Intervertebral somatic dysfunction: A discussion of the manipulable spinal lesion
Gary Fryer B.App.Sc.(Osteo), N.D.
School of Health Science, Victoria University, Melbourne, Australia
Fryer G. Intervertebral dysfunction: a discussion of the manipulable spinal lesion. Journal of Osteopathic Medicine. 2003;6(2):64-73.
Address correspondence to Gary Fryer, School of Health Science, City Campus Victoria University, P.O. Box 14428 MCMC, Melbourne 8001, Australia. Email: email@example.com
The concept of the manipulable spinal lesion – a musculoskeletal disturbance that can be detected with manual palpation and corrected with manipulation – is examined and evidence for the theories of the dysfunction is discussed. A model for intervertebral dysfunction is presented that describes both mechanical and neurological sequelae to spinal injury, leading to a deficit in regional proprioception, changes in segmental and polysegmental muscle activity and motor control, and predisposing the segment to further strain. The evidence for the proposed model and mechanisms of manual treatment is discussed. Recommendations and directions are outlined for future research.
14 The assumption of absence of any tissue pathology is neither supported or refuted by evidence. and neural elements. some osteopaths claim that chronic dysfunctions may be nonpainful. and related vascular.
. There is growing evidence of functional15-26 and certain structural changes27-30 associated with low back pain (LBP). Egypt and Greece. 6-10 Somatic dysfunction has been defined as: “Impaired or altered function of related components of the somatic (body framework) system: skeletal. there is no current evidence that directly relates to the nature of intervertebral dysfunction. and myofascial structures. arthroidal. 9 Osteopaths have also claimed that segmental dysfunction may produce distant adverse effects on segmentally related viscera by disturbing the autonomic nervous supply at that level. 1138)
The term “somatic dysfunction” may be used broadly to describe a disturbance in any region of the body. but potentially create a region of altered mobility that can predispose to spinal strain and pain elsewhere. 9 Although acute segmental dysfunctions may create local pain. that is.5 and now may be referred to as the “intervertebral lesion”. “chiropractic subluxation complex” or “manipulable subluxation”.8. 1.4 In the field of osteopathy. it was originally called the “osteopathic lesion” or “osteopathic spinal lesion”. China. 12 Intervertebral dysfunction has been claimed to be a precursor of clinical disease and pain syndromes and so it has been argued that the treatment of intervertebral dysfunction in asymptomatic persons may prevent clinical disease.7.
Intervertebral dysfunction is not synonymous with spinal pain. These professions have stamped their own “brand names” on these allegedly “manipulable” spinal lesions.” The Educational Council on Osteopathic Principles 11(p. There is evidence of the use of manual therapy procedures in ancient Thailand.8.6 “intervertebral dysfunction”. whereas “segmental dysfunction” or “intervertebral dysfunction” is often used to denote a somatic dysfunction that appears to involve a single spinal level. 3 European medical manipulators and physiotherapists have used the term “joint fixation or blockage”. the manipulable spinal lesion is known as the “subluxation”.13 It has been proposed that intervertebral dysfunction does not involve tissue pathology but is a disturbance of function of the related components of the musculo-skeletal system.1 Modern manual therapy professions all have described spinal dysfunctions that are claimed to be detected with manual palpation and corrected with manipulation. lymphatic. For the chiropractic profession. as well as its use by bonesetters from the middle ages to relatively recent times. 9.2. but this may or may not be relevant to the clinical entity that osteopaths claim to detect with palpation.THE MANIPULABLE LESION
Manual therapy and manipulation of the spine is not new.8 “Intervertebral dysfunction” will be used in this article because the author believes it is the most descriptive term and likely to be understood across the manual therapy disciplines. “segmental dysfunction” or “somatic dysfunction”. Osteopaths have argued that intervertebral dysfunction may or may not directly cause spinal pain.
or “end-feel”. It is possible that manual diagnostic techniques vary from osteopathic practitioner to practitioner.41-44 The reliability of palpation for static asymmetry has been reported to be poor in the examination of both the spine and pelvis. and have raised the possibility that intervertebral dysfunction may be a figment of the collective manual therapy imagination. and reproduction of local or referred pain. 34 The acronym “TART” is sometimes used as a memory aid for the features of tissue texture.40. 49 Jull et al. Physiotherapists have placed emphasis on the altered quality of joint motion. asymmetry. but combine multiple findings such as joint range of motion and end-feel.10. 33.
Of all the diagnostic signs of intervertebral dysfunction. Phillips & Twomey49 found that manual palpation was highly sensitive and specific for detecting a symptomatic lumbar segment when they incorporated a subjective pain response from the patient. it seems likely that such a lesion exists. 34 A number of studies have demonstrated that palpation using several criteria can be highly specific and sensitive for diagnosing symptomatic intervertebral joints.35 successfully identified symptomatic cervical zygapophysial joints. but have more recently advocated motion palpation. 7 Some authors also include tenderness.35. segmental motion testing (without pain provocation) of the spine has consistently demonstrated poor concordance. Other manipulative professions use similar diagnostic criteria to diagnose manipulable lesions. 32 The diagnostic indicators of segmental dysfunction are said to be segmental asymmetry of bony landmarks. physiotherapists.
.Diagnostic indicators of intervertebral dysfunction
Authors in the field of osteopathy claim that intervertebral dysfunction can be detected by skilled manual palpation. range of motion abnormality (increased. 37
Reliability of detection of intervertebral dysfunction
Given that the different manual therapy professions – osteopaths. 33. 31. 31. and tissue texture changes. confirmed by diagnostic blocks. Most authors of modern osteopathic texts urge the practitioner not to rely on a single palpatory test. range of motion abnormality and tenderness. and medical manipulators – have all independently described a manipulable spinal lesion. 3.38-40 There is presently an urgent need to develop objective means of examining and validating the aetiology of intervertebral dysfunction and to establish reliable methods for its clinical detection. palpation of soft tissues and tenderness.1. decreased or a change in quality). chiropractors. and tenderness to detect intervertebral dysfunction. 10. school to school. 48. 36 whereas the chiropractic profession have traditionally emphasised static asymmetry. by using the criteria of abnormal endfeel. have recently lamented the lack of inter-examiner reliability in attempting to detect such dysfunctions.47
The methods that osteopaths most commonly use in clinical practice to detect intervertebral dysfunction are largely unknown because there has been no descriptive survey to establish this. and from country to country. 31.1. tissue texture.2.35. Several authors. however. 46 Similarly. abnormal quality of resistance to motion. 45. palpation for tenderness appears to be the most reliable. 7-10.1.
Osteopathic researchers J. Experimental evidence. All activity passing through that segment would become exaggerated. They reported evidence of spontaneous electromyographic (EMG) activity and increased sympathetic output at spinal levels associated with clinically detected segmental dysfunctions. 8. and is cited in most osteopathic texts. 7. pain receptors) were the only proprioceptors capable of producing reflex muscle contraction and sympathetic discharge.13 In 1990.Few studies have examined the reliability of detecting symptomatic joints without tenderness or pain provocation. Although they presented no statistical analysis beyond percentage agreement. 53 is Korr’s neurological concept of the facilitated segment.8 zygapophysial joints. argued Van Buskirk. and tissue texture changes due to sustained muscle contraction and sympathetic induced circulatory changes. The model that appears to be the most accepted in the field of osteopathy. assessment of joint motion and tissue texture are important clinical signs. where he proposed that minor trauma to segmentally innervated musculature could produce a discordant barrage of afferent input from muscle spindle proprioceptors into the dorsal horn of the spinal cord and alter the firing thresholds and excitability of the interconnecting neurones.54-59 Korr developed the “facilitated segment” concept. He proposed that noxious stimuli (from viscera or somatic tissues) would produce axon reflex changes that promote inflammation at all the terminal branches of
. and had a central role in segmental dysfunction. Van Buskirk60 highlighted deficiencies with Korr’s neurological model. while pain provocation improves the reliability of detecting symptomatic joints (a procedure not advocated in any osteopathic text). joint range of motion restriction due to the resistance of shortened and overactive muscles.1. 52as the underlying cause of motion restriction and tissue texture change. and assessment of abnormal tissue stiffness associated with muscle reactivity) when no verbal report of pain was allowed. Jull et al. Denslow and Irwin Korr conducted studies from the 1940s to the early 1960s that they claimed provided evidence of segmental spinal cord hyper-activity.
PROPOSED EXPLANATIONS FOR INTERVERTEBRAL DYSFUNCTION
There has been much speculation on the aetiology of the manipulable lesion with various authors implicating the paraspinal muscles. S.50 and the intervertebral disc51. in particular the proposed role of the muscle spindle. and sympathetic output. their results lend support to the view that. Van Buskirk claimed that the nociceptors (free nerve endings. motion palpation. indicated that the muscle spindle was not capable of producing reflex muscle contraction and spindle silence was common. α and γ motor activity to segmental muscles.36 reported good concordance between examiners detecting symptomatic cervical joints (using passive accessory. Korr’s neurological model was an attempt to explain the clinical findings of segmental dysfunction: tenderness and pain due to facilitated ascending nociception. producing increased nociception (pain).
Denslow appeared to have misgivings about his original research. and thus reproduction of these studies with modern equipment would help verify their significance. not all palpable paraspinal tissue texture changes could be explained by muscle contraction. In 1975.75 Denslow stated that: “However. Over time the muscle would become fibrotic and if stretched or re-strained nociceptors would be activated once again. following further experience with these methods and additional studies by other researchers.63 while other authorities (such as Guyten & Hall 64 in their “Textbook of Medical Physiology”) still describe low level motor activity contributing to resting muscle tone. The issue of EMG activity in relaxed paraspinal muscles that appear to be abnormal to palpation requires further investigation.73 This pilot study should be regarded as inconclusive due to the small sample size. by today’s standards.73 Slosberg74 suggested that the size of the needles used by Denslow were larger and more disruptive than the fine-wire electrodes used today. The assessment of very low level EMG activity in paraspinal muscles is difficult and complicated by electrical noise generated by the heart. and apparent increased activity in the only symptomatic subject. poorly described with insufficient data reported and no statistical analysis.65
The two main problems with the proposal of muscle contraction as a component of intervertebral dysfunction are the lack of evidence of abnormal EMG activity associated with palpatory findings and the large body of evidence that demonstrates decreased EMG activity in deep paraspinal muscles of patients with LBP. the evidence is lacking.22. problems with artefact.61 Lederman62 has recently questioned the concept of “neurological muscle tone” – low level motor activity that contributes to the resting tone of a relaxed muscle – and the popular belief that this tone can be “turned up” to produce muscle spasm. 66-72 Denslow and Korr’s studies54-59 are over fifty years old and were.
. respiratory muscles. it was recognised that if sufficient care was used in bolstering the subject with pillows and sandbags. Although the concepts of “muscle spasm” and “pain-spasm-pain cycle” are popular explanations for hard and tender muscles.60
Both these models attribute the restricted range of segmental motion and palpable tissue changes principally as a result of sustained paraspinal muscle contraction. The only recent investigation of EMG activity of abnormal to palpation paraspinal muscles found no significant increased activity. “Neurological” muscle tone appears to be controversial. 23. the electromyographic evidence of muscle contraction in some of the abnormal areas disappeared. thirty-four years after the publication of his original article that described increased paraspinal EMG activity. Afferents reaching the dorsal horn would produce reflex muscle contraction and sympathetic discharge (producing visceral and immune effects).that axon. although there appeared to be muscles in the region of clinically detected osteopathic lesions that displayed increased EMG activity. and extraneous sources. further sensitising other nociceptors.”75 (p155) Denslow conceded that. as some authorities in the field of EMG claim that relaxed muscles have no motor activity.
Various authors have speculated that it may be possible for the meniscus to become entrapped (swollen and inflamed from minor trauma. and tissue texture changes (spread of inflammation to the peri-articular muscles and tissues). but the nature of the lesion remains elusive.76 Bogduk reported that zygapophysial joint capsule tears. it does not account for the more commonly diagnosed sub-acute or chronic intervertebral dysfunction. and projects from the superior and inferior margins of the joint capsule. is a plausible cause of the “acute locked back” that responds to manipulation.81 have published the only quality study investigating the potential of diagnostic ultrasound for detecting signs of cervical and lumbar zygapophysial joint inflammation in symptomatic patients and were unable to demonstrate abnormal echogenicity in or adjacent to these joints.Meniscoid entrapment and extrapment
Three commonly occurring meniscoid-like inclusions found within the zygapophysial joints of the spine have been well described. 34. which may prevent the superior joint surface from gliding downwards and backwards). and these lesions may underlie zygapophysial joint pain. is a fibro-fatty vascular structure up to 5mm long.76 Although meniscoid extrapment may explain the acute locked back that prevents the sufferer from standing upright. that this theory is likely to be difficult to prove because meniscoid structures are most probably impossible to detect with diagnostic imaging.80 Nazarian et al. and intra-articular haemorrhages have been found in biomechanical and postmortem studies. 76
Extrapment of meniscoid structures. Bogduk argues. capsular avulsion.76 The largest of these. reported a study whose author claimed to visualise inflammation of the zygapophysial capsular ligaments in a small number of low back pain patients. the restricted joint motion and end-feel (tense joint effusion). The quoted study has been criticised for its poorly described methods. Bogduk states.78 Sprain and effusion may account for the diagnostic signs of segmental dysfunction: pain and deep paraspinal tenderness (capsule inflammation).10. Rhodes and Bishop. however. lack of illustrated ultrasound images and statistical analysis.76 It has been suggested that minor trauma may cause zygapophysial joint capsule sprains and produce joint effusion.
Zygapophysial joint sprain
Sprains of the zygapophysial joint have been postulated as a cause of spinal pain and intervertebral dysfunction. insufficient data. the fibro-adipose meniscoid.76-78 Studies using diagnostic blocks have confirmed that the zygapophysial joint is a common source of low back pain and can produce both local spinal and referred pain. subchondral fractures. which may prevent the gliding of the opposing joint surfaces) or extrapped (buckled and caught on the joint margin during full flexion.79 in a review of the use of diagnostic ultrasound of the spine.
82 and this could be responsible for palpable paraspinal tissue change. most with little evidence to support them.2.78 This mechanism. creating a change in joint pressure.2. vascular and neurological consequences. 52 It is feasible that degenerative changes in the disc may affect the quality of passive motion at that segment.
A number of other theories have been advanced to explain intervertebral dysfunction.Peri-articular adhesions
Adhesions within the zygapophysial joint and thickening of the joint capsule has been suggested as a cause of restricted segmental mobility. would be difficult to investigate and the proposal remains purely speculative.
. 78 Although this may not account for dysfunctions of short duration or the associated tissue texture changes. resistance to motion and altered end-feel. 51. The chiropractic profession originally believed that the manipulable “subluxation” was a malposition of bones but modern chiropractic authors have largely moved away from the concept of static malposition and embraced a more complex definition with similarities to somatic dysfunction encompassing motion restriction. although the evidence for abnormal EMG activity associated with palpatory findings is lacking. however. 3.
Intra-discal nuclear displacement
There is no question that intervertebral discs are innervated and are a common source of chronic low back pain. The disc is capable of producing reflex multifidus contraction. 83. 77. 84
Axial rotation of cadaver lumbar spines has been observed to produce movement of joint fat pads (within the joint but external to the synovium) in and out of the joint capsule. adhesion formation and capsule thickening may be logical consequences of capsule sprain and explain the long-term changes to passive range and quality of joint motion following joint injury.76 Some authors have attributed the signs of segmental dysfunction to internal disruption of the disc and migration of the nucleus. or how manipulation might improve restricted passive motion as claimed by osteopaths.85 It has been suggested that sprain and capsule inflammation may narrow the communicating foramen and prevent the fat pad moving in and out of the capsule. Nonetheless. the disc has the potential to produce some of the cardinal signs of intervertebral dysfunction.2. presumably to keep the joint volume relatively constant. but it is uncertain if changes in the disc would produce segmental tissue texture change.
Sprain of the intervertebral joint complex
As previously discussed. like others before it. and create a cycle which predisposes the segment to ongoing strain (Figure 1). Zygapophysial joint capsule sprain and effusion could potentially cause typical symptoms of the acute intervertebral dysfunction: local pain and tenderness. and altered end-feel. painful limitation of motion.
Sprain of the anulus fibrosus. and muscles would also produce local pain and tenderness. subsequent changes in segmental and polysegmental muscle activity and motor control. subchondral fractures. it was likely that the subjects were suffering from sub-acute or chronic pain. clearly demonstrate synovial effusion and subsequent pain and limitation of motion.
Zygapophysial joint effusion has not yet been demonstrated as a cause of acute spinal pain. and intra-articular haemorrhages have been found in biomechanical and post-mortem studies and are likely to underlie joint pain.76 Injuries to synovial joints. intervertebral ligaments. The only well designed study81 that has attempted to detect signs of zygapophysial joint inflammation failed to locate evidence of inflammation in the cervical and lumbar regions. The existence – let alone the nature – of intervertebral dysfunction is largely speculative and the following model.A PROPRIOCEPTIVE-DEFICIT MODEL FOR INTERVERTEBRAL DYSFUNCTION
This proposed model describes concurrent patho-anatomical and functional changes that may be initiated by minor injury. and produce a deficit in local proprioception.
It is likely that intervertebral dysfunction is initiated by minor trauma and tissue damage as this would activate nociceptors. The clinical signs produced by tissue damage would predominate in the acute stage of dysfunction.
. such as the knee. zygapophysial joint pain has been demonstrated to be a common source of LBP and zygapophysial joint capsule tears.60 Increased tissue fluid may limit the capacity of the peri-articular soft tissues to stretch and deform with movement. which appear necessary to produce the functional changes. making it vulnerable to further injury and recurring acute and sub-acute episodes of pain. as the researchers did not report the average duration of symptoms. This study examined patients with neck and LBP and. capsular avulsion. The resulting neurological disturbance would lead to impaired coordination and stability of the region. is also speculative and in need of further corroborating evidence. It is quite possible that zygapophysial joint effusion may only be evident in the acute stage of joint injury. and so may contribute to altered range of motion and end-feel. Peripheral sensitisation of the nociceptors could enhance segmental tissue inflammation and potentially produce tissue texture change identifiable with palpation.
This peripheral sensitisation would produce local pain and tenderness. or the anulus fibrosus of the disc would produce release of inflammatory chemicals and sensitise nociceptors (pain receptors). 16
Activation of the sympathetic nervous system
Osteopaths have claimed that intervertebral dysfunction is capable of producing long-term adverse effects on segmentally innervated viscera.93 Volunteers suffering with pain have demonstrated decreased awareness of direction of lumbar motion and position. 22.88. without any longer a tissue basis.88. Depending on the intensity of the afferent bombardment and the susceptibility of the individual. 26 The increased activity
.Activation of nociceptive pathways
Sprain and inflammation of the zygapophysial joint capsule. may have detrimental effects on the patient’s health.25. neuroplastic changes in the dorsal horn of the spinal cord may eventuate. 93 and jaw muscle spindle afferent activity. 9. 86 Some limited experimental evidence supports the concept that noxious somatic afferents can modify visceral activity via segmental sympathetic efferent activity. For most individuals. the peri-articular tissues. known as somato-visceral reflexes.7. despite the fact that tissues may be tender when palpated. 12. Recent studies have demonstrated decreased proprioception in association with experimental muscle pain. producing chemical and physical changes in the pain processing regions of the dorsal horn and creating the phenomena known as “central sensitisation”. and result in permanent hyperalgesia (increased sensitivity to painful stimuli) and allodynia (pain evoked from normally nonpainful stimuli). 24 and as a reaction to stress. 89 lumbar muscle fatigue.17-23 relaxed standing. in the long-term.62 Although there is no convincing evidence of segmental sympathetic hyper-activity associated with the manipulable lesion. the pain and tenderness would progressively diminish as the injured tissues healed.92 and chronic cervicobrachialgia.91 lumbar spinal stenosis.89 Intervertebral sprains could potentially activate joint and muscle nociceptors and result in diminished proprioception from that segment.90 subjects with LBP.90-92 cutaneous touch perception.87 but this theory has been challenged. it is likely that pain and emotional distress can certainly produce general sympathetic arousal that.19. It is likely that most chronic pain is centrally generated.
Spinal pain and disturbed proprioception produce a change in CNS strategy and increased “guarding” activity in polysegmental paraspinal muscles
Increased lumbar paraspinal activity has been demonstrated in volunteers with LBP in full flexion (lack of flexion-relaxation).15. These changes to pain processing may long outlast the original tissue injury.
Nociceptor activity disturbs proprioception
There is growing evidence that pain interferes with normal joint and muscle proprioception.
non-specific activity may further adversely affect the control and proprioception of that region.23 demonstrated that decreased flexion-relaxation occurred as a result of experimental paraspinal muscle pain alone and the increased paraspinal muscle activity was virtually unchanged even when subjects were carefully guided to perform movement at pre-experimental pain range and velocity.95 demonstrated reflex inhibition of multifidus activity after injecting saline into a porcine zygapophysial joint.96-98 The deep paraspinal muscles. Although much of this change in muscle activity can be attributed to de-conditioning associated with modified patient activity and behaviour. do not automatically recover once back pain has resolved. This process may likely occur following zygapophysial joint sprain and effusion. patients often remark that their injured region “feels like it does not belong to them” and often have trouble relaxing and allowing the region to “let go”. some studies have reported rapid and selective atrophy of the multifidus that suggests reflex inhibition. This attempt to compensate with increased. which may be a result of impaired proprioception and control. Hides et al. 67 reduced muscle strength.27 used diagnostic ultrasound to study the cross-sectional area of the lumbar multifidus muscles of patients suffering from their first episode of unilateral acute/subacute LBP and found that specific wasting of multifidus was evident at the spinal level and side determined symptomatic by clinical examination. together with the transversus abdominus muscle.23 Zedka et al. 66.22. Multifidus atrophy has also been observed in subjects with chronic LBP using MRI28 and computer tomography.
Reflex inhibition of paraspinal activity appears to target the deep paraspinal muscles. are believed to be a critical factor in lumbar stability. which resulted in the muscle working in “pain mode” to protect the spine from extreme movement whenever pain was signalled. Many studies have demonstrated reduced activity in free dynamic movements. and the “pain mode” CNS strategy appears to activate the more superficial musculature spanning several spinal segments. In the author’s experience. They concluded that pain from any spinal structure (joint. and may leave the spine vulnerable to normally
. 71. 21 and a complex change in motor control strategy. probably caused by reflex inhibition following a stretch of the joint capsule.
Spinal pain produces inhibition and atrophy of deep segmental muscles
There is a large body of evidence that clearly demonstrates that lumbar paraspinal muscles of subjects with LBP operate sub-maximally.68-70 and increased muscular fatigability67. 23. ligament or muscle) may produce a change in CNS strategy. but a combination of voluntary ‘guarding’ behaviour18. which are the muscles that contribute most to intervertebral stability.
Spinal pain and a regional deficit in proprioception may result in the inability to execute coordinated contractions of deep segmental musculature. 72 of paraspinal muscles in volunteers with LBP.is not likely due to reflex contraction.94 Indahl et al.
rather than end range of motion.
Zygapophysial joint capsule fibrosis and intervertebral disc resorption
Repeated sprain and inflammation of the joint capsule may result in proliferation of fibroblasts and shortening and thickening of the capsule.104 and these fluctuations are likely to increase the rate of trans-synovial flow. as a rhythmic movement would likely be needed to move fluid across a membrane and allow filling and re-filling of peri-articular lymphatics. It may be possible that manual techniques produce physiological effects – such as hypoalgesia. Intervertebral disc disruption and degradation may result in isolated disc resorption. will therefore increase the likelihood of further spinal strain.27.
THERAPEUTIC MECHANISMS OF MANUAL TREATMENT
The mechanisms responsible for the therapeutic effect of manual techniques are poorly understood and largely speculative. 96. rhythmic stretching (as performed with articulation) is
.101-103 Active and passive spinal movements have been demonstrated to produce pressure fluctuations in zygapophysial joints. If acute and sub-acute intervertebral dysfunctions involve capsule sprain.
Reducing zygapophysial joint effusion and peri-articular oedema
Movement of synovial joints has been shown to promote "trans-synovial flow". as well as stimulating lymphatic and blood flow around the joint. or plastic changes in connective tissue – whether or not an intervertebral dysfunction exists.76 These long-term changes could potentially produce decreased range of motion. such as muscle energy. synovial effusion.62
Stretching zygapophysial joint capsule
It has been proposed that multiple sprains to a intervertebral joint may result in zygapophysial joint capsule fibrosis and shortening. because muscle contraction and relaxation would assist lymphatic drainage from the peri-articular lymphatics. combined with impaired proprioception and non-specific guarding activity. High velocity low amplitude techniques (HVLA) or indirect techniques would probably have little effect. and peri-articular oedema.96 Lack of active control from the deep stabilising muscles. manual techniques such as passive articulation may produce pressure fluctuations and stimulate trans-synovial flow and move the excess fluid across the membrane and out of the joint. 99. possibly in mid-range motion and in the absence of any obvious strain or trauma. 97. decreased accessory ‘joint play’ and altered joint ‘end-feel’. may help drain fluid from the periarticular tissues. The following proposed mechanisms of action are based on the author’s model of intervertebral dysfunction and are consistent with available evidence. 100 These deep paraspinal muscles appear to offer most stability in the spinal mid-range “neutral zone”.trivial episodes of trauma. improvement of motor recruitment. Active techniques.78 Repetitive. moving fluids in and out of the joint through the synovial membrane.
17-26 and it is hypothesised that this impairment may occur regionally as a result of intervertebral sprain. 115 Similarly. and allow the CNS to normalise the proprioceptive and motor coordination from that segment. where mechanoreceptor afferents carried by large diameter axons inhibit nociceptor afferents at the dorsal horn. following treatment. and greater capsule elongation and stretch during passive articulation.
Improvement of proprioception and motor control
Changes in proprioception and motor control may underlie both short and long term benefits for patients receiving manual therapy. There is a rationale. Researchers have demonstrated reductions in pain using cervical mobilisation.111 One study110 found that HVLA was more effective than muscle energy in reducing pain.likely to be the most effective means to elongate the capsule. or inhibition of pain at the spinal cord. it is not unusual for patients to volunteer feelings of being more “balanced”. Christian et al.108. which will stimulate joint and muscle proprioceptors. and purposeful joint movement in a relaxed patient will stimulate joint proprioceptors. with the painful region “back in place” and “part of the body again”.105 allow greater joint surface separation. however.106-108 cervical HVLA. may be less likely to produce viscoelastic or plastic changes to the connective tissue. such as functional and counterstrain. such as HVLA. ballistic stretches. and specific mobilisation of spinal articulations.
In the author’s experience.114 Any technique that produces movement of the joint and stretch of the capsule will stimulate joint proprioceptors. Although active exercise is considered more effective than passive treatment for
.108. Manual techniques often involve applying gentle stretch and pressure to muscles.
Manipulation induced hypoalgesia
Manipulative therapy is commonly employed to relieve spinal pain. 110 and thoracic HVLA technique. short. for performing HVLA before other techniques. 112 Experimental evidence supports the possibility of inhibition at the spinal cord according to the Gate-control theory. and potentially may be capable of producing inhibition of pain. but more research is required to confirm this. but also suggest an improvement in proprioception and motor control. Such comments could be attributed to a placebo response. It has been proposed that manipulation may produce hypoalgesia by activating descending inhibitory pathways from the dorsal periaqueductal gray area (dPAG) of the midbrain. indirect techniques.109.113 failed to demonstrate elevated plasma levels of endorphins following manipulation. as the cavitation and subsequent gas bubble formation would increase joint volume. 112 release of endorphins. but the dPAG appears to have a role due to the observation of concurrent sympathetic nervous system activation with manipulation induced hypoalgesia. specific.78. highlight a different pattern of afferent activity in the proprioceptive-impaired region. may highlight a different pattern of afferent feedback to alter and improve regional proprioception and motor control. Quick. It has been proposed that careful. Researchers have demonstrated that LBP patients exhibit impaired proprioception90-92 and altered muscle recruitment.
Diagnostic imaging of zygapophysial joint effusion
Zygapophysial joint sprain and effusion has been proposed as a potential component in intervertebral dysfunction.76-78 Diagnostic imaging.117 Cervical mobilisation has been demonstrated to improve body sway in patients with whiplash trauma.118 and decrease superficial neck muscle recruitment during staged cervical flexion. 46 motion palpation.81 but it could be possible that effusion may be visualised only in acute episodes of sprain. but more research is needed.
Few studies have attempted to investigate the effect of manipulation on proprioception and motor control.120 These studies support the proposition that manual therapy can influence proprioception and motor control.motor learning. 49 but these studies may simply be confirming the reliability of pain provocation rather than the TART criteria.
DIRECTIONS FOR RESEARCH
Reliable detection of intervertebral dysfunction
The reliability of the clinical detection of intervertebral dysfunction has not been clearly established. which would support joint sprain and effusion as having a role in spinal pain and the manipulable lesion.62 minor specific regions of impaired proprioception may respond to specific passive stimulation. 39 The detection of symptomatic segments using combined criteria (including pain provocation) has been found to be sensitive and reliable.116 and patients with vertigo and dizziness. 48. 45.40. and subsequent normal patient activity may be sufficient for improved proprioceptive integration and motor learning. Recent studies have failed to show acceptable inter-examiner agreement for detection of static asymmetry of bony landmarks.
.35.108 HVLA has been claimed to diminish quadriceps muscle inhibition. such as diagnostic ultrasound.47 or which segment to manipulate. Cervical HVLA has been reported to improve head re-positioning after active displacement in patients with chronic neck pain.119 and mechanical spinal manipulation (activator) has been claimed to increase the mean voluntary contraction of the paraspinal muscles.38. One study found no sign of inflammation in the cervical and lumbar regions of patients with neck and LBP. MRI and CT. Only after acceptable reliability has been established can the validity of the diagnosis be tested. may be capable of detecting signs of peri-articular inflammation or zygapophysial joint effusion in patients with symptomatic intervertebral dysfunctions. Researchers need to re-examine the diagnostic criteria of the manipulable lesion and find ways to make the detection of dysfunction more reliable.
researchers can accurately investigate the efficacy of manual therapy. and postural balance and sway can be used to confirm proprioceptive deficit of patients and as outcome measures to determine the efficacy of osteopathic treatment. theories and supporting evidence for the manipulable spinal lesion have been reviewed.
Acknowledgments The author wishes to thank Peter Gibbons for his constructive comments during preparation of this manuscript.Determine the nature of altered tissue texture associated with the manipulable lesion Denslow and Korr’s54-57 observations that “lesioned” segments displayed spontaneous paraspinal muscle activity at rest provided the foundation of much osteopathic theory.
. Diagnostic imaging could be employed to determine if the size or shape of these muscles was different to the surrounding musculature. changes in associated paraspinal muscle size and activity.
Investigate the effect of spinal pain on proprioception and the efficacy of osteopathic treatment to improve it
Further evidence is needed to confirm that patients with spinal pain or clinically detected intervertebral dysfunction have a deficit in proprioception and motor control. The nature of relaxed paraspinal muscles Detected as tender and abnormal with palpation needs re-investigation with EMG. signs of joint effusion. A model for intervertebral dysfunction has been presented that details mechanical and functional changes following minor trauma and it is hoped this will stimulate discussion and research into the nature of intervertebral dysfunction and the mechanisms of manual therapy. Head re-positioning. during quiet sitting and standing. Future research should examine methods for reliable detection of intervertebral dysfunction. these studies are dated and inadequate and have not been verified by any study since. Such regions could be examined at rest. As previously discussed. and the effect of spinal pain on proprioception. awareness of body position and motion. and during dynamic movements to determine if these muscles are abnormally overactive or under-active relative to normal regions. Once objective signs of dysfunction are established.
Peri-articular soft tissue inflammation
Decrease in control & stability
Impairment of proprioception
Zygapophysial capsule fibrosis (time) Isolated disc resorption (time) Central sensitisation Sympathetic activation
Altered “pain mode” motor recruitment
Increased “guarding” activity of superficial paraspinal muscles
Reflex inhibition of deep segmental “stabilising” paraspinal muscles
Altered visceral & immune function?
Minor sprain of intervertebral joint complex
Zygapophysial joint synovitis & effusion
Anulus tear. altered end-feel
Tissue texture change
Pain and tenderness
Tissue texture change
Figure 1: A Proprioceptive-Deficit Model of Intervertebral Dysfunction
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