Bookmark and Share
logo

Call us now at: 02 9922 6806

appointment times

Neurophysiological effects of mechanical traction

Mechanical Traction and the assessment of signs and symptoms to ascertain effective dose

Martin Krause (1995, 1999, 2004, 2006) M.Appl.Sc(Manip Physio), Grad.Dip.Hlth.Sc(Sport & Ex), Grad.Cert.Hlth.Sc.Edu

Table of Contents

- Introduction

- Slide Presentation

- Indications

- Dose

- Force Closure

- Dorsal Root Ganglion

- Sympathetic Sensory Coupling

- Mind Map

- Descending Modulation

- Biomechnical Considerations

- Conditioned & Unconditioned Stimuli

- Placebo and Nocebo affect

- The Neuromatrix

- Modulation of Mechanoceptor Acitivity

- The Locus Coeruleus response to treatment stress

- The role of feedback to descending modulation of pain and inflammation

- Conclusions

- Impaired Brain Processing w.r.t emotions and catastrophising

- Theoretical Explanations - original paper on the effect of mechanical traction on neurogenic inflammation (1995)

- Sensory Discriminative - Motivational Affective Components of Pain Processing

- Ectopic Impulse Generation by the DRG

- Normalisation of Signs and Symptoms using Traction

- Clinical Implication of Neurophysiology on a 'Two Threshold' hypothesis

- Validity of using the normalisation of signs and symptoms to establish the dose

- Neurogenic inflammation and the cytokine immune response

- Reduction of Venous Congestion

- Sinuvertebral Nerve and Sympathetic Somatic coupling for healing

- Duration of Efficacy

- References

 

Introduction

The brain's neural processing has been likened to a symphony orchestra playing in tune (Goldstein JA 2004).  A type of resonance termed 'neural synchrony' has been related to arousal, attentional selection, and working memory.  Grossberg (2000) highlights the relationship between matching top-down expectations with bottom-up data, a process which focuses attention on those features of the bottom-up input that are expected.  The interaction of attention-learning and orienting-search subsystems and how they interact has been developed into adaptive resonance theory (ART).  If there is appropriate stimulus generalisation then amplified representation can, in turn, attentionally block or inhibit the representations of irrelevant sensory events (Goldstein JA 2004).  Therefore, radicular pain may represent a disturbance to CNS data processing and appropriate treatment may represent the attentional block which can help re-establish neural synchrony ?

 

See Cochrane report (2006)

amazingly, a decade after the realisation that immediate normalisation of neurological signs and symptoms can occur if the appropriate dose of traction is applied, the research evidence still doesn't justify it's use.

 

Note that the sinuvertebral nerve is a peripheral nerve

Through the normalisation of muscle spasm, the amount of 'force closure' around the spine should reduce. Consequently, such a reduction in muscle tension should reduce compressive forces on the intervertebral discs and blood vesels of the intervertebral foramen as well as the spinal canal (Batson's venous plexus).

Normalisation of pressure around the dorsal root ganglion (DRG) should reduce the propagation of ectopic impulses to the spinal cord and moreover improve the afferent-efferent interaction in the periphery. The latter would improve the modulation of blood flow as well as the modulation of neurogenic inflammation. It should be remembered that the sinuvertebral nerve is a peripheral nerve responsible for these effects within the intervertebral foramen and spinal canal.

Sympathetic-sensory coupling after L5 spinal nerve lesion in the rat and its relation to changes in dorsal root ganglion blood flow

H. -J. Haebler, S. Eschenfelder, X. -G. Liu and W. Jaenig
Physiologisches Institut, Christian-Albrechts-Universität, Olshausenstrasse 40, 24098 Kiel, Germany
Received 6 December 1999; revised 2 March 2000; accepted 17 March 2000. Available online 9 October 2000.

Abstract

Transection of the L5 spinal nerve in rats results in allodynia- and hyperalgesia-like behavior to mechanical stimulation which are thought to be mediated by ectopic activity arising in lesioned afferent neurons mainly in the dorsal root ganglion (DRG). It has been suggested that the neuropathic pain behavior is dependent on the sympathetic nervous system. In rats 3–56 days after L5 spinal nerve lesion, we tested responses of axotomized afferent fibers recorded in the dorsal root of the lesioned segment to norepinephrine (NE, 0.5 small mu, Greekg/kg) injected intravenously and to selective electrical stimulation of the lumbar sympathetic trunk (LST). In some experiments we measured blood flow in the DRG by laser Doppler flowmetry. The majority of lesioned afferent fibers with spontaneous activity responded to neither LST stimulation (82.4%) nor NE (71.4%). In those which did react to LST stimulation, responses occurred only at high stimulation frequencies (likely to be above the physiological range), and they could be mimicked by non-adrenergic vasoconstrictor drugs (angiotensin II, vasopressin). Excitatory responses to LST stimulation were closely correlated with the stimulation-induced phasic vasoconstrictions in the DRG. We therefore hypothesized that the activation of lesioned afferents might be brought about indirectly by an impaired blood supply to the DRG. To test this hypothesis we induced a strong and sustained baseline vasoconstriction in the DRG by blocking endothelial nitric oxide synthesis with N G -nitro- -arginine methyl ester ( -NAME) applied systemically. -NAME enhanced baseline vascular resistance in the DRG about threefold and also increased stimulation-induced vasoconstrictions. After -NAME, the majority of axotomized neurons with spontaneous activity were activated by LST stimulation (76%) or NE (75%). Again, activations closely followed stimulation-induced phasic vasoconstrictions in the DRG provided that a critical level of vasoconstriction was exceeded. In the present study, inhibitory responses to LST stimulation were generally rare and could be reversed to activation by prolonged stimulation or after -NAME. These results show that sympathetic-sensory coupling occurs only in a minority of axotomized afferents after L5 spinal nerve injury. Like previous studies, they cast doubt on the notion that the L5 spinal nerve lesion is a good model for sympathetically maintained pain. Since responses of lesioned afferent neurons to LST stimulation and NE could be provoked with high reliability after inducing vasoconstriction in the DRG, and since they mirrored stimulation-induced vasoconstrictions in the DRG, it appears that in this model the association of sympathetic activity with afferent discharge occurs mainly when perfusion of the DRG is impaired.

Author Keywords: Neuropathic pain; L5 spinal nerve injury; Sympathetically maintained pain; Dorsal root ganglion; Neurogenic vasoconstriction; Sympathetic nervous system

If one considers the sinuvertebral nerve to be a peripheral nerve then inudction of inflammation around the DRG can in turn create changes within the DRG which leads to hyperalgesia. Clearly a viscious cycle may ensue.

Induction of high mobility group box-1 in dorsal root ganglion contributes to pain hypersensitivity after peripheral nerve injury

Pain, Volume 149, Issue 3, Pages 514-521 (June 2010)

Masayuki Shibasaki1, Mika Sasaki1, Mayumi Miura1, Keiko Mizukoshi1, Hiroshi Ueno, Satoru Hashimoto, Yoshifumi Tanaka, Fumimasa AmayaCorresponding Author Information1email address

Received 3 June 2009; received in revised form 21 January 2010; accepted 17 March 2010. published online 14 April 2010.

Abstract

Pro-inflammatory cytokine high mobility group box-1 (HMGB-1) is involved in inflammation in the central nervous system, but less is known about its biological effects in the peripheral nervous system. In the present study, the role of HMGB-1 in the primary afferent nerve was investigated in the context of the pathophysiology of peripheral nerve injury-induced pain hypersensitivity. Real-time PCR confirmed an increase in HMGB-1 mRNA expression in the dorsal root ganglion (DRG) and spinal nerve at 1day after spinal nerve ligation (SNL). Induction of HMGB-1 mRNA was observed in both injured L5 and uninjured L4. Immunohistochemistry for HMGB-1 revealed that SNL-induced HMGB-1 expression in the primary afferent neurons and satellite glial cells (SGCs) in the DRG, and in Schwann cells in the spinal nerve. Up-regulation of HMGB-1 was associated with translocation of its signal from the nucleus to the cytoplasm. Injection of HMGB-1 into the sciatic nerve produces transient behavioural hyperalgesia. Neutralizing antibody against HMGB-1 successfully alleviated the mechanical allodynia observed after SNL treatment. Receptor for advanced glycation end products (RAGE), one of the major receptors for HMGB-1, was expressed in the primary afferent neurons and SGCs in the DRG, as well as in Schwann cells in the spinal nerve. These results indicate that HMGB-1 is synthesized and secreted into the DRG and spinal nerve, and contributes to the development of neuropathic pain after nerve injury. Blocking HMGB-1/RAGE signalling might thus be a promising therapeutic strategy for the management of neuropathic pain.


Conditioned stimulus and unconditioned stimulus inputs converge on individual cells in the lateral amygdala, which is the principal output nucleus of fear system projects to areas of the hypothalamus and brainstem that control behavioural, endocrine, and autonomic conditional responses associated with fear learning (Goldstein JA 2004).  In neurosomatic disorders, an accentuation of the attentional weighting is given to elements of a stimulus that, in actuality, have a very tenuous relationship to the state of activation of the long-term memory store.  Unlike the individual with a normally functioning neural network for associated learning, the activated memory store to which the stimulus is associated does not rapidly decay but continues to be highly weighted, even if this weighting is outside the individual's attention (Newport DJ, Nemeroff CV 2000; in Goldstein JA 2004).

Attentional resources are allocated in favour of unexpected salient events.  The term 'switching' is used to denote reallocation processes, and 'salient' is used to refer to stimuli with special biological significance.  Dopaminergic output is involved in 'behavioural orienting', the allocation of attention to a particular stimulus.  This response normally extinguishes rapidly.  Unexpected rewards or punishments lead to the acquisition of new conditioned responses.  Dopaminergic activity is suppressed when expected rewards fail to materialize.  Basal ganglia have evolved to resolve conflicts of multiple subsystems competing for access to limited motor or cognitive resources ( see orienteering section of website for more details ).  The frontal eye fields brings visual stimuli into the most active perceptual area of the retina, so it's potential reward significance can be determined.  The computations of the possible reward occur before the behavioural switch occurs, and a signal is often lost before the identity of the stimulus is fully known (Goldstein JA 2004).

The prefrontal cortex (PFC) and noradrenergic systems are both important for attentional regulation. Lesions of the PFC impair the ability to sustain attention to relevant information and to inhibit processing of irrelevant stimuli. Neurones in the locus coereleus (LC) fire in relation to the attentional state, and the PFC is one of the few high-order inputs to the LC and is an important regulator of it's activity.  Noradrenaline is known to enhance signal-to-noise ratio in sensory cortices.  With insufficient noradrenergic stimulation, small signals may be obscured (targets) while potent stimuli may be processed (distractors).  If noradrenaline is hypersecreted, it would take the PFC 'off line'.  The PFC may be responsible for exploratory responses in a fear-inducing environment (Goldstein JA 2004).  Therefore, higher centres are most probably involved in assessing the visual input during the assessment of signs and symptoms.

Placebo versus Nocebo effect

 

Mechanisms of placebo analgesia: rACC recruitment of a subcortical antinociceptive network

U. Bingel a, b,, J. Lorenz c, E. Schoell a, C. Weiller d and C. Büchel
a NeuroImage Nord, Institute for Systems Neuroscience, University Medical Center Hamburg Eppendorf, Germany
b NeuroImage Nord, Department of Neurology, University Medical Center Hamburg Eppendorf, Germany
c Department of Physiology, University Medical Center Hamburg Eppendorf, Germany
d Department of Neurology, University of Freiburg, Germany

Received 31 January 2005;  revised 19 July 2005;  accepted 18 August 2005.  AIB-05768.  Available online 20 December 2005

Abstract

Placebo analgesia is one of the most striking examples of the cognitive modulation of pain perception and the underlying mechanisms are finally beginning to be understood. According to pharmacological studies, the endogenous opioid system is essential for placebo analgesia. Recent functional imaging data provides evidence that the rostral anterior cingulate cortex (rACC) represents a crucial cortical area for this type of endogenous pain control. We therefore hypothesized that placebo analgesia recruits other brain areas outside the rACC and that interactions of the rACC with these brain areas mediate opioid-dependent endogenous antinociception as part of a top–down mechanism. Nineteen healthy subjects received and rated painful laser stimuli to the dorsum of both hands, one of them treated with a fake analgesic cream (placebo). Painful stimulation was preceded by an auditory cue, indicating the side of the next laser stimulation. BOLD-responses to the painful laser-stimulation during the placebo and no-placebo condition were assessed using event-related fMRI. After having confirmed placebo related activity in the rACC, a connectivity analysis identified placebo dependent contributions of rACC activity with bilateral amygdalae and the periaqueductal gray (PAG). This finding supports the view that placebo analgesia depends on the enhanced functional connectivity of the rACC with subcortical brain structures that are crucial for conditioned learning and descending inhibition of nociception.

Keywords: Pain; Placebo; rACC; fMRI; PAG; Amygdala; PPI

Corresponding author. Address: NeuroImage Nord, Bldg. S 10, University Medical Center Hamburg Eppendorf, Martinistr. 52, D-20246 Hamburg , Germany . Tel.: +49 40 42803 9962; fax: +49 40 42803 9955.

Link to Pain Journal : Volume 120, Issues 1-2 , January 2006, Pages 8-15

Dissection of perceptual, motor and autonomic components of brain activity evoked by noxious stimulation

Pain, Volume 149, Issue 3, Pages 453-462 (June 2010)

M. Pichéacef, M. Arsenaultcde, P. Rainville

Received 15 April 2009; received in revised form 29 December 2009; accepted 11 January 2010. published online 23 April 2010.
Abstract

In the past two decades, functional brain imaging has considerably advanced our knowledge of cerebral pain processing. However, many important links are still missing in our understanding of brain activity in relation to the regulation of pain-related physiological responses. This fMRI study investigates the cerebral correlates of pain (rating), motor responses (RIII-reflex) and autonomic activity (skin conductance response; SCR) evoked by noxious electrical stimulation. Stimulus intensity was adjusted individually based on the RIII threshold to control for differences in peripheral processes and baseline spinal activation. Covariance analyses were used to reveal individual differences in brain activity uniquely associated with individual differences in pain, RIII and SCR. Shock-evoked activity in cingulate, medial orbitofrontal and parahippocampal regions predicted pain sensitivity. Moreover, lateral orbitofrontal and cingulate areas showed strong positive associations with individual differences in motor reactivity but negative associations with autonomic reactivity. Notably, individual differences in OFC activation was almost fully accounted by the combination of individual measures of autonomic and motor reactivity (R2=0.93). Additionally, trial-to-trial fluctuations of RIII-reflex and SCR (within-subjects) were proportional to shock-evoked responses in subgenual cingulate cortex (RIII), anterior insula (SCR) and midcingulate cortex (SCR and RIII). Together, these results confirm that individual differences in perceptual, motor, and autonomic components of pain reflect robust individual differences in brain activity. Furthermore, the brain correlates of trial-to-trial fluctuations in pain responses provide additional evidence for a partial segregation of sub-systems involved more specifically in the ongoing monitoring, and possibly the regulation, of pain-related motor and autonomic responses.

Abbreviations: ACC, anterior cingulate cortex, aINS, anterior insula, AMY, amygdala, BA, Brodmann area, BOLD, blood oxygen level dependant, dlPFC, dorsolateral prefrontal cortex, dPCC, dorsal posterior cingulate cortex, EMG, electromyographic recording, IFG, inferior frontal gyrus, INS, insula, IPL, inferior parietal lobule, MCC, midcingulate cortex, mPFC, medial prefrontal cortex, OFC, orbitofrontal cortex, PAG, periacqueductal gray matter, PCC, posterior cingulate cortex, PCG, precentral gyrus, PCL, paracentral lobule, PFC, prefrontal cortex, pgACC, perigenual anterior cingulate cortex, PHG, parahippocampal gyrus, PMC, premotor cortex, PVA, parietal ventral area, sACC, subgenual anterior cingulate cortex, SCR, skin conductance response, SI, primary somatosensory cortex, SII, second somatosensory cortex, SMA, supplementary motor cortex, VAS, visual analogue scale

The Neuromatrix

According to Melzack (1999) the sensory-discriminative, affective-motivational and evaluative-cognitive dimensions of pain experience are determined by the multiple inputs that act on the neuromatrix programmes.  These include sensory inputs, visual inputs which influence the cognitive interpretation of the situation, phasic and tonic cognitive inputs from other areas of the brain, intrinsic neural inhibitory modulation, activity of the body's stress-regulation systems including cytokines, as well as endocrine, autonomic, immune and opioid systems. Therefore, the role of mechanical traction within a multi-modal approach would be a useful clinical research paradigm.

Multimodal approach to treatment of musculoskeletal conditions.

Chronic stress may have a direct influence on pain.

Increased basal mechanical pain sensitivity but decreased perceptual wind-up in a human model of relative hypocortisolism

Pain, Volume 149, Issue 3, Pages 539-546 (June 2010)

Linn K. Kuehla, Gilles P. MichauxbCorresponding Author Informationemail address, Steffen Richtera, Hartmut Schächingera, Fernand Antonb

Received 5 October 2009; received in revised form 18 March 2010; accepted 19 March 2010. published online 09 April 2010.

Abstract

Clinical data have accumulated showing that relative hypocortisolism, which may be regarded as a neuroendocrinological correlate of chronic stress, may be a characteristic of some functional pain syndromes. However, it has not been clarified yet whether deregulations of the hypothalamus–pituitary–adrenal (HPA) axis may directly alter pain perception and thus be causally involved in the pathophysiology of these disorders. To test this hypothesis, we performed a randomized placebo-controlled crossover trial in N=20 healthy drug-free volunteers (median age 24yrs) and analyzed the effects of metyrapone-induced hypocortisolism on quantitatively assessed basal mechanical pain sensitivity (1.5–13m/s impact stimuli), perceptual wind-up (9m/s impact stimuli at 1Hz) and temporal summation of pain elicited by inter-digital web pinching (IWP; 10N pressure stimuli for 2min). Experimentally induced hypocortisolism significantly decreased pain detection thresholds and augmented temporal summation of IWP-induced pain (p<.05). The latter effect was dependent on the relative reduction in cortisol levels, and seemed to rely on a potentiated sensitization and not merely on the observed changes in basal pain sensitivity. Perceptual wind-up by contrast was reduced when cortisol synthesis was blocked (p<.05). This result is reminiscent of findings from animal studies showing a reversal of NMDA receptor activation by glucocorticoid receptor antagonists in neuropathic pain models. Our results speak in favor of a potential causal role of HPA axis alterations in pain chronicity.

The 2 threshold hypothesis of dose suggests that a therpeutic dose (normalisation of signs and symptoms) for lumbar spine traction occurs at a very low threshold of around 12-14kg and another threshold occurs with a deterioration of signs and symptoms at around 20-25kg. These values vary to some extent depending on the stage, stability, irritability and stability of the disorder.

Therefore, it appears to be important to engage the client in the clinical reasoning process.  In so doing, they are not passive recipients of treatment.  Rather, their cognitive processes are involved with the aims and objectives of treatment as well as expected outcome.  Additionally, their motor systems are involved not only in the re-evaluation of signs, but also in the re-establish of correct muscle co-ordination and stability post traction.  Importantly, general consensus suggests that multi-modal treatment approaches within the clinical reasoning frame of reference is more efficacious than using one modality alone.  Hence, treatment with mechanical traction should be integrated with other techniques such as joint mobilisations of the hip & thoracic spine, muscle energy techniques, soft tissue massage, trigger point massage, fascial release, dry needling, taping, and exercise regimes appropriate for the stage, stability, severity, &  irritability of the disorder, whilst respecting biomechanical principles of inverse dynamics.

It should be noted however, that patients who have high scores on the Catastrophizing Scale of the CSQ (Coping Stratagies Questionnaire : Rosentiel & Keefe 1983), who endorse passive coping strategies on the PMI (Pain Management Inventory : Brown et al 1989), who demonstrate low self efficacy regarding their ability to manage their pain on the PSEQ (Pain self efficacy questionnaire : Lorig et al 1989), who describe themselves as disabled by their pain on the SOPA (Survey of pain attitudes : Jensen et al 1987), and who report negative thoughts about their pain on the INTRP (Inventory of negative thoughts in response to pain : Gil et al 1990) are at greatest risk for poor treatment outcome (Jamison 2004).

For more information on Musculoskeletal Low Back Pain and treatments LBP Treatment Progress.

Further evidence regarding psychological aspects of pain and impaired brain processing come from the following recent investigations :

Chronic pain patients are impaired on an emotional decision-making task

A. Vania Apkariana, Yamaya Sosa a, Beth R. Krauss b, P. Sebastian Thomas c, Bruce E. Fredrickson d, Robert E. Levy e, R. Norman Harden f and Dante R. Chialvo a

a Department of Physiology, Northwestern University Medical School, 303 E Chicago Avenue, Chicago, IL 60611, USA
b Department of Neurosurgery, Upstate Medical University SUNY Syracuse, Syracuse, NY 13210, USA
c Department of Anesthesia, Upstate Medical University SUNY Syracuse, Syracuse, NY 13210, USA
d Department of Orthopedics, Upstate Medical University SUNY Syracuse, Syracuse, NY 13210, USA
e Neurosurgery Department, Northwestern University Medical School, Chicago, IL 60611, USA
f Rehabilitation Institute, Northwestern University Medical School, Chicago, IL 60611, USA

Received 26 June 2003;  Revised 4 November 2003;  accepted 15 December 2003 AIB-16048  Available online 20 April 2004.

Abstract

Chronic pain can result in anxiety, depression and reduced quality of life. However, its effects on cognitive abilities have remained unclear although many studies attempted to psychologically profile chronic pain. We hypothesized that performance on an emotional decision-making task may be impaired in chronic pain since human brain imaging studies show that brain regions critical for this ability are also involved in chronic pain. Chronic back pain (CBP) patients, chronic complex regional pain syndrome (CRPS) patients, and normal volunteers (matched for age, sex, and education) were studied on the Iowa Gambling Task, a card game developed to study emotional decision-making. Outcomes on the gambling task were contrasted to performance on other cognitive tasks. The net number of choices made from advantageous decks after subtracting choices made from disadvantageous decks on average was 22.6 in normal subjects ( n =26), 13.4 in CBP patients ( n =26), and -9.5 in CRPS patients ( n =12), indicating poor performance in the patient groups as compared to the normal controls ( P <0.004). Only pain intensity assessed during the gambling task was correlated with task outcome and only in CBP patients ( r =-0.75, P <0.003). Other cognitive abilities, such as attention, short-term memory, and general intelligence tested normal in the chronic pain patients. Our evidence indicates that chronic pain is associated with a specific cognitive deficit, which may impact everyday behavior especially in risky, emotionally laden, situations.

Pain (2004) 108, 129-136


Dimensions of catastrophic thinking associated with pain experience and disability in patients with neuropathic pain conditions.

Michael J.L. Sullivan a, Mary E. Lynch b and A.J. Clark b, c

a Department of Psychology, University of Montreal, C.P. 6128 Succ Centre Ville, Montreal, Que., Canada H3C 3J7
b Pain Management Unit, Queen Elizabeth II Health Sciences Centre, Dalhousie University, Halifax, NS, Canada
c Department Anesthesia, Pain Management Unit, Queen Elizabeth II Health Sciences Centre, Dalhousie University, Halifax, NS, Canada

Received 3 July 2004;  revised 13 October 2004;  accepted 1 November 2004.  Available online 9 December 2004.

Abstract

The objective of the present study was to examine the relative contributions of different dimensions of catastrophic thinking (i.e. rumination, magnification, helplessness) to the pain experience and disability associated with neuropathic pain. Eighty patients with diabetic neuropathy, post-herpetic neuralgia, post-surgical or post-traumatic neuropathic pain who had volunteered for participation in a clinical trial formed the basis of the present analyses. Spontaneous pain was assessed with the sensory and affective subscales of the McGill Pain Questionnaire. Pinprick hyperalgesia and dynamic tactile allodynia were used as measures of evoked pain. Consistent with previous research, individuals who scored higher on a measure of catastrophic thinking (Pain Catastrophizing Scale; PCS) also rated their pain as more intense, and rated themselves to be more disabled due to their pain. Follow up analyses revealed that the PCS was significantly correlated with the affective subscale of the MPQ but not with the sensory subscale. The helplessness subscale of the PCS was the only dimension of catastrophizing to contribute significant unique variance to the prediction of pain. The PCS was not significantly correlated with measures of evoked pain. Catastrophizing predicted pain-related disability over and above the variance accounted for by pain severity. The findings are discussed in terms of mechanisms linking catastrophic thinking to pain experience. Treatment implications are addressed.

Keywords: Catastrophizing; Helplessness; Neuropathic pain; Affective pain

Pain (2005) 113, 310-315


Self-management of chronic pain: a population-based study

Fiona M. Blyth a, Lyn M. March b, Michael K. Nicholas a and Michael J. Cousins b

a Pain Management and Research Institute, University of Sydney, Royal North Shore Hospital, St Leonards, NSW 2065, Australia
b Department of Rheumatology, University of Sydney, Royal North Shore Hospital, St Leonards, NSW 2065, Australia

Received 3 May 2004;  revised 6 September 2004;  accepted 22 October 2004.  AIB-400572.  Available online 25 December 2004.

Abstract

While effective self-management of chronic pain is important, clinic-based studies exclude the more typical pattern of self-management that occurs in the community, often without reference to health professionals. We examined specific hypotheses about the use of self-management strategies in a population-based study of chronic pain subjects. Data came from an Australian population-based random digit dialling computer-assisted telephone survey and included 474 adults aged 18 or over with chronic pain (response rate 73.4%). Passive strategies were more often reported than active ones: passive strategies such as taking medication (47%), resting (31.5%), and using hot/cold packs (23.4%) were most commonly reported, while the most commonly reported active strategy was exercising (25.8%). Only 33.5% of those who used active behavioural and/or cognitive strategies used them exclusively, while 67.7% of those who used passive behavioural and/or conventional medical strategies did so exclusively. Self-management strategies were associated with both pain-related disability and use of health services in multiple logistic regression models. Using passive strategies increased the likelihood of having high levels of pain-related disability (adjusted OR 2.59) and more pain-related health care visits (adjusted OR 2.9); using active strategies substantially reduced the likelihood of having high levels of pain-related disability (adjusted OR 0.2). In conclusion, we have shown in a population-based study that clinical findings regarding self-management strategies apply to the broader population and advocate that more attention be given to community-based strategies for improving awareness and uptake of active self-management strategies for chronic pain.

Keywords: Self-care; Chronic pain; Epidemiology

Pain (2005) 113, 285-292

 


Also see the following investigations into the role of neuro-immune substances in pain modulation

Tumor necrosis factor a and interleukin-1ß stimulate the expression of cyclooxygenase II but do not alter prostaglandin E 2 receptor mRNA levels in cultured dorsal root ganglia cells

Jill C. Fehrenbacher, Thomas H. Burkey, Grant D. Nicol and Michael R. Vasko E-mail The Corresponding Author

Department of Pharmacology and Toxicology, Indiana University School of Medicine, Medical Science Bldg-MS A401, 635 Barnhill Drive, Indianapolis, IN 46202, USA

Received 3 July 2004;  revised 15 September 2004;  accepted 28 September 2004.  . Available online 11 November 2004.

Abstract

Tumor necrosis factor a (TNFa) and interleukin 1ß (IL-1ß) are pro-inflammatory cytokines capable of altering the sensitivity of sensory neurons. Because sensitization elicited by IL-1ß and TNFa is blocked by inhibition of the inducible enzyme, cyclooxygenase-II (COX-2), we examined whether these cytokines could increase COX-2 expression in dorsal root ganglion (DRG) cultures. Treatment of cell cultures with either IL-1ß or TNFa increases immunoreactive COX-2, as measured by immunoblotting, in a time- and concentration-dependent manner. A 24-h pretreatment with 10 ng/ml IL-1ß or 50 ng/ml TNFa augmented COX-2 expression 50- and 8-fold over basal levels, respectively. Immunohistochemistry established the presence of COX-2-like immunoreactivity in both neuronal and non-neuronal cells in culture. The addition of IL-1 receptor antagonist blocked the induction of COX-2 expression by IL-1ß, but did not alter TNFa-stimulated increases in COX-2, indicating that the mechanism of TNFa is not limited to increasing the expression of IL-1ß. The basal and TNFa-induced expression of COX-2 was not dependent on the presence of NGF in the growth media. IL-1ß and TNFa treatment for 24 h enhanced prostaglandin E 2 (PGE 2 ) production 2–4-fold, which was blocked by pretreatment with the COX-2 inhibitor, NS-398. Exposing cultures to PGE 2 , IL-1ß, or TNFa for 24 h did not alter PGE 2 receptor (EP) mRNA levels. These results indicate that TNFa and IL-1ß induce the functional expression of COX-2 but not EP receptors in DRG cells in culture and suggest that cytokine-induced sensitization of sensory neurons is secondary to prostaglandin production and not alterations in EP receptors.

Link to article at on-line Pain journal at Elsevier.com


Excitatory and modulatory effects of inflammatory cytokines and neurotrophins on mechanosensitive group IV muscle afferents in the rat

Ulrich Hoheisel b, Thomas Unger b and Siegfried Mense a,

a Institut für Anatomie und Zellbiologie, Universität Heidelberg, Im Neuenheimer Feld 307, D-69120 Heidelberg, Germany
b Institut für Pharmakologie und Toxikologie, Charité, Humboldt Universität, Dorotheenstraße 94, D-10117 Berlin, Germany

Received 16 June 2004;  revised 22 October 2004;  accepted 13 December 2004.  AIB-400013.  Available online 1 February 2005.

Abstract

In inflamed tissue – including skeletal muscle – the concentrations of cytokines and neurotrophins are known to increase. However, nothing is known about a possible contribution of these agents to muscle pain and hyperalgesia. The present study investigated acute effects of cytokines and neurotrophins on response properties of slowly conducting muscle afferents. In anaesthetised rats, the impulse activity of single mechanosensitive group IV fibres innervating the gastrocnemius–soleus muscle was recorded and tumour necrosis factor-a (TNF-a), interleukin-6 (IL-6), nerve growth factor (NGF), or brain-derived neurotrophic factor (BDNF) were injected into the muscle. Changes in the mechanosensibility of the endings following administration of the agents were tested with repeated pressure stimuli of defined forces. A low mechanical threshold in the innocuous range was found in 44.4% of the units tested, 55.6% required strong, potentially tissue-damaging pressure stimuli for activation. NGF excited only units that had a high mechanical threshold, while IL-6 was a stimulant for low-threshold mechanosensitive units only. TNF-a and BDNF did not excite group IV units but had a desensitising action: after TNF-a or BDNF, the response magnitudes to pressure stimuli decreased significantly. The data indicate that cytokines and neurotrophins influence the impulse activity and mechanosensitivity of group IV muscle afferent units. These effects could be of functional significance when the agents are released from muscle cells under pathophysiological circumstances.

Keywords: Group IV afferent units; Skeletal muscle; Cytokines; Neurotrophins; Nociception

Link to Pain Journal


Spinal nerve lesion-induced mechanoallodynia and adrenergic sprouting in sensory ganglia are attenuated in interleukin-6 knockout mice

Matt S. Ramer a, Patricia G. Murphy b, Peter M. Richardson b and Mark A. Bisby a

a Department of Physiology, Queen's University, Kingston, Ontario, K7L 3N6 Canada
b Division of Neurosurgery, McGill University and Montreal General Hospital, Montreal, Quebec, H3G 1A4 Canada

Received 24 March 1998; revised 25 June 1998; accepted 1 July 1998. Available online 20 November 1998.

Abstract

Tight ligation and transection of the L5 spinal nerve (SNL) gives rise to pain which is dependent upon activity in the sympathetic nervous system. It also results in novel adrenergic sympathetic innervation of the dorsal root ganglion (DRG) with the formation of pericellular axonal basket structures around some DRG neurons. Since the sympathetic sprouting and basket formation may represent an anatomical basis for pain-generating interactions between the sympathetic efferent neurons and sensory afferent neurons, it is of great interest to determine possible chemical mediators of this phenomenon. Previous findings have shown that IL-6 can contribute to sympathetically-independent pain, and can give rise to thermal hyperalgesia when injected intrathecally. We have now investigated a possible contributory role of the pleiotropic cytokine interleukin-6 (IL-6) in sympathetically-mediated pain: we gave IL-6 knockout mice and mice of the parent strain c57B6/129 a SNL, assessed their resulting pain behavior for 10 days post-surgery, and used tyrosine-hydroxylase immunohistochemistry to compare sympathetic sprouting in the DRG at the end of the testing period. We found that thermal allodynia (as assessed by measuring the latency to withdrawal from radiant heat) did not differ significantly between strains. On the other hand, in the IL-6 mice, mechanoallodynia (as assessed with von Frey filaments) was markedly delayed. Sympathetic invasion of the fiber tract and cell layer of the DRG, and the formation of pericellular axonal baskets were all significantly reduced in the IL-6 knockout mice compared to the control strain. These results imply a facilitatory role for IL-6 in pain and sympathetic sprouting induced by nerve injury, and add to the growing list of roles for IL-6 in neuropathological events.

Author Keywords: Sympathetic sprouting; Allodynia; Hyperalgesia; DRG; Cytokines; Mice

Index Terms: spinal nerve; nerve injury; allodynia; hyperalgesia; interleukin 6

link to Pain Journal

Neurophysiology of Pain and Inflammation

Clinical example using mechanical traction

Presentation on Stress, Exercise and the Immune System

Mechanical traction neurophysiology conceptualised and conceived predominantly during early 1995 as part of my Masters treatise at Sydney University - for references see below as well as the paper on pain and inflammation elsewhere on this site.

Melzack R (1999)  From the gate to the neuromatrix.  Pain Supplementation 6; S121-S126

Newport DJ, Nemeroff CB (2000)  Neurobiology of post traumatic stress disorder.  Current Opinion in Neurobiology 10; 211-218

Goldstein JA (2004)  Tuning the Brain.   Principles and practice of neurosomatic medicine.  The Hawthorn Press New York

Grossberg S (2000).  The complimentary brain: unifying brain dynamics and modularity.  Trends in Cognitive Sciences 4, 233-246

The Dorsal Root Ganglion, the Intervertebral Foramen and Musculoskeletal Physiotherapy

by Martin Krause, 1995 & 2000.

SUMMARY

The efficacy of manual therapy interventions has been extensively criticised in recent years. Serious charges of physiotherapy induced conviction of disease (nocebo) leading to chronicity have been raised. Paradoxically, the omission of higher centre processing in the design of double blind investigations, results in a dichotomy of interpretation which, either justifies the determination of inefficacy or alternatively, predicts an important role for higher centre involvement during the selection and application of manual therapy techniques. Specifically, the sensory-discriminative and motivational-affective responses require dissemination if hypotheses regarding the efficacy of manual therapy treatment, for acute radicular pain, are to be made. Currently, the majority of pain research has established immune-nervous system responses associated with post-traumatic inflammation rather than repair. Recently, dysfunction of the dorsal root ganglion (DRG), which lies in the intervertebral foramen (IVF), has been implicated in both the genesis and chronicity of radicular pain. Previously, manual therapy techniques to the IVF, such as traction, have been anecdotally advocated to normalise signs and symptoms in acute radicular pain. Clinicians use the presenting signs and symptoms, to guide their clinical reasoning processes. Additionally, the normalisation of signs and symptoms is used to demonstrate the usefulness of a treatment technique to their clients. Investigations demonstrate higher centre involvement in the reduction of pain and inflammation. Clearly, if the efficacy of manual therapy is to be determined, then the differentiation between a treatment dependent descending inhibition of pain and inflammation, with that of a placebo or nocebo, is required.

INTRODUCTION: HIGHER CENTRE SENSORY-DISCRIMINATIVE AND MOTIVATIONAL-AFFECTIVE SENSORY PROCESSING BY THE NERVOUS SYSTEM

Recently, sensory-discriminative (Ploner et al. 1999) and motivational-affective (Vogt et al 1993) pathways for pain have been demonstrated in humans. The main constituents of the sensory-discriminative aspects of pain (Aδ fibre activity) include the lateral thalamic, primary (I) and secondary (II) somatosensory cortices. Conversely, the motivational affective aspects of pain consists predominantly of the medial thalamic nuclei and the anterior cingulate cortex. Importantly, this structural differentiation suggests that the specificity of treatment and the demonstration of efficacy are important aspects in the nervous systems responses to treatment. Frequently, the practitioner uses the normalisation of signs and symptoms to demonstrate efficacy, in addition to guiding their clinical reasoning processes (Higgs & Jones 1995). However, such an approach could be dangerous as it reinforces the conviction of disease and could result in a nocebo effect (Bogduk 1997; Cohen 1995). Hence, what role does the sensory-discriminative aspect of pain have on the motivational-affective response to manual therapy techniques?

Positron Emission Tomography (PET) has demonstrated that higher centres of the nervous system may be actively involved in, the descending inhibition of acute pain and inflammation in humans (Hsieh et al. 1995; Petrovic et al. 1999). Animal investigations of supraspinal opioids found a block in the perception of pain, through a 64% reduction in superficial laminae dorsal horn activity (Gogas et al. (1991) (usually associated with a predominance of nociceptive specific neurones {Lima et al. 1994}), and a 85% reduction in ventral horn activity (usually associated with motor neurones) in animals (Schomburg & Steffens 1991). One source of descending inhibition involves pontine noradrenergic projections, in animals (Janig 1985; Martin et al. 1999; Post et al. 1986; Morgan et al. 1989; Nakagawa et al. 1990; Ren et al. 1990; Proudfit 1992). Although descending noradrenergic inhibition is considered to be an opioid-independent form of analgesia (Proudfit 1992), evidence supports the view that m-opioid and a-2 noradrenergic receptors are functionally linked to pain modulation (Gebhart et al 1994). Higher centres have been implicated in sympathetic responses, to spinal manual therapy techniques, in humans (Petersen et al. 1993; Vicenzino et al. 1998). Plausibly, the sensory-discriminative pathway was involved in the reduction of secondary hyperalgesia, as these techniques were applied to the neck for lateral elbow pain.

Evidence for important motivational-affective responses are from animal investigations which, substantiate the finding that higher centres can act in an antinociceptive manner (Sandkuehler et al. 1995). Importantly, a "behavioural set" has been defined as 'a state of readiness or preparation to receive a stimulus that has not yet arrived, or a state of readiness or preparation to make a movement' (Woodworth 1958 c.f. Dubner & Ken 1999). Therefore, the net effect of descending inhibition in animals from the Locus Coeruleus/Subcoeruleus, Nucleus Raphe Magnus, and Nucleus Gigantocellularis is to "dampen or counteract the cascade of events that ultimately lead to the development of inflammatory hyperalgesia" (Dubner and Ken 1999) (see figure 1). Attention and cognitive factors such as previous experience of manual therapy or possibly even the apparent normalisation of signs and symptoms could modulate noxious stimuli in the primary somatosensory cortex (Bushnell et al. 1999; Dubner & Ken 1999). These motivational-affective responses presumably occur with the interaction of the client and the therapist during the clinical reasoning process.

Together, these investigations represent very powerful arguments for assessment of the signs and symptoms during the clinical reasoning process, thereby involving higher centres in the neuromodulation of pain and inflammation. Additionally, the activation of higher centres through the re-setting of stabilising muscles, after the person receives passive joint mobilisation treatment, may be necessary for even greater involvement of higher centres. Confirmation of motivational-affective responses to treatment would require the use of psychometric pain questionnaires, positron emission tomography (PET) and functional MRI to demonstrate the temporal changes in cerebral activity (Casey & Minoshima 1997; Svensson et al. 1997) before, during and after treatment

ECTOPIC IMPULSE GENERATION IN THE DORSAL ROOT GANGLION (DRG) AND NEUROGENIC INFLAMMATION IN THE SENSORY NERVE ENDINGS OF THE SINUVERTEBRAL (SNV) NERVE – A ROLE FOR LOCALISATION OF TREATMENT?

To justify an important localised sensory-discriminative response to injury and hence treatment requires an appreciation of dorsal root ganglion (DRG) dysfunction. Inflamed structures demonstrate increased excitability of sensory nerve endings (Raja et al. 1988; Schmidt et al. 1994). A cause of acute radicular spinal pain may be the generation of excessive electrical activity (ectopic impulses) from inflamed structures. Passive joint mobilisations may be useful in the treatment of radicular spinal pain by 'unloading' those structures (e.g. DRG) whose functions include the modulation of ectopic impulse generation. Ectopic discharge can occur in the DRG following damage that occurs distally in the neural pathway and in the presence of endoneural oedema in animals (Howe et al. 1977), and humans (Nordin et al. 1984). Essentially, endoneural oedema of the DRG resulting from compression by extraneural inflammatory exudate (Chatani et al. 1995) in the intervertebral foramen (IVF) generates ectopic electrical impulses (Bandalamente et al. 1987). These ectopic impulses originating in the DRG are thought to propagate into the spinal cord and into peripheral receptor sites (Wall & Devor 1983; Bandalamente et al. 1987). Consequently, the extent of spinal cord sensitisation, oedema and neurogenic inflammation may in some cases be more significant than the physical size of an intervertebral disc (IVD) protrusion (Garfin et al. 1991; Thelander et al. 1992). Interestingly, Bogduk (1997) advocates radiofrequency neurotomy in the treatment of chronic spinal pain. However, in acute radicular pain it becomes apparent that the DRG is likely to regulate the excitability of the sensory nerve endings (Devor 1999). Therefore, 'unloading' of mechanical compromise (extraneural inflammation) around the DRG in the IVF, by for example traction, could plausibly reduce ectopic impulse generation (see figure 2).

Ectopic impulse generation from the DRG may propagate throughout the innervation of the sinuvertebral (SNV) nerve. The SNV nerve is a peripheral nerve formed by the recurrent branch of the ventral ramus and a branch of the grey ramus communicantes of the somatic and peripheral sympathetic nervous systems respectively (Bogduk & Twomey 1997). Since the SNV nerve does not innervate superficial structures of the body, it may play a sensory-discriminative role such as mechanoception and nociception (Ahmed et al. 1993). Certainly, the types of receptors innervating the ligamentous structures, suggests such roles (Korkula et al. 1985; Weinstein et al. 1988a). Similar to other peripheral nerves, a vasoactive role on blood vessels may be a function of the sympathetic component of the SNV nerve (Appenzeller et al. 1984; Selander et al. 1985; Weinstein et al. 1988b; Zochodne et al. 1990). Importantly, the terminals of the SNV nerve appear anatomically well placed to transmit ectopic impulses to the IVD, posterior longitudinal ligament, Hoffman ligaments, and the dura mater (Weinstein et al. 1988a, Bogduk & Twomey 1997). This increased ectopic impulse propagation increases neurogenic inflammation, possibly at the SNV nerve receptor sites (Markowitz et al. 1989; Xavier et al. 1990; Chatani et al. 1995). Arborization of the SNV nerve terminals can cause neurogenic inflammation in an expanded receptive field (LaMotte et al. 1991). Furthermore, expansion of spinal cord neuronal hypersensitivity may arise from the propagation of ectopic impulses into the spinal cord from the periphery (Wall & Devor 1983). This expansion is called secondary hyperalgesia and possibly explains the severity of referred limb pain, which is a frequent manifestation of radicular pain. Therefore, a dual role of the SNV nerve in the detection of nociception, in addition to the propagation of ectopic impulses to structures of the IVF and spinal canal is plausible. Presumably, specific manual therapy techniques will induce a sensory-discriminative response, which is likely to activate a motivational-affective response that either increases or decreases secondary hyperalgesia depending upon the perceived appropriateness of the treatment.

THE HYPOTHESIS: SPINAL TECHNIQUES AFFECT THE DORSAL ROOT GANGLION (DRG) IN THE INTERVERTEBRAL FORAMEN (IVF)

Clearly the expansion of the hypersensitive receptive field, underlie the importance of investigating the sensory-discriminative aspects of treatment techniques. Variation of techniques to the IVF, such as the type of load (stretch vs. compression, active vs. passive), the position, and the duration are probably detected by SNV nerve terminals, innervating inflamed structures. Since the SNV nerve appears to innervate the DRG itself (Cuartico et al. 1988; Groen et al. 1988), the ramifications of extraneural inflammation in the IVF are vascular compromise inducing intraneural oedema in the DRG. Consequently, intraneural oedema causes ectopic impulse generation, which increases the intensity of the existing extraneural neurogenic inflammation. Hence, an ongoing self-perpetuating cycle of neurogenic inflammation ensues, which potentially impoverishes any regulation in excitability of sensory nerve endings by the DRG. Thus, if a treatment technique affects the vascular compromise (and extraneural inflammation) surrounding the DRG, in the IVF, then a resultant reduction in endoneural oedema in the DRG would interrupt this self-perpetuating cycle of neurogenic inflammation. Significantly, reduced ectopic impulse generation and enhanced modulation of excitability of sensory nerve endings, by the DRG, may substantiate the validity of using the immediate normalisation of signs and symptoms for the determination of the appropriate technique (Larsson et al. 1980; Maitland 1986; Eggertz 1986; Pal et al. 1986; Knutsson et al. 1988) (see figure 3). Thus, any measured changes in sensory-discriminative function may imply an activation of higher centre responses. In turn, the subsequent motivational-affective response may be indirectly determined through autonomic testing of that innervation field (Sandroni 1998).

A MODEL: MECHANICAL TRACTION FOR THE NORMALISATION OF SIGNS AND SYMPTOMS IN ACUTE RADICULAR SPINAL PAIN

A recent review suggested some people with acute radicular spinal pain responded well to traction with the normalisation of signs and symptoms (Krause et al. 2000). Specifically, to determine an important sensory-discriminative response then the predictive validity of the current model is the normalisation of signs and symptoms within a narrow band of loading tolerance. Since the valid dose of traction would be the normalisation of signs and symptoms, then the inappropriate dose will be the deterioration of signs and symptoms. In considering ectopic impulse generation, 'unloading' of the contents of the IVF (i.e. Nerve Root/Dorsal Root Ganglion/Spinal Nerve, intra-foraminal blood vessels, sinuvertebral nerve) may be a logical explanation for the first observation of the normalisation of signs and symptoms. Reduction in ectopic impulse generation and simultaneously enhanced modulation of inflammation could be expected from the mechanical 'unloading' of the DRG in particular. Similarly, if the inflamed structures comprising the IVF (i.e. IVD, Zygapophyseal joint, Hoffman ligaments, etc) (Groen et al. 1988; Park & Watanabe 1990; Wiltse et al. 1993; Bogduk & Twomey 1997) are 'overloaded', then ectopic impulse generation (Raja et al. 1988; Schmidt et al. 1994) with the deterioration of signs and symptoms can be expected during excessive traction. The normalisation-deterioration of signs and symptoms can be referred to as a two-threshold hypothesis.

The clinical implications of the sensory-discriminative and motivational-affective aspects of pain highlight the importance of differentiating a specific neurophysiological effect from the placebo and nocebo. Clearly the demonstration of efficacy and expectations of outcome are an essential aspect of any treatment protocol. Presumably, some people will deteriorate or not respond to traction at all. In these people, the loading threshold has not been reached or another form of treatment is more appropriate. Importantly, lack of improvement or deterioration may induce a nocebo response. Therefore, the clinical reasoning process needs to identify the responders from the non-responders in a manner, which expedites appropriate treatment. Hence, a correlation with psychometric questionnaires and the temporal aspects of functional MRI and PET diagnostic imaging would be required before conclusions of efficacy are drawn. Since it is unlikely that a person could guess their threshold for their normalisation of signs and symptoms, then a method of investigation for a differentiation of the neurophysiological, placebo and nocebo effect may include the use of the two-threshold hypothesis.

THE VALIDITY OF USING THE NORMALISATION OF SIGNS AND SYMPTOMS

The validity of testing procedures underlie the ability of the examiner to make a clinical prediction (Payton 1988). Clinical reasoning uses signs and symptoms to determine the appropriateness of a treatment strategy (Higgs & Jones 1995). However, is the reduction in ectopic impulse generation and the modulation of excitability in sensory nerve endings correlated with the observable normalisation of signs and symptoms? Significantly, the incidence of the normalisation of signs and symptoms is not clear. Therefore, is the normalisation of signs and symptoms useful for making consistent decisions on the appropriateness of treatment technique for acute radicular pain? Finally, does the use of this methodology impart conviction of disease?

The pain response and range of motion (ROM) of straight leg raise (SLR) is a variable used to assess the effects of treatment using traction (Larsson et al. 1980; Eggertz 1986; Mathews et al. 1987; Pal et al. 1986; Tesio et al. 1989). The load and position of the patient have been defined by the improvement in the pain free ROM of SLR (Larsson et al. 1980). During SLR, the direct contact pressure of the DRG against the structures of the IVF (Smith et al. 1993) and tension generated in inflamed nerve roots are thought to cause sufficient ectopic impulse generation to stimulate the reflexogenic drive to the alpha-motor neurones, as demonstrated in animals (Woolf et al. 1994). Clinically, this reflexogenic drive may represent increased muscle activity that reduces ROM. Since ectopic impulse generation from the DRG also propagates into the spinal cord, then neuronal hypersensitivity could explain alterations in signs and symptoms on the contralateral side seen in humans and animals (Larsson et al. 1980; Woolf 1984; Woolf & Swett 1984; Woolf & MacMahon 1985; Woolf & Wall 1986b; Schmidt 1990; Eckert et al. 1999). Confirmation of such findings require, fine needle electromyography (EMG). Obviously, solely comparing ROM of SLR to the opposite side without due consideration of other variables may lead to errors in the clinical reasoning process.

Other variables inferring some validity when correlated with the normalisation of SLR, during treatment, include reduction in pain intensity, normalisation of muscle strength, and restoration of somatosensory evoked potentials (Knutsson et al. 1988). Additionally, improved asymmetric skin temperatures and sensation testing has been demonstrated (Knutsson et al. 1988; Onel et al. 1989). Although, the incidence of the normalisation of signs and symptoms was high, methodological problems exist which suggest caution in the interpretation of these results. Never the less, normalisation of muscle power, skin sensation, skin temperature, and pain intensity may be correlated with ROM of SLR to predict appropriate technique during the clinical reasoning process.

Normalisation of tendon reflexes has been used to assess patients, during auto-traction, and is thought to correlate with the normalisation of conduction along nerve fibres (Larsson et al. 1980; Pal et al. 1986; Knutsson et al. 1988; Onel et al. 1989; Sabbahi & Khalil 1990b). However, hypersensitivity in spinal cord reflexes can cause tendon reflexes to increase or decrease during neurogenic inflammation and ectopic impulse generation (Ferrell et al. 1988; Rees et al. 1994). Evidence for variable hyper- and hyporeflexia during inflammation comes from Hoffman-reflex investigations where increasing stimulus intensity increases the reflex until a given stimulus threshold is reached where a decrease or complete block in the Hoffman-reflex amplitude occurs (Sabbahi & Khalil 1990a). Since inflamed tissues have reduced receptor threshold, then excessive electrical activity during loading may alter reflex activity (Raja et al. 1988). Whether the hypersensitivity of spinal cord reflexes from neurogenic inflammation and ectopic impulse generation represent a decrease rather than an increase in tendon reflex awaits confirmation in the clinical situation. Importantly, this stimulus-dependent phenomenon may explain the deterioration of signs and symptoms when a technique is applied indiscriminately. Paradoxically, rather than demonstrating efficacy, such sensory-discriminative methodology has been seen to impart conviction of disease, which negatively influences the motivational-affective aspects of the pain (Bogduk 1997: Cohen 1995, Zusman 1998). Therefore, clinical reasoning based upon the normalisation of signs and symptoms would only be justified if a reduction in chronicity could be demonstrated. Epidemiology, using large numbers of subjects, would be required to validate these opinions.

RESTORATION OF NERVE CONDUCTION THROUGH THE MODULATION OF NEUROGENIC INFLAMMATION AND CYTOKINE-IMMUNE RESPONSES BY THE DRG AND PERIPHERAL SYMPATHETIC NERVOUS SYSTEM (SNS)

Peripheral nerve injury results in morphological changes in the DRG (Dib-Hajj et al. 1999; Eckert et al. 1999; Ramer et al. 1999). Although these morphological changes relate to chronic constriction, the onset and perpetuation of neurogenic inflammatory responses appear to begin within hours of the acute phase of injury (Schmidt et al. 1994). Notably, the SNV nerve and spinal nerve may represent the peripheral nerves susceptible to constriction irritation. The proposed genesis of these morphological changes are Wallerian degeneration in the periphery releasing nerve growth factor, leukaemia inhibitory factor and Interleukin (IL) - 6 (Ramer et al. 1999). The activation of similar cytokines is also associated with immune responses during exercise induced musculoskeletal damage (Pedersen et al. 1999) (SEE : Immune function and muscle mass or slide presentation for more detail). The disruption of the fibroblast endothelium is considered the 'trigger' for the release of tumour necrosis factor, IL-1, IL-6, IL-8. Subsequently, there is an activation of prostaglandin driven release of Substance P, with its consequential further release of cytokines from macrophages and mast cells, which completes a self-perpetuating cycle of inflammation (Groenblad et al. 1991; Rothwell & Hopkins 1995). Generally, inflammation and mast cell degranulation affects blood-nerve permeability and nerve conduction (Harvey et al. 1994). If, the interaction between the DRG and peripheral SNS is responsible for these immune responses during inflammation, then a treatment technique like traction may aid in reducing constriction of the affected peripheral nerves. In turn, the re-establishment of DRG function will enhance the modulation of cytokine activity. It is difficult to conceive any methodology, which may directly image these morphological changes in humans. Interestingly, some of the resultant restitution of nerve conduction is predicted to occur beyond the immediate application of the treatment technique. Therefore, the extent by which manual therapy techniques can prevent such morphological changes from occurring could justify early and appropriate treatment interventions. Certainly, pharmacological investigations have demonstrated greater treatment efficacy when early intervention was instigated (Bhala et al. 1988).

REDUCTION OF VENOUS CONGESTION AND THE MODULATION OF HOMEOSTASIS BY THE DRG IN THE INTERVERTEBRAL FORAMEN (IVF).

Reduction in mechanical irritation from venous congestion around the DRG may be an explanation for the efficacy of a treatment technique such as traction. Cadaveric studies demonstrate that mechanical abnormalities within the spine, such as IVD extrusion, result in dilatation, congestion, and thrombosus of veins contributing to disruption of the vascular endothelium and consequent fibrin deposition (Hoyland et al. 1989). Importantly, intraforaminal blood flow may represent part of the sensory-discriminative function of the DRG. The unusual location of the DRG between the peripheral and central nervous systems has been related to its hypothesised function as a sensor of background information such as homeostasis of the IVF milieu (Devor 1999). Besides location, evidence supporting a homeostatic function of the DRG is the lack of blood-nerve barrier around the cells of the DRG and the highly convoluted nature of its vasculature (Devor 1999). Obviously, sufficient blood flow would be required to detect homeostasis. Arguably, techniques such as traction achieve reduction in mechanical irritation by increasing the space for the intra-foraminal blood vessels of the IVF. Apparently, improved IVF space has been demonstrated by merely positioning a person to reduce their lumbar lordosis (Panjabi et al. 1983). The implications are that the function of the DRG may be susceptible to vascular and mechanical compromise in the IVF. Since venous pressure is quite low, the advocacy of using positions of comfort in acute radicular pain may be justified (Maitland 1986), as the required restitution of homeostasis in the IVF may occur.

Additional explanations for the effectiveness of using the 'positions of comfort' or low dose traction reside in the effect of neural irritation from compression at two locations. Besides swelling in the IVF from inflammatory exudate, the zygapophyseal (Z) joint may be swollen and inflamed. Histological changes suggestive of inflammation have been demonstrated in the Z-joint (Cooper et al. 1995). Since the Z-joint represents the posterior aspect of the IVF then presumably some decompression of the IVF may result from stretching of the Z-joint capsule during traction (Krause et al. 2000). Interestingly, nutrient transport to the nerve roots from both the intraneural blood vessels and from diffusion from the cerebrospinal fluid is affected in the intermediate zone between the two sites of compression almost as much as at the compression sites themselves, in rats. Even low pressure (10mmHg) is sufficient to induce a significant reduction in total blood flow possibly from retrograde capillary stasis due to venous occlusion (Rydevik et al. 1984a,b; Olmarker et al. 1989a,b; Cornefjord et al. 1992; Matsui et al. 1992; Takahashi et al. 1993). Clinically, pressure from extruded IVD material, in the IVF, and swelling of the Z-joint may represent a similar situation to the animal model. Importantly, relatively small traction loads or 'positions of comfort' may be required to reduce compromise at one site, thus resulting in the restoration of venous flow necessary for any homeostatic function of the DRG in the IVF. Perhaps, ultrasound imaging may be useful for demonstrating alterations in the dimensions of the Z-joint capsule. Certainly, ultrasound has been effective in demonstrating changes to the size or shape of the multifidus muscle which inserts into the Z-joint capsule (Hides et al. 1994). MRI of the IVF, doppler ultrasound of intraforaminal flow and computer modelling may be investigative procedures, of the future, for determining the biomechanical response to the treatment technique.

HEALING: THE ROLE OF THE VASCULATURE AND PERIPHERAL SYMPATHETIC NERVOUS SYSTEM IN THE MODULATION OF NEUROGENIC INFLAMMATION AT THE SINUVERTEBRAL (SNV) NERVE TERMINALS: A MOTIVATIONAL – AFFECTIVE RESPONSE TO SOMATOSENSORY STIMULI?

The sympathetic efferents are postulated to be important to the healing process since the activation of peripheral terminals of sympathetic postganglionic neurones contributes to neurogenic inflammation (Levine et al. 1986). Since emotions and somatosensory inputs profoundly influence the autonomic nervous system, non-invasive autonomic testing has been advocated in people with pain (Sandroni 1998). Sympathetic postganglionic neurones release inflammatory mediators that increase plasma extravasation, including prostaglandins (Coderre et al. 1989; Gonzales et al. 1989; Gonzales et al. 1991; Green et al. 1991a,b). Additionally, under conditions of sympathetic postganglionic neuronal modulation, bradykinin has been found to increase plasma extravasation (Green et al. 1992). Importantly, the interaction between primary afferent nociceptors (associated with the DRG) and sympathetic efferents during inflammation appears to be increased for intact nociceptors with axons travelling in damaged nerve (Sato & Perl 1991). Conversely, the sympathetic postganglionic neurones also release mediators, which decrease plasma extravasation, including neuropeptide Y and noradrenaline (Green et al. 1991; 1992). Apart from modulating plasma extravasation these substances may also interact with endothelial relaxing factor (Greenberg et al. 1991) and platelet-activating factor (Heller et al. 1994) in the blood vessels. Significantly, agents that enhance synovial plasma extravasation have been demonstrated to decrease tissue injury during inflammation (Coderre et al. 1991). The mechanisms by which sympathetic nerves decrease tissue injury are unclear. However, an increased plasma extravasation would be expected to reduce the concentration of inflammatory substances through the facilitation of venous drainage thereby improving healing (Heller et al. 1994) at the terminals of the SNV nerve. These animal investigations suggest that in addition to non-invasive autonomic testing, the motivational-affective responses need to be monitored using psychometric pain questionnaires.

DURATION OF EFFICACY: THE 'SILENCING' OF ECTOPIC IMPULSE GENERATORS COULD LEAD TO A PROLONGED EFFECT SIMILAR TO LOCAL ANAESTHETICS.

The relief of pressure from extraneural inflammatory compromise at SNV nerve receptor sites surrounding the DRG could 'silence' ectopic impulse discharges. Ideally, this 'silencing' would last for a similar duration to that demonstrated by local anaesthetics. Local anaesthetics 'silence' the neurones at the site of ectopic impulse generation for a period outlasting the pharmacological effect of the local anaesthetic (Devor et al. 1992). It has been hypothesised that any silencing of ectopic discharges should allow the autoinhibitory interneurones of the spinal cord to recover from the neurotoxic effects of increased large diameter afferent bombardment (Sugimoto et al. 1990; Dubner 1991). Alternatively, this 'silencing' may provide the sensory-discriminative pathway an opportunity to activate powerful descending inhibition of pain and inflammation. A reduction in ectopic discharge has been shown in cats when the compression stimulus was removed (Howe et al. 1977). Thus, if a technique reduces endoneurial oedema by assisting in the removal of extraneural inflammatory exudate from around the DRG and SNV nerve, then this may explain any normalisation of neurological signs and symptoms for a duration outlasting the period of the technique. Importantly, the demonstration of such temporal responses, once the biomechanical stimuli of our techniques has been removed, would highlight the overwhelming influence of the neurophysiological processes in healing.

CONCLUSION

Reduced mechanical irritation of the DRG in the IVF may be responsible for the immediate and long lasting effects of the appropriate treatment for acute radicular pain, in some people. Consequently, reduced ectopic impulse generation and enhanced modulation of pain and inflammation should be accompanied by the normalisation of signs and symptoms. Sensory-discriminative and motivational-affective nervous system responses are likely mechanisms required for the prolonged normalisation of signs and symptoms. Clearly, future investigations into the efficacy of manual therapy, requires the incorporation of higher centre processing into the methodology. Vascular changes as a result of inflammation are probably modulated by the sympathetic nervous system (SNS). Improved blood flow allows the restoration of the homeostatic function of the DRG. Additionally, the modulation of the excitability of sensory nerve terminals, by the DRG, involves its interaction with the SNS. Enhanced modulation of prostaglandin activity through the interaction of the DRG and SNS with the cytokine-immune system at the sites of innervation of the SNV nerve may restore nerve conduction. The two-threshold hypothesis for the dose of traction could represent a novel experimental method, as it is unlikely that a person can guess the threshold of their normalisation of signs and symptoms. A promising investigative model, using the dose of traction, psychometric analysis, computer modelling, in addition to diagnostic imaging, represents a potential methodology for unravelling the mysteries of radicular pain. The effect of appropriate early intervention to the incidence of chronicity requires investigation, since the validity and precise incidence of the normalisation of signs and symptoms during the treatment of acute radicular pain has not been clearly established. Hereby, charges of physiotherapy induced conviction of disease leading to chronicity can be addressed.

all intellectual property rights should be observed; written predominantly in early 1995 as part of my Masters in Applied Science (Manipulative Physiotherapy)

uploaded by Martin Krause 2000

 

Descending modulation of pain hypothesis vindicated by recent research:

Skyba DA, Radhakrishnan R, Rohlwing JJ, Wright A, Sluka KA (2003)  Joint manipulation reduces hyperalgesia by activation of monoamine receptors but not opioid or GABA receptors in the spinal cord.  Pain, 106, 159-168

Ren & Dubner (2002). Descending Modulation of Pain:  Pain, 100, 1-6

see also

Tumor necrosis factor α and interleukin-1β stimulate the expression of cyclooxygenase II but do not alter prostaglandin E2 receptor mRNA levels in cultured dorsal root ganglia cells

Jill C. Fehrenbacher, Thomas H. Burkey, Grant D. Nicol and Michael R. VaskoE-mail The Corresponding Author

Department of Pharmacology and Toxicology, Indiana University School of Medicine, Medical Science Bldg-MS A401, 635 Barnhill Drive, Indianapolis, IN 46202, USA

Received 3 July 2004;  revised 15 September 2004;  accepted 28 September 2004.  . Available online 11 November 2004.

Abstract

Tumor necrosis factor α (TNFα) and interleukin 1β (IL-1β) are pro-inflammatory cytokines capable of altering the sensitivity of sensory neurons. Because sensitization elicited by IL-1β and TNFα is blocked by inhibition of the inducible enzyme, cyclooxygenase-II (COX-2), we examined whether these cytokines could increase COX-2 expression in dorsal root ganglion (DRG) cultures. Treatment of cell cultures with either IL-1β or TNFα increases immunoreactive COX-2, as measured by immunoblotting, in a time- and concentration-dependent manner. A 24-h pretreatment with 10 ng/ml IL-1β or 50 ng/ml TNFα augmented COX-2 expression 50- and 8-fold over basal levels, respectively. Immunohistochemistry established the presence of COX-2-like immunoreactivity in both neuronal and non-neuronal cells in culture. The addition of IL-1 receptor antagonist blocked the induction of COX-2 expression by IL-1β, but did not alter TNFα-stimulated increases in COX-2, indicating that the mechanism of TNFα is not limited to increasing the expression of IL-1β. The basal and TNFα-induced expression of COX-2 was not dependent on the presence of NGF in the growth media. IL-1β and TNFα treatment for 24 h enhanced prostaglandin E2 (PGE2) production 2–4-fold, which was blocked by pretreatment with the COX-2 inhibitor, NS-398. Exposing cultures to PGE2, IL-1β, or TNFα for 24 h did not alter PGE2 receptor (EP) mRNA levels. These results indicate that TNFα and IL-1β induce the functional expression of COX-2 but not EP receptors in DRG cells in culture and suggest that cytokine-induced sensitization of sensory neurons is secondary to prostaglandin production and not alterations in EP receptors.

Link to article at on-line Pain journal at Elsevier.com

Late in 2007 DeLeo, Sorkin & Watkins in their IASP publication Immune and glial regulation of pain devoted 5 chapters (of 23) to the DRG. Chapter 9 described DRG signaling and erythropoietin as a protective agent against neuropathic pain development (Campana, WM), chapter 10 cited the recognition that DRG satellite cells and trafficking leukocytes into the DRG may directly affect primary afferent signaling which enhances the complexity of glial - immune reactions within the CNS (McLachlan E). Chapter 21 described the ischaemic compromise due to the metabolic demands of immune - inflammatory processes in the DRG, as well as describing both pro-inflammatory (IL-1, IL-6, TNF-alpha) and anti-inflammatory (IL-10) cytokines found in the Nucleus Pulposus of the disk.

McLachlan EM, Hu P (2007). Inflammation of DRG: Satellite cell activation and immune cell recruitment after nerve injury. In : Immune and Glial Regulation of Pain Ed DeLeo JA, Sorkin LS, Watkins LR. IASP Press, Seattle. Ch 10

  • Neuropathic pain generally developes following lesions of the blood-nerve barrier. Neurogenic inflammation as a result of mechanical irritation leading to chemical irritants and oedema can precipitate the conditions required for the development of neuropathic pain. Retrograde axonal signalling from nociceptors that surround the DRG itself can propagate inflammatory reactions around the somata of motor, sympathetic and sensory neurones triggering the release of chemokines from the glia of satellite cells within the DRG and astrocytes in the ventral horn.
  • In contrast to the CNS, the blood-nerve barrier around the DRG is very permeable thus allowing the the neurones to be exposed to circulating proteins (and potentially the extruded disk material such as the nucleus pulposus (NP) - my thoughts).
  • Transection or ligation of the L5 spinal nerve is followed by degeneration of axons in the distal branches of the sciatic nerve. Interestingly, the L4 DRG shows mild but distinct inflammatory responses with invasion of macrophages and lymphocytes. This finding indicates that DRG inflammation can be triggered by signals independent of axotomy of it's sensory neurones.
  • The chronic constriction injury model using loose ligatures around the sciatic nerve there is recruitment of alpha-beat T-lymphocytes into the DRG and the spinal cord. Amost all are CD8+ T cells. Unless T cells and macrophages in the subarachnoid angle are intravascular, penetration of the capsule is likely to require the upregulation of chondroitin sulphate proteoglycan degrading enzymes such as metalloproteinases, as has been shown in sympathetic ganglia (Leone et al 2005).
  • The most likely effect of inflammation within the DRG is to reduce discharge threshold of injured and non-injured neurones that project centrally in pain pathways.Another factor that may raise neuronal excitability and initiate discharge is the relative ischaemia resulting from the higher metabolic demands of inflammation.

Karppinen J (2007). New perspectives on Sciatica. In : Immune and Glial Regulation of Pain Ed DeLeo JA, Sorkin LS, Watkins LR. IASP Press, Seattle. Ch 21

  • A sharp 40-98% decrease in intraradicular blood flow in the L5 and L4 was elicited by an intraoperative straight leg raising test at the angle which produced symptoms of sciatica. Removal of adhesions normalised blood flow highlighting the importance of mechanical compression in the induction of ischaemia.
  • However, inflammation may induce ischaemia through increased endoneurial pressure from capillary leakage similar to a 'compartment syndrome' of the DRG.
  • In contrast to nerve roots, the DRG are very sensitive to mechanical compression.
  • Both mechanical and chemical irritation produce more severe histological damage to the nerve roots than either factor alone.
  • Hypoxia-inducible factor (HIF), a transcription factor that responds to low oxygen levels, probably triggers mitogen-activated protein kinase (MAPK) expression and erythropoietin synthesis.
  • Tumor necrosis factor alpha is crucial in MAPK activation
  • Exposure of the DRG to IL-1beta, TNF-alpha, and IL-6 increased mechanosensitivity of DRG and it's receptive fields
  • Antereograde activation of spinal cord glial cells (astrocytes and microglia) by cytokines can result in extra-territorial pain and mirror image pain
  • Herniated disk material contains pro-inflammatory as well as anti-inflammatory (IL-10) cytokines.

See the following link for a greater explanation of the neuro-immune-inflammatory cascade as it relates to exercise, muscle protein, apoptosis and cognitive behavioural therapy.

Immune System and Musculoskeletal Dysfunction

References

Adams, M.A., Dolan, P.& Hutton, W.C. (1986). The stages of disc degeneration as revealed by discogram. Journal of Bone and Joint Surgery 68B, 36.

Ahmed, M., Bjurholm, A., Kreicbergs, A.& Schultzberg, M. (1993). Sensory and autonomic innervation of the facet joint in the rat lumbar spine. Spine 18(14), 2121 to 2126.

Alkon, D.L.& Rasmussen, H.A. (1988). A spatial-temporal model of cell activation. Science 239, 998 to 1005.

Attal, N., Filliatreau, G., Perrot, S., Jazat, F., Di Giamberardino, L.& Guilbaud, G. (1994). Behavioural pain-related disorders and contribution of the saphenous nerve in crush and chronic constriction injury of the rat sciatic nerve. Pain 59, 301 to 312.

Badalemente, M.A., Dee, R., Ghillani, R., Chien, P-F. & Daniels, K. (1987). Mechanical stimulation of dorsal root ganglia induces increased production of substance P : A mechanism for pain following nerve root compromise? Spine 12, 552 to 555.

Barasi, S.& Lynn, B. (1986). Effects of sympathetic stimulation on mechanoreceptive and nociceptive afferent units from the rabbit pinna. Brain Research 378, 21 to 27.

Barker, J.N., Mitra, R.S., Griffiths, C.E., Dixit, V.M.& Nicholoff, B.J. (1991). Keratinocytes as initiators of inflammation. Lancet 337, 211 to 214.

Barrows, H.S., Tamblyn, R.N., (1980). Problem-based learning: an approach o medical education. Springer, New York.

Blottner, D.& Baumgarten, H.G. (1994). Neurotrophy and regeneration in vivo. Acta Anatomica 150, 235 to 245.

Bogduk, N. (1993). The anatomy and physiology of nociception. In : Crosbie J.& McConnell, J.(Eds.) (1993). Key Issues in Musculoskeletal Physiotherapy(Ch.3). Oxford : Butterworth-Heinemann Ltd.

Butler, D.S., (1991). Mobilisation of the Nervous System. Churchill Livingstone : Melbourne.

Chatani, K., Kawakami, M., Weinstein, J.N., Meller, S.T.& Gebhart, G.F. (1995). Characterization of thermal hyperalgesia, c-fos expression, and alterations in neuropeptides after mechanical irritation of the dorsal root ganglion. Spine 20(3), 277 to 290.

Coderre, T.J., Basbaum, A.I.& Levine, J.D. (1989). Neural control of vascular permeability : interactions between primary afferents, as cells, and sympathetic efferents. Journal of Neurophysiology 62, 48 to 58

Coderre, T.J., Chan, A.K., Helms, C.& Levine, J.D. (1991). Increasing sympathetic nerve terminal-dependent plasma extravasation correlates with decreased arthritic joint injury in rats. Neuroscience 40, 185 to 189.

Coghill, R.C., Mayer, D.J., Price, D.D., (1993). Spinal cord coding of pain : The role of spatial recruitment and discharge frequency in nociception. Pain, 53, 295 to 309.

Cohen, M.L., (1995). The clinical challenge of secondary hyperalgesia. Moving in on Pain (Abstracts). Adelaide, Australia.

Cohen, M.L., Quintner, J.L., (1993). Fibromyalgia syndrome, a problem of tautology. Lancet, 342, 906-909.

Collingride, G.L.& Singer, W. (1990). Excitatory amino acid receptors and synaptic plasticity. Trends in Pharmacological Science 11, 290 to 296.

Cornefjord, M., Takahashi, K., Matsui, H., Olmarker, K., Holm, S.& Rydevik, B. (1992). Impairment of nutritional transport at double level cauda equina compression: An experimental study. Neuro Orthopedics 13, 107 to 112.

Dickenson, A.H.& Sullivan, A.F. (1987). Evidence for a role of the NMDA receptor in the frequency dependent potentiation of deep rat dorsal horn nociceptive neurons following C-fibre stimulation. Neuropharmacology 26, 1235 to 1238.

Donnerer, J., Amann, R. & Lembeck, F. (1991). Neurogenic and non-neurogenic inflammation in the rat paw following chemical sympathectomy. Neuroscience 45(3), 761 to 765.

Enwemeka, C.S. & Spielholz, N.I. (1992). Modulation of tendon growth and regeneration by electrical fields and currents. In : Currier, D.P.& Nelson, R.M. (Eds.) (1992). Dynamics of Human Biologic Tissues (ch10). Philadelphia : F.A. Davis Company.

Ferrell, W.R., Wood, L. & Baxendale, R.H. (1988). The effect on acute joint inflammation on flexion reflex excitability in the decerebrate, low-spinal cat. Quarterly Journal Of Experimental Physiology 73, 95 to 102.

Galea, M.P. & Darien-Smith, I. (1995). Voluntary movement and pain : Focussing on action rather than perception. Moving in on Pain. Adelaide.

Gallin, J.I., Goldstein, I.M. & Snyderman, R. (Eds.) (1992). Inflammation : Basic Principles and Clinical Correlates (2nd ed.). New York : Raven Press.

Gogas, K.R., Presley, R.W., Levine, J.D. & Basbaum, A.,I., (1991). The antinociceptive action of supraspinal opioids results from an increase in descending inhibitory control : Correlation of nociceptive behaviour and C-fos expression. Neuroscience 42(3), 617 to 628.

Gracely, R.H., Lynch, S.L. & Bennett, G.,J. (1992). Painful neuropathy : Altered central processing, maintained dynamically by peripheral input. Pain 51, 175 to 194.

Greenbag, P.E., Brown, M.D., Pallares, V.S., Tompkins, J.S. & Mann, N.,H., (1988). Epidural anesthesia for lumbar spine surgery. Journal of Spinal Disorders 1, 139 to 143.

Gonzales, R., Goldyne, M.E., Taiwo, Y.O. & Levine, J.D. (1989). Production of hyperalgesic prostaglandins by sympathetic postganglionic neurons. Journal of Neurochemistry 53, 1595 to 1598.

Gonzales, R., Sherbourne, C.D., Goldyne, M.E. & Levine, J.D., (1991). Noradrenaline-induced prostaglandin production by sympathetic postganglionic neurons is mediated by alpha-2-adrenergic receptors. Journal of Neurochemistry 57, 1145 to 1150.

Green, P.G., Basbaum, A.I., Helms, C. & Levine, J.D. (1991). Purinergic regulation of bradykinin-induced plasma extravasation and adjuvant-induced arthritis in the rat. Proceedings of the National Academy of Science, U.S.A. 88, 4162 to 4165.

Green, P.G., Luo, J., Heller, P.H. & Levine, J.D. (1992). Modulation of bradykinin-induced plasma extravasation in the rat knee joint by sympathetic co-transmitters. Neuroscience 52, 451 to 458.

Groen, G.J., Balget, B. & Drukker, J. (1988). The innervation of the spinal dura mater: anatomy and clinical considerations. Acta Neurochirurgica 92, 39 to 46.

Groenblad, M., Weinstein, J.N. & Santavirta, S. (1991). Immunohistochemical observation on spinal tissue innervation. Acta Orthopaedic Scandinavia 62(6), 614 to 622.

Groenblad, M., Virri, J., Tolonen, J., Seitsalo, S., Kaeaepae, E., Kankare, J., Myllynen, P. & Karaharju, E. (1994). A controlled immunohistochemical study of inflammatory cells in disc herniation tissue. Spine 19(24), 2744 to 2751.

Handwerker, H.O., Forster, C. & Kirchhoff, C., (1991). Discharge patterns of human C-fibres induced by itching and burning stimuli. Journal of Neurophysiology 66, 307 to 317.

Harvey, G.K., Toyka, K.V. & Hartung, H.-P. (1994). Effects of mast cell degranulation on blood-nerve barrier permeability and nerve conduction in vivo. Journal of the Neurological Sciences 125, 102 to 109.

Heller, P.H., Green, P.G., Tanner, K.D., Miao, F.J.-P. & Levine, J.D. (1994). Peripheral neural contributions to inflammation. Progress in Pain Management (1st ed.)(pp31 to 42). Seattle : IASP Press.

Hodges, P., Richardson, C., (1996). Inefficient muscular stabilisation of the lumbar spine associated with low back pain : A motor control evaluation of transverse abdominis. Spine, 21, 2640 to 2650.

Hodges, P., Richardson, C., Jull, G., (1996). Evaluation of the relationship between laboratory and clinical tests of transverse abdominis function. Physiotherapy Research International, 1, 30 to 40.

Hu, S. & Zhu, J. (1989). Sympathetic facilitation of sustained discharges of polymodal nociceptors. Pain 38, 85 to 90.

Hsieh, J-C., Stahle-Backdahl, M., Hagermark, O., Stone-Elander, S., Rosenquist, G., Ingvar, M., (1995). Traumatic nociceptive pain activates the hypothalamus and the periaqueductal gray: a positron emission tomography study. Pain, 64, 303 to 314.

Issekutz, T.B. (1992). Inhibition of lymphocyte endothelial adhesion and in vivo lymphocyte migration to cutaneous inflammation by TA-3, a new monoclonal antibody to rat LFA-1. Journal of Immunology 149, 3392 to 3402.

Jaenig, W. (1985). Organization of the lumbar sympathetic outflow to skeletal muscle and skin of the cat hindlimb and tail. Review of Physiology, Biochemistry, Pharmacology 102, 119 to 213.

Jaenig, W. & Koltzenberg, M. (1991). Receptive properties of pial afferents. Pain 45, 77 to 85.

Jones, M., (1995). Clinical Reasoning and Pain. Manual Therapy, 1, 17 to 24.

Jull, G., Zito, G., Trott, P., Potter, H., Shirley, D., Richardson, C., (1997). Inter-examiner reliability to detect painful upper cervical joint dysfunction. Australian Journal of Physiotherapy, 43, 2, 125 to 129.

Kalso, E.A., Sullivan, A.F., McQuay, H.J., Dickenson, A.H., Roques, B.P., (1993). Cross-tolerance between Mu Opioid and alpha-2 Adrenergic receptors, but not between Mu and Delta receptors in the spinal cord of the rat. The Journal of Pharmacology and Experimental Therapeutics, 265 (2), 551 to 558.

Kambin, P., Abda, S. & Kurpici, F. (1980). Intradiskal pressure and volume recording : Evaluation of normal and abnormal intervertebral disks. Clinical Orthopedics 146, 140.

Kawakami, M., Weinstein, J.N., Chatani, K.-I., Spratt, K.F., Meller, S.T. & Gebhart, G.F. (1994a). Experimental lumbar radiculopathy : Behavioural and histologic changes in a model of radicular pain after spinal nerve root irritation with chromic gut ligatures in the rat. Spine 19(16), 1795 to 1802.

Kawakami, M., Weinstein, J.N., Spratt, K.F., Chatani, K-I., Traub, R.J., Meller, S.T. & Gebhart, G.F. (1994b). Experimental lumbar radiculopathy : Immunohistochemical and quantitative demonstrations of pain induced by lumbar nerve root irritation of the rat. Spine 19(16), 1780-1794.

Kobayashi, S., Yoshizawa, H., Hachiya, Y., Ukai, T. & Morita, T. (1993). Vasogenic edema induced by compression injury to the spinal nerve root: Distribution of intravenously injected protein tracers and Gadolinium-Enhanced Magnetic Resonance Imaging. Spine 18(11), 1410 to 1424.

Koltzenburg, M., Kees, S., Budweiser, S., Ochs, G. & Toyka, K.V. (1994). The properties of unmyelinated nociceptive afferents change in a painful chronic constriction neuropathy. In : Gebhart, G.F., Hammond, D.L. & Jensen, T. S. (Eds.) (1994). Proceedings of the 7th World Congress on Pain : Progress in Pain and Management (2nd ed.) (Ch.35). Seattle : IASP Press.

Korkala, O., Gronblad, M., Liesi, P. & Karaharju, E. (1985). Immunohistochemical demonstration of nociceptors in the ligamentous structures of the lumbar spine. Spine 10, 156 to 157.

Kuslich, S.D., Ulstrom, C.L. & Michael, C.J. (1991). The tissue origin of low back pain and sciatica: A report of pain response to tissue stimulation during operation on the lumbar spine using local anaesthesia. Orthopedic Clinics North America 22, 181 to 187.

Laird, J.M.A. & Bennett, G.J. (1993). An electrophysiological study of dorsal horn neurons in the spinal cord of rats with an experimental peripheral neuropathy. Journal of Neurophysiology 69, 2072 to 2085.

Laird, J.M.A. & Cervero, F. (1990). Tonic descending infuences on receptive-field properties of nociceptive dorsal horn neurons in sacral spinal cord of rat. Journal of Neurophysiology 63(5), 1022 to 1032.

LaMotte, R.H., Shane, C.N., Simone, D.A. & Tsai, E.F.P. (1991). Neurogenic hyperalgesia : Psychophysical studies of underlying mechanisms. Journal of Neurophysiology, 66, 190 to 211.

Levine, J.D., Dardick, S.J., Roizen, M.F., Helms, C. & Basbaum, A.I. (1986). The contribution of sensory afferents and sympathetic efferents to joint injury in experimental arthritis. Journal of Neuroscience 6, 3923 to 3929.

Levine, J.D., Goldstine, J., Mayes, M., Moskowitz, M.A. & Basbaum, A.I. (1986). The neurotoxic effect of gold sodium thiomalate on the peripheral nerves of the rat. Arthritis and Rheumatism 29, 897 to 901.

Levine, J.D., Taiwo, Y.O., Collins, S.D. & Tam, J.K. (1986a). Noradrenaline hyperalgesia is mediated through interaction with sympathetic postganglionic neurone terminals rather than activation of primary afferent nociceptors. Nature 323, 158 to 160.

Lotz, M., Vaughn, J.H. & Carson, D. (1988). Effect of neuropeptides on production of inflammatory cytokines by human monocytes. Science 241, 1218 to 1221.

Lovick, T.A., (1991). Interactions between descending pathways from the dorsal and ventrolateral periaquaductal gray matter in the rat. In ; Depaulis, A., Bandler, R.,(eds). The Midbrain Periaqueductal Gray Matter. Plenium Press, New York, 101 to 120.

Lima, D., Esteves, F. & Coimbra, A., (1994). C-fos activation by noxious input of spinal neurons projecting to the nucleus of the tractus solitarius in the rat. In : Gebhart, G.F., Hammond, D.L. & Jensen, T.S. (Eds.) (1994). Proceedings of the 7th World Congress on Pain : Progress in Pain and Management (2nd ed.) (Ch.30). Seattle : IASP Press.

Liu, J., Roughley, P.J. & Mort, J.S. (1991). Identification of human intervertebral disc stromelysin and its involvement in matrix degeneration. Journal of Orthopedic Research 9, 568 to 575.

Lundborg, G., (1988). Nerve Injury and Repair. Edinburgh : Churchill Livingstone

MacMillan, J., Schaffer, J.L. & Kambin, P. (1991). Routes and incidence of communication of lumbar discs with surrounding neural structures. Spine 16, 2, 167 to 171.

Magal, E.L. (1990). Gangliosides prevent ischemia-induced down-regulation of protein kinase C in fetal rat brain. Journal of Neurochemistry 55, 2126 to 2131.

Maitland, G.D. (Ed.) (1986). Vertebral Manipulation (5th ed.). London : Butterworths.

Maitland, G.,D., (Ed) (1991). Peripheral Manipulation. London : Butterworths.

Mao, J., Price, D.D., Coghill, R.C., Mayer, D.J. & Hayes, R.L. (1992). Spatial patterns of spinal cord [14C]-2-deoxyglucose metabolic activity in a rat model of painful peripheral mononeuropathy. Pain 50, 89 to 100.

Markowitz, S., Saito, K., Buzzi, M.G. & Moskowitz, M.A. (1989). The development of neurogenic plasma extravasation in the rat dura mater does not depend upon the degranulation of mast cells. Brain Research 477, 157 to 165.

Matsui, H., Olmarker, K., Cornefjord, M., Takahashi, K. & Rydevik, B. (1992). Local electrophysiological stimulation in experimental double level cauda equina compression. Spine, 17(9), 1075 to 1078.

Maixner, W., Gracely, R.H., Zuniga, J.R., Humphrey, C.B & Bloodworth, G.R. (1990). Cardiovascular and sensory responses to forearm ischemia and dynamic hand exercise. American Journal of Physiology 259, R1156 to R1163.

McKenzie, R.C. & Sauder, D.N. (1990). The role of keratinocyte cytokines in inflammation and immunity. Journal of Investigative Dermatology 95, S105 to 107.

Morton, C.R., Siegel, J., Xiao, H.-M., Zimmermann, M., (1997). Modulation of cutaneous nociceptor activity by electrical stimulation in the brain stem does not inhibit the nociceptive excitation of dorsal horn neurons. Pain, 71, 65 to 70.

Morgan, M.M., Sohn, J.-H., Lohof, A.M. Ben-Eliyahu, S. & Liebeskind, J.C. (1989). Characterization of stimulation-produced analgesia from the nucleus tractus solitarius in the rat. Brain Research 486, 175 to 180.

Nakagawa, I., Omote, K., Kitahata, L.M., Collins, J.G. & Murata, K. (1990). Serotonergic mediation of spinal analgesia and its interaction with noradrenergic systems. Anesthesiology 73, 474 to 478.

Nishizuka, Y. (1989). The family of protein kinase C for signal transduction. JAMA 262, 1826 to 1833.

Ochoa, J.L. & Yarnitsky, D. (1993). Mechanical hyperalgesia in neuropathic pain patients : Dynamic and static subtypes. Annals of Neurology 33, 465 to 472.

Olmarker, K., Rydevik, B., Holm, S. & Bagge, U. (1989). Effects of experimental, graded compression on blood flow in spinal nerve roots. A vital microscope study on the porcine cauda equina. Journal of Orthopedic Research 7, 817 to 823.

Olmarker, K., Rydevik, B. & Nordborg, C. (1993). Autologous Nucleus Pulposus induces neurophysiological and histological changes in porcine cauda equina nerve roots. Spine 18(11), 1425 to 1432.

Petersen, N.,P., Vicenzino, B., Wright, A., (1993). The effects of a cervical mobilisation technique on sympathetic outflow to the upper limb in normal subjects. Physiotherapy Theory and Practice, 9, 149 to 156.

O'Sullivan, P., Twomey, L., Allison, G., Sinclair, J., Miller, K., Knox, J., (1997). Altered patterns of abdominal muscle activation in patients with chronic low back pain. Australian Journal of Physiotherapy, 43, 91 to 98.

Post, C., Minor, B.G., Davies, M. & Archer, T. (1986). Analgesia induced by 5-hydroxytryptamine-depletion in rats. Brain Research 363, 18 to 27.

Price, D.D., Long, S. & Huitt, C. (1992). Sensory testing of pathophysiological mechanisms of pain in patients with reflex sympathetic dystrophy. Pain 49, 163 to 173.

Price, D.D., Mao, J. & Mayer, D.J. (1994). Central neural mechanisms of normal and abnormal pain states. In Fields, H.L. & Liebeskind, J.C. (Eds.)(1994). Progress in Pain Research and Management(1st ed.)(pp61 to 84). Seattle : IASP Press.

Proudfit, H.K. (1992). The behavioural pharmacology of the noradrenergic descending system. In : Besson, J.M. & Guilbaud, G. (Eds.)(1992). Towards the use of Noradrenergic Agonists for the Treatment of Pain(1st ed.). Amsterdam : Elsevier Science Publishers B.V.

Quintner, J.L., Cohen, M.L., (1994). Referred pain of peripheral nerve origin : an alternative to the 'myofascial pain construct'. Clinical Journal of Pain, 10, 243 to 251.

Raja, S.N., Meyer, R.A. & Campbell, J.N. (1988). Peripheral mechanisms of somatic pain. Anesthesiology 68, 571 to 590.

Rees, H., Sluka, K.A., Westlund, K.N. & Willis, W.D. (1994). Do dorsal root reflexes augment peripheral inflammation ? NeuroReport 5, 821 to 824.

Ren, K., Randich, A. & Gebhart, G.F. (1990). Modulation of spinal nociceptive transmission from nuclei tractus solitarii : A relay for effects of vagal afferent stimulation. Journal of Neurophysiology 63(5), 971-986.

Roberts, W.J. & Elardo, S.M. (1985). Sympathetic activation of unmyelinated mechanoceptors in cat skin. Brain Research 339, 123 to 125.

Rothwell, N.J. & Hopkins, S.J. (1995). Cytokines and the nervous system II : actions and mechanisms of action. Trends in Neuroscience 18, 130 to 136.

Rydevik, B.L., Brown, M.D. & Lundborg, G. (1984). Pathoanatomy and pathophysiology of nerve root compression. Spine 9, 7 to 15.

Rydevik, B.L., Myers, R.R. & Powell, H.C. (1989). Pressure increase in the dorsal root ganglion following mechanical compression: Closed compartment syndrome in nerve roots. Spine 14(6), 574 to 576.

Sandkuehler, J., Eblien-Zajjur, A., Fu, Q.-G. & Forster, C. (1995). Differential effects of spinilization on discharge patterns and discharge rates of simultaneously recorded nociceptive and non-nociceptive spinal dorsal horn neurons. Pain 60, 55 to 65.

Sanjue, H. & Jun, Z. (1989). Sympathetic facilitation of sustained discharges of polymodal nociceptors. Pain 38, 85 to 90.

Schmidt, R.F. (1990). Experimental arthritis. Pain(supp) 5, S215.

Schmidt, R.F., Schaible, H.-G., Messlinger, K., Heppelmann, B., Hanesch, U. & Pawlak, M. (1994). Silent and active nociceptors : Structure, functions, and clinical implications. In : Gebhart, G.F., Hammond, D.L. & Jensen, T. S. (Eds.) (1994). Proceedings of the 7th World Congress on Pain : Progress in Pain and Management (Ch.16) (2nd ed.). Seattle : IASP Press.

Shindo, K., Tsunoda, S-T.& Shiozawa, Z. (1994). Muscle spasm induced sympathetic reflex bursts on microneurography in a case with pontine demyelination. Clinical Autonomic Research 4, 299 to 302.

Schomburg, E.,D. & Steffens, H. (1992). On the spinal motor function of nociceptive afferents and enkephalins. In : Jami, L., Pierrot-Deseilligny, E. & Zytnicki, D. (Eds.)(1992). Muscle Afferents and Spinal Control of Movement(pp.395-400)(1st ed.). Oxford : Pergamon Press.

Suval, W.D., Duran, W.N., Boric, M.P., Hobson, R.W., Berendsen, P.B. & Ritter, A.B. (1987). Microvascular transport and endothelial cell alterations preceding skeletal muscle damage in ischemia and reperfusion injury. The American Journal of Surgery 154, 211 to 218.

Taiwo, Y.O. & Levine, J.D. (1989). Prostaglandin effects after elimination of indirect hyperalgesic mechanisms in the skin of the rat. Brain Research 492, 397 to 399.

Takahashi, K., Olmarker, K., Holm, S., Porter, R.W. & Rydevik, B. (1993). Double level cauda equina compression. An experimental study with continuous monitoring of intraneural blood flow in the porcine cauda equina. Journal of Orthopedic Research 11(1), 104 to 109.

Thompson, S.W.N. & Woolf, C.J. (1991). Primary afferent-evoked prolonged potentials in the spinal cord and their central summation : Role of the NMDA receptor. In : Bond, M.R., Charlton, J.E. & Woolf, C.J. (Eds). Proceedings of the VIth World Congress on Pain(pp291-298). Amsterdam : Elsevier

Tillman, L.J. & Cummings, G.S. (1992). Biologic mechanisms of connective tissue mutability. In : Currier, D.P. & Nelson, R.M. (Eds.) (1992). Dynamics of Human Biologic Tissues (pp1-44). Philadelphia : F.A. Davis Company.

Torebjoerk, E. (1994). Nociceptor dynamics in humans. In : Gebhart, G.F., Hammond, D.L. & Jensen, T. S. (Eds.) (1994). Proceedings of the 7th World Congress on Pain : Progress in Pain and Management (Ch.19) (2nd ed.). Seattle : IASP Press.

Troisier, O. & Cypel, D. (1986). Discography: An element of decision. Clinical Orthopedics 206, 70.

Urban, L. & Randic, M. (1984). Slow excitatory transmission in rat dorsal horn : Possible mediation by peptides. Brain Research 290, 336 to 341.

Vaccarino, F., Guidotti, A. & Costa, E. (1987). Ganglioside inhibition of glutamate-mediated protein kinase C translocation in primary cultures of cerebellar neurons. Proceedings of the National Academy of Science, U.S.A. 34, 8707.

Wall, P.D. (1995). Treatment of pain. Moving in on Pain. Adelaide.

Wall, P.D. & Devor, M. (1983). Sensory afferent impulse originate from dorsal root ganglia as well as from the periphery in normal and nerve injured rats. Pain 17, 321-339.

Wall, P.D. & Melzak, R. (1989) (Eds.). Textbook of Pain, (2nd. ed.). Edinburgh : Churchill Livingstone.

Weinstein, J.N., Claverie, W. & Gibson, S. (1988). The pain of discography. Spine 13(12), 1344 to 1348.

Williams, T.J. & Hellewell, P.G. (1992). Endothelial cell biology. Adhesions molecules involved in the microvascular inflammatory response. American Review of Respiratory Disease 146, S45 to 50.

Wiltse, L.L., Fonseca, A.S., Amster, J., Dimartino, P. & Ravessoud, F.A. (1993). Relationship of the dura, Hofmann's ligaments, Batson's plexus, and a fibrovascular membrane lying on the posterior surface of the vertebral bodies and attaching to the deep layer of the posterior longitudinal ligament: An anatomical, radiological, and clinical study. Spine 18(8), 1030 to 1043.

Woolf, C.J. (1983). Evidence for a central component of post-injury pain hypersensitivity. Nature 306, 686 to 688.

Woolf, C.J. (1984). Long-term alterations in the excitability of the flexion reflex produced by peripheral tissue injury in the chronic decerebrate rat. Pain 18, 325 to 343.

Woolf, C.J. & McMahon, S.B. (1985). Injury-induced plasticity of the fexor reflex in chronic decerebrate rats. Neuroscience 16, 395-404.

Woolf, C.J., Shortland, P. & Sivilotti, L.G. (1994). Sensitization of high mechanothreshold superficial dorsal horn and flexor motor neurones following chemosensitive primary afferent activation. Pain 58, 141 to 155.

Woolf, C.J. & Swett, J.E. (1984). The cutaneous contribution to the hamstring flexor reflex in the rat : an electrophysiological and anatomical study. Brain Research 303, 299 to 312.

Woolf, C.J. & Wall, P.D. (1986). Relative effectivenss of C primary afferent fibres in evoking a prolonged facilitation of the flexor reflex in the rat. The Journal of Neuroscience 6, 1433 to 1442.

Wright, A., Vicenzino, B., (1995). Cervical mobilisation techniques, sympathetic nervous system effects and their relationship to analgesia. In : Schacklock, M.,O., (ed.). (1995). Moving in on Pain, Butterworth-Heineman, 164 to 173.

Xavier, A.V., Farrell, C.E., McDanal, J. & Kissin, I. (1990). Does antidromic activation of nociceptors play a role in sciatic radicular pain? Pain 40, 77 to 79.

Zochodne, D.W. (1993). Epineural peptides : A role in neuropathic pain? Canadian Journal of Neurological Sciences 20(1), 69 to 72.

Last update : 2 August 2010


 

Trending @ Back in B Physio

  • Sat 18 Nov 2017

    Beetroot Juice Increases Human Muscle Force

    Beetroot juice increases human muscle force Beetroot juice has been shown to improve low frequency muscle force independent of Calcium-handling-proteins or REDOX reaction (Whitefield et al 2017, Med Sc Sp Ex, 49, 10, 2016-2024). Further benefits of beetroot juice are thought to include reduction of blood pressure protection from pre-mature aging aiding cancer survival lowering serveral inflammatory markers including interleukin-6, C-reactive protein and tumor necrosis factor alpha stabilising blood suger improving sexual performance anti-arthritic effects blood purification and enhanced red blood cells removing 'bad' estrogens from our blood stream Uploaded : 18 November 2017 F Read More
  • Wed 01 Nov 2017

    YouTube videos

    Take a look at our YouTube channel Read More
  • Sun 15 Oct 2017

    Neuroplasticity in Tendon Dysfunction

    Neuroplasticity in Tendinopathy by Martin Krause A multitude of contributing factors to altered motor control must be addressed when treating tendon dysfunction. What we have failed to consider in the past when dealing with chronic or recurrent tendon issues are motor control problems encompassing corticospinal control of excitation and inhibition as well as belief systems about pain and contextual factors related to imaging.  Research by Ebonie Rio et al (2015) (BJSM Sept 25, 10.1136/bjsports-2015-095215) suggest that the pain state sets up an adaptive pathway whereby the ipsilateral kinetic chain is directly inhibited by reflexogenic pathways, as well as being inhibited by contralateral hemispheric activity. Simultaneously excitation is enhanced in the opposite limb as well as in antagonists...at least in the case of enhanced excitation of the hamstrings in quadricep tendinopathy. If this is true, then so much for training the contralateral limb for 'cross training' purposes! This may also explain why a lot of people seem to have "all their injuries on the same side" (of the body). Furthermore, they recommend enhancing corticospinal drive through the use of 30-60 second isometric holds at 70-80% MVC to load the muscle whilst using isokinetics to load the tendon. Moreover, they recommend the use of a metronome at 60bpm (stages 1 and 2) with a count of 3 up, 2 down for quads, and 2 up, 3 down for calf isokinetics to optimally engage corticospinal drive through the visual and auditory stimuli (also shown by Kohei et al 2012 for motor imagery and M1 stimulation) .....read more Cortical mapping of infraspinatus muscle in chronic shoulder pain demonstrating higher motor thresholds (aMT= activation MT) and hence reduced excitability on the affected side (39 vs 35) (Ngomo et al 2015 Clinical Neurophysiol, 126, 2, 365-371) Cortical mapping of pain and fear. Lots of overlap suggesting that taking away the fear from the pain with clear clinical explanations and a focused goal directed program using specific functional outcomes is important.  Individuals with patellofemoral pain (PFP) had reduced map volumes and an anterior shift in the M1 representations, greater overlap of the M1 representation and a reduction in cortical peaks across all three quadriceps (RF, VL, VMO) muscles compared with controls.(Te et al 2017 Pain Medicine, pnx036, https://doi.org/10.1093/pm/pnx036)  Uploaded : 18 October 2017 Read More
  • Mon 09 Oct 2017

    Imaging

    Do I need a scan? "a picture tells a thousand words" - not really! by Martin Krause A scan, in it's self, will not improve anyone's condition. The purpose of a scan is to gain more information about the pathology. Sometimes this information may be irrelevant to the management of a patient's condition. For example, if you knocked your elbow on a door frame and suffered a bruise, which was already beginning to resolve, an ultrasound scan may show some minor soft tissue damage, but that was already obvious by the fact of the bruise, and the information gained from the scan has not helped nor changed the management of the bruise. Therefore, the main reason for getting a scan would be because there is concern that the presence of certain pathologies may lead to a change in the medical management. For example, sometimes a rolled ankle can be more than sprained ligaments, and may require surgey or immobilisation in a boot. If the therapists suspects this might be the case, then they will recommend or refer for a scan (probably an X-Ray) to check the integrity of the bones (especially the fibular and talar dome), because if there is no bony damage then the patient can be managed conservatively with taping, exercises, ultrasound, massage, joint mobilisations etc. However, if there is boney damage, for example, then it might be necessary for the ankle to be immobilised in a boot for three - six weeks, for example. This dramatically different medical management depends on the results of a scan, and it is therefore worth doing. However, scans have no predictive value to the presence or severity of pain. Thirty-three articles reporting imaging findings, in the low back, for 3110 asymptomatic individuals were investigated for pathology. The prevalence of disk degeneration in asymptomatic individuals increased from 37% of 20-year-old individuals to 96% of 80-year-old individuals. Disk bulge prevalence increased from 30% of those 20 years of age to 84% of those 80 years of age. Disk protrusion prevalence increased from 29% of those 20 years of age to 43% of those 80 years of age. The prevalence of annular fissure increased from 19% of those 20 years of age to 29% of those 80 years of age. (Brinjikji, W et al Spine Published November 27, 2014 as 10.3174/ajnr.A4173). Hence, the results of imaging need to be assessed within the context of the entire clinical picture. Frequently too much emphasis is placed on the imaging not only by the clinician but also by the patient. Some people react to pathology seen on scanning as an affirmation of their problem and can either use it to gain clarity and become better or conversely become worse. Moreover, some people find imaging with inconclusive results as a 'panic moment' - "no one knows what is wrong". Similarly, ultrasound imaging of the tendond has good predictive diagnostic and aids in clinical reasoning when it comes to full tears. However, with partial tears it is a totally different 'ball game'. Ultrasound is highly user dependent, with specifically trained musculoskeletal radiologists able to produce high-quality images that may provide more clinically relevant information than those produced by clinicians with less experience in imaging. Sean Docking, a leading tendon researcher at Monash University, cited 7 authors who found pathological tendon chnages in 59% of asymptomatic individuals, whereas he found that 52% of asymptomatic elite AFL sportsmen had tendon pathology on imaging! Furthermore, symptomatic individuals who improved clinically to the point of resuming play, weren't shown to have improvements on imaging. Again, the clinical context and the clinical reasoning can in many instances prove to be the 'gold standard' not the imaging itself, when considering management options. Shoulder supraspintatus tendon pathology, in the abscence of trauma, is known, in many instances, to be a disorder of immune-metabolic compromise of the tendon and bursa. Imaging may show some changes in signal intensity but, unless it's a complete tear, it can reveal neither the intensity nor the severity of pain when taken outside of the clinical context. A thorough physical and subjective examination integrating all the clinical dimensions of the problem will have far greater value than any one single imaging modality. Yet, imaging still should be used in instances of progressive rapid deterioration and suspected serious pathology which may require surgery and/or immediate medical intervention. In summary, sometimes it is worthwhile getting a scan, because the information gained from that scan will determined the type of medical management that is employed. However, at other times, the scan may be unneccessary, because the information may be irrelevant or lead to an incorrect change in medical management, due to over-reporting of 'false positives'. You will be able to make this decision on the advice of your health care professional. On occasions it can actually be detrimental to have a scan, because some patients can become overly obsessed with the medical terms used to describe their scan results, which then can become the major focus for the clinician and the patient, rather than the more prefereable focus on their symptoms and functional abilities. For example, many people have lumbar buldging discs yet have no symptoms, yet sometimes when these patients have an MRI or CT scan, they can develop symptoms because they think they should have pain if the scan says so! Conversely, for some people the results of imaging can have a positive and reassuring affect. Therefore, it is very important to assess a clients attitude to scans before prescibing them so that the patient's expectations are managed appropriately, and not burdened by the additional, sometimes confusing, information supplied by a scan. Uploaded : 10 October 2017 Read More
  • Thu 14 Sep 2017

    Cervical Spine implications in concussion

    Neck aetiology, autonomic and immune implications, exercise and diet in the musculoskeletal physiotherapy management of Post Concussion Syndrome (PCS) by Martin Krause, MAPA, Titled member Musculoskeletal Physiotherapy Association of Australia  A 14 year old boy presented to A&E, in August 2016, after receiving an impact to the head during AFL (Australian Rules Football). Although his SCAT3 scores were relatively mild, he went on to suffer severe lethergy, resulting in a lengthy abscence from school, culminating in a return to school for exams in the first week of December 2016. Even by December, even a 30 minute walk was extremely fatiguing. To place this into perspective, he had been playing elite academy grade AFL for several seasons and was an extremely fit outdoor adventurer. Confounding Variables : end of season injury and hence no follow up from the academy suffers from Hypermobile Joint Syndrome (HJS) and possibly Ehlers Danlos Syndrome (EDS), however Beighton score 4/9. suffers from food intolerances, particularly to Glutin and diary, but also some other foods. Potential IBS and autoimmune issues. had just gone through a growth spurt (190cm) Imaging : Brain MRI normal Medical Examination : Balance remained impaired to tandem walking and single leg stance. The vestibular occular motor scale showed significant accomodation deficit of 15cm and there was a mild exacerbation of symptoms. ImPACT testing revealed adequate scores and reaction time of 0.65 which is within acceptable range. History : School holidays December - January. Return to school and was placed in the lower classes. Prior to his concussion he was a top 10 student at an academically selective high school. Took up basketball and rowing as summer sports. Academic results tanked. Several Basketball injuries (Feb - April 17') as a result of what apppeared to be muscular imbalances from the relatively recent growth spurt, as well as taking on a new sport. Showed little interest in returning to AFL as no-one had followed him up during the previous year.  Current History : September 2017 showed a continued decline in academic levels. School teachers noted an inability to concentrate. Academic results still well below pre-concussion levels. Fatigue continuing to be problematic.  Literature Review : Post Concussion Syndrom (PCS) is defined as "cognitive deficits in attention or memory and at least three or more of the following symptoms: fatigue, sleep disturbances, headache, dizziness, irritability, affective disturbance, apathy, or personality change"  Further complications of PCS also appear to be an increased risk of musculoskeletal injury Nordstrom et al (2014, BMJ Sports Med, 48, 19, http://bjsm.bmj.com/content/48/19/1447) Predictors of PCS are uncertain. However, the following clinical variables are considered factors at increasing risk. These include prior history of concussion, sex (females more prominant), younger age, history of cognitive dysfunction, and affective disorders such as anxiety and depression (Leddy et al 2012, Sports Health, 4, 2, 147-154). Unlike the 'good old days' which recommended a dark room and rest for several weeks post concussion, the consensus appears to be a graded return to exercise in order to restore metabolic homeostasis. Incredibly, highly trained young individuals can find even exercises in bed extremely demanding. Kozlowski et al (2013, J Ath Train, 48, 5, 627-635) used 34 people 226 days post injury to conclude significant physiological annomalies in response to exercise which may be the result of 'diffuse cerebral swelling'. Researchers have noted lower systolic and higher diastolic blood pressure in PCS (Leddy et al 2010, Clin J Sports Med, 20, 1, 21-27). Due to autonomic dysfunction manifested in altered cardiovascular and pulmonary responses (Mossberg et 2007, Arch Phys Med Rehab, 88, 3, 15-320) some clinicians have recommended the use of the exercise program for POTS (Postural Orthostatic Tachycardia Syndrome). This is a 5 month program which recommends mainly exercise in the horizontal and sitting positions for 1-4 months, including recumbent bike, rowing ergometer and swimming laps or kicking laps with a kick board. Month 4 upright bike and Month 5 upright training such as a elliptical trainer or treadmill.  http://www.dysautonomiainternational.org/pdf/CHOP_Modified_Dallas_POTS_Exercise_Program.pdf Other progressive exercise therapies have also included 20 minutes per day, 6 days per week, for 12 weeks of either treadmill or home gym exercises at 80% of the heart rate at which their concussion symtoms are exacerbated. Their programs were individually modified as the heart rate provoking symptoms increased. When compared to the 'control group', this intervention was shown to improve cerebral perfusion on fMRI, increase exercise tolerance at a higher heart rate, less fatigue and were showing activation patterns in areas of the brain on performing math processing test which were now normalised (Leddy et al 2010, Clin J Sports Med, 20, 1, 21-27). Graded exercises could also have included 'motor imagery' as espouse by the NOI group and the work of Lorrimer Moseley (University South Australia) when dealing with chronic pain. Ongoing Symptoms : The literature review by Leddy et al (2012) found that ongoing symptoms are either a prolonged version of concussion pathophysiology or a manifestation of other processes, such as cervical injury, migraine headaches, depression, chronic pain, vestibular dysfunction, visual disturbance, or some combination of conditions. Physiotherapy Assessment : One year PCS, fatigue continued to persist. Cognitive deficits with school work were reported to becoming more apparent. Assessment using various one leg standing tests employing oscillatory movement aroud the hips and knees for kinetic limb stability and lumbopelvic stability, which had been employed 6 months previously for his Basketball injuries were exhibiting deficits, despite these being 'somewhat good' previously. Physical Examination : cervical and thoracic spine Due to the Joint Hypermobility Syndrome (JHS) it was difficult to ascertain neck dysfunction based on range of movement testing. ROM were unremarkable except for lateral flexion which demonstrated altered intervertebral motion in both directions. Palpation using Australian and New Zealand manual therapy techniques such as passive accessory glides (upslopes and downslopes and traction) exhibited muscles spasms in the upper right cervical spine. In particular, the right C1/2 regions demonstrated most marked restrictions in movement. Eye - Neck proprioceptive assessment using blind folds and laser pointer also  revealed marked variance from the normal. Repositioning error using the laser pointer with rotation demonstrated marked inability to reposition accurately from the left, tending to be short and at times completely missing the bullseye. Gaze stability with body rotation was NAD. Gaze stability whilst walking displayed some difficulty. Laser pointer tracing of the alphabet was wildly inaccurate. Thoracic ring relocation testing also revealed several annomalies, which may have also accounted for some autonomic dysfunction.  Occulomotor assessment and training Upper Cervical Spine : The upper cervical spine (atlas and axis) represents approximately 50% of the available rotation. An investigation into the environmental and physiological factors affecting football head impct biomechanics found that rotational acceleration was one of the few factors approaching significance and concluded that more research should be undertaken to evaluate this (Mihalik et al 2017 Med Sc Sp Ex, 49, 10, 2093-2101). Headache : Commonly referred to as cervicogenic headaches, one in five headaches in the general population are thought to be due to the cervical spine. The Upper Cervical Spine is particularly vulnerable to trauma because it is the most mobile part of the vertebral column, with a complex proprioceptive system connecting the vestibular apparatus and visual systems. It also coincides with the lower region of the brainstem and fourth ventricle. The brainstem houses many neurones associated with autonomic responses to pain and balance. Imaging of the fourth ventricle for swelling of the 'tonsils' and Arnold Chiari malformations are recommended when symptoms persist. In particular, children and adolescents are more vulnerable to neck contusions due to the proportionately larger head and less developed musculature. Cervical vertigo and dizziness after whiplash can mimic symptoms of PCS.. Mechanoreceptor dysfunction and vertebrobasilar artery insufficiency should be part of the differential diagnosis. Mechanical instability of the Upper Cervical Spine should also not be missed. Cervicogenic Headaches Further Interventions : Neurocognitive rehabilitation of attention processes. Psychological intervention using cognitive behavioural therapy (CBT). Neuro-opthalmologist to assess and treat smooth pursuit eye tracking. Naturopath for food intolerances and dietician for the optimisation of diet. Diet :  In cases with chronic fatiguing factors, nutrition can be become a vital aspect into the reparative process. This may include energy and mineral rich foods such as bananas, green leafy vegetables for iron and magnesium (200-300mg), oranges for vitamin C (anit-oxidant and helps with the absorption of iron), anti-oxidant rich foods such as EPA/DHA (1000mg) fish oil, curcumin (tumeric), Cats Claw, Devils Claw, Chia seeds, fruits of the forest (berries), and CoQ10 with Vitamin B. Folate and Ferritin levels should also be checked. Calorific energy intake should balance with energy exependiture. However, as we are often dealing with young individuals, as in this case, some form of comfort food may be appropriate such as, nuts, legumes, homus and sushi. Protein intake prior to carbohydrate intake may help ameliorate any blood suger fluctuations due to Glycemic Index factors, however simple carbohydrates (high GI) should be avoided wherever practical. Even oats need to be soaked overnight and cooked briefly, otherwise they become a high GI food and may even affect the absorption of iron. The type of rice used can also influence GI, hence the addition of protein such as fish. Protein supplementations are generally over-used. Daily protein intake should not exceed 1.2g per kg of body weight per day. Dosage for children is less than that for adults. See Nutritional Section of this Site Conclusion  Investigations, into people with persisting PCS, demonstrated that they applied more force over time to control balance. Helmich et al (2016, Med Sc Ex Sp, 48,  12, 2362-2368) proposed that in regard to cognitive processes, the increase of cerebral activation indicates an increase of attention demanding processes during postural control in altered environments. This is relevant in so far as individuals with post concussive symptomatology have a variety of symptoms including headache, dizziness, and cognitive difficulties that usually resolve over a few days to weeks. However, a subgroup of patients can have persistent symptoms which last months and even years. Complications in differential diagnosis, can arise clinically, when neck dysfunction and altered motor control occur concurrently due to both neck and cerebral pathology. For example, Whiplash and other traumatic head and neck injuries can result in pathology to both regions, whereas, more discreet altered cognitive processing from concussion can result in altered neck motor control. Musculoskelatal Physiotherapy can play a vital part in the treatment of neck dysfunction including the re-establishment of occulomotor proprioception and managing localized strength and cardiovascular exercise regimes. A total body, multi-disciplinary approach which is well co-ordinated amongst practitioners is vital to an optimal outcome.    Uploaded : 17 November 2017 Read More
  • Thu 24 Aug 2017

    Pain in the Brain - neural plasticity

    Pain in the Brain and Neural Plasticity by Martin Krause There are several mechanisms that can create a sensation of pain, which has been described as 'an unpleasent sensory and emotional experience in response to perceived or potential tissue damage'. Pain can be the result of peripheral sensitisation from peripheral inflammation, vascular compromise, necrosis, swelling, etc. Importantly, higher centres of the central nervous system not only perceive such sensitization of the peripheral nerve receptors, they can also modulate and control the intensity and tolerability of the perceived sensation through descending modulation at the peripheral receptor and in the spinal cord and through transcortical mechanisms depending on the 'meaning' and 'context given to the pain. Moreoever, the higher centres can create a 'state' of perceived 'threat' to the body through emotions such as fear and anxiety. Rather than the brain acting as a filter of unwanted sensation, in the higher centre induced pain state, rumination and magnification of sensations occur to create a pathological state.  Paradoxically, representation of body parts such as limbs and individual muscles can reduce in perceived size. In such instances the pain doesn't represent the sensation of pathology but rather pain has become the pathology. Hence, the brain generates pain in the brain, where the pain is perceived to be some sort of non-existant inflammatory or pathological sensation in the periphery. Evidence for this neural plasticity comes from imaging studies, where brain white matter structural properties have been shown to predict transition to chronic pain (Mansour et al 2013, Pain, 154, 10, 2160-2168). Specifically, differential structural connectivity to medial vs lateral prefrontal cortex and connectivity between medial prefrontal cortex and nucleus accumbens has been shown in people with persistent low back pain. In this case the back pain becomes the inciting event and given the persons' structural propensity, establishes specific functional coonectivity strength.  further reading Peripheral input is a powerful driver to neuroplasticity. Information gathered by touch, movement and vision, in the context of pain can lead to mal-adaptive plasticity, including the reorganisation of the somatosensory, and motor cortices, altered cortical excitability and central sensitisation. Examples of somatosensory reorganisation come from the work of Abrahao Baptista when investigating chronic anterior knee pain, who not only demonstrated reduced volume of Vastus Medialis but also is cortical translocation to another part of the cortex. ndividuals with patellofemoral pain (PFP) had reduced map volumes and an anterior shift in the M1 representations, greater overlap of the M1 representation and a reduction in cortical peaks across all three quadriceps (RF, VL, VMO) muscles compared with controls.(Te et al 2017 Pain Medicine, pnx036, https://doi.org/10.1093/pm/pnx036)   AKP = anterior knee pain The same researcher (Abrahao Baptista) has shown that maximal tolerable electrical stimulation (eg TENS) of muscles can induce normalisation of the cortical changes through a process called 'smudging'. Transcortical stumilation has also been applied as a cortical 'primer' prior to the application of more traditional therapy such as motor re-training, exercise, and manipulation. Body illusions are another novel way to promote the normalisation of cortical function through adaptive neuroplasticity. Examples come from people with hand athritis, whose perception of their hand size is underestimated (Gilpin et al 2015 Rheumatology, 54, 4, 678-682). Using a curved mirror, similar to that in theme parks, the visual input can be increased to perceive the body part as larger (Preston et al 2011 DOI: 10.1093/rheumatology/ker104 · Source:PubMed ) . Irrespective of size, watching a reflection of the hand while performing synchronised movements enhances the embodiment of the reflection of the hand (Whitkopf et al 2017, Exp Brain res, 23, 5, 1933-1944). These visual inputs are thought to affect the altered functional connectivity between areas of the brain thereby affecting the 'pain matrix'. Another, novel way of looking at movement and pain perception is the concept of the motor engram. This has been defined as motor skill acquisition through the modification and organisation of muscle synergies into effective movement sequences. The learning process is thought to be acquired as a child through experientially based play activity. The specific neural mechanisms involved are unknown, however they are thought to include motor map topography reflecting the capacity for skilled movement reorganisation of motor maps in a manner that reflects the kinematics of aquired skilled movement map plasticity is supported by a reorganisation of cortical microcircuitry involving changes in synaptic efficacy motor map integrity and topography are influenced by various neurochemical signals that coordinate changes in cortical circuitry to encode motor experience (Monfils 2005 Neuroscientist, 11, 5, 471-483). Interestingly, it is an intriguing notion that accessing motor engrams from patterns aquired prior to the pain experience might lead a normalisation of brain activity. My personal experience of severe sciatica with leg pain, sleepness nights and a SLR of less than 30 degrees, happened to coincide with training my 9 year old sons soccer training. I was noticing that the nights after i trained the children, I slept much better and my range of movement improved. I commenced a daily program of soccer ball tricks which i had been showing the kids, including 'juggling', 'rainbows' and 'around the worlds'. Eventually, I even took up playing soccer again after a 30 year abscence from the sport. Other than new activity related pain issues (DOMS), four years on, the sciatica hasn't returned. I can only conclude that this activity activated dormant childhood motor engram, worked on global balance, mobilised my nerve, encouraged cross cortical activity and turned my focus into finctional improvement. Further explainations for my expereience comes from evidence suggesting that a peripheral adaptive pain state is initiated, whereby transcortical inhibiton occurs by the contralaleral hemisphere to the one which controls the affected limb. Additionally, excitation cortical (M1) drive of the muscles of the contralateral limb to the one which is in pain also occurs. In such cases re-establishement of motor drive to the affected side is important. In terms of tendon rehabilitation, external audtory and visual cues using a metronome have been employed and are showing promising results (Ebonie Rio et al 2017 Personal communication). In terms of my experience with the soccer ball tricks, the external visual cues and the cross talk from using left and right feet, head, shoulders, and chest during ball juggling manouvers, whilst calling the rhythm to the kids may have been the crucial factor to overcome the dysfunctional brain induced pain - muscle inco-ordination cycle, which I was in. Additionally, I was cycling which allowed me to focus on motor drive into the affected.limb. However, work by Lorrimer Moseley on CRPS has established that 'brain laterality' must be established before commencing trans-cortical rehabilitation techniques. Lorrimer's clinical interventions use 'mirror imaging' techniques which are only effective once the patient is able to discriminate the left and right sides of the affected body parts, presented visually, in various twists and angles.   Alternatively, the altered pain state can result in a hostage like situation, whereby the pain takes control. Similar to the 'Stockholm Syndrome' where the hostage begins to sympathise with their captors, so do some peoples brain states, where it begin to sympathise with the pain, creating an intractable bondage and dysfunctional state. One screening question which may reflect commitment to the process of rehabilitatation is to question whether they were able to resist the cookie jar when they were a child? Or were they committed to any sporting endeavours as a child? This may give some indication for the presence of motor engrams which can be used to overcome dysfunctional pain induced muscle synergies (neurotags), but also indicate an ability to be self disciplined, as well as being able to reconcile and identify goal oriented objectives, in spite of the cognitive pain processes? Remember that neurons that fire together, wire together. Uploaded : 18 October 2017 Read More
  • Thu 03 Aug 2017

    Sickle Cell Trait and Acute Low Back Pain

    Researchers believe that lumbar paraspinal myonecrosis (LPSMN) may contribute to the uncommon paraspinal compartment syndrome and that sickle cell trait (SCT) may play a role. Sustained, intense exertion of these lumbar paraspinal muscles can acutely increase muscle size and compartment pressure and so decrease arterial perfusion pressure. This same exertion can evoke diverse metabolic forces that in concert can lead to sickling in SCT that can compromise perfusion in the microvasculature of working muscles. In this manner, they believe that SCT may represent an additional risk factor for LPSMN. Accordingly, they presented six cases of LPSMN in elite African American football players with SCT. See link below http://journals.lww.com/acsm-msse/Fulltext/2017/04000/Acute_Lumbar_Paraspinal_Myonecrosis_in_Football.1.aspx Read More
  • Thu 03 Aug 2017

    Ibuprofen, Resistance Training, Bone Density

    Taking Ibuprofen immediately after resistance training has a deleterious effect on bone mineral content at the distal radius, whereas taking Ibuprofen or undertaking resistance training individually prevented bone mineral loss. http://journals.lww.com/acsm-msse/Fulltext/2017/04000/Effects_of_Ibuprofen_and_Resistance_Training_on.2.aspx Read More
  • Tue 11 Jul 2017

    Mitochondrial Health and Sarcopenia

    The aging process (AKA 30 years of age onwards), in the presence of high ROS (reactive oxygen species) and/or damaged mitochondrial DNA, can induce widespred mitochondrial dysfunction. In the healthy cell, mitophagy results in the removal of dysfunctional mitochondria and related material. In the abscence of functional removal of unwanted mitochondrial material, a retrograde and anterograde signalling process is potentially instigated, which results in both motor neuronal and muscle fibre apoptosis (death) (Alway, Mohamed, Myers 2017, Ex Sp Sc Rev, 45, 2, 58-69). This process is irreversible. Investigations in healthy populations, have shown that regular exercise improves the ability to cope with regular oxidative stress by the buffering and 'mopping up' of ROS agents which are induced as a result of exercise. It is plausible and highly probable that regular exercise throughout life can mitigate against muscle fibre death (Sarcopenia). Importantly, this process of muscle fibre death can commence in the 4th decade of life. and be as much as 1% per year. Reduction of muscle mass can result in immune and metabolic compromise, including subclinical inflammation, type II diabetes as well as the obvious reduction in functional capacity for activities of daily living. Published 11 July 2017 Read More
  • Thu 22 Dec 2016

    Ehlers Danlos Syndrome

    Is your child suffering Ehlers Danlos Syndrome? Hypermobile joints, frequent bruising, recurrent sprains and pains? Although a difficult manifestation to treat, physiotherapy can help. Joint Hypermobility Syndrome (JHS) by Martin Krause When joint hypermobility coexists with arthralgias in >4 joints or other signs of connective tissue disorder (CTD), it is termed Joint Hypermobility Syndrome (JHS). This includes conditions such as Marfan's Syndrome and Ehlers-Danlos Syndrome and Osteogenesis imperfecta. These people are thought to have a higher proportion of type III to type I collagen, where type I collagen exhibits highly organised fibres resulting in high tensile strength, whereas type III collagen fibres are much more extensible, disorganised and occurring primarily in organs such as the gut, skin and blood vessels. The predominant presenting complaint is widespread pain lasting from a day to decades. Additional symptoms associated with joints, such as stiffness, 'feeling like a 90 year old', clicking, clunking, popping, subluxations, dislocations, instability, feeling that the joints are vulnerable, as well as symptoms affecting other tissue such as paraesthesia, tiredness, faintness, feeling unwell and suffering flu-like symptoms. Autonomic nervous system dysfunction in the form of 'dysautonomia' frequently occur. Broad paper like scars appear in the skin where wounds have healed. Other extra-articular manifestations include ocular ptosis, varicose veins, Raynauds phenomenon, neuropathies, tarsal and carpal tunnel syndrome, alterations in neuromuscular reflex action, development motor co-ordination delay (DCD), fibromyalgia, low bone density, anxiety and panic states and depression. Age, sex and gender play a role in presentaton as it appears more common in African and Asian females with a prevalence rate of between 5% and 25% . Despite this relatively high prevalence, JHS continues to be under-recognised, poorly understood and inadequately managed (Simmonds & Kerr, Manual Therapy, 2007, 12, 298-309). In my clinical experience, these people tend to move fast, rely on inertia for stability, have long muscles creating large degrees of freedom and potential kinetic energy, resembling ballistic 'floppies', and are either highly co-ordinated or clumsy. Stabilisation strategies consist of fast movements using large muscle groups. They tend to activities such as swimming, yoga, gymnastics, sprinting, strikers at soccer. Treatment has consisted of soft tissue techniques similar to those used in fibromyalgia, including but not limited to, dry needling, myofascial release and trigger point massage, kinesiotape, strapping for stability in sporting endeavours, pressure garment use such as SKINS, BSc, 2XU, venous stockings. Effectiveness of massage has been shown to be usefull in people suffering from chronic fatigue syndrome (Njjs et al 2006, Man Ther, 11, 187-91), a condition displaying several clinical similarities to people suffering from EDS-HT. Specific exercise regimes more attuned to co-ordination and stability (proprioception) than to excessive non-stabilising stretching. A multi-modal approach including muscle energy techniques, dry needling, mobilisations with movement (Mulligans), thoracic ring relocations (especially good with autonomic symptoms), hydrotherapy, herbal supplementaion such as Devils Claw, Cats Claw, Curcumin and Green Tee can all be useful in the management of this condition. Additionally, Arnica cream can also be used for bruising. Encouragment of non-weight bearing endurance activities such as swimming, and cycling to stimulate the endurance red muscle fibres over the ballistic white muscles fibres, since the latter are preferably used in this movement population. End of range movements are either avoided or done with care where stability is emphasized over mobility. People frequently complain of subluxation and dislocating knee caps and shoulders whilst undertaking a spectrum of activities from sleeping to sporting endeavours. A good friend of mine, Brazilian Physiotherapist and Researcher, Dr Abrahao Baptista, has used muscle electrical stimulation on knees and shoulders to retrain the brain to enhance muscular cortical representation which reduce the incidence of subluxations and dislocations. Abrahao wrote : "my daughter has a mild EDS III and used to dislocate her shoulder many times during sleeping.  I tried many alternatives with her, including strenghtening exercises and education to prevent bad postures before sleeping (e.g. positioning her arm over her head).  What we found to really help her was electrostimulation of the supraspinatus and posterior deltoid.  I followed the ideas of some works from Michael Ridding and others (Clinical Neurophysiology, 112, 1461-1469, 2001; Exp Brain Research, 143, 342-349 ,2002), which show that 30Hz electrostim, provoking mild muscle contractions for 45' leads to increased excitability of the muscle representation in the brain (at the primary motor cortex).  Stimulation of the supraspinatus and deltoid is an old technique to hemiplegic painful shoulder, but used with a little different parameters.  Previous studies showed that this type of stimulation increases brain excitability for 3 days, and so we used two times a week, for two weeks.  After that, her discolcations improved a lot.  It is important to note that, during stimulation, you have to clearly see the humerus head going up to the glenoid fossa" Surgery : The effect of surgical intervention has been shown to be favourable in only a limited percentage of patients (33.9% Rombaut et al 2011, Arch Phys Med Rehab, 92, 1106-1112). Three basic problems arise. First, tissues are less robust; Second, blood vessel fragility can cause technical problems in wound closure; Third, healing is often delayed and may remain incomplete.  Voluntary Posterior Shoulder Subluxation : Clinical Presentation A 27 year old male presented with a history of posterior shoulder weakness, characterised by severe fatigue and heaviness when 'working out' at the gym. His usual routine was one which involved sets of 15 repetitions, hence endurance oriented rather than power oriented. He described major problems when trying to execute bench presses and Japanese style push ups.  https://youtu.be/4rj-4TWogFU In a comprehensive review of 300 articles on shoulder instability, Heller et al. (Heller, K. D., J. Forst, R. Forst, and B. Cohen. Posterior dislocation of the shoulder: recommendations for a classification. Arch. Orthop. Trauma Surg. 113:228-231, 1994) concluded that posterior dislocation constitutes only 2.1% of all shoulder dislocations. The differential diagnosis in patients with posterior instability of the shoulder includes traumatic posterior instability, atraumatic posterior instability, voluntary posterior instability, and posterior instability associated with multidirectional instability. Laxity testing was performed with a posterior draw sign. The laxity was graded with a modified Hawkins scale : grade I, humeral head displacement that locks out beyond the glenoid rim; grade II, humeral displacement that is over the glenoid rim but is easily reducable; and grade III, humeral head displacement that locks out beyond the glenoid rim. This client had grade III laxity in both shoulders. A sulcus sign test was performed on both shoulders and graded to commonly accepted grading scales: grade I, a depression <1cm: grade 2, between 1.5 and 2cm; and grade 3, a depression > 2cm. The client had a grade 3 sulcus sign bilaterally regardless if the arm was in neutral or external rotation. The client met the criteria of Carter and Wilkinson for generalized liagmentous laxity by exhibiting hyperextension of both elbows > 10o, genu recurvatum of both knees > 19o, and the ability to touch his thumbto his forearm Headaches Jacome (1999, Cephalagia, 19, 791-796) reported that migraine headaches occured in 11/18 patients with EDS. Hakim et al (2004, Rheumatology, 43, 1194-1195) found 40% of 170 patients with EDS-HT/JHS had previously been diagnosed with migraine compared with 20% of the control population. in addition, the frequency of migraine attacks was 1.7 times increased and the headache related disability was 3.0 times greater in migraineurs with EDS-HT/JHS as compared to controls with migraine (Bendick et al 2011, Cephalgia, 31, 603-613). People suffering from soft tissue hypermobility, connective tissue disorder, Marfans Syndrome, and Ehler Danlos syndrome may be predisposed to upper cervical spine instability. Dural laxity, vascular irregularities and ligamentous laxity with or without Arnold Chiari Malformations may be accompanied by symptoms of intracranial hypotension, POTS (postural orthostatic tachycardia syndrome), dysautonomia, suboccipital "Coat Hanger" headaches (Martin & Neilson 2014 Headaches, September, 1403-1411). Scoliosis and spondylolisthesis occurs in 63% and 6-15% of patients with Marfans syndrome repsectively (Sponseller et al 1995, JBJS Am, 77, 867-876). These manifestations need to be borne in mind as not all upper cervical spine instabilities are the result of trauma. Clinically, serious neurological complications can arise in the presence of upper cervical spine instability, including a stroke or even death. Additionally, vertebral artery and even carotid artery dissections have been reported during and after chiropractic manipulation. Added caution may be needed after Whiplash type injuries. The clinician needs to be aware of this possibility in the presence of these symptoms, assess upper cervical joint hypermobility with manual therapy techniques and treat appropriately, including exercises to improve the control of musculature around the cervical and thoracic spine. Atlantoaxial instability can be diagnosed by flexion/extension X-rays or MRI's, but is best evaluated by using rotational 3D CT scanning. Surgical intervention is sometimes necessary. An interesting case of EDS and it's affect on post concussion syndrome can be read elsewhere on this site. Temperomandibular Joint (TMJ) Disorders The prevelence of TMJ disorders have been reported to be as high as 80% in people with JHD (Kavucu et al 2006, Rheum Int., 26, 257-260). Joint clicking of the TMJ was 1.7 times more likely in JHD than in controls (Hirsch et al 2008, Eur J Oral Sci, 116, 525-539). Headaches associated with TMJ disorders tend to be in the temporal/masseter (side of head) region. TMJ issues increase in prevelence in the presence of both migraine and chronic daily headache (Goncalves et al 2011, Clin J Pain, 27, 611-615). I've treated a colleague who spontaneously dislocated her jaw whilst yawning at work one morning. stressful for me and her! Generally, people with JHD have increased jaw opening (>40mm from upper to lower incisors). Updated 17 October 2017  Read More
  • Fri 09 Dec 2016

    Physiotherapy with Sharna Hinchliff

    Physiotherapy with Sharna Hinchliff    Martin is pleased to welcome the very experienced physiotherapist Sharna Hinchliff to Back in Business Physiotherapy for one on one physiotherapy sessions with clients in 2017.  Sharna is a passionate triathelete and mother and has had several years experience working locally and internationally (New York and London) in the field of physiotherapy. Originally from Western Australia, Sharna graduated from the world renowned Masters of Manipulative Physiotherapy at Curtin University. read more Read More

Funding, Advertising and Linking Policy

This site is set up as a free of charge service to the community. Back in Business Physiotherapy pays for all aspects of this website and does not endorse any paid advertising on this site. Back in Business Physiotherapy does have an affiliate program with Lunar pages who host this website. Additionally, the links to Human Kinetics and Amazon may result in Back in Business Physiotherapy receiving a small commission for precisely those books if purchased on those sites. Links to other sites are based on the relevance of that sites information to the principles of this websites desire to enhance the standards of Physiotherapy. Unless I am the author of the content of a linked site, these links are not based on reciprocal agreements. No banner adds or pop-ups should appear on your browser as a result of browsing this website. However, if you leave this website to a related one, Back in Business Physiotherapy cannot accept responsibility for neither changes in their contents nor their advertising or privacy policies.

image removed

Updated : 10 May 2014

No responsibility is assumed by Back in Business Physiotherapy for any injury and/or damage to persons or property as a matter of product liability, negligence, or from any use of any methods, products, instruction, or ideas contained in the material in this and it's related websites. Because of rapid advances in the medical sciences, the author recommends that there should be independent verification of diagnoses and exercise prescription. The information provided on Back in Business Physiotherapy is designed to support, not replace, the relationship that exists between a patient/site visitor and their treating health professional.

Copyright Martin Krause 1999 - material is presented as a free educational resource however all intellectual property rights should be acknowledged and respected