Pain Science and Biomechanics
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1 Pain Science and Biomechanics Key messages to reconceptualize pain Reconceptualizing Biomechanics Explanations for how pain persists and how it can change
2 The Point of Pain Science Greg Lehman MSc, DC, MScPT Physiotherapist & Chiropractor
3 Why pain science? Pain science helps the patient think differently about their predicament
4 Changing Cognitions First interplay between nociception and the central processing we still want to decrease the nociceptive trigger but we are uncertain how much nociception is involved when we have changed beliefs about pain we can then begin to desensitize with graded exposure, specific exercise and movement alterations Treatment addresses all aspects of pain because we can t be certain what is most dominant
5 addressing the psychosocial
6 Linton 2011
7 We need to reinforce that our patients are strong the goal of education is to change how our patients view their condition this gives hope and builds self efficacy starts the path to re-activation and control
8 enforcing the key messages
9 pain is an alarm
10 pain is an alarm the brain perceives real or perceived damage How do we explain this to our patients? what is your analogy and story?
11 what does an alarm tell us?
12 pain is an alarm can alarms become more sensitive? sure - consider the sentry on duty protecting warehouse. if there has been a rash of break-ins is she more likely to pull the alarm? how is this like pain?
13 pain is not just in your head
14 the brain is involved with pain but it is real can you think of other examples where the brain constructs or limits what we do? sports and exercise? vision?
15 WHAT CAN WE LEARN FROM VISION draw the lines for your patients
16 WHAT CAN WE LEARN FROM TASTE? what happens when you drink orange juice but expected milk? What does this illustrate to the patient about context and expectations?
17 pain is not a damage indicator
18 break into groups of 3-4 what examples of alarm reactions that are disproportionate to the stimulus
19 pain is poorly linked with damage initially pain is good at telling us about damage but over time the link becomes poor How do we explain this to our patients? does broken bone hurt in a cast? what happens when your hand approaches fire? why does pain move around - its not a GPS why does a heart attack cause a painful arm?
20 questions to ask what is the purpose of an alarm or pain? do alarms tell us why it was activated? does a fire alarm tell us how bad the fire is? can you think of times where your pain was less or more for no apparent reason? when do you feel better? does your pain change on vacation?
21 pain is a protective as are other responses
22 pain is a protective response like other responses how we move changes with pain stress responses change with pain immune reactions are involved swelling can occur all can persist and continue to promote ongoing sensitivity. we reframe the symptoms patients have to being about unnecessary protective responses
23 teaching about pain processing helps give hope for change
24 the steps of processing (strongly from Explain Pain) Step 1: Danger signalling (Nociception) Step 2: Nociceptive Modulation the drug cabinet in the brain Butler Step 3: The Brain s Opinion how dangerous is this really Moseley
25 How do we teach that all of these areas can be modulated? aka: Selling Therapy
26 Nociception sensors let us know they are irritated temporarily avoiding aggravating postures loading tissue to create adaptation manual therapy desensitizes changing how we move to move fluidly with less stress
27 Nociceptive Modulation centrally produced desensitizing chemicals general exercise isometric exercise manual therapy goal setting and re-activation learning about pain - decreasing the threat **all of these interact with Brain Processing as the brain influences the spinal cord excitability
28 Brain Processing an opinion is made whether we need protection changing contexts and environments learning about pain stress, sleep and lifestyle fear, anxiety, catastrophizing, anger, injustice recognizing factors may be helpful we ask questions about these areas
29 Pain is multifactorial everything in the patient s life that can sensitize the ecosystem can be a factor in perpetuating or initiating pain we know that we don t need to remove all these factors but perhaps its the action of addressing, recognizing or accepting them that influences pain
30 pain persists past healing
31 pain persistence pain becomes its own problem and is poorly connected to tissue disruption the body/brain/person still feels the need to protect pain is now more about sensitivity than damage often seen when people continue to limp without the need for it KEY MESSAGE HURT DOES NOT EQUAL HARM
32 PAIN IS ABOUT SENSITIVITY draw the graphs for your patients
33 Adaptability & Sensitivity Tissue strength Changing Pain Threshold Loading on the ecosystem
34 Answering the tough questions why does it continue to hurt?
35 Practical using the BPS as a framework come up with simple explanations for why pain persists
36 Psychological models of persistence pain and disability Linton 2011
37 some background to address those false beliefs about damage and pain
38 A reliance on structural pathology and pain is false and may increase the pain and suffering of our patients
39 Damage and Pain (knowpainmike)
40 Damage and Pain
41 Fibrosis and Reinjury
42 Damage and Pain
43
44 Psychosocial variables strongly predicted both long- and short-term disability events, duration and health-care visits for LBP problems (p< ). The likelihood of a sustained remission from the baseline persistent (subclinical) LBP appeared to be linked to occupation factors (leaving a heavy labor occupation; p=0.0001), neurophysiologic variables (chronic nonlumbar pain; p=0.0002) and psychometric profiles at baseline (DRAM and FABQ-PA; p= ). Of the structural findings measured only moderate or severe Modic changes of the vertebral end plate were weakly associated with an adverse outcome. A positive provocative discogram at baseline did not predict any future adverse event. CONCLUSION: The development of serious LBP disability in a cohort of subjects with both structural and psychosocial risk factors was strongly predicted by baseline psychosocial variables. Structural variables on both MRI and discography testing at baseline had only weak association with back pain episodes and no association with disability or future medical care.
45 Increased load not associated with disc degeneration (Videman 2010) Higher body weight was associated with 6.2% higher bone density in the lumbar spine, confirming an effective discordance (p<.0001). Disc signal variation was 5.4% higher ("better") among the heavier MZ co-twins (p=.005), but the 2.6% higher disc heights and 2.9% higher adjusted disc signals were not statistically significant. CONCLUSIONS: Contrary to common beliefs, our findings suggest that cumulative or repetitive loading because of higher body mass (nearly 30 pounds on average) was not harmful to the discs. In fact, a slight delay in L1-L4 disc desiccation was observed in the heavier men, as compared with their lighter twin brothers
46 Battie (2009) Twin Spine Study More recent results indicate that the effect of anthropometric factors, such as body weight and muscle strength on disc degeneration, although modest, appear in this work to be greater than those of occupational physical demands. In fact, some indications were found that routine loading may actually have some benefits to the disc. CONCLUSIONS: The once commonly held view that disc degeneration is primarily a result of aging and "wear and tear" from mechanical insults and injuries was not supported by this series of studies. Instead, disc degeneration appears to be determined in great part by genetic influences. Although environmental factors also play a role, it is not primarily through routine physical loading exposures (eg, heavy vs. light physical demands) as once suspected.
47 Why are the previous slides important? We give our patients permission to move.
48 but loading may not be irrelevant
49 Cases showed significantly higher loading on all biomechanical variables. Four independent risk factors were identified: integrated lumbar moment (over a shift), 'usual' hand force, peak shear force at the level of L(4)/L(5) and peak trunk velocity. Substituting lumbar compression or moment for shear did not appreciably alter odds ratios because of high correlations among these variables. CONCLUSIONS: Cumulative biomechanical variables are important risk factors in the reporting of LBP. Spinal tissue loading estimates from a biomechanical model provide information not included in the trunk kinematics and hand force inputs to the model alone. Workers in the top 25% of loading exposure on all risk factors are at about six times the risk of reporting LBP when compared with those in the bottom 25%. RELEVANCE: Primary prevention, treatment, and return to work efforts for individuals reporting LBP all require understanding of risk factors. The results suggest that cumulative loading of the low back is important etiologically and highlight the need for better information on the response of spinal tissues to cumulative loading.
50 maximizing the clinical encounter
51 what questions do we need to ask?
52 What have they been told about their pain? What do they think is wrong with them? Are there activities they are afraid to do? What holds them back from doing what they want?
53 What happens if we can make a shift in our mindset of how we view the body and pain?
54 what happens if no activity is off limits?
55 if we shift to thinking the body is strong and adaptable, not frail, not misaligned, not full of adhesions and not damaged what does this permit?
56 If we shift our explanation to one of sensitivity and lacking in movement options what does that shift permit?
57 More information to change patient s cognitions
58 Academic Stress and Injury We found that the odds of an injury restriction during training camp (high physical stress) were greatest compared to weeks of high academic stress (OR=2.05, p=0.0003) and low academic stress (OR=3.65, p<0.001). However, the odds of an injury restriction during weeks of high academic stress were nearly twice as high than during weeks of low academic stress (OR=1.78, p=0.0088)
59 Psychosocial and Loading Psychosocial stress increased spine compression and lateral shear, but not in all subjects. Differences in muscle coactivation accounted for these stress reactions. Gender also influenced spine loading; Women's anterior-posterior shear forces increased in response to stress, whereas men's decreased. Certain personality traits were associated with increased spine loading compared with those with an opposing personality trait and explained loading differences between subjects. CONCLUSIONS: A potential pathway between psychosocial stress and spine loading has been identified that may explain how psychosocial stress increases risk of low back disorders. Psychosocially stressful environments solicited more of a coactivity response in people with certain personality traits, making them more susceptible to spine loading increases and suspected low back disorder risk.
60 Patients with low back pain experienced 26% greater spine compression and 75% greater lateral shear (normalized to moment) than the asymptomatic group during the controlled exertions. The increased spine loading resulted from muscle coactivation. When permitted to move freely, the patients with low back pain compensated kinematically in an attempt to minimize external moment exposure. Increased muscle coactivation and greater body mass resulted in significantly increased absolute spine loading for the patients with low back pain, especially when lifting from low vertical heights. CONCLUSIONS: The findings suggest a significant mechanical spine loading cost is associated with low back pain resulting from trunk muscle coactivation. This loading is further exacerbated by the increases in body weight that often accompany low back pain. Patient weight control and proper workplace design can minimize the additional spine loading associated with low back pain.
61
62 Factors significantly associated with membership of the MTA group included greater anger-hostility (P = 0.003), more subjective health complaints (P = 0.026), more severe previous pain/injury (P = 0.017), more general everyday pain (P = 0.020), more body parts affected by pain/injury (P = 0.028), always/often dancing in pain (P = 0.028), and insufficient sleep (P = 0.043). Several biopsychosocial factors appear to be associated with absence from ID because of pain/injury. Biopsychosocial screening protocols and prevention strategies may best identify at-risk dancers
63 The creation of Catastrophe catastrophizing is negatively associated with outcomes these beliefs can be driven by our words and words of others when we change these beliefs we change the meaning of pain with certain movements USE WHATEVER MODEL OF TREATMENT YOU WANT BUT CONSIDER HOW THE PATIENT UNDERSTANDS YOUR EXPLANATION
64 Are you afraid of this? from thesciencept.com
65 or this?
66
67
68 or this?
69 are any of those movements inherently injurious under all conditions?
70 BUT
71 Movement Quality Still Matters it might matter but is it important during the majority of our activities? can we really say that there is an ideal way to move? we must find the certain situations where it is important and look to researchers for help
72 everything we do and say influences the patients opinion of themselves
73 How should you jump or land?
74 Ballet Jump
75 Alternative to Faulty Patterns Is a pattern simply faulty because it is sensitive? Is it faulty because it is linked with pain in the patients mind, past experiences, beliefs etc?
76 Alternative to Correcting Patterns Break the Pain Habit with new movement options
77 how do we explain this to the patient?
78 ask how much they move ask if they try to assume an ideal posture? ask why they don t slump ask if they cross their arms or legs do they brace/stiffen with pain or go loose and relaxed?
79 The Habit/Memory of Pain the painful neurotag can become coupled with a movement neurotag the protective pain memory is coupled with protective movement behaviours (bracing, avoidance, decreased variety our treatment breaks this coupling but we have to do it along with changing beliefs about their pain
80 An alternative to ideal movement Comprehensive Capacity
81 Comprehensive Capacity Assumes that the body should be able to tolerate all forms of stress and we need to train the body to tolerate these stressors. If there are few faulty movements then we train to adapt and tolerate all movements and under different parameters. encapsulates variety, fluidity, exploration demands the most out of every joint assumes the body gets into bad positions and we learn to handle them
82 Providing Movement Alternatives creates variety creates options shows the patient they can move without fear demonstrates the idea that they have ability builds self efficacy and confidence in movement modifies symptoms establishing control desensitizes while the body adapts
83 Teach people to move pain free using variety and novelty you can modify movements that were once painful this starts to desensitize movements start with same principles of slow progression
84 Sixteen subjects performed arm movements during control trials, when the movement evoked back pain and then when it did not. Variability in the postural strategy of the abdominal muscles and pain-related cognitions were evaluated. Only those subjects for whom pain induced a reduction in variability of the postural strategy failed to return to a normal strategy when pain stopped. They were also characterized by their pain-related cognitions. Ongoing perception of threat to the back may exert tighter evaluative control over variability of the postural strategy.
85 more from Moseley That is poignant because when a movement becomes painful, the meaning of that movement changes. Thus, perhaps when people who perceive their back to be vulnerable experience back pain, they continue to exert tighter evaluative control over variability, even when the back pain has resolved. That asymptomatic controls demonstrate a protective postural strategy when they expect their back to hurt (Moseley et al., 2004a) and that recurrent back pain patients demonstrate it even when they are pain free (Hodges & Richardson, 1996) seem consistent with that possibility
86 The participants with LBP exhibited significantly less variability of their IO muscle onset latencies, confirming that the decreased variability of postural coordination that is evident following acutely induced LBP is also evident in people with chronic LBP. Thus, people with chronic LBP may be less capable of adapting their APAs to ensure postural stability during movement.
87 Practical Break - Adding Variety 1. Modifications to a Bird Dog 2. How many different ways to get your arm over your head 3. How can you train your hip rotators 4. Different ways to one leg squat 5. The dynamic bridging series
88 Break into groups of three take a simple exercise find three different modifications to that exercise
89 up next when biomechanics matters
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