Search
Close this search box.

The OSTEOPATHYST

Canadian Journal of Osteopathy

scroll

A Full Body Osteopathic Approach Part 2: Compensation Strategies

Written by Lee Jarvis. Proofreading and editing by Bobby-Jean Marrandino.

In this second article in our series on the justification for an Osteopathic full body treatment, we will continue with our discussion regarding how the body works together and how this should be applied in Osteopathic Manual Therapy (OMT). In the first article we explained the historical significance of exploration and treatment of the whole body by Dr. Andrew Taylor Still, the founder of Osteopathy. In this article we will further discuss the concept of the body working together through the concept of what is often called “compensation”.

On the idea that the body works together (often Osteopathically referred to as a “dynamic unit of function”), it would be, at this point in the understanding of how the human body works, very difficult to disprove that the body does just that. In just the known, shared functions between the Autonomic Nervous System (ANS), Hypothalamus, and Pituitary gland we can say that every tissue has multiple pathways to communicate and adjust the functions of the body. We can certainly say that the workings of the body are complex, confusing, and possibly beyond our full comprehension, but at no point can we say that anything is truly an island of function in the body.

That being said, in dire situations, certain specific organs or tissues will cause a lethal amount of trouble and must be focused on in exclusion of others (hence the great importance of medical specializations). Though, this type of pathology should not happen in the relatively healthy individual and is not the subject of this article.

When the term “compensation” is used, it is a product of an understanding that the body is working together in some capacity. Even the general public seems to have an idea of what compensation is; however, this understanding is typically in simplistic terms. Likely this is because compensation is not always well explained or even understood by those explaining it. In fact, at times the concept of compensation can be used to excuse a behaviour as opposed to explaining it. For that reason, let’s see if we can review the idea of compensation, first in a simplistic and straightforward way so it is accessible to anyone and second, to build a full body concept (that is still accessible to most readers).

The concept of compensation would suggest that the lack of movement of a single tissue will affect all other tissues. As well, compensation suggests that movement of every tissue must be taken into account when trying to change the movement of a single tissue. Even if the previous statements are true, taking this concept as completely true and equal in all movements would be incorrect. Imagine if even a slight change in your finger would change the position of every other tissue in your body to a proportionate degree. In this scenario, the bending of the toes would then require the disarticulation of the skull (amongst other areas of the body). If the previous point was true, we would not be capable of any kind of controlled or smooth movement that is required for something as simple as walking. As much as everything works together in the body, the tissues need some level of independence in movement or flexibility relative to the other parts. The reality should be that everything is connected and affected by each other, but only to varying degrees. Much of the time, the effect of one tissue on a distal tissue is minimal. However, the degree to which one tissue can affect another by movement can be changed by contraction and/or stiffness of the tissue.

Before explaining the smaller and larger potentials of compensation, let’s talk about what’s commonly described as compensation. The most frequently used example seems to be to describe compensation in terms of over using one appendage when the other is not available. For instance, should a person fracture an ankle and have to use crutches, they use the non-fractured leg to weight bear/walk on; Eventually the non-injured leg starts to hurt and often it said by the patient that they are “compensating” by over using non-injured leg. This is actually a very reasonable explanation of how the leg became painful, but only a very “wide-shot” or “big picture” of what we see in terms of the body’s capacity for compensating (making it a good place to start our explanation as we “zoom in”). It is likely that the non-fractured leg is now painful because it is being used for more weight bearing as well as in a different way than it was previously used to. A very similar process happens frequently when a person takes on a new exercise routine. Whenever we introduce a new way of moving and an increase in weight bearing capacity (for instance, a new weight lifting routine or exercise class) we expect the tissue growth and soreness that often comes along with that [14, 19]. Though real tissue injuries do occur at times with new exercise practices, much of the soreness will be created by the growth process of the body being asked to take on a new job with increasing weight and frequency. Just as exercise will not always create soreness, not all compensation causes pain, however, the two can be related in the right circumstances.

At some point and for some reason, the tissue (muscle, tendon, ligament, fascia, etc) moves less than it once did. This decreased mobility could be due to an injury such as a sprain or strain [5, 8, 9, 18], age [13, 20], a degenerative disease [1, 17], or a long enough time in a sedentary environment [2, 4, 6, 7, 21]. When a tissue moves less, this means that anything directly attached to the tissue will move less as well. Perhaps it will only move a little less, perhaps a lot less, but movement will be decreased. Examples of these attached tissues could be other muscles in the same functional group of muscles, fascia within the local region, and the joint/multiple joints that a muscle crosses. The affected person who desires to move is, however, largely unaware that motion capacity (or flexibility) has changed and to what extent it has changed. The affected may be in pain after the initial loss of motion (in cases of injury and certain degenerative diseases), which may temporarily make them do less with the part that hurts. An interesting element to immobility is that, though immobile or degenerating tissue can cause C-fibre type pain, it is typically not the type of sharp pain that greatly halts our movement. Compared to the pain from new injuries, such as a strain or sprain, the A Delta fibre pain is usually sharp enough to stop us immediately. However, after the initial pain(s) have reduced or been ignored, we will attempt to continue the same type of activities as before. For the sake of clarity, examples of the previous idea can be as simple as an injured person continuing to walk on a sore leg or in pathology wherein a sufferer of chronic pain will learn to adapt to and ignore their pain [11, 12, 15, 16]

To continue to achieve the same goals or complete the same activities that are normal of the affected person, other tissues must then be asked to move more than or in different ways than previously needed to make up for the loss in motion. Perhaps there are other joints and tissues made to easily move in the ways that are now needed and so this requires less extra effort even though there have been changes made. For instance, if the end range of extension is lost in the elbow, some shoulder flexion can be added to reach the same height if we need to reach up high. In this way, the shoulder “compensates” for the lack of full motion of the elbow. In this isolated example, the arm is largely fine, the body is made for this type of small compensation and does this compensation likely without the user of the arm knowing. In this example, this compensation is a very beneficial thing. Much like in our example of the fractured leg and crutches, the fact that the person‘s non-fractured leg is now hurting still means that they’re capable of moving around and completing at least some of their typical daily activities. The capacity of the body to do this compensation effectively is, however, dependent on the capacity for one part to be strong and flexible enough to support another.

Though individual tissues or a small area of motion loss may not be a problem, let’s discuss how motion losses amongst larger areas could create a problem. When it comes to compensating for loss of motion, the other tissues in the body that might make up for the lack of mobility in one part may not necessarily be directly connected. The tissue that is limited in motion may not have any local (directly attached) areas that can compensate and so, the movement adjustments may come from more distant parts of the body. Let’s take a look at the simple act of bending over to pick something up.

Without question, bending over is a full body motion involving numerous joint position changes and tissues lengthening. For this example, let’s say that flexion of the hip is limited, therefore the hip stays comparatively extended when bending over.

This person cannot drop down as far because of this limited hip flexion and so may push other areas further to extend their reach. For instance, increased knee extension may slightly tilt the pelvis forward causing the body to drop down more.

In addition, Lumbar and Thoracic flexion could be increased to bring the head and arms closer to the ground. Scapular protraction could also be increased to extend the reach of the arm.

Much like the previous arm example, individually these compensations would not necessarily cause problems. However, as a group, they represent a greater need for flexibility throughout the body. Like in our fractured ankle or exercise examples above, asking a body part to do a movement it is not used to doing, possibly body parts having to weight bearing more than they previously were, can be uncomfortable and even painful. In an optimal environment where the affected person was given time to adapt to this change in movement, the tissues could grow and adapt to the new movement(s) required of them. However, an ideal environment with ample time to adapt, optimal nutrition for growth, minimal stress, as well as no additional motion reductions occurring, is not always realistic.

If we acquire reduced movement/flexibility in any of these other contributing areas, we then have a reduced capacity for compensation. Furthermore, should any of these supplementary areas be reduced in their ability for movement, we may instinctively call on the others to lengthen even more. With this increased need, further lengthening may then cause strain and pain in the area. This strain and the pain that goes along with it could occur as a singular event or a repeated event that could take some time to be fully experienced. As previously stated, much of this occurs without our awareness and so, painful experiences may arise from what seems to be without cause.

We feel it necessary to, again say, that even if the above were the case, it does not mean this person is going to fall apart into a disassembled skeleton shortly after their hip tightens slightly. Those types of connotations discount the tremendous capacity of the body to manage and heal injuries in the short and long term. We have to be reasonable and understand that you can have small motion losses in parts of the body and if they are never challenged, the person affected may be fine (potentially for their entire life). One thing, however, that most can agree on is that the increased capacity for movement is generally healthier than reduced capacity for movement. With that, we can say that because many parts can add to overall motion, when we improve the movement of one part of the body, other parts improve also. When we use OMT on the whole body, not just the part that hurts, we have a greater tendency to move the whole person. This gives us a greater chance to get the patient moving better as a complete person; being more active and involved in their life and community (again, some things most would agree are signs of health).

In part 3 of this series, we will discuss how pain changes movement, how pain can be experienced widely and subtly, how pain affects stress levels, and how OMT can affect pain [3, 10].

References

  1. Di Nicola V. Degenerative osteoarthritis a reversible chronic disease. Regen Ther. 2020 Aug 15;15:149-160. doi: 10.1016/j.reth.2020.07.007. PMID: 33426213; PMCID: PMC7770340.
  1. Gaffney CJ, Drinkwater A, Joshi SD, O’Hanlon B, Robinson A, Sands KA, Slade K, Braithwaite JJ, Nuttall HE. Short-Term Immobilization Promotes a Rapid Loss of Motor Evoked Potentials and Strength That Is Not Rescued by rTMS Treatment. Front Hum Neurosci. 2021 Apr 26;15:640642. doi: 10.3389/fnhum.2021.640642. PMID: 33981206; PMCID: PMC8107283.
  1. Haller H, Lauche R, Sundberg T, Dobos G, Cramer H. Craniosacral therapy for chronic pain: a systematic review and meta-analysis of randomized controlled trials. BMC Musculoskelet Disord. 2019 Dec 31;21(1):1. doi: 10.1186/s12891-019-3017-y. PMID: 31892357; PMCID: PMC6937867.
  1. Hamaue Y, Nakano J, Sekino Y, Chuganji S, Sakamoto J, Yoshimura T, Origuchi T, Okita M. Immobilization-induced hypersensitivity associated with spinal cord sensitization during cast immobilization and after cast removal in rats. J Physiol Sci. 2013 Nov;63(6):401-8. doi: 10.1007/s12576-013-0277-4. Epub 2013 Jul 2. PMID: 23818166; PMCID: PMC10717811.
  1. Handorf AM, Zhou Y, Halanski MA, Li WJ. Tissue stiffness dictates development, homeostasis, and disease progression. Organogenesis. 2015;11(1):1-15. doi: 10.1080/15476278.2015.1019687. PMID: 25915734; PMCID: PMC4594591.
  1. Kishikawa Y, Kawahara Y, Ohnishi YN, Sotogaku N, Koeda T, Kawahara H, Nishi A. Dysregulation of dopamine neurotransmission in the nucleus accumbens in immobilization-induced hypersensitivity. Front Pharmacol. 2022 Sep 8;13:988178. doi: 10.3389/fphar.2022.988178. PMID: 36160381; PMCID: PMC9493457.
  1. Knight J et al (2019) Effects of bedrest 5: the muscles, joints and mobility. Nursing Times [online]; 115: 4, 54-57.
  1. Lee DR, Therrien E, Song BM, Camp CL, Krych AJ, Stuart MJ, Abdel MP, Levy BA. Arthrofibrosis Nightmares: Prevention and Management Strategies. Sports Med Arthrosc Rev. 2022 Mar 1;30(1):29-41. doi: 10.1097/JSA.0000000000000324. PMID: 35113841; PMCID: PMC8830598.
  1. Ramos MS, Pasqualini I, Surace PA, Molloy RM, Deren ME, Piuzzi NS. Arthrofibrosis After Total Knee Arthroplasty: A Critical Analysis Review. JBJS Rev. 2023 Dec 11;11(12). doi: 10.2106/JBJS.RVW.23.00140. PMID: 38079496.
  1. Rehman, Yasir, Ferguson, Hannah, Bozek, Adelina, Blair, Joshua, Allison, Ashley and Johnston, Robert. “Osteopathic Manual Treatment for Pain Severity, Functional Improvement, and Return to Work in Patients With Chronic Pain” Journal of Osteopathic Medicine, vol. 120, no. 12, 2020, pp. 888-906.
  1. Salduker S, Allers E, Bechan S, Hodgson RE, Meyer F, Meyer H, Smuts J, Vuong E, Webb D. Practical approach to a patient with chronic pain of uncertain etiology in primary care. J Pain Res. 2019 Sep 3;12:2651-2662. doi: 10.2147/JPR.S205570. PMID: 31564957; PMCID: PMC6731975.
  1. Solan, Matthew. “Stopping pain before it turns chronic.” Harvard Health Publishing, Jan. 2023, www.health.harvard.edu/pain/stopping-pain-before-it-turns-chronic?utm_source=chatgpt.com. Accessed 29 Jan. 2025.
  1. Stathokostas L, McDonald MW, Little RM, Paterson DH. Flexibility of older adults aged 55-86 years and the influence of physical activity. J Aging Res. 2013;2013:743843. doi: 10.1155/2013/743843. Epub 2013 Jun 19. PMID: 23862064; PMCID: PMC3703899.
  1. Stožer A, Vodopivc P, Križančić Bombek L. Pathophysiology of exercise-induced muscle damage and its structural, functional, metabolic, and clinical consequences. Physiol Res. 2020 Aug 31;69(4):565-598. doi: 10.33549/physiolres.934371. Epub 2020 Jul 16. PMID: 32672048; PMCID: PMC8549894.
  1. van der Miesen, Maite M.a,*; Joosten, Elbert A.a,b; Kaas, Amanda L.c; Linden, David E.J.d; Peters, Judith C.c; Vossen, Catherine J.a,b. Habituation to pain: self-report, electroencephalography, and functional magnetic resonance imaging in healthy individuals. A scoping review and future recommendations. PAIN 165(3):p 500-522, March 2024. | DOI: 10.1097/j.pain.0000000000003052
  1. van der Miesen MM, Vossen CJ, Joosten EA. Habituation to Pain in Patients with Chronic Pain: Clinical Implications and Future Directions. J Clin Med. 2023 Jun 27;12(13):4305. doi: 10.3390/jcm12134305. PMID: 37445339; PMCID: PMC10342770.
  1. Verhaar J. B | Degenerative and Inflammatory Joint Diseases. In: Verhaar JAN, Kjærsgaard-Andersen P, Limb D, et al., editors. The EFORT White Book: “Orthopaedics and Traumatology in Europe” [Internet]. Lowestoft (UK): Dennis Barber Ltd; 2021. Available from: https://www.ncbi.nlm.nih.gov/books/NBK585963/
  1. Wang B, Zhong JL, Xu XH, Shang J, Lin N, Lu HD. Incidence and risk factors of joint stiffness after Anterior Cruciate Ligament reconstruction. J Orthop Surg Res. 2020 May 14;15(1):175. doi: 10.1186/s13018-020-01694-7. PMID: 32410648; PMCID: PMC7227360.
  1. Wilke, J., & Behringer, M. (2021). Is “Delayed Onset Muscle Soreness” a False Friend? The Potential Implication of the Fascial Connective Tissue in Post-Exercise Discomfort. International Journal of Molecular Sciences, 22(17), 9482. https://doi.org/10.3390/ijms22179482
  1. Wilke J, Macchi V, De Caro R, Stecco C. Fascia thickness, aging and flexibility: is there an association? J Anat. 2019 Jan;234(1):43-49. doi: 10.1111/joa.12902. Epub 2018 Nov 11. PMID: 30417344; PMCID: PMC6284431.
  1. Yohei Hamaue, Jiro Nakano, Yuki Sekino, Sayaka Chuganji, Junya Sakamoto, Toshiro Yoshimura, Minoru Okita, Tomoki Origuchi, Effects of Vibration Therapy on Immobilization-Induced Hypersensitivity in Rats, Physical Therapy, Volume 95, Issue 7, 1 July 2015, Pages 1015–1026, https://doi.org/10.2522/ptj.20140137