U.S. flag

An official website of the United States government

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

Cover of StatPearls

StatPearls [Internet].

Show details

Lumbar Stabilization

; .

Author Information and Affiliations

Last Update: August 14, 2023.

Continuing Education Activity

Lumbar stabilization is the natural ability of the spinal column to maintain its anatomical structure on physiological loading. The stability is maintained by the interaction between the bony structure with ligaments, the attached muscles, and the nervous system that connects the above two. Natural disc degeneration combined with sedentary behavior can lead to weakness of the muscles, which can then cause segmental instability. Back pain is the largest cause of disability-adjusted living years based on the WHO survey of the global burden of disease. This article reviews the components that contribute to stability, details how the lack of interaction between the various elements can cause abnormal mobility and pain, details the clinical tests required to identify lack of strength and endurance of the lumbar muscles and provides one of the standard methods (motor control exercises) available to increase muscle strength and regain stability.


  • Identify the anatomical structures contributing to lumbar stability.
  • Describe the tests required to determine the strength and endurance of the lumbar muscles.
  • Review appropriate therapeutic exercises to rectify low back pain from segmental instability.
  • Outline simple exercises to retrain the muscles that surround the lumbar spine to activate in the right sequence to provide stability and thereby pain-free movement.
Access free multiple choice questions on this topic.


Spinal stability is the spine's ability to maintain its structure and anatomical relationship with normal physiological loading. In the 1990s, Manohar Panjabi postulated that the following three interacting systems were responsible for the maintenance of spinal stability[1]:

  • The passive system comprising of the vertebral bodies, the intervertebral discs, the zygapophyseal joints, the zygapophyseal joint capsules, and the spinal ligaments
  • The active system comprising of the muscles and
  • The neutral system that interacts between these two systems

In a normal healthy spine, the above three systems interact and allow normal function and a pain-free range of movement. With stress loading of the passive system (vertebrae, disc, ligaments, and joints), the active system (muscles) come into play and prevent abnormal deformation. The contribution of the passive system in the neutral spine is minimal. Cadaveric experiments show that when the muscles are removed, and only the bones, discs, and the ligaments are left in situ, the spine buckles under low loads of 20 lbs (9 kg).[2] 

The neural control subsystem receives input both from the passive and the active subsystems and then direct the spinal musculature to stabilize the spine. The neural system should act at the right time and the right amount to protect the spine from injury and to allow the desired movement.[3] 

An inability of the active system to maintain the relationship between different elements of the passive system during physiological loading can lead to spinal pain. Based on this, clinical instability can be defined as the abnormal displacement that occurs within the motion segment when a normal physiological load is applied.[4] In a healthy state, if the three systems interact and provide stability, then following injury or degeneration to the passive system, the active system needs to work harder to compensate for the decreased contribution from the passive system.[1]


The range of movement in the spine can subdivide into a neutral zone and an elastic zone. The neutral zone is the normal functional range of movement. There is very little stiffness of movement within the neutral zone. At the ends of the range of motion is the elastic zone, where the stiffness of the system increases. Because of the increased stiffness at the end ranges of movement, the load-displacement curve of the spine is non-linear with increased flexibility around the neutral position of the spine and increased passive resistance and decreased flexibility in the end ranges of motion.  Hence lumbar stability is the ability to maintain the spinal neutral zones during routine functional activity without causing the neurological deficit, significant deformity, or incapacitating pain. 

Muscles provide stability in the neutral zone. Both strength and endurance are equally important. These factors contribute to endurance to maintain stability over long periods of static postures and increased strength when the spine is subject to suddenly increased stress like a fall or a sudden loading of the spine: both muscular strength and endurance decrease in patients with low back pain. The importance of the active system becomes apparent when attempting to link between clinically measurable parameters and back pain. Measures of lumbar lordosis, pelvic tilt, and leg length discrepancy, which measure the passive system does not seem to be as important as muscle strength and endurance, which are measures of the active system [5]. Also, the evidence suggests that the weakness of muscles can lead to segmental instability and cause back pain even in the absence of structural defects.[6]

Maintaining the spine in the neutral zone is important to prevent injury. In the elastic zone or at extremes of motion, there is likely a chance of injury when the spine is loaded. The work by Cholewicki and McGill on powerlifters with fluoroscopy showed that the active system prevents the spine from entering the elastic zone. Even when the powerlifters were in global full flexion, the individual lumbar segments were not in full flexion and remained in the neutral zone to protect the spine.[7] 

The mainstay of treatment in chronic low back pain is exercise and retraining to improve the strength and endurance of the muscles to provide stability during trunkal perturbations. Also, it is crucial to facilitate the proper and sequential firing of muscles. In a minority of patients, when non-surgical methods fail to address lumbar segmental instability, then surgical intervention through fusion may be necessary.[8][9]


A global review including 165 studies conducted in 54 different countries estimated the point prevalence of low back pain as 18.3% and the 1-month prevalence as 30.8%.[10] Females are affected more than men, and the complaint of back pain was more common between the ages of 40 and 69.[10] Higher-income countries (median 30.3%) had a greater prevalence than middle income (median 21.4%) or low-income countries (median 18.2%).[10] There was no difference between urban and rural areas.

Low back pain is the leading cause of years lived with disability in both developed and developing countries. A review that included data from 28 countries showed that low back pain even affected children. There seemed to be an increased prevalence with increasing age. The prevalence was 27.4% in the 11 years old age group, which rose to 46.7% among 15-year-olds.[10] There is also a significant economic burden due to back pain—direct costs from care and indirect costs from lost productivity. 

However, estimating the cost of back pain is difficult. In 1996 two different studies predicted different indirect costs as a result of back pain in the USA. One predicted the cost as being US$ 18.5 billion while another predicted the cost to be US$ 28.2 billion.[10] The costs from spinal issues had, however, increased to US$ 102 billion by 2005.[11]


The core is a box structure made up of the abdominal muscles in the front and the sides, the paraspinal and gluteal muscles at the back, the diaphragm at the roof, and the pelvic floor and the hip girdle muscles as the floor.[12] The abdominal muscles create a rigid cylinder around the spine during movement and provide stability. The activity of the transverse abdominis is recorded during the entire range of flexion and extension of the spine. This co-activation of the abdominal muscles during spinal movement is necessary to maintain spinal stability.[13][14] 

The pelvic floor muscles also form part of the core. The increased effort by the abdominal muscles can only increase intra-abdominal pressure during spinal movement if there is co-contraction of the pelvic floor musculature.[15]

The muscles in the back of the core or that which envelope the vertebrae can be subdivided into the deeper uni-segmental muscles, i.e., the multifidus and the superficial large multisegmental muscles i.e., the erector spinae.[16] The larger multisegmental muscles like the erector spinae are involved in lifting, and the oblique abdominal muscles are involved in rotational movements of the spine.[17] 

These larger muscles do not have a direct attachment to the spinal segment and hence are unable to stabilize the individual segments. The multifidus, which is deeper, has direct attachments to the spinal segments, and allows stabilization of the motion segment during lifting and rotational movements of the spine.[9] The deeper uni segment muscles being close to the axis of the spine act as force transducers. Higher concentrations of muscle spindles are located in the smaller uni-segmental muscles.[18]

The neural subsystem anticipates the loading of the spine and activates contraction of the transverse abdominis and multifidus muscle ahead of the loading. Electrophysiological studies have identified that the activity in the transverse abdominis and multifidus precedes movement in the extremities; this then allows the individual segments of the lumbar spine to become stabilized before movement initiates. Hodges and Richardson identified that in patients with low back pain, there was a delay in the contraction of the transversus abdominis and multifidus.[19]

When there is a delay in the contraction of the multifidus, the larger and global superficial muscles like the erector spinae contract to compensate for the delay in increasing the stiffness of the lumbar spine. Unfortunately, the activation of the large global muscles creates abnormal forces across the individual segments resulting in back pain.[20] This situation is why patients say that any movement causes spasmodic pain. Rehabilitation involves correcting this delayed activation of the deep muscles. If therapy only involves strengthening the muscles without correction of the delay, then it can result in recurrence and chronicity.[21]

History and Physical


The most relevant component of history is the history of pain. Pain should undergo analysis by the SOCRATES method (Sight, Onset, Characteristics, Radiation, Associated factors, Timing, Exacerbating factors, and Severity).[22] Additionally, history should exclude the presence of red flags.[23] Some of the red flags include; Onset of pain <20 or >50 years old, No relief of pain with bed rest, night pain, history of cancer, unexplained weight loss, fever, trauma, intravenous drug abuse, history of steroids or immunosuppressant intake, perineal numbness, bladder dysfunction, and gait disturbance. 

Examination Findings

The standard clinical examination taught in medical schools involves inspection, short evaluation of gait, testing the range of motion, neurological examination, tenderness to palpation, special tests like straight leg raising, Spurlings, Fabers, and Scobers.[24] This method of examination is ideal for identifying severe disorders like cancer or infection and for evaluating radiculopathy and myelopathy. However, they fail to identify weaknesses in the stabilizing systems of the spine.[4] The majority of patients presenting to a doctor do not have serious pathology in the spine. The commonest condition presenting to a physician is mechanical back pain from instability.

Unfortunately, the standard spinal examination taught in medical schools does not include any clinical test to identify the weakness of the muscle, which could cause segmental instability. A physician's report to a patient with mechanical low back pain, at the end of a standard clinical examination, is that no abnormal pathology has been identified. This both frustrates the patient and also does not provide the answers required to help the patient. Ideally, some of the following tests should be included in all health professionals' armamentarium who are involved in assessing and treating spinal disorders. 

Clinical Tests for Instability

Aberrant movement on flexion-extension [25]

The standard examination involves documenting the range of movement. The quantitative range of movement may not be as significant as the qualitative range of movement. The important feature of spinal instability is the aberrant motion that occurs when flexing and extending the spine. A catch, a painful arc, supporting the arms on the thighs, or a reversal of the lumbopelvic rhythm when standing from the flexed posture indicates instability.

Passive lumbar extension test [26]

The subject lies on the examination couch. The examiner passively lifts the lower limbs to a height of 30 cm from the coach while maintaining the knee in extension and applying gentle traction on the legs. A positive test is recorded if the patient complains of "pain in the lower back region" or complains of "heaviness in the lower back" or complains that, "the lower back is coming off." These experiences should return to normal when the leg returned to the couch. The passive lumbar extension test has the highest combined sensitivity and specificity and may be comparable to radiological findings to identify lumbosacral structural instability.

The prone instability test [27]

The patient stands at the foot end of the examination couch. The patient then lowers his/her upper body to rest on the examination couch. The iliac crest should rest on the edge of the examination couch. The patient holds the sides of the examination couch for increased stability. In the first part of the test, the feet of the patient is resting on the ground. The examiner with the heel of his/her hand creates a small posterior to anterior trust at each segment of the lumbar spine. Pain, if experienced by the patient, is recorded. In the second part of the test, the patient is asked to lift the feet of the floor and steady himself /herself by holding onto the sides of the examination couch. The examiner again repeats the posterior to anterior trust with the heel of his/her hand at each lumbar segment. The test is positive if the pain created in the initial part of the test subsides when the extensor muscles of the spine are tensed by lifting the feet of the floor.

Clinical tests for endurance

Sorensen test[28]

The legs of the patient are strapped onto a low platform, which is only 25 cms above the floor.  The upper end of the iliac crest is aligned to the edge of the table. The upper torso rests on the floor. At the commencement of the test, the patient extends the spine and lifts the upper torso off the floor with the arms crossed across the chest and is asked to maintain the horizontal position. The record of the time, the patient can maintain this position is documented.  Normative values: Men 146 +/- 51. Women 189 +/- 60.

Prone isometric chest raise[29]:

The patient lies prone on the examination couch with a pad underneath the abdomen and the arms along the sides. The patient is instructed to lift the upper trunk about 30 degrees from the table while keeping the neck flexed, and the intention is to hold the sternum of the surface of the couch. The clinician records the maximum time that the patient can hold this position. Normative values: Men 40 +/- 9. Women 52 +/- 18.[30]

Prone double straight leg raise[30]:

The patient lies prone on the examination couch with the hips extended and the hands underneath the forehead. The arms are perpendicular to the body. The patient is then requested to lift both the legs off the couch until the knee is cleared off the couch. The patient should maintain normal breathing during the entire test procedure. The examiner can monitor the knee clearance by sliding a hand under the knee. The clinician records the maximum time that the patient can hold this position. Normative values: Men 38 +/- 6. Women 35 +/- 5. The prone double straight leg raise has shown to have great sensitivity and specificity. 

Supine static chest raise[30]:

The patient lies supine on the couch with the legs extended. The hands are placed on the temples with the elbows pointing to the ceiling.  The patient is then instructed to lift the head, the arms and upper trunk of the couch. The patient should maintain normal breathing during the entire test procedure. The clinician records the maximum time that the patient can hold this position. Normative values: Men 43 +/- 9. Women 32 +/- 5. 

Supine double straight leg raise[30]:

The patient lies supine with the legs extended, and the arms crossed in front of the chest. The pelvis is tilted forward to increase the lumbar lordosis. The patient is then requested to lift both the legs of the floor for 30 degrees while maintaining normal breathing during the entire test procedure. To monitor the pelvic tilt, the examiner can place one hand under the lumbar spine.  The clinician records the maximum time that the patient can hold this position. Normative values: Men 28 +/- 4. Women 28 +/- 4. 

Flexor endurance test[31]:

The patient is supine on the couch with the upper part of the body propped up on a support. The support is at an angle of 60 degrees. The legs are flexed so that the knee is at a 90-degree angle with the foot flat on the couch. The toes and feet are strapped to the couch to provide a counterbalance. In a modified procedure, the examiner sits on the edge of the couch and over the toes of the patient to provide a counterbalance. The arms are crossed across the chest towards the opposite shoulder. The support is moved back by 10 cms, and the patient is instructed to maintain the original position. The clinician records the maximum time that the patient can hold this position. Normal values: Men 144 +/- 76, Women 149 +/- 99 in normal subjects.

Prone Plank/Bridge[32]

The patient lies prone on a mat. Initially, the patient lifts his / her upper torso off the mat and steadies on the elbows and forearms. The elbow is directly below the shoulder, and the forearms are straight with hands in front of the elbow. The patient then lifts the pelvis off the mat. The body is now supported on the elbow/forearm and the tips of the toes. The patient maintains a rigid horizontal position parallel to the floor. The clinician records the maximum time that the patient can hold this position. Normative values: Men 124 +/- 72s, Women 83 +/- 63s.

Supine Bridge[33]:

The patient lies supine with the legs flexed so that the knee is at a 90-degree angle, and the foot is flat on the couch but not touching each other. The elbows are bent, and the hands are placed on the ears. The patient then lifts the pelvis so that the shoulders, hips, and knees are in a straight line. A rigid position is maintained, and the clinician records the maximum time that the patient can hold this position. Normative values: Men 188 +/- 45s, Women 152 +/- 30s.

Side Plank/Bridge[33]:

The patient lies on the side on a mat. The upper part of the body is lifted off the mat and supported on the elbow of the arm below. The opposite (upper) arm crosses across the chest onto the lower shoulder. The top foot is positioned in front of the lower foot. The patient is then instructed to lift the pelvis off the floor and to maintain the trunk and the legs in a straight line. A rigid position is maintained, and the clinician records the maximum time that the patient can hold this position. Normative values: Men 95 +/- 35s, Women 74 +/- 33s.


Segmental instability is also identifiable on dynamic radiographs. White and Punjabi suggested that any of the following criteria on a flexion-extension radiograph could be considered as segmental instability. A sagittal plane translation of greater than 4.5 mm or a sagittal plane translation greater than 15% of the vertebral body width or a sagittal plane rotation greater than 15 degrees at either L1/L2, L2/L3 or L3/L4, or greater than 20 degrees at L4/L5, or greater than 25 degrees at L5/S1.[34]

Ultrasound examination has shown that the cross-sectional area of the multifidus muscle becomes decreased in patients with low back pain.[35] Computed tomography has identified the correlation between fat infiltration of the multifidus muscle and the presence of low back pain.[36] Similarly, magnetic resonance imaging has also identified the correlation between low back pain and the decreased cross-sectional area of the muscle.[37]

Treatment / Management

Exercises have become the cornerstone of treating and preventing back pain. Evidence suggests that the lack of muscle strength can itself contribute to low back pain even in the absence of degeneration. A study of adolescents aged between 14 to 16 and who had minimal to no degenerative changes showed that weakness of the lumbar spine extension was a risk factor for developing low back pain.[38] The exercise regimes for treating and preventing low back pain vary from stretching, strengthening, endurance, aerobic fitness, walking, yoga, pilates, and motor control exercises. All these active interventions reduce back pain, but there is no evidence that one form of exercise is superior to the other.[39] 

Though there are many modalities of exercise therapies that are beneficial for back pain, this article will only discuss the motor control exercises here because motor control exercises allow regaining the stability and control of the spine, which patients who have low back pain lose.[40]

Among the paraspinal muscles, the deeper uni-segmental multifidus muscle control stiffness and intervertebral relationship. The larger multi-segmental and global erector spinae are torque generators and aid in lifting. The deep fibers of the multifidus are the first to become active when a limb is moved because a limb can only move on a stable axial skeleton. Hence co-activation of the spinal and abdominal muscles is required before limb movement or any activity that involves perturbation of the trunk and spine.[41]

The dysfunction of the multifidus muscle results in delay and reduced activity.  When there is a delay or reduced activity in the deeper multifidus, the larger multi-segmental muscles compensate by co-activation. Motor control errors or lack of the abdominals and the multifidus acting before larger global muscles increase compressive forces across spinal segments and result in pain.[41][42] Motor control exercises involve retraining the deep local muscle system i.e., the multifidus and the transverse abdominis, to become active before the larger global multisegment muscles become active.[43]

The Motor control exercise (MCE) program involves three stages.[44] In the first stage, the local stabilizing muscles (i.e., the lumbar multifidus and the transversus abdominis) are activated by an abdominal drawing-in maneuver (ADIM) while maintaining normal breathing. The abdominal drawing-in maneuver is maintained for 8 seconds. The ADIM is performed in 4 different body positions, sitting, standing, supine lying, and quadruped positions.

The target to aim for is 30 repetitions in each position. After reaching the goal by the second week, then the second stage of the program starts. In the second stage, increased loads are placed on the trunk by placing the upper and lower limbs and the trunk in various positions while continuing with the ADIM. This activity may involve heel slide in supine, curls in supine, side bridge with knees bent, the side bridge with knees straight, prone plank, supine bridge, a quadruped with raised contralateral arm and leg. The second stage continues from the second week to the fourth week. From the fifth week, the patient can progress to the third stage of the program; this involves using functional positions like rolling, sit to stand transfer, squatting, and sit to stand transfer. Rabin et al. provide a detailed description of images.[29]

The lack of ability in patients with low back pain to compensate for unexpected balance challenges can be improved with rehabilitation. Also, retraining increases the cross-sectional area of the multifidus, which is usually maintained in the long term and helps to decrease recurrence and chronicity.[21][45] There is very low to moderate-quality evidence that MCE has a clinically important effect compared with a minimal intervention for chronic low back pain.[46]

Differential Diagnosis

rThe potential differential diagnoses are leaking aortic aneurysm, epidural abscess, spondylodiscitis, compression fracture, spondyloarthropathy, malignancy, disc prolapse causing radiculopathy spinal canal stenosis, and cauda equina syndrome.[10] History, examination, and investigations will help to identify the cause of low back pain.

Non-specific low back pain is a diagnosis of exclusion when no serious pathology or cause for the low back pain ae identifiable. Among patients with low back pain who present to primary care, more than 90% have non-specific low back pain, 4% have a compression fracture, 3% have spinal stenosis, 2% have a visceral disease and 0.7% have a tumor or metastasis, and 0.01% have an infection.[47]


Most of the patients with low back pain improve quickly. The difficulty, however, is that in some, the pain becomes chronic and persistent. A systematic review, which included 4994 patients from 24 studies, showed that patients with acute pain made good progress. The pain score on a scale of 0 to 100 was 52 at baseline. It decreased to 23 at six weeks, 12 at 26 weeks, and 6 at 52 weeks. However, the cohorts with persistent pain decreased only to 23 at 52 weeks.[48] Older age, poor general health, psychological or psychosocial distress, discordant relationships, physically heavy work, poor baseline functional disability, sciatica, and litigation/compensation were indicators of poor prognosis is.[49]


Progression to chronicity and the lack of improvement in patient outcomes or disability is worrying; this is despite a 629% increase in medicare expenditure for an epidural steroid injection, a 423% increase in opioids, a 307% increase in MRI scans, and a 220% increase in spinal fusion surgery rates.[50] Overprescription of opioid analgesics results in mortality.[51]  Surgery is also increasingly recommended for chronic low back pain, but scientific evidence unequivocally shows that surgery is not superior to non-operative management for chronic low back pain.[52]

Deterrence and Patient Education

Patients need to understand that majority of low back pain is harmless and spontaneously resolves. Fear-avoidance can be detrimental. There is no role for bed rest, and it is essential to remain active.[53] Sedentary behavior has weakened our muscles.  Health professions have a profound effect on patients, and they should positively influence attitudes and beliefs during their interaction with patients.[54]

Enhancing Healthcare Team Outcomes

Exercise has been the mainstay of treatment for mechanical low back pain. All healthcare professionals involved in the care of back pain must be able to identify mechanical back pain due to lumbar instability and provide validated exercise protocols to correct the same.

Family practitioners, physiotherapists, and orthopedic surgeons should be able to communicate to patients the benefits of involvement in a regular exercise program in the treatment and prevention of lower back pain secondary to mechanical instability. 

Pharmacological analgesia should only be a supplement of the good rehabilitation regime. There is no role for surgical intervention in mechanical low back pain. 

Review Questions


Panjabi MM. The stabilizing system of the spine. Part I. Function, dysfunction, adaptation, and enhancement. J Spinal Disord. 1992 Dec;5(4):383-9; discussion 397. [PubMed: 1490034]
Crisco JJ, Panjabi MM. Euler stability of the human ligamentous lumbar spine. Part I: Theory. Clin Biomech (Bristol, Avon). 1992 Feb;7(1):19-26. [PubMed: 23915612]
Gardner-Morse M, Stokes IA, Laible JP. Role of muscles in lumbar spine stability in maximum extension efforts. J Orthop Res. 1995 Sep;13(5):802-8. [PubMed: 7472760]
Barr KP, Griggs M, Cadby T. Lumbar stabilization: core concepts and current literature, Part 1. Am J Phys Med Rehabil. 2005 Jun;84(6):473-80. [PubMed: 15905663]
Nourbakhsh MR, Arab AM. Relationship between mechanical factors and incidence of low back pain. J Orthop Sports Phys Ther. 2002 Sep;32(9):447-60. [PubMed: 12322811]
Delitto A, George SZ, Van Dillen L, Whitman JM, Sowa G, Shekelle P, Denninger TR, Godges JJ., Orthopaedic Section of the American Physical Therapy Association. Low back pain. J Orthop Sports Phys Ther. 2012 Apr;42(4):A1-57. [PMC free article: PMC4893951] [PubMed: 22466247]
Cholewicki J, McGill SM. Lumbar posterior ligament involvement during extremely heavy lifts estimated from fluoroscopic measurements. J Biomech. 1992 Jan;25(1):17-28. [PubMed: 1733981]
Slosar PJ. Indications and outcomes of reconstructive surgery in chronic pain of spinal origin. Spine (Phila Pa 1976). 2002 Nov 15;27(22):2555-62; discussion 2563. [PubMed: 12435993]
Macintosh JE, Bogduk N. The biomechanics of the lumbar multifidus. Clin Biomech (Bristol, Avon). 1986 Nov;1(4):205-13. [PubMed: 23915551]
Maher C, Underwood M, Buchbinder R. Non-specific low back pain. Lancet. 2017 Feb 18;389(10070):736-747. [PubMed: 27745712]
Martin BI, Deyo RA, Mirza SK, Turner JA, Comstock BA, Hollingworth W, Sullivan SD. Expenditures and health status among adults with back and neck problems. JAMA. 2008 Feb 13;299(6):656-64. [PubMed: 18270354]
Akuthota V, Nadler SF. Core strengthening. Arch Phys Med Rehabil. 2004 Mar;85(3 Suppl 1):S86-92. [PubMed: 15034861]
Gardner-Morse MG, Stokes IA. The effects of abdominal muscle coactivation on lumbar spine stability. Spine (Phila Pa 1976). 1998 Jan 01;23(1):86-91; discussion 91-2. [PubMed: 9460158]
Cresswell AG, Grundström H, Thorstensson A. Observations on intra-abdominal pressure and patterns of abdominal intra-muscular activity in man. Acta Physiol Scand. 1992 Apr;144(4):409-18. [PubMed: 1534959]
Sapsford RR, Hodges PW. Contraction of the pelvic floor muscles during abdominal maneuvers. Arch Phys Med Rehabil. 2001 Aug;82(8):1081-8. [PubMed: 11494188]
Crisco JJ, Panjabi MM. The intersegmental and multisegmental muscles of the lumbar spine. A biomechanical model comparing lateral stabilizing potential. Spine (Phila Pa 1976). 1991 Jul;16(7):793-9. [PubMed: 1925756]
Bogduk N, Macintosh JE, Pearcy MJ. A universal model of the lumbar back muscles in the upright position. Spine (Phila Pa 1976). 1992 Aug;17(8):897-913. [PubMed: 1523493]
Peck D, Buxton DF, Nitz A. A comparison of spindle concentrations in large and small muscles acting in parallel combinations. J Morphol. 1984 Jun;180(3):243-52. [PubMed: 6235379]
Hodges PW, Richardson CA. Inefficient muscular stabilization of the lumbar spine associated with low back pain. A motor control evaluation of transversus abdominis. Spine (Phila Pa 1976). 1996 Nov 15;21(22):2640-50. [PubMed: 8961451]
van Dieën JH, Selen LP, Cholewicki J. Trunk muscle activation in low-back pain patients, an analysis of the literature. J Electromyogr Kinesiol. 2003 Aug;13(4):333-51. [PubMed: 12832164]
Hides JA, Jull GA, Richardson CA. Long-term effects of specific stabilizing exercises for first-episode low back pain. Spine (Phila Pa 1976). 2001 Jun 01;26(11):E243-8. [PubMed: 11389408]
Sayma M, Williams HR. A new method for teaching physical examination to junior medical students. Adv Med Educ Pract. 2016;7:91-7. [PMC free article: PMC4762462] [PubMed: 26937208]
Verhagen AP, Downie A, Popal N, Maher C, Koes BW. Red flags presented in current low back pain guidelines: a review. Eur Spine J. 2016 Sep;25(9):2788-802. [PubMed: 27376890]
Davenport D, Colaco HB, Kavarthapu V. Examination of the adult spine. Br J Hosp Med (Lond). 2015 Dec;76(12):C182-5. [PubMed: 26646344]
Fritz JM, Piva SR, Childs JD. Accuracy of the clinical examination to predict radiographic instability of the lumbar spine. Eur Spine J. 2005 Oct;14(8):743-50. [PMC free article: PMC3489248] [PubMed: 16047211]
Kasai Y, Morishita K, Kawakita E, Kondo T, Uchida A. A new evaluation method for lumbar spinal instability: passive lumbar extension test. Phys Ther. 2006 Dec;86(12):1661-7. [PubMed: 17033040]
Alqarni AM, Schneiders AG, Hendrick PA. Clinical tests to diagnose lumbar segmental instability: a systematic review. J Orthop Sports Phys Ther. 2011 Mar;41(3):130-40. [PubMed: 21289452]
Biering-Sørensen F. Physical measurements as risk indicators for low-back trouble over a one-year period. Spine (Phila Pa 1976). 1984 Mar;9(2):106-19. [PubMed: 6233709]
Ito T, Shirado O, Suzuki H, Takahashi M, Kaneda K, Strax TE. Lumbar trunk muscle endurance testing: an inexpensive alternative to a machine for evaluation. Arch Phys Med Rehabil. 1996 Jan;77(1):75-9. [PubMed: 8554479]
Arab AM, Salavati M, Ebrahimi I, Ebrahim Mousavi M. Sensitivity, specificity and predictive value of the clinical trunk muscle endurance tests in low back pain. Clin Rehabil. 2007 Jul;21(7):640-7. [PubMed: 17702706]
McGill SM, Childs A, Liebenson C. Endurance times for low back stabilization exercises: clinical targets for testing and training from a normal database. Arch Phys Med Rehabil. 1999 Aug;80(8):941-4. [PubMed: 10453772]
Strand SL, Hjelm J, Shoepe TC, Fajardo MA. Norms for an isometric muscle endurance test. J Hum Kinet. 2014 Mar 27;40:93-102. [PMC free article: PMC4096102] [PubMed: 25031677]
Schellenberg KL, Lang JM, Chan KM, Burnham RS. A clinical tool for office assessment of lumbar spine stabilization endurance: prone and supine bridge maneuvers. Am J Phys Med Rehabil. 2007 May;86(5):380-386. [PubMed: 17303961]
Leone A, Guglielmi G, Cassar-Pullicino VN, Bonomo L. Lumbar intervertebral instability: a review. Radiology. 2007 Oct;245(1):62-77. [PubMed: 17885181]
Hides JA, Stokes MJ, Saide M, Jull GA, Cooper DH. Evidence of lumbar multifidus muscle wasting ipsilateral to symptoms in patients with acute/subacute low back pain. Spine (Phila Pa 1976). 1994 Jan 15;19(2):165-72. [PubMed: 8153825]
Alaranta H, Tallroth K, Soukka A, Heliövaara M. Fat content of lumbar extensor muscles and low back disability: a radiographic and clinical comparison. J Spinal Disord. 1993 Apr;6(2):137-40. [PubMed: 8504225]
Ranger TA, Cicuttini FM, Jensen TS, Peiris WL, Hussain SM, Fairley J, Urquhart DM. Are the size and composition of the paraspinal muscles associated with low back pain? A systematic review. Spine J. 2017 Nov;17(11):1729-1748. [PubMed: 28756299]
Sjölie AN, Ljunggren AE. The significance of high lumbar mobility and low lumbar strength for current and future low back pain in adolescents. Spine (Phila Pa 1976). 2001 Dec 01;26(23):2629-36. [PubMed: 11725246]
Shiri R, Coggon D, Falah-Hassani K. Exercise for the Prevention of Low Back Pain: Systematic Review and Meta-Analysis of Controlled Trials. Am J Epidemiol. 2018 May 01;187(5):1093-1101. [PubMed: 29053873]
Bergmark A. Stability of the lumbar spine. A study in mechanical engineering. Acta Orthop Scand Suppl. 1989;230:1-54. [PubMed: 2658468]
McGill SM. Low back stability: from formal description to issues for performance and rehabilitation. Exerc Sport Sci Rev. 2001;29(1):26-31. [PubMed: 11210443]
Ferreira PH, Ferreira ML, Hodges PW. Changes in recruitment of the abdominal muscles in people with low back pain: ultrasound measurement of muscle activity. Spine (Phila Pa 1976). 2004 Nov 15;29(22):2560-6. [PubMed: 15543074]
Wilder DG, Aleksiev AR, Magnusson ML, Pope MH, Spratt KF, Goel VK. Muscular response to sudden load. A tool to evaluate fatigue and rehabilitation. Spine (Phila Pa 1976). 1996 Nov 15;21(22):2628-39. [PubMed: 9045348]
Rabin A, Shashua A, Pizem K, Dickstein R, Dar G. A clinical prediction rule to identify patients with low back pain who are likely to experience short-term success following lumbar stabilization exercises: a randomized controlled validation study. J Orthop Sports Phys Ther. 2014 Jan;44(1):6-B13. [PubMed: 24261926]
O'Sullivan PB, Phyty GD, Twomey LT, Allison GT. Evaluation of specific stabilizing exercise in the treatment of chronic low back pain with radiologic diagnosis of spondylolysis or spondylolisthesis. Spine (Phila Pa 1976). 1997 Dec 15;22(24):2959-67. [PubMed: 9431633]
Saragiotto BT, Maher CG, Yamato TP, Costa LO, Menezes Costa LC, Ostelo RW, Macedo LG. Motor control exercise for chronic non-specific low-back pain. Cochrane Database Syst Rev. 2016 Jan 08;2016(1):CD012004. [PMC free article: PMC8761501] [PubMed: 26742533]
Deyo RA, Weinstein JN. Low back pain. N Engl J Med. 2001 Feb 01;344(5):363-70. [PubMed: 11172169]
da C Menezes Costa L, Maher CG, Hancock MJ, McAuley JH, Herbert RD, Costa LO. The prognosis of acute and persistent low-back pain: a meta-analysis. CMAJ. 2012 Aug 07;184(11):E613-24. [PMC free article: PMC3414626] [PubMed: 22586331]
Hayden JA, Chou R, Hogg-Johnson S, Bombardier C. Systematic reviews of low back pain prognosis had variable methods and results: guidance for future prognosis reviews. J Clin Epidemiol. 2009 Aug;62(8):781-796.e1. [PubMed: 19136234]
Deyo RA, Mirza SK, Turner JA, Martin BI. Overtreating chronic back pain: time to back off? J Am Board Fam Med. 2009 Jan-Feb;22(1):62-8. [PMC free article: PMC2729142] [PubMed: 19124635]
Paulozzi LJ, Budnitz DS, Xi Y. Increasing deaths from opioid analgesics in the United States. Pharmacoepidemiol Drug Saf. 2006 Sep;15(9):618-27. [PubMed: 16862602]
Mannion AF, Brox JI, Fairbank JC. Consensus at last! Long-term results of all randomized controlled trials show that fusion is no better than non-operative care in improving pain and disability in chronic low back pain. Spine J. 2016 May;16(5):588-90. [PubMed: 27261844]
Wilkes MS. Chronic back pain: does bed rest help? West J Med. 2000 Feb;172(2):121. [PMC free article: PMC1070772] [PubMed: 10693375]
Darlow B, Dowell A, Baxter GD, Mathieson F, Perry M, Dean S. The enduring impact of what clinicians say to people with low back pain. Ann Fam Med. 2013 Nov-Dec;11(6):527-34. [PMC free article: PMC3823723] [PubMed: 24218376]

Disclosure: Katarzyna Studnicka declares no relevant financial relationships with ineligible companies.

Disclosure: George Ampat declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK562179PMID: 32965850


  • PubReader
  • Print View
  • Cite this Page

Related information

  • PMC
    PubMed Central citations
  • PubMed
    Links to PubMed

Similar articles in PubMed

See reviews...See all...

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...