UNDERSTANDING CHRONIC PAIN

The Low Back Pain Algorithm; Kieran Macphail

2 days ago

6.8 Posture and Chronic Low Back Pain

The links between posture and low back pain is contentious at best (Hamberg-van Reenen et al 2007).
Diek et al (1985) investigated elevation of one shoulder, elevation of one hip, and deviation of the spine from the midline of the body in adolescents. None of these parameters nor the physical education department evaluations were associated with a subsequent report of low-back pain, mid-back pain, or neck pain.
Chaléat-Valayer et al. (2011) evaluated sagittal spino-pelvic alignment in 198 patients with chronic LBP and 709 normal subjects. The two cohorts were compared with respect to the sacral slope, pelvic tilt, pelvic incidence, lumbar lordosis, lumbar tilt, lordotic levels, thoracic kyphosis, thoracic tilt, kyphotic levels, and lumbosacral joint angle. They found sacral slope, pelvic incidence, lumbar tilt, lordotic levels, thoracic tilt and lumbosacral angle were significantly different in chronic low back pain patients compared to healthy subjects. Pelvic tilt, lumbar lordosis and kyphotic levels were not. In particular a greater proportion of patients with chronic low back pain had low sacral slope and lordotic levels associated with a small pelvic incidence, while a greater proportion of normal subjects presented normal or high sacral slope associated with normal or high pelvic incidence.
Laird et al (2018) identified 4 different sub groups of lumbar kinematics in a mixed sample of those with and without LBP. These patterns could be described as standard (26% LBP), lumbar dominant (71% LBP), pelvic dominant (83%) and guarded (100%). Significant post-hoc differences were seen between subgroups for most lumbo-pelvic kinematic and EMG parameters. There was greater direction-specific pain and activity limitation scores for subgroup 4 compared to other groups, and a greater percentage of people with leg pain in subgroups 2 and 4.
Misir et al (2018) measured spinal parameters in 20 standing-induced low back pain developers and 18 non-pain developers. They tookplain radiographs to assess upright standing posture, lumbar lordosis, lumbosacral lordosis, L1/L2 and L5/S1 intervertebral (IV) joint angles, pelvic incidence, pelvic tilt and sacral slope. There were no significant differences in terms of age, BMI, SF-36 score, or Oswestry Disability Index scores between groups. Pain developers had significantly larger lumbar lordosis, larger L1/L2 intervertebral angles, larger pelvic incidences and sacral slopes in all postures. The contribution of L5/S1 intervertebral angle to lumbar flexion was higher than that of the L1/L2 intervertebral angle during stair descent, the sitting and the leaning forward while sitting postures.
Nowotny et al (2011) assessed body posture in 125 persons: 39 adults with a childhood history of scoliosis, 39 midwives, and 47 physiotherapists. In midwives and physiotherapists, body position during work-related tasks was also evaluated. Over 80% of the participants suffered from spinal pain, with 85% in those with a history of scoliosis. In most cases, the pain was located in the lumbar spine and intermittent. The occurrence of pain among midwives and physiotherapists was not directly associated with the body position during work-related tasks.

6.8.1 Adult Spinal Deformity
Pellisé et al (2015) defined adult spinal deformity as scoliosis >20°, sagittal vertical axis >5 cm, pelvic tilt >25° or thoracic kyphosis >60°.
Pellisé et al (2015) used the International Quality of Life Assessment project data. This included data from 24,936 people, SF-36 scores of patients with self-reported arthritis, chronic lung disease, diabetes and congestive heart failure from 8 industrialized countries, 3 continents (Alonso et al. 2004). They compared this date with the SF-36 baseline data of consecutive patients with adult spinal deformity enrolled in a prospective multicentre international database in patients age >18 years that met their criteria above for adult spinal deformity. 766 patients (mean age 45.8 years) met the inclusion criteria for adult spinal deformity. The scores on all SF-36 domains were lower in adult spinal deformity patients than in any other chronic condition. Differences between adult spinal deformity and the other chronic conditions were always greater than the reported minimal clinically important differences. Physical function, role physical and pain domains showed the worst scores. Surgical candidates with adult spinal deformity displayed the worst health related quality of life scores and patients previously operated the best, however, even the latter remained worse than any scores for the other self-reported chronic conditions.
Although, the severity of the deformity is not associated with health related quality of life (Takemoto et al 2017).

References
Alonso et al 2004. Qual Life Res Int J Qual Life Asp Treat Care Rehabil 13:283-298.
Chaléat-Valayer, E., Mac-Thiong, J.M., Paquet, J., Berthonnaud, E., Siani, F. and Roussouly, P., 2011. Sagittal spino-pelvic alignment in chronic low back pain. European spine journal, 20(5), p.634.
Dieck, G.S., Kelsey, J.L., Goel, V.K., Panjabi, M.M., Walter, S.D. and Laprade, M.H., 1985. An epidemiologic study of the relationship between postural asymmetry in the teen years and subsequent back and neck pain. Spine, 10(10), pp.872-877.
Hamberg-van Reenen, H.H., Ariëns, G.A., Blatter, B.M., van Mechelen, W. and Bongers, P.M., 2007. A systematic review of the relation between physical capacity and future low back and neck/shoulder pain. Pain, 130(1-2), pp.93-107.
Laird, R.A., Keating, J.L. and Kent, P., 2018. Subgroups of lumbo-pelvic flexion kinematics are present in people with and without persistent low back pain. BMC musculoskeletal disorders, 19(1), p.309.
Misir, A., Kizkapan, T.B., Tas, S.K. et al. Lumbar spine posture and spinopelvic parameters change in various standing and sitting postures. Eur Spine J (2018). doi.org/10.1007/s00586-018-5846-z
Nowotny, J., Nowotny-Czupryna, O., Brzęk, A., Kowalczyk, A. and Czupryna, K., 2011. Body posture and syndromes of back pain. Ortopedia, traumatologia, rehabilitacja, 13(1), pp.59-71.
Pellisé, F., Vila-Casademunt, A., Ferrer, M., Domingo-Sàbat, M., Bagó, J., Pérez-Grueso, F.J., Alanay, A., Mannion, A.F., Acaroglu, E. and European Spine Study Group, 2015. Impact on health related quality of life of adult spinal deformity (ASD) compared with other chronic conditions. European Spine Journal, 24(1), pp.3-11.
Takemoto, M., Boissière, L., Vital, J.M., Pellisé, F., Perez-Grueso, F.J.S., Kleinstück, F., Acaroglu, E.R., Alanay, A. and Obeid, I., 2017. Are sagittal spinopelvic radiographic parameters significantly associated with quality of life of adult spinal deformity patients? Multivariate linear regression analyses for pre-operative and short-term post-operative health-related quality of life. European Spine Journal, 26(8), pp.2176-2186. ...

The Low Back Pain Algorithm; Kieran Macphail

1 week ago

1.3.3.3 Theoretical Basis for Aerobic and anaerobic Exercise for Chronic Low Back Pain

Of the lifestyle components physical activity is the best researched and the superiority of advice to stay active over bed rest has been discussed extensively (Waddel et al. 1997, Hilde et al. 2002). A 2017 Cochrane review of exercise for CLBP found a reduction in pain severity and improved physical function with few adverse events, though these were mostly of small‐to‐moderate effect, and were not consistent across the reviews (Geneen et al 2017). There were variable effects for psychological function and quality of life. Unfortunately the quality of the evidence examining physical activity and exercise for chronic pain is low. Furthermore the specifics and methods for individualising exercise selection are contentious (Van Middlekoop et al. 2010). The modern guidelines are placing more emphasis on early return to work even when pain persists (Koes et al. 2010). Similarly, ergonomic interventions are commonly recommended and assist in return to work (Anema et al. 2004), improving posture and reducing LBP incidence (Pillastrini et al. 2010). ...

The Low Back Pain Algorithm; Kieran Macphail

2 weeks ago

From 9.4.4 Inflammation and Psychosocial Symptoms in Low Back Pain in causes

Inflammation signals the brain to induce sickness behaviours and negative affect (Walker et al. 2014). This partially occurs, as there is some active transport of cytokines across the blood brain barrier. With increased levels of systemic inflammation, active transport of cytokines across the blood brain barrier is increased further. Peripherally cytokines interact with afferent nerves which propogate signals to their primary projection area. For example the nucleus of the tractus solitarius for vagal afferents. From here it propagates to secondary projections including the paraventricular nucleus of the hypothalamus and the central nucleus of the amygdala. In addition microglial cells produce cytokines in response to peripheral inflammation via volume transmission (Brady et al. 1994).
Tissue damage in the body is responded to by two main systems, pathogen associated molecular patterns (PAMPs) and damage associated molecular patterns (DAMPs). In a cold it is PAMPs that give rise to the illness behaviour associated with having cold symptoms. With back pain it is DAMPs that give rise to the illness behaviours.
The association between peripheral inflammation and depression was initially established in patients undergoing cytokine therapy. Immune stimulating therapies such interferon therapy in those with hepatitis C or malignant melanoma produced initial sickness behaviour and then a transition to depression in many patients (Raison et al. 2007). Capuron et al. (2002) established that the anti-depressant paroxetine only reduces sickness behaviours and not the cognitive and affective aspects of depression. It appears that it is prolonged elevated levels of inflammation that are required for the transition of sickness behaviour in to depression. Obviously there are multiple mechanisms interacting here and to focus on one to the exclusion of others would be negligent clinically.
In healthy individuals typhoid vaccination induces negative mood post-vaccination (Wright et al., 2005), stops the normally occurring improvement in mood as the day progresses (Strike et al., 2004), increases brain activity in depression-related regions such as the subgenual cingulate cortex, and decreases its connectivity to the amygdala, medial prefrontal cortex, and nucleus accumbens (Harrison et al., 2009). Similarly, in healthy mice increasing levels of inflammation induce initial sickness behaviours which subside and transition to depressive symptoms following prolonged increased inflammatory levels (O’Connor et al. 2009).
Inflamamtion is closely linked to the pain experience. Whilst peripheral inflammation can propogate signals to key brain areas involved in pain discussed above such as the central nucleus of the amygdala, pro-inflammatory cytokines lower nociceptor thresholds (Walker et al. 2014). Further low levels of anti-inflammatory cytokines, such as Il-10 may also lower nociceptor thresholds (Uceyler et al. 2006).

Norman et al (2010) investigated the effects of social isolation on depressive symptoms in mice post nerve injury. Only the socially isolated mice developed depression and increased inflammation in the brain seven days later as measured by Interleukin-1β. Mice that underwent social isolation but received oxytocin did not develop increased inflammation or depression. Conversely, mice that were socialising but received an oxytocin antagonist developed depression and elevated brain Interleukin-1β.
Eisenberg et al (2010) exposed participants to an endotoxin or placebo and measured hourly reports of “fatigue”, “I feel disconnected from others” and “I feel unhappy”, as well as TNF-α and IL-6. The endotoxin increased feelings of fatigue and unhappiness in relation to the increase in inflammatory markers. Feelings of social disconnection and unhappiness peaked at the same time. Controlling for social disconnection eliminated the relationship between fatigue and unhappiness, suggesting a mediating role for social disconnection from increased peripheral inflammation in sickness behaviour.
Tryptophan is required for the production of the “happy” neurotransmitter serotonin. Decreases in tryptophan have been theorised cause depressive symptoms and there is some support for this (Research). Under increased levels of systemic inflammation there is increased activity of indoleamine 2,3-dioxygenase, an enzyme that converts tryptophan in to kynurenine, Thus there is less available for serotonin production. In animal studies the induction of inflammation has been shown to produce increase indoleamine 2,3-dioxygenase activity, decreased circulating tryptophan and a progression from sickness behaviour to depression (O’Connor 2009).
Increased activity of indoleamine 2,3-dioxygenase ultimately leads to an increase in the NMDA receptor agonist quinolinic acid. Increased glutamate and its receptor subtypes including NMDA have been implicated in the development of both chronic pain and depression (Mitani et al 2006). Glutamate is primary neurotransmitter in nociceptor afferents.
Slavich and Irwin (2014) outline a social signal transduction theory of depression. They highlight how the conserved transcriptional response to adversity, which allowed us to survive threats in our past environment, is now activated in response to social stresses. The conserved transcriptional response causes up-regulation of proinflammatory immune response genes, which combat extracellular pathogens and wound-related bacterial infections, and down-regulation of antiviral immune response genes, which target intracellular pathogens such as viruses. This redeployment of the leukocyte basal transcriptome is adaptive in the context of actual physical threat because it enhances wound healing and recovery from injury and infection. The conserved transcriptional response can also be activated by modern-day social, symbolic, anticipated, and imagined threats, contributing to chronic inflammation.
(see Antoni et al., 2012; S. W. Cole et al., 2012; Fredrickson et al., 2013; Irwin & Cole, 2011; Powell et al., 2013; Slavich & Cole, 2013).
www.ncbi.nlm.nih.gov/pmc/articles/PMC4006295/

This evidence clearly indicates the role of peripheral inflammation to directly impact our behaviour. This needs to be viewed within a broad context and the central process contributing to illness behaviours must also be considered. Nonetheless this information can be powerful for patients in taking the pressure off themselves to change these behaviours under the illusion that they are 100% under our control. This can be quite empowering in a perverse way and allows for a more open and honest discussion of these behaviours with patients as the pressure for responsibility and feelings of being judged are decreased.

References
Butler, D.S., Moseley, G.L. (2013) Explain Pain. London: Noigroup Publications.
Capuron, L., Ravaud, A., Neveu, P.J., Miller, A.H., Maes, M. and Dantzer, R., 2002. Association between decreased serum tryptophan concentrations and depressive symptoms in cancer patients undergoing cytokine therapy. Molecular psychiatry, 7(5), 468.
Dell’Osso, L., Carmassi, C., Mucci, F. and Marazziti, D., 2016. Depression, Serotonin and Tryptophan. Current pharmaceutical design, 22(8), 949-954.
Eisenberger, N.I., Inagaki, T.K., Mashal, N.M. and Irwin, M.R., 2010. Inflammation and social experience: an inflammatory challenge induces feelings of social disconnection in addition to depressed mood. Brain, behavior, and immunity, 24(4), pp.558-563.
Gallagher, P.J., Castro, V., Fava, M., Weilburg, J.B., Murphy, S.N., Gainer, V.S., Churchill, S.E., Kohane, I.S., Iosifescu, D.V., Smoller, J.W. and Perlis, R.H., 2012. Antidepressant response in patients with major depression exposed to NSAIDs: a pharmacovigilance study. American Journal of Psychiatry, 169(10), 1065-1072.
Glattacker, M., Heyduck, K., Meffert, C. (2013) Illness beliefs and treatment beliefs as predictors of short-term and medium-term outcome in chronic back pain. Rehabilitation Medicine, 45(3): 268-76.
Grimmer-Somers, K., Prior, M., Robertson, J. (2008) Yellow flag scores in a compensable New Zealand cohort suffering acute low back pain. Journal of pain Research, 1:15-25.
Hänsel, A., Hong, S., Cámara, R.J. and Von Kaenel, R., 2010. Inflammation as a psychophysiological biomarker in chronic psychosocial stress. Neuroscience & Biobehavioral Reviews, 35(1), 115-121.
Harrison, N.A., Brydon, L., Walker, C., Gray, M.A., Steptoe, A. and Critchley, H.D., 2009. Inflammation causes mood changes through alterations in subgenual cingulate activity and mesolimbic connectivity. Biological psychiatry, 66(5), 407-414.
Iyengar, R.L., Gandhi, S., Aneja, A., Thorpe, K., Razzouk, L., Greenberg, J., Mosovich, S. and Farkouh, M.E., 2013. NSAIDs are associated with lower depression scores in patients with osteoarthritis. The American journal of medicine, 126(11), 1017-e11.
Koes, B.W., van Tulder, M., Lin, C.W.C., Macedo, L.G., McAuley, J., Maher, C. (2010) An updated overview of clinical guidelines for the management of non-specific low back pain in primary care. European Spine Journal, 19(12): 2075-2094.
Miller, G.E., Brody, G.H., Yu, T. and Chen, E., 2014. A family-oriented psychosocial intervention reduces inflammation in low-SES African American youth. Proceedings of the National Academy of Sciences, 111(31), 11287-11292.
Mitani, H., Shirayama, Y., Yamada, T., Maeda, K., Ashby, C. R., & Kawahara, R. (2006). Correlation between plasma levels of glutamate, alanine and serine with severity of depression. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 30(6), 1155-1158.
Moseley, G.L. (2007) Reconceptualising pain according to modern pain science. Physical Therapy Reviews, 12(3): 169-178.
Norman, G. J., Karelina, K., Morris, J. S., Zhang, N., Cochran, M., & DeVries, A. C. (2010). Social interaction prevents the development of depressive-like behavior post nerve injury in mice: a potential role for oxytocin. Psychosomatic medicine, 72(6), 519-526.
Nicholas, M. K., Linton, S. J., Watson, P. J., Main, C. J. (2011) Early identification and management of psychological risk factors (“yellow flags”) in patients with low back pain: a reappraisal. Physical Therapy, 91 (5): 737-753.
O’Connor JC, André C, Wang Y, Lawson MA, Szegedi SS, Lestage J, Castanon N, Kelley KW, and Dantzer R
(2009) Interferon-γ and tumor necrosis factor-α mediate the upregulation of indoleamine 2,3-dioxygenase and the induction of depressive-like behavior in mice in response to bacillus Calmette-Guerin. J Neurosci 29:4200–4209.
Raison, C.L., Woolwine, B.J., Demetrashvili, M.F., Borisov, A.S., Weinreib, R., Staab, J.P., Zajecka, J.M., Bruno, C.J., Henderson, M.A., Reinus, J.F. and Evans, D.L., 2007. Paroxetine for prevention of depressive symptoms induced by interferon‐alpha and ribavirin for hepatitis C. Alimentary pharmacology & therapeutics, 25(10), 1163-1174.
Slavich, G.M. and Irwin, M.R., 2014. From stress to inflammation and major depressive disorder: a social signal transduction theory of depression. Psychological bulletin, 140(3), p.774.
Strike, P.C., Wardle, J. and Steptoe, A., 2004. Mild acute inflammatory stimulation induces transient negative mood. Journal of psychosomatic research, 57(2), 189-194.
Üçeyler, N., Valenza, R., Stock, M., Schedel, R., Sprotte, G., & Sommer, C. (2006). Reduced levels of antiinflammatory cytokines in patients with chronic widespread pain. Arthritis & Rheumatology, 54(8), 2656-2664.
Walker, A.K., Kavelaars, A., Heijnen, C.J. and Dantzer, R., 2014. Neuroinflammation and comorbidity of pain and depression. Pharmacological reviews, 66(1), 80-101.
Watson, P., Kendall, N. (2000) Assessing psychosocial yellow flags. Topical issues in pain, 2: 111-129.
Wright, C.E., Strike, P.C., Brydon, L. and Steptoe, A., 2005. Acute inflammation and negative mood: mediation by cytokine activation. Brain, behavior, and immunity, 19(4), 345-350. ...