A Hypothesis of Chronic Back Pain Ligament Subfailure Injuries Lead to Muscle Control Dysfunction

8/12/2019 A Hypothesis of Chronic Back Pain Ligament Subfailure Injuries Lead to Muscle Control Dysfunction

1/9

Introduction

Low back pain is an important societal problem withsignicant costs. Up to 7085% of the population inindustrialized societies experience low back pain at leastonce in their lifetime, with point prevalence of about30% [ 1, 24]. The total cost of low back pain has beenestimated to exceed 50 billion dollars per year in theUSA [ 17]. Although neck pain due to whiplash-associ-ated disorder is less common and less costly, awarenessof this disorder, diagnosis and treatment are equally

baffling [ 63]. The term back pain as used here does notinclude back pain due to known infections, tumor, sys-

temic disease, fractures or fracture dislocations [ 73].Further, the term used here refers generally to the entirespine but in particular to the cervical and lumbar re-gions.

Back pain is complex. The exact cause of most back(low back and neck) pain remains unproven [ 72]. Themulti-factorial nature of back pain is well recognizedwith respect to its causes, diagnosis, chronicity, disabil-ity and treatment [ 73]. Abnormal mechanics of the

Manohar M. Panjabi A hypothesis of chronic back pain: ligamentsubfailure injuries lead to muscle controldysfunction

Received: 13 November 2004Revised: 25 January 2005Accepted: 28 February 2005Published online: 27 July 2005

Springer-Verlag 2005

Abstract Clinical reports and re-search studies have documented thebehavior of chronic low back andneck pain patients. A few hypotheseshave attempted to explain thesevaried clinical and research ndings.A new hypothesis, based upon theconcept that subfailure injuries of ligaments (spinal ligaments, discannulus and facet capsules) maycause chronic back pain due tomuscle control dysfunction, is pre-sented. The hypothesis has the fol-lowing sequential steps. Singletrauma or cumulative microtraumacauses subfailure injuries of the lig-aments and embedded mechanore-ceptors. The injuredmechanoreceptors generate cor-rupted transducer signals, whichlead to corrupted muscle responsepattern produced by the neuromus-cular control unit. Muscle coordi-nation and individual muscle force

characteristics, i.e. onset, magnitude,and shut-off, are disrupted. This re-sults in abnormal stresses and strainsin the ligaments, mechanoreceptorsand muscles, and excessive loadingof the facet joints. Due to inherentlypoor healing of spinal ligaments,accelerated degeneration of disc andfacet joints may occur. The abnor-mal conditions may persist, and,over time, may lead to chronic backpain via inammation of neural tis-sues. The hypothesis explains manyof the clinical observations and re-search ndings about the back painpatients. The hypothesis may help ina better understanding of chroniclow back and neck pain patients,and in improved clinical manage-ment.

Keywords Low back pain Neckpain Whiplash Biomechanics Hypothesis

Eur Spine J (2006) 15: 668676DOI 10.1007/s00586-005-0925-3 ORIGINAL ARTICLE

M. M. PanjabiBiomechanics Research Laboratory,Department of Orthopaedics andRehabilitation, Yale UniversitySchool of Medicine, New Haven,Box 208071, CT 06520-8071, USAE-mail: [email protected].: +203-785-2812Fax: +203-785-7069


2/9

spinal column has been hypothesized to lead to backpain via nociceptive sensors [ 72]. The path fromabnormal mechanics to nociceptive sensation may go viainammation [ 8, 11], biochemical and nutritional chan-ges [6], immunological factors [ 44], and changes in thestructure and material of the endplates [ 6] and discs [ 40,41], and neural structures, such as nerve ingrowth into

diseased intervertebral disc [ 15, 16]. The abnormalmechanics of the spine may be due to degenerativechanges of the spinal column [ 18] and/or injury of theligaments [ 43]. Most likely, the initiating event is somekind of trauma involving the spine. It may be a singletrauma due to an accident or microtrauma caused byrepetitive motion over a long time. It is also possible thatspinal muscles will re in an uncoordinated way in re-sponse to sudden fear of injury, such as when one mis- judges the depth of a step. All these events may causespinal ligament injury. Adverse psychosocial factorsmay also play an important role in transforming theback pain into disability [ 3].

The research literature on chronic back pain is vast.However, there are some important and commonobservations. Chronic low back pain patients have de-layed muscle response when asked to perform a task [ 65]or when the spine is suddenly loaded [ 35], or in antici-pation of raising an arm to horizontal position [ 20], andalso delayed muscle shut-off after the external challengehas been withdrawn [ 52]. Further, they show poorerspinal posture control and balance, especially duringcomplex tasks, when compared to subjects without backpain [ 10, 33, 53]. The ndings in neck pain patients aresimilar, although the number of studies is fewer. Patientswith whiplash-associated disorders have disrupted neck

motion [ 2, 4, 14, 27, 34, 49, 51] and less efficient musclecontrol [ 14, 19, 22, 31, 34].A few hypotheses have attempted to explain the

clinical observations and research ndings in back painpatients. As the nociceptive sensors are present in mostcomponents of the spinal column, the hypotheses havefocused on disruption of the spinal column and itscomponents, such as spinal column degeneration [ 25],injury and clinical instability [ 47, 73]; facet joint injury[13], and inferior facet-tip impingement on the lamina[77], and Schmorls nodes [ 29]. Others have focused onspinal muscles. The pain adaptation [ 32] and pain spasmpain [ 54] hypotheses were evaluated in a recentreview article [ 69]. The evidence was mixed, and authorssuggested that other models, such as spinal instability[46, 47], may be explored. The role played by the injuryto the mechanoreceptors embedded in the ligaments of the spinal column has not been explored by anyhypothesis.

The spinal column, consisting of ligaments (spinalligaments, discs annulus and facet capsules) and verte-brae, is one of the three subsystems of the spinal stabi-lizing system [ 46]. The other two are the spinal muscles

and neuromuscular control unit, Fig. 1. The spinal col-umn has two functions: structural and transducer . Thestructural function provides stiffness to the spine. Thetransducer function provides the information needed toprecisely characterize the spinal posture, vertebral mo-tions, spinal loads etc. to the neuromuscular control unitvia innumerable mechanoreceptors present in the spinal

column ligaments [ 26, 58], facet capsules [ 11 , 36, 76] andthe disc annulus [ 26]. These mechanical transducersprovide information to the neuromuscular control unitwhich helps to generate muscular spinal stability via thespinal muscle system and neuromuscular control unit.[46] The criterion used by the neuromuscular unit ishypothesized to be the need for adequate and overallmechanical stability of the spine. If the structural func-tion is compromised, due to injury or degeneration, thenthe muscular stability is increased to compensate theloss. What happens if the transducer function of theligaments of the spinal column is compromised? This hasnot been explored. There is evidence from animal studies

that the stimulation of the ligaments of the spine (discand facets [ 21], and ligaments [ 59, 62]) results in spinalmuscle ring. The mechanoreceptor-muscle ring rela-tionships are modulated by several factors, such as lig-ament fatigue [ 61], static exed posture [ 60], andcumulative microtrauma [ 75].

The observations from animal studies just mentioned,together with the possibility of transducer dysfunction inback pain patients, form the basis of a new back painhypothesis. The purpose is to describe the hypothesis,use the hypothesis to explain the various important re-search ndings, and suggest possible treatment options.

The hypothesis

The hypothesis consists of the following sequential steps:

1. Single trauma or cumulative microtrauma causessubfailure injury of the spinal ligaments and injury tothe mechanoreceptors embedded in the ligaments.

2. When the injured spine performs a task or it ischallenged by an external load, the transducer signalsgenerated by the mechanoreceptors are corrupted.

3. Neuromuscular control unit has difficulty in inter-preting the corrupted transducer signals becausethere is spatial and temporal mismatch between thenormally expected and the corrupted signals received.

4. The muscle response pattern generated by the neu-romuscular control unit is corrupted, affecting thespatial and temporal coordination and activation of each spinal muscle.

5. The corrupted muscle response pattern leads to cor-rupted feedback to the control unit via tendon organsof muscles and injured mechanoreceptors, furthercorrupting the muscle response pattern.

669


3/9

6. The corrupted muscle response pattern produces highstresses and strains in spinal components leading tofurther subfailure injury of the spinal ligaments, me-chanoreceptors and muscles, and overload of facet joints.

7. The abnormal stresses and strains produce inam-

mation of spinal tissues, which have abundant supplyof nociceptive sensors and neural structures.

8. Consequently, over time, chronic back pain may de-velop. The subfailure injury of the spinal ligament isdened as an injury caused by stretching of the tissuebeyond its physiological limit, but less than its failurepoint [ 48].

Under normal circumstances, to perform a task or torespond to an external challenge, the mechanoreceptorsgenerate a complex and redundant set of transducersignals describing vertebral position, spinal motion,spinal load, and so forth, at each spinal level (Fig. 2).The signals are transmitted to the neuromuscular con-trol unit for interpretation and action. The neuromus-cular control unit evaluates the signals and produces anormal muscle response pattern, based upon severalfactors, including the need for spinal stability, posturalcontrol, balance, minimal stress/stain in various spinalcomponents, and so forth. This is achieved via feedbackfrom the muscle spindles and golgi tendon organs of themuscles as well as the mechanoreceptors of the liga-ments. The muscle response pattern includes all the

information needed to dynamically orchestrate themuscles: to choose the individual muscles needed, and toactivate each muscle in a dened sequence with respectto its onset, activation level and shut-off. The entiredynamic procedure is relatively quick, non-injurious andleads to no adverse consequences.

The injured spine behaves differently (Fig. 3). Thesubfailure injuries of the ligaments disrupt and/or injurethe embedded mechanoreceptors. When the spine per-forms a routine task or responds to an external challenge,the disrupted/injured mechanoreceptors produce cor-rupted transducer signals, describing vertebral position,motion, spinal loads etc. for each spinal level. There isloss of spatial and temporal integrity of the transducersignals received from multiple redundant mechanore-ceptors distributed through the spinal column. Theneuromuscular control unit, not affected by the injuryitself, senses a mismatch between the normally expectedand the received transducer signals, and, therefore, hasdifficulty in choosing the appropriate muscle responsepattern. However, it must act. Consequently, the neu-romuscular control unit produces a corrupted muscleresponse pattern, which is the closest match it candetermine to the corrupted transducer signals. The cor-rupted muscle response pattern affects the choice of thespinal muscles to activate, and the individual muscleactivation: force onset, intensity and shut-off. Theorchestration of the various spinal muscles responsiblefor spinal stability, posture and motion is disrupted.

Fig. 1 Spinal stabilizing system.It consists of three subsystems:spinal column, spinal muscles,and neuromuscular controlunit. The spinal column has twofunctions: structuralto pro-vide intrinsic mechanical stabil-ity, and transducertogenerate signals describingspinal posture, motions, loadsetc. via the mechanoreceptors.The neuromuscular control unitgenerates muscle response pat-tern to activate and coordinatethe spinal muscles to providemuscle mechanical stability.There is feedback from thespinal muscles and mechanore-ceptors to the control unit.(Adapted from Panjabi 1992)

670


4/9

Additionally, the feedback to the neuromuscular controlunit and mechanoreceptors is also negatively affected,further corrupting the muscle response pattern. This hasseveral adverse effects. Higher stresses, and strains andinjuries may develop in the spinal ligaments, and me-chanoreceptors. The facet joints may be overloaded, andthe spinal muscles may fatigue or be injured. Over time,these injurious stresses and strains can initiate inam-mation of neural tissues [ 12], and accelerate disc [ 40] andfacet joint [ 9] degeneration. Thus, a vicious cycle is set up,leading to chronic dysfunction of the entire spinal sys-tem, resulting in back pain.

Discussion

The underlying concept of the spinal instabilityhypothesis was the need for adequate spinal stabilityprovided by vertebrae and ligaments of the spinal col-umn, and augmented by the spinal muscles under theneuromuscular control [ 46, 47]. In the present hypoth-esis, the focus is on the disruption of the mechanore-ceptors due to ligament injury leading to corruptedtransducer signals and muscle response pattern, andoverall system dysfunction. What follows is an attempt,using the new hypothesis, to explain some of theobservations concerning low back and neck pain pa-tients, and to suggest treatment options.

Delayed muscle response is a common observation inlow back pain patients. When low back pain patients

were challenged by a sudden external load, the delayedmuscle onset was observed [ 35], and delayed muscleshut-off was seen when the load was removed [ 52].Similarly, the anticipatory response of the transverseabdominis was delayed [ 20]. These ndings can be ex-plained by the hypothesis. An individual with intactspinal system, when challenged by a sudden change in itsload or posture, will produce a quick and normal muscleresponse pattern, specic to the challenge (Fig. 2).However, when the neuromuscular control unit receivescorrupted transducer signals, it may take a longer timeto choose a muscle response pattern that most closelymatches the corrupted transducer signals, taking intoaccount a multitude of factors such as spinal stability,postural balance, tissue overload and so forth (Fig. 3).Additional factors, such as muscle fatigue, complexity of the task, mental distraction, and so forth, may furtherdecrease the efficiency of the neuromuscular control unitleading to the delayed muscle system response.

Balance and postural control are decient in low backpain patients [ 10, 33, 53]. The balance and posturalcontrol includes a three-step process: generation of transducer signals by the mechanoreceptors; selection of appropriate muscle response pattern by the neuromus-cular control unit based up mechanoreceptor signals;and feedback from the mechanoreceptors and musclespindles and golgi tendon organs (Fig. 2). Therefore,subfailure injuries of the ligaments disrupt all the threesteps involving the mechanoreceptors thereby resultingin poor balance and postural control.

Fig. 2 Normal circumstances.The intact mechanoreceptorssend transducer signals to theneuromuscular control unit,which evaluates the transducersignals and sends out muscleresponse pattern to coordinatethe activation of individualspinal muscles. There is feed-back from the muscle spindlesand golgi tendon organs of themuscles and mechanoreceptorsof the ligaments to the neuro-muscular control unit. Undernormal circumstances, there areno adverse consequences

671


5/9

Re-positioning error has been consistently found inboth low back pain [ 7, 38, 42] and whiplash [ 19, 31] pa-tients. The error occurs when the patient is asked, start-ing from an initial posture, to rst bend or twist the spineto a certain posture, and then to return to the initialposture. Based upon the hypothesis presented, this is tobe expected. The muscle response pattern generated tobring back the trunk or head to the initial posture makesuse of the mechanoreceptor transducer signals, in thethree-step process described above. With the ligamentinjury in back pain patients, the corrupted mechanore-ceptor information and the corrupted muscle responsepattern will both lead to the re-positioning error.

Among chronic whiplash patients, decreased neckmotion has been observed in most studies [ 2, 4, 14, 34,49, 51]. These were active motion studies in which thesubject was encouraged to produce the motion. How-ever, when the subject was relaxed and the motion wasproduced passively by the examiner, the motion wasfound to be increased in the whiplash patients comparedto the control group [ 27]. How can one explain thesecontrasting ndings? In the active motion studies, cor-rupted muscle response pattern (generated due to cor-rupted mechanoreceptor signals) applies higher muscleforces on the cervical spine. Such forces stiffen the spine

and reduce the motion [ 50, 68, 74]. In the relaxed passivemotion studies, care was taken to decrease the inuenceof muscle guarding, pain and lack of motivation byrelaxing the neck and shoulder muscles with applicationof vapor coolant, and then letting the examiner move thepatients head into maximum exion. Thus, when theabnormal muscle forces were minimized in the passiveexamination, the intrinsic injury of the spinal columnwas exhibited as the increased motion.

Muscle spasm is commonly observed in both low backpain [ 5, 30] and whiplash patients [ 39, 55, 67]. Musclecoordination may be thought of as an orchestratedactivation of various spinal muscles to stabilize the spinalcolumn and accomplish a certain task. The orchestrationconsists of activation of individual muscles with respectto the onset, magnitude of the force generated, and offset.With the injury of the ligaments, the mechanoreceptorsgenerate corrupted transducer signals, and therefore,there is a mismatch between the expected and the re-ceived corrupted transducer signals. The neuromuscularcontrol unit senses the mismatch and may re simulta-neously both the agonist and antagonist muscles at itscommand to temporarily stabilize the spine and minimizethe intervertebral motions, corrupted transducer signals,and pain. If the situation does not improve with time,

Fig. 3 Subfailure injuries of theligaments. The injured me-chanoreceptors send out cor-rupted transducer signals to theneuromuscular control unit,which nds spatial and tempo-ral mismatch between the ex-pected and received transducersignals, and, as a result, there ismuscle system dysfunction andcorrupted muscle response pat-tern is generated. Consequently,there are adverse consequenses:higher stresses, strains, andeven injuries, in the ligaments,mechanoreceptors, and mus-cles. There may also be musclefatigue, and excessive facetloads. These abnormal condi-tions produce neural and liga-ment inammation, and overtime, chronic back pain

672


6/9

then the muscle action may become chronic. Suchsimultaneous ring of agonistic and antagonist muscleshas been observed in low back pain patients.

Greater variability has been observed in almost allparameters measured in low back [ 28, 33, 37, 42, 53] andwhiplash [ 14, 34] patients. The new hypothesis can ex-plain this increased variability. The subfailure injuries of

ligaments are incomplete injuries, which may range be-tween tearing of a few bers to a nearly complete ruptureof a ligament. Importantly, a complex joint, such as afunctional spinal unit, includes many ligament struc-tures. This collection of ligament structures mayencompass a wide range of injuries, each structure withdifferent injury severity, depending upon the magnitudeand mode of the trauma. The density of the mechano-receptors imbedded in the various ligament structuresmay also vary. The result of all these numerous varia-tions can produce a wide spectrum of corrupted muscleresponse patterns for seemingly similar injury-causingevents. Further, each low back pain patient is unique,

for example with respect to the anatomy, mechanicalproperties of ligaments, and muscle response to thetrauma, adding further to the muscle response patternvariability.

There are limitations to the hypothesis. Back pain is acomplex multifactorial problem, and a single hypothesiscannot explain each and every clinical and researchobservation, and there may also be alternative explana-tions, such as instability [ 46, 47], and/or pain [ 32, 54]. It isrecognized that the pain is a subjective experience. Be-sides affecting the muscle system via the corruptedmechanoreceptor signals, ligament injury may also resultin muscle atrophy and weakness due to disuse, thus di-

rectly affecting the spinal system function. Additionally,muscle injury, fatigue, atrophy, and so forth mayaggravate the spinal system dysfunction. As the musclesparticipate in the feedback loop via the mechanorecep-tors in the form of muscle spindles and golgi tendonorgans (Fig. 3), their disruption could further corrupt themuscle response pattern. However, an injured musclemay heal relatively quickly due to abundant blood sup-ply, and, therefore, may not be the main cause of chronicback pain. In contrast, the ligament injuries heal poorlyand, therefore, may lead to tissue degeneration over time[40, 41]. Thus, the ligament injuries are more likely to bethe major cause of the chronic back pain. The corruptedtransducer signals may be the result not only of the lig-ament injury, but also due to ligament fatigue and vis-coelastic creep stretch [ 61], but such an effect is oftenreversible given sufficient rest, and, therefore, may notalways lead to chronic back pain. The clinical and re-search studies presented constitute only a small, but animportant and quite representative sample, of the vastliterature available on the subject of back pain. It isrecognized that there may be other studies whoseexplanation may or may not t the new hypothesis. In

general, hypotheses and models are extremely difficult, if not impossible, to fully validate [ 45]. They can only at-tempt to explain the available ndings, and may be usedto predict outcomes in specic situations.

Can the system adapt to the subfailure injury of themechanoreceptors? A minor subfailure injury is proba-bly repaired or compensated with no long-term conse-

quences. A mild subfailure injury, on the other hand,may be successfully compensated in the short-term bytemporarily modifying the chosen muscle response pat-tern. However, the modication may be difficult tomaintain overtime, as it is likely to produce excessivetissue loads and muscle fatigue. Lapses in the mainte-nance of the modied muscle response pattern may oc-cur from time to time. Could this be the mechanism forrecurrent episodes of back pain that many patientsexperience? [ 57, 71] On the other hand, if the corruptedmuscle response pattern becomes permanent, then itmay result in abnormal posture, disturbed intervertebralmotion pattern, altered gait, and, in general, a less effi-

cient system to perform every day spinal functions.One can speculate as to the possible treatment op-tions based upon the hypothesis. The incoming cor-rupted transducer data may never become normal, eventhough the ligaments, incorporating the injured me-chanoreceptors, may heal/scar over time. After breakingthe cascade of injury, inammation, and pain by suitabledrug treatment, the patient may be encouraged to re-train the neuromuscular control unit to produce an al-tered muscle response pattern that is suited to both thecorrupted transducer signals and activities of daily liv-ing. The criterion for the altered muscle response patternmay be the reduction of stresses and strains of the lig-

aments, loads on facet joints, and muscle forces, whichmay reduce the back pain. A set of tasks may be de-signed for this purpose. The tasks may be repeated andvaried. Improvement in the efficiency of the neuromus-cular control unit may develop over time, with con-comitant relief of back pain. Several clinical studies haveincorporated these and similar ideas. Re-training exer-cises involving muscle control have shown promisingresults in both chronic low back pain [ 22, 23, 70], andneck pain [ 56, 64, 66] patients, compared to traditionaltherapies. More research is needed in this area. I hopethat the presentation of this hypothesis will stimulatediscussion among clinicians and researchers in biome-chanics to evaluate the usefulness of the hypothesis to-wards better understanding of back pain, developmentof more precise diagnostic methods, and design of moreefficient treatments for back pain patients.

Conclusions

A new hypothesis of chronic back pain based uponmuscle system dysfunction due to ligament injuries is

673


7/9

described. Subfailure injuries of the ligaments andembedded mechanoreceptors generate corrupted mech-anoreceptor signals. Consequently, the neuromuscularcontrol unit produces corrupted muscle response pattern,resulting in excessive loading and, possibly, injuries of the spinal structures, including additional injuries of themechanoreceptors. The hypothesis accounts for many of

the common and important experimental observationsand clinical ndings seen in low back pain and whiplashpatients. In the low back pain patients, it explainsndings of delayed muscle response, poor balance,inefficient postural control, greater error in re-position-ing the trunk, muscle spasm, and greater variability

in the tasks performed. In the whiplash patients, boththe decreased motion in active testing and increasedmotion in passive-relaxed testing are explained. Thehypothesis proposes that the dysfunction of the musclesystem over time may lead to chronic back pain viaadditional mechanoreceptor injury, and neural tissueinammation.

Acknowledgements I would like to express my sincere thanks toElena Gimenez, Paul Ivancic, Kim Reid, and James Yue for theirvaluable advice, and assistance. I also want to thank the anony-mous reviewers for their thoughtful suggestions to improve themanuscript. Further, I would like to acknowledge the grant sup-port over many years from the National Institutes of Health.

References

1. Andersson GB (1997) The epidemilogyof spinal disorders, 2nd edn. Lippincott-Raven, Philadelphia

2. Antonaci F, Bulgheroni M, Ghirmai Set al (2002) 3D kinematic analysis andclinical evaluation of neck movementsin patients with whiplash injury. Cep-halalgia 22:533542

3. Bigos SJ, Spengler DM, Martin NAet al (1986) Back injuries in industry: aretrospective study. III. Employee-re-lated factors. Spine 11:252256

4. Bonelli A, Donati P, Maltoni G et al(2000) Neck motion evaluation afterwhiplash: a radiographic and kinematicprotocol. Ital J Anat Embryol 105:51 62

5. Borenstein DG, Korn S (2003) Efficacyof a low-dose regimen of cyclobenzap-rine hydrochloride in acute skeletalmuscle spasm: results of two placebo-controlled trials. Clin Ther 25:1056 1073

6. Brown MF, Hukkanen MV, McCarthyID et al (1997) Sensory and sympatheticinnervation of the vertebral endplate inpatients with degenerative disc disease.J Bone Joint Surg Br 79:147153

7. Brumagne S, Cordo P, Lysens R et al(2000) The role of paraspinal musclespindles in lumbosacral position sensein individuals with and without lowback pain. Spine 25:989994

8. Burke JG, Watson RW, McCormack Det al (2002) Intervertebral discs whichcause low back pain secrete high levelsof proinammatory mediators. J BoneJoint Surg Br 84:196201

9. Butler D, Tramow JH, Andersson GBet al (1990) Discs degenerate beforefacets. Spine 15:111113

10. Byl NN, Sinnott PL (1991) Variationsin balance and body sway in middle-aged adults: subjects with healthy backscompared with subjects with low-backdysfunction. Spine 16:325330

11. Cavanaugh JM, Ozaktay AC, Ya-mashita T et al (1997) Mechanisms of low back pain: a neurophysiologic andneuroanatomic study. Clin Orthop 166 180

12. Cornefjord M, Olmarker K,Otani K et al (2002) Nucleus pulposus-induced nerve root injury: effects of diclofenac and ketoprofen. Eur SpineJ 11:5761

13. Farfan HF, Sullivan JD (1967) Therelation of facet orientation to inter-vertebral disc failure. Can J Surg10:179185

14. Feipel V, Rondelet B, LePallec JP et al(1999) The use of disharmonic motioncurves in problems of the cervical spine.Int Orthop 23:205209

15. Freemont AJ, Peacock TE, Goupille Pet al (1997) Nerve ingrowth into dis-eased intervertebral disc in chronic backpain. Lancet 350:178181

16. Freemont AJ, Watkins A, Le Maitre Cet al (2002) Nerve growth factorexpression and innervation of the pain-ful intervertebral disc. J Pathol 197:286 292

17. Frymoyer JW, Cats-Baril WL (1991)An overview of the incidences and costsof low back pain. Orthop Clin NorthAm 22:263271

18. Fujiwara A, Tamai K, An HS et al(2000) The relationship betweendisc degeneration, facet joint osteoar-thritis, and stability of the degenerativelumbar spine. J Spinal Disord 13:444 450

19. Heikkila H, Astrom PG (1996) Cervic-ocephalic kinesthetic sensibility in pa-tients with whiplash injury. ScandJ Rehabil Med 28:133138

20. Hodges PW, Richardson CA (1996)Inefficient muscular stabilization of thelumbar spine associated with low backpain. A motor control evaluation of transversus abdominis. Spine 21:2640 2650

21. Indahl A, Kaigle AM, Reikeras O et al(1997) Interaction between the porcinelumbar intervertebral disc, zygapophy-sial joints, and paraspinal muscles.Spine 22:28342840

22. Jull GA, Richardson CA (2000) Motorcontrol problems in patients with spinalpain: a new direction for therapeuticexercise. J Manipulative Physiol Ther23:115117

23. Kankaanpaa M, Taimela S, AiraksinenO et al (1999) The efficacy of activerehabilitation in chronic low back pain.Effect on pain intensity, self-experienceddisability, and lumbar fatigability. Spine24:10341042

24. Kelsey JL, White AA III (1980) Epide-miology and impact of low-back pain.Spine 5:133142

25. Kirkaldy-Willis WH, Wedge JH, Yong-Hing K et al (1978) Pathology andpathogenesis of lumbar spondylosis andstenosis. Spine 3:319328

26. Kojima Y, Maeda T, Arai R et al (1990)Nerve supply to the posterior longitu-dinal ligament and the intervertebraldisc of the rat vertebral column asstudied by acetylcholinesterase histo-chemistry. I. Distribution in the lumbarregion. J Anat 169:237246

27. Kristjansson E, Leivseth G, Brinck-mann P et al (2003) Increased sagittalplane segmental motion in the lowercervical spine in women with chronicwhiplash-associated disorders, GradesI-II: a case-control study using a newmeasurement protocol. Spine 28:2215 2221

28. Lariviere C, Gagnon D, Loisel P (2000)The comparison of trunk musclesEMG activation between subjects withand without chronic low back painduring exion-extension and lateralbending tasks. J Electromyogr Kinesiol10:7991

674


8/9

29. Lipson SJ, Fox DA, Sosman JL (1985)Symptomatic intravertebral discherniation (Schmorls node) in thecervical spine. Ann Rheum Dis 44:857 859

30. Long DM, BenDebba M, TorgersonWS et al (1996) Persistent back pain andsciatica in the United States: patientcharacteristics. J Spinal Disord 9:4058

31. Loudon JK, Ruhl M, Field E (1997)Ability to reproduce head position afterwhiplash injury. Spine 22:865868

32. Lund JP, Donga R, Widmer CG et al(1991) The pain-adaptation model: adiscussion of the relationship betweenchronic musculoskeletal pain and motoractivity. Can J Physiol Pharmacol69:683694

33. Luoto S, Aalto H, Taimela S et al(1998) One-footed and externally dis-turbed two-footed postural control inpatients with chronic low back pain andhealthy control subjects. A controlledstudy with follow-up (discussion 990).Spine 23:20812089

34. Madeleine P, Prietzel H, Svarrer H et al(2004) Quantitative posturography inaltered sensory conditions: a way toassess balance instability in patientswith chronic whiplash injury. Arch PhysMed Rehabil 85:432438

35. Magnusson ML, Aleksiev A, WilderDG et al (1996) European Spine Soci-etythe AcroMed Prize for Spinal Re-search 1995. Unexpected load andasymmetric posture as etiologic factorsin low back pain. Eur Spine J 5:2335

36. McLain RF (1994) Mechanoreceptorendings in human cervical facet joints.Spine 19:495501

37. Newcomer KL, Jacobson TD, Gabriel

DA et al (2002) Muscle activation pat-terns in subjects with and without lowback pain. Arch Phys Med Rehabil83:816821

38. Newcomer KL, Laskowski ER, Yu Bet al (2000) Differences in repositioningerror among patients with low backpain compared with control subjects.Spine 25:24882493

39. Norris SH, Watt I (1983) The prognosisof neck injuries resulting from rear-endvehicle collisions. J Bone Joint Surg Br65:608611

40. Osti OL, Vernon-Roberts B, Fraser RD(1990) 1990 Volvo Award in experi-mental studies. Anulus tears and inter-

vertebral disc degeneration. Anexperimental study using an animalmodel. Spine 15:762767

41. Osti OL, Vernon-Roberts B, Moore Ret al (1992) Annular tears and discdegeneration in the lumbar spine. Apost-mortem study of 135 discs. J BoneJoint Surg Br 74:678682

42. OSullivan PB, Burnett A, Floyd ANet al (2003) Lumbar repositioning decitin a specic low back pain population.Spine 28:10741079

43. Oxland TR, Crisco JJ III, Panjabi MMet al (1992) The effect of injury onrotational coupling at the lumbosacral joint. A biomechanical investigation.Spine 17:7480

44. Palmgren T, Gronblad M, Virri J et al(1996) Immunohistochemical demon-stration of sensory and autonomic nerveterminals in herniated lumbar disc tis-sue. Spine 21:13011306

45. Panjabi M (1979) Validation of mathematical models. J Biomech12:238

46. Panjabi MM (1992) The stabilizingsystem of the spine. Part I. Function,dysfunction, adaptation, and enhance-ment (discussion 97). J Spinal Disord5:383389

47. Panjabi MM (1992) The stabilizingsystem of the spine. Part II. Neutralzone and instability hypothesis

(discussion 7). J Spinal Disord 5:390 396

48. Panjabi MM, Yoldas E, Oxland TRet al (1996) Subfailure injury of therabbit anterior cruciate ligament.J Orthop Res 14:216222

49. Patijn J, Wilmink J, ter Linden FH et al(2001) CT study of craniovertebralrotation in whiplash injury. Eur SpineJ 10:3843

50. Patwardhan AG, Havey RM,Ghanayem AJ et al (2000) Load-carry-ing capacity of the human cervicalspine in compression is increasedunder a follower load. Spine 25:1548 1554

51. Puglisi F, Ridi R, Cecchi F et al (2004)Segmental vertebral motion in theassessment of neck range of motion inwhiplash patients. Int J Legal Med118:235239

52. Radebold A, Cholewicki J, PanjabiMM et al (2000) Muscle responsepattern to sudden trunk loading inhealthy individuals and in patients withchronic low back pain. Spine 25:947 954

53. Radebold A, Cholewicki J, PolzhoferGK et al (2001) Impaired posturalcontrol of the lumbar spine isassociated with delayed muscleresponse times in patients with chronic

idiopathic low back pain. Spine 26:724 73054. Roland MO (1986) A critical review of

the evidence for a pain-spasm-pain cyclein spinal disorders. Clin Biomech(Bristol, Avon) 1:102109

55. Ronnen HR, de Korte PJ, Brink PRet al (1996) Acute whiplash injury: isthere a role for MR imaging?a pro-spective study of 100 patients. Radiol-ogy 201:9396

56. Rosenfeld M, Seferiadis A, Carlsson Jet al (2003) Active intervention inpatients with whiplash-associated dis-orders improves long-term prognosis: arandomized controlled clinical trial.Spine 28:24912498

57. Salminen JJ, Erkintalo MO, Pentti Jet al (1999) Recurrent low back painand early disc degeneration in theyoung. Spine 24:13161321

58. Sekine M, Yamashita T, Takebayashi Tet al (2001) Mechanosensitive afferentunits in the lumbar posterior longitudi-nal ligament. Spine 26:15161521

59. Solomonow M, Zhou B, Baratta RVet al (2002) Neuromuscular disordersassociated with static lumbar exion: afeline model. J Electromyogr Kinesiol12:8190

60. Solomonow M, Zhou BH, Baratta RVet al (2003) Biomechanics and electro-myography of a cumulative lumbardisorder: response to static exion. ClinBiomech (Bristol, Avon) 18:890898

61. Solomonow M, Zhou BH, Baratta RV

et al (1999) Biomechanics of increasedexposure to lumbar injury caused bycyclic loading: Part 1. Loss of reexivemuscular stabilization. Spine 24:2426 2434

62. Solomonow M, Zhou BH, Harris Met al (1998) The ligamento-muscularstabilizing system of the spine. Spine23:25522562

63. Spitzer WO, Skovron ML, Salmi LRet al (1995) Scientic monograph of theQuebec Task Force on Whiplash-Asso-ciated Disorders: redening whiplashand its management. Spine 20:1S73S

64. Taimela S, Diederich C, Hubsch M et al(2000) The role of physical exercise and

inactivity in pain recurrence andabsenteeism from work after activeoutpatient rehabilitation for recurrentor chronic low back pain: a follow-upstudy. Spine 25:18091816

65. Taimela S, Osterman K, Alaranta Het al (1993) Long psychomotor reactiontime in patients with chronic low-backpain: preliminary report. Arch PhysMed Rehabil 74:11611164

66. Taimela S, Takala EP, Asklof T et al(2000) Active treatment of chronic neckpain: a prospective randomized inter-vention. Spine 25:10211027

67. Tarsy D (1998) Comparison of acute-and delayed-onset posttraumatic cervi-

cal dystonia. Mov Disord 13:48148568. Tawackoli W, Marco R, LiebschnerMA (2004) The effect of compressiveaxial preload on the exibility of thethoracolumbar spine. Spine 29:988993

69. van Dieen JH, Selen LP, Cholewicki J(2003) Trunk muscle activation in low-back pain patients, an analysis of theliterature. J Electromyogr Kinesiol13:333351

675


9/9

70. Vezina MJ, Hubley-Kozey CL (2000)Muscle activation in therapeutic exer-cises to improve trunk stability. ArchPhys Med Rehabil 81:13701379

71. Wasiak R, Pransky G, Verma S et al(2003) Recurrence of low back pain:denition-sensitivity analysis usingadministrative data. Spine 28:2283 2291

72. White AA III, Gordon SL (1982) Sym-posium on idiopathic low back pained.C.V. Mosby, St. Louis

73. White AA III, Panjabi MM (1990)Clinical Biomechanics of the Spine, 2ndedn. Lippincott, Philadelphia

74. Wilke HJ, Wolf S, Claes LE et al (1995)Stability increase of the lumbar spinewith different muscle groups. A biome-chanical in vitro study. Spine 20:192 198

75. Williams M, Solomonow M, Zhou BHet al (2000) Multidus spasms elicitedby prolonged lumbar exion. Spine25:29162924

76. Yamashita T, Cavanaugh JM, el-BohyAA et al (1990) Mechanosensitiveafferent units in the lumbar facet joint.J Bone Joint Surg Am 72:865870

77. Yang KH, King AI (1984) Mechanismof facet load transmission as a hypoth-esis for low-back pain. Spine 9:557565

676

A Hypothesis of Chronic Back Pain Ligament Subfailure Injuries Lead to Muscle Control Dysfunction

Documents

Transcript of A Hypothesis of Chronic Back Pain Ligament Subfailure Injuries Lead to Muscle Control Dysfunction