interest, Factor V Leiden, is an abnormal version of the clotting factor that is resistant to the action of activated protein C (APC); a substance that inactivates Factor V preventing an excessive growth of the clot [18]. Since the mutation results in APC being unable to inhibit the effects of Factor V, clots are more prone to develop, hence their correlation to the development of DVTs. This statement is supported by a study which indicated that Factor V Leiden mice had faster growing thrombi compared with non-Factor V Leiden mice [19]. There are two forms of the genetic mutation, either heterozygous or homozygous, with an increased risk of DVT found in homozygous carriers (an increased risk of about 25-50 fold) [20]. The athlete in this case tested as a heterozygous carrier of the genetic mutation. The risk of venous thrombosis once again increases in women using oral contraceptive pills or on hormone replacement therapy that also have Factor V Leiden, as there is a 35-fold increased risk of developing a DVT [20].

Conclusion
Each of the previously mentioned risk factors contributed to the etiology of this athlete’s extensive DVT, reinforcing the importance of obtaining a thorough medical history to assist the medical team with the diagnosis. Using these risk factors as a guide, the following questions should be asked of an athlete presenting with a lower leg trauma:

  • Have you had any period of immobilization or weight bearing restrictions recently?
  • Have you recently traveled or intend to travel in the near future (specifically air travel lasting longer than four hours)?
  • Are you currently taking oral contraceptives or receiving hormonal therapy? If so, what kind?
  • Do you or any members of your family have a history of DVTs or clotting disorders?

Although young, otherwise healthy athletes are not typical candidates for DVT following mild to moderate orthopedic trauma, the risk for developing thrombi should be at the forefront of a clinician’s thought process when other risk and contributing factors are present. After the initial trauma, this athlete presented with only two known risk factors for a DVT (limb trauma and oral contraceptive use). At this point in the diagnostic process, suspicion of a DVT would be limited, but should not be eliminated as a potential sequela to the injury. Yet, the exacerbation of symptoms shortly following a period of prolonged travel should serve as a red flag to the diagnostic team.

Well’s Clinical Prediction Rules inform us that a history of cancer, presence of paralysis, and/or lengthy immobilization are major criteria for increasing the risk for DVTs. In young athletic populations, none of these criteria are typically in the mix, nor were they in our case presentation except for the 10 hours of air and bus travel that forced her into immobilization. However, it turned out that the athlete actually had a genetic risk factor for the condition, and presented with 3 of the key clinical features upon her return trip. Collectively, our case supports the robustness of the Well’s Clinical Prediction Rules and reinforces the need for the attending clinicians to perform a thorough history and pay attention to subtle clinical findings, regardless of the relatively low risk in college aged athletes. Well’s Clinical Prediction Rules can be used as a diagnostic guideline for DVTs in the athletic population, but further development of research-based guidelines for return to play in athletic populations is worthy of future investigation.

References
1. American Association of Hip and Knee Surgeries (2009) Deep Vein
Thrombosis. American Academy of Orthopaedic Surgeons.
2. Deep Vein Thrombosis (2010) APS Foundation of America, Inc.
3. White RH (2003) Four Topics in Venous Thromboembolism: The Epidemiology
of Venous Thromboembolism. Circulation 107: I-4-I-8.
4. Deep Vein Thrombosis Overview (2012) Society of Interventional Radiology.
5. Young BA, Flynn TW (2005) Pulmonary emboli: the differential diagnosis
dilemma. J Orthop Sports Phys Ther 35: 637-644.
6. Wells PS, Hirsh J, Anderson DR, Lensing AW, Foster G, et al. (1995)
Accuracy of clinical assessment of deep-vein thrombosis. Lancet 345: 1326-
1330.
7. Prandoni P, Kahn SR (2009) Post-thrombotic syndrome: prevalence,
prognostication and need for progress. Br J Haematol 145: 286-295.
8. Martinelli I, Taioli E, Battaglioli T, Podda GM, Passamonti SM, et al. (2003)
Risk of venous thromboembolism after air travel: interaction with thrombophilia
and oral contraceptives. Arch Intern Med 163: 2771-2774.
9. Cranley JJ, Canos AJ, Sull WJ (1976) The diagnosis of deep venous
thrombosis. Fallibility of clinical symptoms and signs. Arch Surg 111: 34-36.
10. Goodman C, Fuller K (2009) Pathology Implications for the Physical Therapist
(3rdedn) St. Louis: Saunders 2009: 625-626.
11. Hirsh J, Hoak J (1996) Management of deep vein thrombosis and pulmonary
embolism. A statement for healthcare professionals. Council on Thrombosis
(in consultation with the Council on Cardiovascular Radiology), American
Heart Association. Circulation 93: 2212-2245.
12. Ferrari E, Chevallier T, Chapelier A, Baudouy M (1999) Travel as a risk factor
for venous thromboembolic disease: a case-control study. Chest 115: 440-444.
13. Moyses C (1988) Economy class syndrome. Lancet 2: 1077.
14. Bragshaw M (2001) Traveller’s thrombosis: a review of deep vein thrombosis
associated with travel. The Air Transport Medicine Committee, Aerospace
Medical Association. Aviat Space Environ Med 72: 848-851.
15. Gertler JP, Perry L, L’Italien G, Chung-Welch N, Cambria RP, et al. (1993)
Ambient oxygen tension modulates endothelial fibrinolysis. J Vasc Surg 18:939–945.
16. Kelman CW, Kortt MA, Becker NG, Li Z, Mathews JD, et al. (2003) Deep vein
thrombosis and air travel: record linkage study. BMJ 327: 1072.
17. Conard J (1999) Biological coagulation findings in third-generation oral
contraceptives. Hum Reprod Update 5: 672-680.
18. Ornstein DL, Cushman M (2003) Cardiology patient page. Factor V Leiden.
Circulation 107: e94-e97.
19. Cooley BC, Szema L, Chen CY, Schwab JP, Schmeling G (2005) A murine
model of deep vein thrombosis: characterization and validation in transgenic
mice. Thromb Haemost 94: 498-503.
20. Van Stralen KJ, Doggen CJ, Bezemer ID, Pomp ER, Lisman T, et al. (2008)
Mechanisms of the factor V Leiden paradox. Arterioscler Thromb Vasc Biol
28: 1872-1877.

Red Lights or Blue Lights: What Color Do You See?

Can you think of a time when your thoughts influenced how you felt about a situation? For example; have you ever heard a sound at night while you’ve been home alone? In a matter of seconds you can go from being relaxed on the couch to having a mild panic attack thinking that there is an intruder in the house with you. Did you actually see something? No, but your brain processed that information as potentially dangerous and kick started your body’s “fight or flight” response just in case.

This hypothetical situation can be applied to a variety of scenarios, including our perceptions of pain. In fact, Mosely and Arntz published a study in 2007 looking at how the context in which a noxious stimulus is delivered can alter the way people perceive pain. During the study, a cold metal rod (-20 degrees Celsius) was applied very briefly to the subject’s hand while they received various contextual information about the stimulus. This information was in the form of a light: red or blue. The subjects were told that the red light meant “hot” and the blue light stood for “cold.” The subjects were then asked to rate their pain intensity, pain unpleasantness, and the temperature that they perceived (on a 0-10 scale, with 0 indicating both no pain/unpleasantness, as well as being extreme cold).

Now the study was a little more complicated than just looking at the color light; the subjects were given different scenarios in which they rated their perception of the stimulus. For example, they either were provided a warning as to the color of the light versus no warning, or were allowed to look at the application of the rod versus being blinded to it (see the image below for a representation of the different scenarios).

 

blue light study

So what did they find? Well long story short, the subjects rated their pain intensity and unpleasantness as higher when looking at the red light versus the blue. In case you forgot…THE STIMULUS NEVER CHANGED! The rod stayed the same temperature; all that changed was the color of the light (see the graph below for the results of the study).

blue light graph

So what does this mean? Well Mosely and Arntz made the following conclusion, “the tissue damaging meaning of a noxious stimulus, warning about the stimulus and visual attention to the stimulus all affect the evoked experience.” That being said, our perceptions about an injury (whether they are accurate or not), can play a huge role in regards to our pain. This can be a game changer for us as physical therapists, as we have the opportunity to educate our patients not only about their injury, but about other factors that may be exacerbating their symptoms as well.

So what can we do about it? How many times have you had a patient tell you that they have imaging that shows they have arthritis, a torn rotator cuff, or a disc herniation? And obviously since there is evidence of these pathological tissues it must be the source of their pain, right? WRONG! One recent study published in 2015 by Nakashima et al examined the prevalence of abnormal findings on cervical spine MRIs. Over 1,200 healthy volunteers (key word, healthy, aka no symptoms) ranging in ages from 20 to 70 years were imaged. The findings? Over 85% of the subjects presented with disc bulges (even those subjects in their 20s, with over 70% of this population having evidence of some degree of bulging). Why is this information important? Well if you were a patient and you were told by a medical doctor that your MRI found degenerative changes, disc protrusions/herniations/bulges, narrowing, etc…what would you think? All of these words have such negative connotations associated with them, which may also serve as a “red light.” Could these “issues in your tissues” be causing the pain? Maybe, but we just saw how many “abnormal” findings were associated with individuals without symptoms. In fact, since the majority of the individuals presented with disc bulges wouldn’t it be “abnormal” not to have these changes…? Think about that.

Be mindful of how you talk to your patients, because the way you communicate to them may have the potential to change a few red lights to blue. For example, I love reviewing lumbar MRIs with my patients, because I feel that this can be a “make or break” point in regards to their fear of their prognosis. Often the images look like the following:

lumbar mriI choose my words very carefully at this point, and instead of pointing out the disc protrusions at L4/L5 and L5/S1 or the degenerative disc disease that they have, I may say that they have some “grey hairs” in their back (metaphorically speaking) which can be found in individuals without any symptoms at all. Now a once potentially red light may be slightly bluer. What I may highlight a little more closely would their multifidi, as you can see in the following example:

multifidi

The above image shows fatty infiltration of the lumbar multifidi; a common finding in individuals with low back pain. Now I tend to describe these changes to their multifidi in regards to hamburger meat (once again, metaphorically speaking); image on the left has the good stuff, high quality lean beef. Image on the right on the other hand, may be closer to 60/40 beef. Which would you prefer to eat? Why do I show them these muscles? If their impairments include lumbopelvic stability (not all patients with low back pain need “core” exercises though, see the following post), then we can address this through physical therapy. BLUE LIGHT! The once depressing, scary MRI now shows the potential for an improvement in their symptoms, and you may have a better adherence to your plan of care now that the patient understands more about their “tissue issue.” Remember, knowledge is power.

Check out the following statements that I’ve heard used by patients or other medical professionals, and see how they could potentially switch from a red light to a blue:

  • “I have bone on bone arthritis that the doctor said was the worst he has ever seen.”
    • Thank you for instilling fear avoidant behaviors. Educating the patient that arthritic changes are a normal part of the aging process, and that they probably have had these changes for several years. Maybe discussing some of the research behind “abnormal” imaging findings in asymptomatic individuals can drive home the point that pain does not always equal tissue damage.
  • I hurt my back 20 years ago lifting a box off of the ground, so my doctor told me never to lift anything over 10 pounds again.
    • Sounds like a red light to me. Using words like “never,” “always,” or “worst,” really stick in a patient’s mind, so try and be mindful when making suggestions or recommendations (even if it is regarding something like posture or exercise technique). This would be a perfect patient to talk about tissue healing rates, and dive into some more pain science education (ex: their tissues have healed at this point, but their nervous system may still perceive lifting as a dangerous stimuli…aka red light).
  • “That knot in your muscle is as hard as a rock and keeps coming back.”
    • So now the patient thinks of their muscles as rocks, and that there symptoms are resilient. I often have patient’s ask if things “feel tight” when I’m performing soft tissue mobilizations, and if applicable, I tell them how it is normal for certain muscle groups to be “tighter” or “stiffer” than others (ex: upper trapezius when doing myofascial work, or thoracic spine when performing joint mobilizations). While each patient is special and unique, we do not necessarily want to verbalize that their tissues are that way.
  • “I was told that since I tore my rotator cuff I’d never be able to swim again.”
    • A few things to address in this one. Once again, discussing the normal “abnormalities” found during imaging would be a good start. Also, never say never. Never. Automatically the thought of not being able to return to a sport, work, or life activities can prove to be a huge blinking red light. Now this patient may not be able to swim for hours, but talking about the benefits of addressing the potential impairments that they may have, and relating that back to their ability to achieve their goals may increase their confidence.

Each time a patient walks into your clinic, they may have a few red lights in the back of their mind. While some may be brighter than others, cumulatively they can add up, and when they do, your patient’s symptoms may go through the roof. Thankfully we have the potential to turn these lights off, and maybe switch on a few of the blue ones while we are at it.