Lumbar Spine Current Concepts PDF

The Lumbar Spine: Evidence-Informed Physical Therapy Patient Management Independent Study Course 31.2.8 Max Jordon, PT, DPT, PhD Assistant Professor...

The Lumbar Spine: Evidence-Informed Physical Therapy Patient Management Independent Study Course 31.2.8 Max Jordon, PT, DPT, PhD Assistant Professor Department of Physical Therapy College of Health Education and Professional Studies University of Tennessee at Chattanooga Chattanooga, Tennessee  The Lumbar Spine: Evidence-Informed Physical Therapy Patient Management Guy G. Simoneau, PT, PhD, FAPTA—Editor Gordon Riddle, PT, DPT, ATC, OCS, SCS, CSCS—Associate Editor Cover Illustration by Joseph Kinstler Dear Colleagues, I am pleased to welcome you to The Lumbar Spine: Evidence-Informed Physical Therapy Patient Management monograph written by Max Jordon, PT, DPT, PhD. This work is part of the Academy of Orthopaedic Physical Therapy Independent Study Course series 31.2, Cur- rent Concepts of Orthopaedic Physical Therapy, 5th Edition. Dr. Jordon graduated with his Doctor of Physical Therapy degree from the University of South Carolina in 2011. After working as a full- time clinician in an outpatient orthopedic practice, he returned to the University of South Carolina to work on his PhD in Rehabilitation Sciences. His predoctoral work focused primarily on the interactions between pain and motor control using functional magnetic reso- nance imaging in individuals with chronic low back pain. While he was working on his PhD, he continued to work in the clinic where he started to specialize in chronic pain and low back pain management. Dr. Jordon completed his PhD in 2019, at which time he joined the University of Tennessee at Chattanooga as an Assistant Professor of Physical Therapy. At the University of Tennessee at Chattanooga, he is part of the orthopedic faculty with a focus on teaching spine and upper extremity disorders. He continues to see patients in the student pro bono clinic and is actively engaged in research as it relates to motor control in the lumbar spine. In this monograph, the author provides a contemporary, evidence-based perspective on the management of acute and chronic low back pain. The monograph begins with practical information on screening for red and yellow flags. Incorporated in the discussion of yellow flags are the limitations of the pathoanatomical model for the treatment of low back pain and strategies to manage these patients effi- ciently within a biopsychosocial context. The author then presents factors that contribute to the transition from acute to chronic low back pain, with a particular focus on preventing that transition. A discussion of the physical examination follows, in the context of the limited ability to make a pathoanatomical diagnosis for most people with acute or chronic low back pain. An overview of evidence-based treat- ment options for low back pain, differentiating between acute and chronic conditions, is then provided. For additional clinical context, the monograph concludes with pertinent clinical scenarios. I am confident that readers will find value in this monograph, which summarizes the management of a common yet complex condition in a practical manner. My sincere thanks to the author for his contribution to the Current Concepts series. Sincerely, Guy Simoneau, PT, PhD, FAPTA Editor 2920 East Avenue South, Suite 200 | La Crosse, WI 54601 | Office 608-788-3982 | Toll Free 800-444-3982 | Fax 608-788-3965  TABLE OF CONTENTS ACRONYM LIST.................................................................................................................................................................................................................5 ABSTRACT...........................................................................................................................................................................................................................7 LEARNING OBJECTIVES...............................................................................................................................................................................................7 BACKGROUND.................................................................................................................................................................................................................7 Prevalence and Chronicity.............................................................................................................................................................. 7 The economic and health burden of low back pain is still on the rise..................................................................................... 7 The burden of low back pain is not borne equally in our society............................................................................................. 8 Take home messages............................................................................................................................................................... 8 Pathophysiology............................................................................................................................................................................. 8 Acute and chronic low back pain are very different................................................................................................................. 8 The natural history of acute low back pain.............................................................................................................................. 8 The natural history of chronic low back pain.......................................................................................................................... 9 Structural changes associated with low back pain.................................................................................................................... 9 The lumbar intervertebral discs are integral to the spine.......................................................................................................... 9 Disc degeneration occurs naturally and does not always result in pain................................................................................... 10 How do we differentiate an asymptomatic degenerative disc from a symptomatic one?......................................................... 10 A disc by any other name….................................................................................................................................................. 11 What role does a herniated (or bulging) disc play in low back pain?...................................................................................... 11 Herniated discs get better with time...................................................................................................................................... 12 The potential role of endplate changes in low back pain........................................................................................................ 12 Structural changes in the central nervous system can occur with low back pain..................................................................... 12 Changes in gray matter volume can reverse with treatment................................................................................................... 13 Wrapping it up: What are the structural causes of low back pain?......................................................................................... 13 Non-structural changes occur in individuals with low back pain........................................................................................... 15 People with low back pain commonly suffer from psychological comorbidities..................................................................... 17 Predictors for transition from acute to chronic low back pain............................................................................................... 18 Take home messages............................................................................................................................................................. 20 EVIDENCE-BASED GUIDELINES...........................................................................................................................................................................20 What Makes the “Best Evidence”?................................................................................................................................................ 20 The Benefits of Evidence-Based Guidelines.................................................................................................................................. 20 Limitations of Evidence-Based Guidelines.................................................................................................................................... 21 Take Home Message.................................................................................................................................................................... 21 PHYSICAL THERAPY EVALUATION.....................................................................................................................................................................21 Physical Therapist Screening Flags................................................................................................................................................ 21 Red flags and their use to screen for serious medical conditions............................................................................................ 21 Academy of Orthopaedic Physical Therapy, APTA. For personal use only. No other uses without permission. 3 © 2021 Academy of Orthopaedic Physical Therapy, APTA, Inc. All rights reserved.  Yellow flags can help with patient prognosis.......................................................................................................................... 22 Components of the Assessment.................................................................................................................................................... 23 The challenge of using special tests to diagnose pathophysiology in the spine........................................................................ 23 Neurological examination..................................................................................................................................................... 24 Physical examination............................................................................................................................................................ 24 Take Home Messages................................................................................................................................................................... 25 Movement-Based Classification Systems....................................................................................................................................... 25 PHYSICAL THERAPY INTERVENTIONS.............................................................................................................................................................26 Physical Therapists are Effective in Treating Low Back Pain.......................................................................................................... 26 The Evidence (For Once) is Conclusive: Exercise is Good............................................................................................................ 26 Manual Therapy to the Lumbar Spine can be a Valuable Addition to Exercise.............................................................................. 27 Mobilization and manipulation............................................................................................................................................. 28 Dry needling......................................................................................................................................................................... 29 Educating Patients is Important in Physical Therapy.................................................................................................................... 30 Patients with chronic low back pain benefit from education that is specific to their condition............................................... 30 Patients with acute low back pain require a different type of education................................................................................. 30 Take Home Message.................................................................................................................................................................... 31 The Environment in Which Physical Therapists Provide Treatment can be a Powerful Factor in Rehabilitation............................ 31 Factors we cannot control: the impact of the built environment and the health care setting in which one works................... 31 Factors we can control: therapeutic alliance can play a key role in a patient’s rehabilitation.................................................. 32 Novel Interventions that are Gaining Popularity......................................................................................................................... 33 FUTURE DIRECTIONS AND ADDITIONAL THOUGHTS.............................................................................................................................34 Take Home Messages................................................................................................................................................................... 35 SUMMARY........................................................................................................................................................................................................................35 CASE SCENARIOS.........................................................................................................................................................................................................35 Case Scenario 1............................................................................................................................................................................ 35 Case Scenario 2............................................................................................................................................................................ 36 Case Scenario 3............................................................................................................................................................................ 37 Case Scenario 4............................................................................................................................................................................ 38 REFERENCES..................................................................................................................................................................................................................39 Opinions expressed by the author are his own and do not necessarily reflect the view of the Academy of Orthopaedic Physical Therapy. The author declares no conflict of interest. The publishers have made every effort to trace the copyright holders for borrowed material. If we have inadvertently overlooked any, we would be willing to correct the situation at the first opportunity. © 2021, Academy of Orthopaedic Physical Therapy. For personal use only. No other uses without permission. Course content is not intended for use by participants outside the scope of their license or regulations. Academy of Orthopaedic Physical Therapy, APTA. 4 For personal use only. No other uses without permission. © 2021 Academy of Orthopaedic Physical Therapy, APTA, Inc. All rights reserved.  ACRONYM LIST aLBP: acute low back pain CBT: cognitive behavioral therapy CI: confidence interval cLBP: chronic low back pain CPM: conditioned pain modulation CS: comparable sign DD: disc degeneration DDD: degenerative disc disease DLPFC: dorsal lateral prefrontal cortex DNIC: diffuse noxious inhibitory control EMG: electromyographic FABQ: Fear-Avoidance Beliefs Questionnaire GM: gray matter GMV: gray matter volume HIZ: high intensity zone HR: hazard ratio IVD: intervertebral disc LBP: low back pain MBC: Movement Based Classification MDQ: Modified low back pain Disability Questionnaire (Oswestry) MDT: Mechanical Diagnosis and Therapy MBSR: Mindfulness Based Stress Reduction mPFC: medial prefrontal cortex MRI: magnetic resonance imaging NA: nucleus accumbens -LR: negative likelihood ratio NPRS: numerical pain rating scale NSAIDs: non-steroidal anti-inflammatory drugs OMPQ: Orebro Musculoskeletal Pain Questionnaire OSPRO: Optimal Screening for Prediction of Referral and Outcome OSPRO-ROS: Optimal Screening for Prediction of Referral and Outcome – Review of Systems OSPRO-YF: Optimal Screening for Prediction of Referral and Outcome – Yellow Flag PCC: posterior cingulate cortex PCS: Pain Catastrophizing Scale PIPT: psychologically informed physical therapy PNE: pain neuroscience education +LR: positive likelihood ratio RCT: randomized controlled trial RMDQ: Roland Morris Disability Questionnaire rLBP: recurrent low back pain ROM: range of motion SBT: STarT Back Screening Tool SES: socioeconomic status SMT: spinal manipulative therapy TBC: Treatment-Based Classification TENS: transcutaneous electrical nerve stimulation TMS: transcranial magnetic stimulation TSK: Tampa Scale for Kinesiophobia Academy of Orthopaedic Physical Therapy, APTA. For personal use only. No other uses without permission. 5 © 2021 Academy of Orthopaedic Physical Therapy, APTA, Inc. All rights reserved. 6 The Lumbar Spine: 5.  escribe the predictors for the transition of acute to cLBP D and how to use the different outcome measures discussed. Evidence-Informed Physical 6. Use evidence-based clinical guidelines in the treatment of Therapy Patient Management patients with acute and cLBP. 7. Detect yellow and red flags and understand their clinical Max K. Jordon, PT, DPT, PhD implications. University of Tennessee at Chattanooga 8. Integrate into clinical practice the research behind common Chattanooga, Tennessee physical therapy interventions such as: motor control ex- ercises, graded activity/exposure, directional-based exercise ABSTRACT approaches, aerobic exercise, spinal manipulation/mobili- Physical therapists are uniquely positioned in the health zation, dry needling, and education. care system to treat individuals with low back pain (LBP). This 9. Differentiate between pathoanatomical education and pain monograph highlights some of the best available evidence as neuroscience education and the clinical utility of each. it relates to the role of physical therapy in the evaluation and 10. Discuss the importance of the therapeutic alliance and management of LBP. The current research suggests that despite strategies to incorporate this alliance into clinical practice. the great advances in treatment, the overall prevalence of LBP and LBP-related disability seem to be largely unchanged. This BACKGROUND monograph will review the evidence regarding the validity and Prevalence and Chronicity importance of structural abnormalities as determined by mag- The economic and health burden of low back pain netic resonance imaging, and what functional changes are com- is still on the rise monly present in patients with chronic LBP (cLBP). Since the As it relates to the musculoskeletal system, there is no con- last edition of Current Concepts for Orthopaedic Physical Therapy dition more prevalent or costly as low back pain (LBP).1,2 The was published, updated evidence-based guidelines have been prevalence and disability rate of LBP continues to rise1,3,4 while published and will be reviewed in this monograph. Up-to-date the economic burden to the United States economy remains information regarding clinical outcome measures like the Opti- great.5,6 It is estimated that the United States spends approxi- mal Screening for Prediction of Referral and Outcome and how mately $90 billion annually on the treatment of LBP alone.7 they can be incorporated into physical therapy practice will be According to the Global Burden of Disease Study,1 LBP was reviewed. The evidence behind a variety of treatment interven- a third-tier cause of disability in 1990. Fast-forward 27 years, tions will be assessed including various exercise approaches and in the 2017 update, disability caused by LBP increased by manual therapy techniques. In addition, the role of education 30% to claim the prominent number 1 condition of disability and emerging treatment strategies will be discussed. Following among industrialized nations. In 2009, Freburger et al4 report- the body of this manuscript the reader will be presented with 4 ed that the percent of the population suffering from chronic case scenarios, each will require strong clinical reasoning skills as LBP (cLBP) rose from 3.9% to 10.2% between 1990 and 2006. well as an understanding of the current evidence for the proper Disability rates have also increased; during a similar time period treatment and evaluation of the patient. These case scenarios years lived with disability increased by almost 25%.8 Chronic will include patients who have both acute and cLBP with ac- LBP is also the most common reason for both physician9 and companying psychosocial risk factors. physical therapy visits.10 For these reasons, LBP remains an im- portant focus of physical therapy practice. Key Words: education, flags, psychosocial, treatment While the impact of LBP is indisputably high, the exact prevalence of the condition at any given time is difficult to de- LEARNING OBJECTIVES termine. A recent systematic review by Hoy et al3 estimated the Upon completion of this monograph, the course partici- point prevalence of LBP (defined as the amount of people with pant will be able to: this condition at any given time) to be 11.9%. However, esti- 1. Describe the prevalence of low back pain (LBP), the dif- mates of LBP can vary widely in the literature and are largely ferences between the point estimates of acute and chronic determined by the window of observation used. For example, LBP (cLBP), and how racial and socioeconomic factors can in 2002, Deyo et al9 reported that 26.4% of the population contribute to the conditions. experienced LBP in the last 3 months. This finding was consis- 2. Discuss the relative role of diagnostic imaging and the clin- tent with findings by Yang et al11 who, using a similar 3-month ical implications of positive findings. window of observation, reported the prevalence of LBP in 2010 3. Discuss the different structural and functional changes that to be 25.7%. However, when one expands the window of ob- can occur with cLBP and the implications of each. servation to 1 year, the incidence of LBP can rise to 65%.12 Life- 4. Understand the impact of psychosocial risk factors in LBP time prevalence of LBP can range between 70% and 84%.12,13 and identify potential treatment approaches to each. Another factor that complicates the estimate of the prevalence Academy of Orthopaedic Physical Therapy, APTA. For personal use only. No other uses without permission. 7 © 2021 Academy of Orthopaedic Physical Therapy, APTA, Inc. All rights reserved. of LBP is the difference between acute and cLBP. While the life- therapists to ensure that equal care and concern is given to all time incidence of LBP is quite high, the prevalence of cLBP is patients regardless of race or sex and that biases, conscious or lower. A recent systematic review of 28 studies by Meucci et al14 unconscious, have no role in the treatment of cLBP. found that the prevalence of cLBP ranged anywhere from 2% to 25.4%. Part of the variability of the reported incidence was secondary to the stratification of different age groups. However, Take Home Messages across the different studies the prevalence in chronic pain typi- The prevalence and burden of LBP continues to rise. cally increased until about the 7th decade of life, at which time Approximately 65% of the population will experience at the prevalence stabilized or reduced slightly. least 1 episode of LBP in a year. The burden of LBP is not borne equally in our soci- The burden of low back pain is not ety, with minorities and women exhibiting greater pain, borne equally in our society greater disability, and poorer treatment. In the above studies, the prevalence of LBP was assessed for the population as a whole. However, there is mounting evidence that the distribution of LBP burden is not equal between race, Pathophysiology sex, and socioeconomic status (SES). While the intent of this Acute and chronic low back pain are very different monograph is not to examine all the interactions between health It should come as no surprise that acute and cLBP are very care and race, sex, and SES, a brief look at some recent studies different conditions. While some arguments exist regarding the is warranted. In 2019, Brandão et al15 found that pain from optimal way to classify pain as “chronic,” according to the re- patients from low-SES was considered less intense and more cent ICD-11 guidelines, chronic pain is “persistent or recurrent likely to be the result of psychological influences compared to pain lasting longer than 3 months.”24 Therefore, throughout patients from high-SES. Viewing someone’s pain as predomi- this monograph we will consider cLBP as pain lasting greater nantely psychological as opposed to physiological might have than 3 months while acute LBP (aLBP) describes a condition the unfortunate side effect of deeming the pain to be less cred- with symptoms occurring for less than 3 months. ible and changing one’s course of treatment. Those with lower SES also experience cLBP and subsequent disability at higher The natural history of acute low back pain rates.16,17 However, low-SES alone does not account for many of The prognosis for aLBP is generally favorable, with reports the inequities in health care as it relates to cLBP. In 2020, An- of complete recovery ranging anywhere from 72% to 90% astas et al18 performed a study where physicians made pain care within a year of diagnosis25-27 (although, it should be mentioned decisions for 12 computer-simulated patients with chronic back that the 90% figure has come under considerable debate).28,29 pain. They found that among patients with low-SES, White pa- One of the most thorough examinations of the typical course of tients were more likely to receive workplace accommodations aLBP was undertaken by Henschke et al in 2008.25 The authors compared to Black patients. Additionally, for patients with high studied a cohort of 973 patients with recent onset LBP and SES, Black patients were more likely to be rated as being in followed their progress over the course of 1 year. As it related distress compared to White patients; indicating greater psycho- to pain, they found that the probability to be pain free after 6 logical influence on their symptoms. While studies have shown weeks was 39.9% and by the end of 1 year that probability rose that White and Black Americans experience cLBP at equal to 72.5%. Interestingly, disability had a better prognosis. By rates19—with the potential of White Americans experiencing the end of 6 weeks the probability of having no disability was cLBP at slightly higher rates13,14—Black Americans experience 54.9% and by the end of 1 year that probability rose to 83.3%. more severe and disabling LBP even independent of SES.19-21 This is an important finding as it highlights that a return-to- Unfortunately, this bias extends into treatment approaches as work criteria for LBP may not need to be a complete resolution well. In 2018, Kohns et al22 assessed treatment outcomes of 600 of symptoms. Rather, it could be argued that individuals with adults from 3 different hospital settings. They found that Black LBP can participate in the workplace even if their pain has yet Americans were less likely to receive advanced imaging and were to completely resolve. less likely to receive opioids. While one might argue that—as Another important concept of aLBP is that recurrence rate will be discussed later on in this monograph—less opioids and is high.28,30,31 Recurrence of aLBP within a year can be as high imaging might inadvertently be better medical care, the paper as 66% to 84%32 with a similar 3-year recurrence rate.33 Even highlighted discrepancies in treatment between races. Black within a shortened time span of 3 months, up to 10.5% of pa- Americans were also found less likely to receive physical therapy tients can have fluctuations in their symptoms.34 This indicates for cLBP.19 Disparities exist across sex as well with females rou- that physical therapy does not necessarily result in a long term tinely experiencing cLBP at higher rates and greater intensities “fix” for LBP for a large portion of patients. Perhaps instead than males.13,14,23 These studies highlight the need for physical physical therapy should be viewed as a means to reduce current Academy of Orthopaedic Physical Therapy, APTA. 8 For personal use only. No other uses without permission. © 2021 Academy of Orthopaedic Physical Therapy, APTA, Inc. All rights reserved. LBP and a potential vehicle by which a patient can improve their self-efficacy in their own pain management. Figure 1. Common Disc Pathologies The natural history of chronic low back pain People with cLBP typically present with more comorbid- ities than do people with aLBP. For example, those with cLBP typically present with symptoms of central sensitization,35,36 structural alterations in the lumbar musculature,37 and even changes in the processing of pain in the brain.38 These changes can make cLBP resistant to treatment,39-42 leading to the long held belief that those with cLBP generally have a poor progno- sis.32,43 However, in 2009, Costa et al44 followed a cohort of 406 patients who developed an initial instance of cLBP. They found that 41% of all participants reported a complete recovery at 1 year and furthermore only 11% were not able to return to work. This information should be used to provide encouragement for those newly diagnosed with cLBP. It shows that many people with cLBP do get better with time and that those experiencing cLBP should not lose hope. For some, however, cLBP continues to be a debilitating condition with which one must live. As is evident from the above examples, these individuals represent the minority of those with back pain. However, they account for an outsized proportion of the health care resources and economic impact. Therefore, the focus of much of this monograph will be on the consequences of cLBP. Structural changes associated with low back pain A, Normal disc. B, Degenerative disc. C, Bulging Structural changes associated with LBP can be thought of disc. D, Herniated (Extruded) disc. E, Tear in poste- in 2 general categories: peripheral and central. Peripheral struc- rior annulus representing pathology of the High In- tures that are thought to be associated with LBP can include tensity Zone. F, Modic change (Type 1). the following: intervertebral disc (IVD), facet joints, ligamen- tous structures (specifically the ligamentum flavum), vertebral bodies (fractures, spondylolysis, etc), and the lumbar paraspinal musculature.45 It is not the intent of this monograph to review A normal, healthy, IVD is composed of 2 primary layers: every possible structural change that can result in LBP. Howev- the outer annulus fibrosus and the inner nucleus pulposus. The er, of the structures listed above, few have been given the atten- outer annulus is comprised of 15-25 concentric layers—lamel- tion that the IVD has (Figure 1). lae—that are primarily composed of Type I cartilage.46,47,49 Each concentric layer is oriented approximately 45o from the trans- The lumbar intervertebral discs are integral to the spine verse plane.47,50 This alternating orientation of the concentric The IVD serves several very important roles in the lumbar layers is what helps the anulus fibrosus resist tensile forces in spine. It helps the spine absorb and transmit shock, maintains each direction as well as providing resistance to torsional forces. flexibility, and under higher loads, helps to stabilize the spine.46 Additionally, between each lamellae, there is a collagen-based The normal disc is composed of an outer layer of fibrocartilage bridging network that provides resistance to any shear forc- that surrounds an inner layer comprised of a well hydrated pro- es.51,52 Therefore, with the combination of the alternating con- teoglycan gel. Working together these 2 layers are able to pro- centric layers, the trans-lamellae bridges, and the tough Type vide resistance in various combinations of compression, shear, I collagen fibers found through the annulus fibrosus, the disc and tensile forces.47 During spinal loading, the IVD is able to is allowed to provide significant resistance against distraction, distribute the load evenly on the vertebral bodies.48 Addition- shearing, and torsional forces. ally, when the IVD is healthy, it provides a “spacer effect.” As The inner portion of the disc, or the nucleus pulposus, is a spacers, the IVDs provide about 25% of the total height of the gelatinous structure that accounts for approximately half of the lumbar spine. The greater the height, the greater the mobility of volume of the IVD.53,54 Approximately 70% to 90% of the nu- the lumbar spine and the greater the space for adequate passage cleus pulposus is comprised of water, creating great hydrostat- for exiting spinal nerve roots. ic pressure.47,50 In fact, intradiscal pressures within the lumbar Academy of Orthopaedic Physical Therapy, APTA. For personal use only. No other uses without permission. 9 © 2021 Academy of Orthopaedic Physical Therapy, APTA, Inc. All rights reserved. spine have been found to range from 100 kPa (laying supine) with at least 1 disc narrowing. Clearly, the implications of a all the way up to 2300 kPa (lifting 20 kg, bent over with round positive finding of DD should be taken with a grain of salt. back).55 Under compressive loads the increasing hydrostatic It should be noted, however, that evidence does exist that, pressure will generate tension in the surrounding anulus fibro- despite the wide spread prevalence of degenerative disc disease sus, increasing the stability of the spine.56 Located within the (DDD), symptomatic individuals are more likely to have DD nucleus pulposus are glycosaminoglycans bound to a proteo- than asymptomatic individuals.65,69 In the same year they pub- glycan molecule that act to thicken the surrounding water.47,57 lished their systematic review of the prevalence of DDD in an The thickening of the water within the nucleus pulposus acts to asymptomatic population, Brinjikji et al69 performed a me- increase the load-bearing capacities of the lumbar spine.47 ta-analysis comparing the prevalence of DDD in symptomatic The vertebral endplate borders the IVD on the superior and asymptomatic individuals. They included 14 studies with and inferior vertebral body. Typically, the endplates are less than a total sample size of 3097 individuals, all were 50 years of age 1 mm thick but it varies from region to region.58,59 They create or less. They reported that individuals with LBP are 2.24 times a semi-permeable barrier between the vertebral body and the more likely to have DD compared to asymptomatic individuals. IVD that allows for the diffusion of some nutrients into the However, it should be noted that due to the high prevalence largely avascular inner nucleus.47 While the portion of the end of naturally occurring degeneration in the spine, the authors plate that borders the IVD is generally comprised of strong fi- did not include individuals older than 50 years of age. This led brocartilage, where the end plate borders the vertebral body it is them to the conclusion that “the association between these en- primarily comprised of hyaline cartilage.47 This creates a poten- tities and LBP [may be] less significant in older age groups.” To tial area of weakness that, when the IVD is exposed to trauma further support the notion that DDD is more prevalent in a or simply over time, might lead to the nuclear material of the symptomatic population, a more recent study has shown that IVD protruding into the vertebral marrow.60 This is thought to DD, especially in the presence of additional degenerative find- contribute to the development of disc degeneration.58 ings in the lower lumbar spine, is more likely to be correlated with LBP. This brings up a very pertinent question: how can Disc degeneration occurs naturally one differentiate between symptomatic and asymptomatic DD? and does not always result in pain Disc degeneration has commonly been associated with How do we differentiate an asymptomatic LBP.61-63 It has been shown that as an individual ages the water degenerative disc from a symptomatic one? content within the nucleus decreases, causing the annulus fibro- Several studies have focused on answering the question sus to resist compression.48 This change can lead to decreases in of how to differentiate a symptomatic versus an asymptomatic both disc flexibility and height.63 With the loss of disc height, degenerative disc. The focus of this work has largely revolved the potential for foraminal narrowing increases as well as in- around the presence of a high intensity zone (HIZ) within the creased facet arthritis63 and spondylosis. However, the impact of posterior aspect of the annulus fibrosus. First discussed in 1992 the mere presence of a degenerated disc is debated. by Aprill and Bogduk,70 the HIZ is defined as the “high sig- There is now substantial evidence that shows as one ages, the incidence of disc degeneration (DD) increases.64-66 In fact, nal contained within the annulus of a disc, separated from the it was found that individuals over the age of 50 had an 88% nucleus pulposus, on lumbar spine MRI.” According to their likelihood of having a degenerated disc in their lumbar spine.65 initial research they deemed the sign as diagnostic of internal However, this naturally occurring phenomenon does not always disc disruption. Since then, significant work has been done to correlate with pain. In 2015, Brinjikji et al67 performed a sys- examine the pathogenesis and clinical significance of the HIZ. tematic review of the literature that assessed the prevalence of In 2006, Peng et al61 performed biopsies on 21 discs that were asymptomatic spinal degeneration across the lifespan. They in- found to have both an HIZ in the posterior region of the annu- cluded 33 articles in their systematic review that had a total of lus and reproduced pain during discography. After performing 3110 asymptomatic individuals. They found that the incidence a histological study of the disc and with supportive data from of lumbar DD was approximately 37% in individuals in their their concurrent study,62 they described a potential mechanism 20s, and that percentage increased to 96% by the time an indi- for how an HIZ might become pathologic. They hypothesized vidual reached their 80s. In fact, that systematic review showed that a tear in the structurally weak71 posterior annulus occurs that by the time an individual is in their 30s, they are more likely from some unspecified trauma. Following the tear, the normal to have a degenerated disc than not. A later study that highlighted structure of the posterior annulus is replaced with granulation the ubiquitous nature of DD was performed in 2019 by Romeo tissue. However, due to the poor vascularization of the IVD the et al.68 In that study they assessed the incidence of spinal ab- healing is defective.62 Therefore, following the injury there is an normalities in a population of 350 asymptomatic young adults “abundance of inflammatory mediators, specifically prostaglan- (between the ages of 18 and 22 years). They found that 30% of din E2, IL-6, and IL-8 that can sensitize the nociceptors in the participants had signs of a disc desiccation and 13% presented disc.”61 With movements of flexion and extension, the increase Academy of Orthopaedic Physical Therapy, APTA. 10 For personal use only. No other uses without permission. © 2021 Academy of Orthopaedic Physical Therapy, APTA, Inc. All rights reserved. in the intradiscal pressure might be enough to elicit a nocicep- that differences in the quantitative measures in IVDs between tive signal from the disc. symptomatic and asymptomatic patients could be attributed to While the work from Peng et al61 provides a plausible the HIZs, but did not explain why asymptomatic patients have biological mechanism for HIZ being related to symptomatic HIZs in the first place. Ultimately, the prevalence of HIZ is too DDD, epidemiologic data supporting the notion that the HIZ great in the asymptomatic population for meaningful clinical is associated with pain is inconclusive. Wang et al72 reviewed use75 and the results of MRI alone is not enough to definitively the lumbar magnetic resonance imaging (MRI) of 637 partici- conclude that a disc is symptomatic or asymptomatic.80 More pants. Of the participants, roughly half had symptoms of LBP work is needed to fully elucidate the clinical relevance of the while the other half were asymptomatic. While they found that HIZ. the rate of HIZ was statistically higher in those with LBP, the difference was not large. Those with LBP had an incidence rate A disc by any other name… of 36% while those without LBP had an incidence rate of 27%. Another potential source of pathoanatomical pain in the Other studies found the prevalence of asymptomatic HIZ to be lumbar spine could be the presence of a bulging disc.81 However, as high as 56%73 although 20% to 32% is more common.74-76 clinicians and medical professionals use different terms for the These studies73-76 also found a correlation between increased age same observed pathology, leading to confusion.82,83 Therefore, and weight with increased prevalence of HIZ, suggesting that this monograph will attempt to use the terminology proposed the development of HIZ could be part of the natural aging pro- by the combined task forces of the North American Spine Soci- cess. In a different study, Campos et al77 assessed the prevalence ety, the American Society of Spine Radiology, and the American of HIZ in adults who underwent an abdominal and pelvic MRI Society of Neuroradiology in their publication “Lumbar Disc as a screening tool. While they found that HIZ was significantly Nomenclature: Version 2.0.”84 With that in mind, the following more prevalent in asymptomatic discs with degeneration, the definitions will be used. A bulging disc, which is not considered overall prevalence was at 11.06%. This was actually a higher a type of herniated disc, is the presence of disc tissue extending prevalence rate than the symptomatic prevalence rate (10.4%) beyond the edges of the ring apophyses throughout the circum- that Brinjikji et al69 reported in their meta-analysis in 2015. ference of the disc (Figure 1C). A herniated disc (Figure 1D) Conversely, to support the use of HIZ as a diagnostic pa- can be subdivided into 2 categories: protrusion or extrusion. A rameter to determine if DD contributes to LBP, Fang et al78 protruded disc is present “if the greatest distance between the performed a meta-analysis combining the data of more than edges of the disc material presenting outside the disc space is 11 studies. They specifically looked at the relationship between less than the distance between the edges of the base of that disc pain reproduction based on provocative discography and the material extending outside the disc space.” A disc extrusion is HIZ. Their sample, by nature of their inquiry, only contained defined when “any one distance between the edges of the disc individuals who had LBP. They reported that the odds are 8.64 material beyond the disc space is greater than the distance be- times greater that a disc with an HIZ will result in a positive tween the edges of the base of the disc material beyond the disc provocative discography compared to a disc without an HIZ. space.” A sequestration can exist if the disc material beyond the This led them to the conclusion that the presence of a HIZ and disc space is no longer connected to the remaining disc and is pain are linked. Furthermore, Waldenburg et al79 examined the considered a subcategory of a disc extrusion. differences in IVD characteristics as measured with quantitative MRI and found that there were small but significant differences What role does a herniated (or bulging) in the tissue composition between asymptomatic and symp- disc play in low back pain? tomatic IVD. Specifically, they found decreased heterogeneity There is strong evidence that both bulging and herniated between the nucleus pulposus and the annulus fibrosis in the discs occur in asymptomatic individuals. Since the early 1990s posterior portion of discs in symptomatic participants. How- the presence of asymptomatic bulging and herniated discs has ever, when they excluded the IVDs which demonstrated HIZs, been described.85,86 Looking back at the systematic review by difference could no longer be found between symptomatic and Brinjikji et al,67 a bulging disc was found in 30% of individ- asymptomatic IVDs. This led them to the conclusion that the uals in their 20s and up to 84% of individuals in their 80s. quantitative differences they found in symptomatic and asymp- Disc protrusions were found in 29% of individuals in their 20s tomatic discs were the result of the presence of the HIZs. and by the time an individual reaches their ninth decade of The shortcoming of both of the above studies is that they life that prevalence increases to 43%. Kim et al87 reviewed the did not address the significant presence of asymptomatic discs MRI of 102 participants and found that the incidence for an that have a HIZ. In the meta-analysis performed by Fang et asymptomatic bulging, protruded, or extruded disc was 61.3%, al,78 the general conclusion is that provocative discs as measured 46.3%, and 31.7%, respectively. Romeo et al68 demonstrated by discography have significantly increased odds of also having the prevalence of asymptomatic bulging and protruding discs in a present HIZ. This does not explain the high proportion of young adults to be as high as 49% and 26%, respectively. What asymptomatic discs having a HIZ. Waldenburg79 demonstrated is interesting is that in 2 more recent publications,68,87 using Academy of Orthopaedic Physical Therapy, APTA. For personal use only. No other uses without permission. 11 © 2021 Academy of Orthopaedic Physical Therapy, APTA, Inc. All rights reserved. a 3T MRI as opposed to the lower strength MRI of previous LBP. When they stratified their data based on Modic change studies, a higher prevalence of asymptomatic discs was found. type, they found no significant differences in the strength of the This raises the question that as technology improves and the ac- associations. Other findings of interest from the study includ- cessibility to better equipment is greater, is the chance of finding ed the fact that the size of the Modic change did not correlate false-positive imaging even higher? with pain intensity, there was no difference in the pain intensity between patients with and without Modic changes, and finally Herniated discs get better with time that there was no support for an association between the Modic One piece of very encouraging news for patients who have changes and activity limitation.92 Interestingly, another system- been diagnosed with a herniated or bulging disc is that, with atic review in the same year, which assessed the relationship be- time, the probability of a spontaneous resolution of the herniat- tween Modic changes and LBP, also found that only half of their ed disc is quite high. Chiu et al88 performed a systematic review studies demonstrated a statistically significant association.93 of the literature assessing the probability of spontaneous regres- Other systematic reviews have attempted to determine the sion of herniated and bulging discs in the lumbar spine. The role of Modic changes in the relationship to LBP, concluding results of their study are astounding. After combining the data that the presence of a type 1 Modic change has a non-significant from 9 separate studies, they found that the rate of spontaneous association with postoperative clinical outcomes;94,95 Modic regression was 96% for a sequestered disc, 70% for an extruded changes are not associated with occupational loading;96 and the disc, 41% for a protruded disc, and 13% for a bulging disc. presence of Modic changes cannot guide treatment.97 Further- While most spontaneous regression occurred within the first more, single studies have also called into question the clinical year—with the initiation of regression being observed as early utility of Modic changes.98,99 Much like HIZ, the prevalence of as 2 to 3 months—it was found to take some individuals up to Modic changes in the population at large can be high and the 40 months to experience full regression. What is interesting is prevalence increases as one ages. Wu et al100 found that approx- that as the severity of the condition increased, the likelihood of imately 45% of individuals in their population-based study had spontaneous resolution also increased. However, it should be Modic changes (although it should be noted that they did not noted that the disc regression did not correlate well to clinical include how many of their participants had LBP) and that the outcome. Since then, this finding has been supported by addi- prevalence increased with age. In fact, after adjusting for age, tional research.89,90 This should come as great relief for patients sex, and body mass index, there were no statistically significant and as a powerful tool for the physical therapist. When patients associations between Modic changes and other lifestyle factors. come into the clinic having been diagnosed with a bulging/her- This helps support the argument that Modic changes can and niated disc, the astute physical therapist can explain to them do occur naturally with age. that not only is their disc likely to recover on its own, but the worse it is on imaging, the more likely the resolution. Structural changes in the central nervous system can occur with low back pain The potential role of endplate changes in low back pain In recent years, more and more researchers are looking at In recent years changes in the vertebral endplates and sub- changes within the brain to help explain some of the symptoms chondral bone have been further evaluated as a potential source associated with LBP. These efforts have largely fallen into 2 cat- of LBP. Commonly referred to as Modic changes, these clus- egories: changes in functional activity and structural morpholo- ters of findings represent changes in the vertebral endplate and gy. Functional activity relates to how different parts of the brain vertebral bone marrow lesions.91,92 Modic changes type 1 are activate or communicate with one another. Structural morphol- hypothesized to represent an inflammatory reaction in the bone ogy, which will be the focus of this section, largely relates to marrow (Figure 1F), Modic changes type 2 are associated with changes in the gray matter volume (GMV). fatty infiltration of the bone marrow, while Modic changes type Two recent systematic reviews have examined the effects 3 are associated with sclerotic change of the vertebral bone mar- of LBP on the structural morphology of the brain. In 2015, row.92 Modic changes, specifically type 1, have been associated Kregel et al101 examined the reported structural organization with the presence of LBP;69 however, the association is not clear. of grey matter (GM) in 10 studies. While there was inconsis- A meta-analysis of 31 studies was performed by Herlin et al92 tent reporting in multiple brain regions, 3 regions stood out. where they attempted to elucidate the relationship between the Reduced GMV was reported for the dorsal lateral prefrontal presence of Modic changes and the presence of pain and/or ac- cortex (DLPFC), temporal lobes, and insula. There were mixed tivity limitation, as well as if this relationship can be modified results for the somatosensory cortex (S1) with studies showing by other factors. First, they found that the association between both increased and decreased GMV. Reduction in the insula Modic changes (all types) and LBP was tenuous. Only approx- makes intuitive sense as it plays an integral role in both senso- imately half of the studies they evaluated demonstrated a statis- ry and emotional component of pain processing.102 However, tically significant association between the Modic changes and the reduction in the gray matter of the DLPFC is of particular Academy of Orthopaedic Physical Therapy, APTA. 12 For personal use only. No other uses without permission. © 2021 Academy of Orthopaedic Physical Therapy, APTA, Inc. All rights reserved. interest because it has been shown to limit the magnitude of The previous systematic reviews also demonstrated that the perceived pain.103 Disruption of this region might signify that cortical thickness of S1 was altered in patients with cLBP.101,104 individuals with cLBP are less able to actively control their pain Kim et al110 recruited 102 participants with cLBP and 50 age- perception and not able to modulate nociception.103 matched controls. Those with cLBP were randomized into 4 A more recent systematic review confirmed several of these groups: traditional acupuncture, sham-acupuncture with and findings. In 2018, Ng et al104 examined the literature and re- without somatosensory afference, and no treatment. The au- viewed the results of 55 imaging studies. They found further thors took MRI scans at baseline and again after treatment (du- evidence of decreased GMV in the DLPFC, insula, and tem- ration between the assessments was a mean ± standard deviation poral lobe, with mixed results for the S1 region. Furthermore, of 7.0 ± 2.7 weeks). At baseline, they found that those with they found evidence of decreased GMV within the cuneus, cLBP demonstrated decreased 2-point discrimination threshold thalamus, medial prefrontal cortex (mPFC), the posterior cin- in the low back but not when testing a finger, indicating site gulate cortex (PCC), as well as the precentral region of the specific decreases in sensation. Furthermore, this decrease in brain. Without examining the specific role of each region and tactile acuity was associated with an increase in S1 region GMV to simply summarize the authors’ remarks, they concluded that (interestingly, Li et al105 in their study in 2018 found a simi- many of the regions demonstrating altered GMV were associ- lar increase in S1 region GMV). Following treatment, those ated with emotion and cognition rather than nociception.104 in the true acupuncture group who responded to treatment Since the publication of this systematic review, another study demonstrated improved 2-point discrimination thresholds and has been published with similar findings of decreased GMV in reduced S1 region GMV. Interestingly, those in the sham acu- the DLPFC.105 puncture groups and in the no treatment group demonstrat- While the results of these 2 systematic reviews indicate ed no significant change. Therefore, they concluded that the structural change following cLBP, it should be noted that change in S1 region GMV was associated with a decrease in their results are not universal. Mansour et al106 performed a 2-point discrimination, and that both improved after treatment region-of-interest analysis to more systematically examine the along with a reduction in symptoms. regions that have been previously found to demonstrate differ- ences in volume. After enrolling a total of 130 participants who Wrapping it up: What are the structural had either subacute or cLBP, or no pain at all, they demon- causes of low back pain? strated no differences in GMV. However, they did not include As is evident by now, it is difficult to determine what the the DLPFC in their assessment. An additional study found that anatomical cause of LBP is. Multiple studies looking at changes after controlling for age, depression/anxiety, pain medication, in GMV, DD, bulging discs, end-plate changes, stenosis, etc and pain phenotype, any reductions in GMV disappeared.107 have found conflicting results as to which degenerative change Assessing morphological changes in GM is a relatively re- is pathologic and which is benign. Part of the problem with cent endeavor with the first study published in 2004.108 While the full extent of the changes that occur during cLBP requires trying to pinpoint a pathoanatomic cause for cLBP is that there further exploration, the bulk of the literature at this moment are so many possible causes for the pain. The HIZ or the DD suggests that there are changes in the GMV for the DLPFC, might be only one of many findings and as such a single source insula, temporal lobe, and the S1 region. The fact that changes cannot be identified. It might be that the patient’s lumbar spine occur in these 4 regions is important as the structural changes MRI is normal, but there have been structural changes within brought on by pain are not necessarily permanent. the GM of the DLPFC that is causing the pain. This would, for example, diminish the association found between a DD and Changes in gray matter volume can reverse with treatment LBP. Additionally, while all patients with LBP have pain, that As previously mentioned, one of the key regions that has pain might be influenced by multiple factors other than noci- been shown to have decreased GMV is the DLPFC.101,104 Sem- ception.92 This would further diminish the correlation between inowicz et al109 performed a longitudinal study of 18 patients any one degenerative change and pain. with cLPB and 14 healthy controls. They performed an MRI The heterogeneous nature of LBP makes it difficult for both before and 6 months after treatment (either surgery or in- the clinician because one of the primary reasons why patients jection). At baseline measure, they found that the cortical thick- seek health care is to obtain information on their condition.111 ness of the DLPFC for those with cLBP was thinner than for Patients desire a clear explanation about the source of their the controls. However, for those with cLBP who responded pos- symptoms,111 and in trying to give an explanation as to what itively to the intervention (n=11), cortical thickness increased, is causing the patient’s symptoms, the clinician may be un- whereas for those who did not respond to treatment (n=3), the derstandably reluctant to say, “the literature is unclear.” The thickness remained the same. The authors observed the initial patient, also understandably, might interpret the clinician to thinning of the cortex and subsequent thickening in responders mean, “I don’t know what is wrong with you” or potentially even after controlling for depression. think, “my therapist doesn’t know what is going on.” A lack of Academy of Orthopaedic Physical Therapy, APTA. For personal use only. No other uses without permission. 13 © 2021 Academy of Orthopaedic Physical Therapy, APTA, Inc. All rights reserved. perceived expertise on the part of the health care provider can and necessary, to treat LBP. As an alternative, a therapist can have detrimental effects on the patient.112 One solution to this provide the patient with the facts regarding their condition (as dilemma might be to discuss some of the commonly promul- written by O’Sullivan et al)113: LBP is not a serious life-threaten- gated myths about LBP. ing medical condition; most episodes of LBP improve and LBP In 2020, O’Sullivan et al113 compiled a list of 10 myths that does not get worse as we age; imaging scans do not determine are commonly believed but not supported by evidence (Table prognosis of the current episode of LBP, the likelihood of future 1). Some examples of myths taken from the article include the LBP disability, and do not improve LBP; and effective care for following: LBP is usually a serious medical condition; persistent LBP is relatively cheap and safe, including engaging in phys- LBP is always related to tissue damage; imaging scans are always ical activity and exercise, social activities, healthy sleep habits needed to detect the cause of LBP; pain related to exercise and and body weight, and remaining employed. By reviewing these movement is always a warning that harm is being done to the “myths” and “facts” about LBP, perhaps the therapist can diffuse spine and a signal to stop or modify activity; and treatments some of the patient’s justified concerns about not knowing ex- such as strong medications, injections, and surgery are effective, actly what is happening in their low back. Table 1. Myths versus Facts Regarding Low Back Pain as Defined by O’Sullivan et al113 Myth Fact LBP is usually a serious medical condition LBP is not a serious life-threatening medical condition LBP will become persistent and deteriorate in later life Most episodes of LBP improve and LBP does not get worse as we age Persistent LBP is always related to tissue damage A negative mindset, fear-avoidance behavior, negative recovery expectations, and poor pain coping behaviors are more strong- ly associated with persistent pain than is tissue damage Scans are always needed to detect the cause of LBP Scans do not determine prognosis of the current episode of LBP, the likelihood of future LBP disability, and do not im- prove LBP clinical outcomes Pain related to exercise and movement is always a warning Graduated exercise and movement in all directions is safe and that harm is being done to the spine and a signal to stop healthy for the spine or modify activity LBP is caused by poor posture when sitting, standing, and Spine posture during sitting, standing, and lifting does not lifting predict LBP or its persistence LBP is caused by weak ‘core’ muscles and having a strong A weak core does not cause LBP, and some people with LBP core protects against future LBP tend to overtense their ‘core’ muscles. While it is good to keep the trunk muscles strong, it is also helpful to relax them when they are not needed Repeated spinal loading results in ‘wear and tear’ and Spine movement and loading is safe and builds structural tissue damage resilience when it is graded Pain flare-ups are a sign of tissue damage and require rest Pain flare-ups are more related to changes in activity, stress, and mood rather than structural damage Treatments such as strong medications, injections, and Effective care for LBP is relatively cheap and safe. This in- surgery are effective, and necessary, to treat LBP cludes education that is patient-centered and fosters a positive mindset, and coaching people to optimize their physical and mental health (such as engaging in physical activity and exer- cise, social activities, healthy sleep habits and bodyweight, and remaining in employment) Abbreviation: LBP, low back pain Academy of Orthopaedic Physical Therapy, APTA. 14 For personal use only. No other uses without permission. © 2021 Academy of Orthopaedic Physical Therapy, APTA, Inc. All rights reserved.  As previously discussed, it is very difficult to pinpoint an have consistently been found in individuals with cLBP at higher exact pathoanatomical cause for LBP. In fact, Deyo and Wein- rates than in asymptomatic controls.122-124 Furthermore, upon stein114 found that 85% of all cLBP has no known anatomical biopsy of the multifidus muscle, evidence of muscle degenera- cause. Consistent with these findings, Hoy et al31 reported that tion, inflammation, and decreased vascularity was common in for 95% of all individuals with cLBP there was no known an- those with cLBP compared to normative data.125 Because the atomical cause. However, not all changes that occur with LBP multifidus is thought to assist with providing segmental stabili- result in structural abnormalities. ty to the vertebra and this promotes stiffness in the spine during movement,126 it is readily apparent how decreases in the struc- Non-structural changes occur in individuals tural integrity of the multifidus might contribute to LBP. Fur- with low back pain thermore, this alteration in the quality of the multifidus muscle could potentially explain the decreased proprioception noted in What is now clear is that LBP cannot consistently be at- individuals with LBP. People with LBP tend to demonstrate de- tributed to an anatomical cause. For this reason, researchers creased positional sense compared to asymptomatic controls127 have looked beyond the anatomy to look for an explanation. while also having greater repositioning error.128,129 As the multif- People with low back pain move differently. Considerable idus is thought to play a strong role in the proprioception of the effort has been made to determine motor control changes as- spine,130 any deficits of the multifidus could help explain poor sociated with LBP. As described by Sung et al,115 motor control positional sense and repositioning error. However, it is unclear changes can be divided into 4 separate categories: altered mus- the extent to which this happens.131 cle timing, changes in muscle quality, altered proprioception, In an attempt to promote a unifying theory on how an and altered stiffness. The phenomenon of altered muscle timing individual in pain moves differently, Hodges and Tucker132 largely revolves around the premise of altered recruitment of the penned a review article that outlined their new theory on how abdominal obliques and transverse abdominis muscles prior to an individual with pain adapts. The authors described 5 basic engagement of distal extremities.116-118 The general premise is elements (Table 2). The first element is that “pain leads to redis- that the transverse abdominis and internal oblique will activate tribution of activity within and between muscles.” They explain in an anticipatory manner to stabilize the trunk prior to distal how people with pain do not always exhibit a uniform increase perturbations.117 This activation, specifically of the transverse or decrease in muscular excitation, but rather a redistribution abdominis, is thought to help support the spine by increasing of activity aimed to protect the painful region. Second, “adap- intra-abdominal pressure without additional compression at the tation to pain changes mechanical behavior.” Specific to the low disc. However, recent data from Morris et al119 suggested that back they indicate how individuals exhibit increases in trunk activation of the transverse abdominis is not a bilateral event to stiffness and move to a more en bloc movement pattern. Third, stiffen the spine, it rather reflected a muscle synergy associat- “adaptation to pain leads to protection from pain or injury, or ed with efficient transfer of momentum from ground to hand. threatened pain or injury.” This element highlights how the Since then, additional research has supported the notion that ability to either excite or inhibit muscular activation protects the feed-forward mechanism might not play the role that it was the injured or irritated tissue. The fourth element states that once thought to play.120,121 “adaptation to pain involves changes at multiple levels of the Other motor control changes are thought to occur through motor system.” The theory postulates that changes can occur at the alterations in the muscle quality. Specifically, multiple stud- the spinal level (eg, the spinal cord can be changed by direct in- ies have investigated the role of fatty infiltrates in the lumbar put of nociceptive afferents), while cortical changes can result in multifidus as a potential source of nociception. Fatty infiltrates changes in motor planning and reorganization of somatotopical Table 2. The 5 Elements of Hodges and Tucker’s132 Theory of Motor Adaptation to Pain Element 1 Pain leads to redistribution of activity within and between muscles Element 2 Adaptation to pain changes mechanical behavior Element 3 Adaptation to pain leads to protection from pain or injury, or threatened pain or injury Element 4 Adaptation to pain involves changes at multiple levels of the motor system Element 5 Adaptation to pain has short-term benefit, but with potential long-term consequences Academy of Orthopaedic Physical Therapy, APTA. For personal use only. No other uses without permission. 15 © 2021 Academy of Orthopaedic Physical Therapy, APTA, Inc. All rights reserved. organization. Finally, the fifth element states that “adaptation to detailed how this mechanism is impaired in individuals with pain has short-term benefit, but with potential long-term con- cLBP and is correlated to pain chronicity, duration, and severi- sequences.” Essentially, the short-term adaptation of movement ty.35,148-150 Furthermore, as will be discussed in a later section, in- to unload or avoid pain due to an irritated tissue can result in an dividuals with cLBP often exhibit catastrophizing, depression, altered movement pattern than can persist even when the initial and fear avoidance. All of these factors have been thought to injury has subsided. This can result in an adapted motor pattern increase descending facilitatory pathways in the central nervous which limits movement variability and results in chronic tissue system.135 stress.133 To summarize, people with cLBP experience pain differ- People with low back pain process nociception differently. ently than the healthy population; nociception pathways, both While a full review of the central changes in pain perception is ascending and descending, are facilitated, processing of pain in beyond the scope of this monograph a few key points are worth the brain is augmented, and descending inhibition of pain is highlighting. Altered nociception processing in cLBP can occur often decreased. Taken together, these phenomena can help ex- in 4 separate arenas: enhanced ascending nociceptive pathways, plain why cLBP can be so debilitating. altered processing in the brain, decreased descending inhibitory Somatotopic organization differs in individuals with chron- pathways, and enhanced descending facilitatory pathways. En- ic low back pain. Somatotopic organization refers to the way hanced ascending nociceptive pathways often present as altered the brain represents movements and sensation of different body temporal wind-up. Temporal wind-up is a spinal mechanism in segments.151 A generalized pattern is present at birth,152 with which repetitive noxious stimulation to a single location results the pelvic floor153 and lower limbs being closer to the midline in a slow temporal summation.134 To the patient it is processed and the hands being represented most laterally. This pattern is as an increased pain experience to an equal stimulus. Studies us- thought to be disrupted in individual’s with cLBP. Tsao et al154 ing thermal quantitative sensory testing has shown that in indi- examined the extent of cortical somatotopical reorganization viduals with cLBP, temporal summation is enhanced compared in individuals with LBP. They recruited 9 individuals with re- to asymptomatic controls, specifically at the site of pain.135-137 current LBP (rLBP) and 11 asymptomatic controls. They in- Once the nociceptive signal reaches the brain, individuals with serted intramuscular electromyographic (EMG) electrodes into cLBP process that signal differently. In a recent study, Li et al105 the deep multifidus and longissimus muscles and used a sin- assessed brain connectivity during a painful stimulus to the low gle-pulse monophasic transcranial magnetic stimulation (TMS) back. They recruited 16 participants with cLBP and 16 healthy to map the motor cortex. They found that for those who had controls to undergo functional MRI while undergoing a pneu- rLBP there were overlapping areas of control for the deep mul- matical induced mechanical quantitative sensory test. Com- tifidus and the longissimus, whereas the asymptomatic individ- pared to asymptomatic individuals, those with cLBP exhibited uals had separate, discrete centers. The authors noted that there increased connectivity between the sensorimotor regions and was a loss of discrete organization in the motor cortex in indi- sensory association cortices when undergoing a painful stimu- viduals with LBP and termed this phenomenon “smudging.” lus. They hypothesized that because this increase in connectiv- Smudging in the motor cortex has also been linked with ity also positively correlated with pain intensity, it might help the severity of LBP. In 2015, Schabrun et al155 recruited 27 in- explain cLBP. Other studies examining brain activity in people dividuals with rLBP and 23 asymptomatic controls to undergo with LBP have found evidence of increased activity in the S1 both surface EMG and TMS. The surface EMG electrodes were region,138 alterations in the resting communication between applied over the L3 and L5 paraspinal muscles to record signals different regions (default mode network),139,140 and increased generated from a single-pulse TMS. Consistent with the results activity in other pain regions of the brain during both mechan- from Tsao et al,154 those with rLBP had a loss of discrete centers ical141,142 and thermal stimulation.143,144 of control compared to healthy individuals. However, the extent Descending pain pathways are also altered in individu- of the loss was dependent on the severity of LBP. For those in- als with cLBP. Evidence of decreased descending inhibitory dividuals with moderate-to-severe LBP (>5/10 on a numerical pathways (eg, pathways that “shut down pain”) is thought to pain rating scale [NPRS]) the lack of discrete centers was uni- be related to a deficit in the diffuse noxious inhibitory control versal, where this was only the case for 53% of those with mild (DNIC) system.145 The DNIC system describes how noxious LBP (NPRS of ≤ 5/10). stimuli applied to various parts of the body could decrease or Changes in cortical organization is not unique to the mo- inhibit the activity of C-fibers distal to the site of the applica- tor cortex. Hotz-Boendermaker et al156 observed evidence of tion of the noxious stimulus.146 Commonly, to assess for chang- cortical smudging in the secondary somatosensory cortex. Us- es in the DNIC, researchers use a technique called “conditioned ing functional MRI, they measured the whole brain activation pain modulation” (CPM) which is a paradigm that consists of while providing nonpainful posteroanterior movement pressure 2 painful stimuli over different, distant regions of the body, and to L1, L3, and L5 in 13 individuals with and without cLBP. evaluating how much one stimulus is reducing the pain elicited They found that for those in the cLBP group there was a blur- by the application of the other stimulus.147 Several authors have ring, or “smudging,” of the S2 region responsible for the repre- Academy of Orthopaedic Physical Therapy, APTA. 16 For personal use only. No other uses without permission. © 2021 Academy of Orthopaedic Physical Therapy, APTA, Inc. All rights reserved. sentation of these different segments. They hypothesized that strongest predictor of future LBP, with a hazard ratio (HR) of the impairments in motor and postural control often observed 2.3 (95% confidence interval [CI] = 1.2, 4.4). Furthermore, in individuals with cLBP could be due to the cortical reorgani- disc protrusions were associated with a lower risk for developing zation of S2, as S2 often exhibits connectivity with the parts of future back pain (HR = 0.5; 95% CI = 0.3, 0.9). One tentative the brain associated with premotor planning. conclusion that can be drawn from this study and supported by Other research has also tried to link smudging of the cortex the research on the prevalence of asymptomatic bulging discs with poor motor control. For example, in 2008, Tsao et al157 is that the psychosocial state of an individual might be a better recruited 11 individuals with rLBP and 11 asymptomatic con- predictor of future pain than the presence of abnormal imaging trols. As in their previous work,154 they measured the muscle findings. activity as generated from the TMS. However, this time, in- Pain catastrophizing is the “tendency to magnify the threat stead of measuring activation in the erector spinae, they assessed value of pain stimulus and to feel helpless in the context of pain, the activity of the transverse abdominis. Additionally, they also and by a relative inability to inhibit pain-related thoughts in measured the latency of the activation of the transverse abdom- anticipation of, during or following a painful encounter.”165 inis following an upper extremity movement to evaluate the One popular approach to measure pain catastrophizing is to feed-forward mechanism. The authors had 3 interesting find- complete the Pain Catastrophizing Scale (PCS),166 which is a ings: first, they found that in the individuals with cLBP, the 13-item outcome measure of pain-related catastrophizing. Sev- cortical representation for the transverse abdominis was broader eral systematic reviews have linked pain catastrophizing with and less pronounced compared to the asymptomatic controls; increased levels of pain and disability, treatment mediation, and second, the feed-forward mechanism was impaired in the group outcomes following physical therapy treatment.167,168 Further- with cLBP (although keep in mind the potential pitfalls of this more, pain catastrophizing has also been linked to decreased assessment);119-121 third, that the cortical reorganization and the GMV in the DLPFC,169 persistent pain, disability following impaired feed-forward mechanism were associated. This led the surgery,170 and even overall psychological distress.171 Pain cata- authors to conclude that the impaired motor control often ob- strophizing has large implications on not only the sta