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Neurophysiology of pain and inflammation

A Neurophysiological and Clinical Reasoning Approach to the selection of Dosage in Manual Therapy

Martin Krause

Bachelor of Applied Science (Physiotherapy), University of Sydney

Masters of Manipulative Physiotherapy, University of Sydney

Graduate Certificate Health Science Education, University of Sydney

Graduate Diploma Health Science (Exercise and Sport), University of Sydney

Certificate IV Workplace Assessment and Training

Private Practitioner, North Sydney, Australia.

Table of Contents

- Introduction

- Inflammation

- Inflammation and Oedema

- Neurogenic and non-neurogenic inflammation

- Sympathetic modulation of inflammation and it's role in repair

- The consequences of reduced receptor threshold to manual therapy

- Secondary mechanical hyperalgesia due to oedema around the dorsal root ganglion

- Spinal cord expansion of sensitised receptive fields

- Manual therapy during peripheral and central expansion of the hypersensitive receptive field

- Reduced movement due to expanded hypersensitive receptive fields

- Effect of manual therapy on muscle acivity around the Intervertebral Foramen

- The importance of dose in manual therapy

- Descending inhibition in the modulation of pain

- Center surround inhibition

- Motor control in the modulation of pain

- Conclusion

- References

 

Introduction

Pain is a dynamic entity, which affects a large number of people around the world. Pain knows no cultural boundaries and people suffering from pain have been treated in various manners by various practitioners with various degrees of success for centuries. Modern medical and paramedical practice has attempted to come to terms with patient's ailments by diagnosing various pathologies with labels such as 'fibromyalgia', 'fibrocytis', 'repetitive strain injury', 'cervico-brachialgia', 'reflex sympathetic dystrophy', etc. However these labels may detract from effective clinical reasoning because

  • the diagnostic criteria become so broad that it becomes difficult to exclude people from that diagnosis (Cohen & Quintner 1993; Quintner & Cohen 1994).
  • the fundamental clinical reasoning principle for the production of symptoms is violated. i.e. a leap is made from signs and symptoms (phenomenology) to the assumption of disease (nosology) without consideration of pathophysiology (Cohen 1995).

To improve clinical reasoning skills it may be important for the clinical practitioner to understand the pathophysiology that underlies the phenomenology (Jones 1995). It is the objective of this paper to elucidate the mechanisms of pain and inflammation in a theoretical and clinical context. Improved understanding of pathology may provide the practitioner the context specific feedback to discover the most effective approach to treatment. Hence, the main argument which will be pursued here is that clinical signs and symptoms correlate with the underlying process of inflammation and repair. Thus, the dossage and type of manual therapy employed in the treatment of pain should reflect the normalisation of clinical signs and symptoms.

 

Inflammation

The reaction of living tissue to injury is called inflammation. Inflammation involves a cascade of events in cells, involving products of cells, enzymes, soluble factors, and blood vessels and their contents (Enwemeka & Spielholz 1992; Schmidt et al 1994; Tillman & Cummings 1992). Trauma to the intervertebral disc (IVD) may result in a focus of inflammation inside the disc (Weinstein et al 1988). Inflammatory substances may diffuse out of the IVD and contact the posterior longitudinal ligament, Batson's venous plexus, Hoffman ligaments and the dura mater (Adams et al 1986; Kambin et al 1980; Liu et al 1991; MacMillan et al 1991; Troisier & Cypel 1986). In contrast to the IVD, these later structures have a good blood supply and are densely innervated by sensory and sympathetic nerve fibres. Consequently, the nerve receptors and blood vessels may become inflamed directly from trauma and/or indirectly from inflammatory substances of IVD trauma (Korkula et al 1985; McLain 1993; Weinstein et al 1988; Wiltse et al 1993). Hence, inflammation and the resolution of inflammation may be synonymous with healing.

 

Inflammation and oedema

Inflammation may cause the formation of oedema and spinal pain (Barker et al 1991; Gallin et at 1992; Groenblad et al 1991;1994b; Kawakami et al 1994a; 1994b; McKenzie & Saunder 1990; Rothwell & Hopkins 1995; Rydevik et al 1989; Williams & Hellewell 1992). As oedema increases, compression of intraneural blood vessels and nerve fibres may preferentially decrease the conduction velocity of myelinated afferents and efferents, whilst probably leaving the conduction velocity along unmyelinated nerve fibres largely unaffected (Cornefjord et al 1992; Kobayashi et al 1993; Matsui et al 1992; Olmarker et al 1989; Rydevik et al 1984; Takahashi et al 1993). Decreased conduction along large diameter myelinated (type II) nerve fibres has been postulated to decrease the modulation (by wide dynamic range neurones [WDR]) of nociception in the spinal cord and thus increase pain (figure 1) (Dickenson & Sullivan 1987; Ochoa & Yarnitsky 1993; Price et al 1994).

Figure 1: Spinal cord modulation of pain. Wide dynamic range (WDR) neurone inhibition of nociceptive specific neurone (NS) in the dorsal horn of the spinal cord (adapted from Wall & Melzack 1989, pp11-13; Bogduk 1993, p59)

By implication, non-noxious mechanical stimuli from joint mobilisations may be ineffective where a decreased conduction along large diameter myelinated (type II) nerve fibres exists. Hence a more effective means of treatment may be one which normalises blood flow to neural tissue (eg. traction or a sustained rotatory technique) .

 

Neurogenic and non-neurogenic inflammation.

Inflammation involves a complex cascade of reactions at the peripheral receptor terminals. These reactions may be divided into two entities: neurogenic and non-neurogenic inflammation. Neurogenic inflammation includes the release of neuropeptides (e.g. substance P, Calcitonin Gene Related Peptide [CGRP], nordrenaline, etc) from C-fibre terminals whereas non-neurogenic inflammation involves the release of inflammatory substances (e.g. histamines, prostaglandins, cytokines, leukotrienes, bradykinin, etc) from the blood vessels and connective tissue. Both processes lead to a decrease in the activation threshold of the mechanoceptors.

Neurogenic inflammation is the process whereby neuropeptides released from C-fibres of primary afferents and sympathetic efferents cause vasculature membrane changes which results in the leakage of proteins from the vasculature into surrounding tissue (Ahmed et al 1991; Blottner & Baumgartner 1994; Donnerer et al 1991; Heller et al 1994; Kobayashi et al 1993; LaMotte et al 1991; Levine et al 1986; Markowitz et al 1989; Suval et al 1987; Zochodne 1993). In the absence of inflammation, sympathetic nerve fibre efferent terminals in experiments with rats (Hu & Zhu 1989) suppress C-fibre afferent receptor evoked discharges. However, during inflammation C-fibre receptors increase their neurogenic inflammatory response and hence increase their discharge frequency with stimulation of the sympathetic nerve terminals (Levine et al 1986). Sensitisation of peripheral nerve terminals by neurogenic and non-neurogenic inflammation may reduce mechanoceptors thresholds and contribute to pain (figure 2 and 3) (Groenblad et al 1991; Jaenig 1985; Lotz et al 1988; Handwerker et al 1991; Levine et al 1986a; Rees et al 1994; Raja et al 1988; Rothwell & Hopkins 1995; Schmidt et al 1994; Taiwo & Levine 1989).

Massive infiltration of macrophages into the dorsal root ganglion (DRG) was demonstrated in both the ipsilateral and contralateral lumbar but not thoracic DRG using the rat model of unilateral antigen-induced arthritis (AIA) in the knee (Segond von Banchet et al 2009). This activation wasn't explainable as a result of nerve cell lesion. During AIA lumbar but not thoracic DRGs exhibited bilateral de novo expression of vascular adhesion molecule (VCAM-1) which is known to be involved with macrophage infiltration. Chemical inhibtion of tumor necrosis factor alpha after induction of AIA significantly inhibited macrophage infiltration as well reduced the expression of VCAM-1. This also reduced mechanical hyperalgesia at the inflammed joint without attenuating the joint inflammation, additionally the mechanical hyperalgesia in the contralateral knee was also reduced. Thus, bilateral segment specific infiltration of macrophages into the DRGs is part of an unilateral inflammatory process in peripheral tissue and may be involved in the generation of peripheral mechanical hyperalgesia in the non-inflammed side (Segond von Banchet et al 2009).

Figure 2 : Schematic representation of the interaction between neurogenic and non-neurogenic inflammation on free nerve endings through the stimulation of mast cells. SNS = sympathetic nervous system. (adapted from Groenblad et al 1991, p617; Jaenig 1985; Lotz et al 1988; Handwerker et al 1991; Levine et al 1986a; Taiwo & Levine 1989).

Figure 3 : Percentageof mechanoceptors (group II, III, IV) responding to movement in the non-inflamed and inflamed states (Raja et al 1988; p576)

 

Sympathetic modulation of inflammation and its role in repair.

The sympathetic postganglionic nerves release inflammatory mediators that increase plasma extravasation, including prostaglandins (Coderre et al 1989; Gonzales et al 1991; Gonzales et al 1989; Green et al 1991). Additionally, under conditions of sympathetic postganglionic neuronal modulation bradykinin has been found to increase plasma extravasation (Green et al 1992). 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. Agents that enhance synovial plasma extravasation have been demonstrated to decrease tissue injury during inflammation (Coderre et al 1991). The mechanisms by which sympathetic nerve terminals decrease tissue injury are unclear. However, an increased plasma extravasation would be expected to reduce the concentration of inflammatory substances through the facilitation of lymphatic and venous drainage, thereby improving repair (figure 4)(Heller et al 1994).

Figure 4 : Sympathetic modulation of peripheral nerve activity

 

The consequences of reduced receptor threshold to manual therapy.

At this stage it would appear that there are 2 mechanisms of modulation of electrical activity in type III and IV nerve fibres. These 2 mechanisms include

  • non-noxious stimuli via the type II nerve fibres and WDR neurones and
  • the peripheral sympathetic nervous system.

Significantly, WDR neurones probably respond specifically to the wide range of frequencies of input from the variations of force, frequency, direction and velocity which gentle oscillatory mobilisation techniques present. Consequently the type and dosage of techniques used need to reflect the normalisation of signs and symptoms. Further, the SNS is likely to respond to techniques which increase blood flow and lymphatic drainage whilst simultaneously being demonstrated to be non-threatening and effective to both the patient and the therapist. Thus, after each treatment technique the 'expected' normalisation of signs and symptoms need to be demonstrated. Similar to the paradox of Schroedingers Catin quantum physics, it is not until we observean effect do we know the effect.  Yet our mere observation can affect clinical outcomes.

 

Secondary mechanical hyperalgesia due to the effect of oedema on the nerve roots/dorsal root ganglia/spinal nerve complex.

Endoneurial oedema of the dorsal root ganglia (DRG) may be the result of compression from inflammatory exudate (Chatani et al 1995). Endoneurial oedema of the DRG may generate ectopic electrical impulses (Bandalamente et al 1987). Ectopic impulses originating in the DRG are thought to propagate into the spinal cord and into peripheral receptor sites (Bandalamente et al 1987; Wall & Devor 1983). Increased neuronal firing may increase neurogenic inflammation at the receptor sites (Chatani et al 1995; Markowitz et al 1989; Xavier et al 1990). Arborization of peripheral nerve terminals may result in neurogenic inflammation in an expanded receptive field (LaMotte et al 1991). This suggests that extraneural inflammation may induce intraneural oedema that in turn may increase the intensity of extraneural neurogenic inflammation. In the case of the sinuvertebral nerve this may mean that receptors at multiple (eight) segments may become sensitised and exhibit decreased mechanical activation thresholds (Groen et al 1988; Koltzenburg et al 1994; Raja et al 1988). This area of neurogenic inflammatory expansion of the sensitised receptive field is termed secondary mechanical hyperalgesia (Raja et al 1988).

During surgery, retraction of the inflamed dura mater has been demonstrated to increase nerve impulse generation (Greenbarg et al 1988; Kuslich et al 1991). Therefore, the clinical implications of decreased activation threshold are a decreased dosage of treatment. Feedback of the effect of treatment on signs and symptoms may be a means of determining the effective dosage of treatment.

Interestingly, a projection of nerve fibres from the DRG to the pia mater of the ventral nerve root has been demonstrated in the cat (Jaenig & Koltzenburg 1991). Since electrical stimulation of the sympathetic nerve fibres has been demonstrated to sensitise mechanoceptors in rats (Barasi & Lynn 1986; Roberts & Elardo 1985; Snajue & Jun 1989), then ectopic impulse propagation due to mechanical irritation of the DRG may result in neurogenic inflammation of the ventral nerve root pia mater (Groenblad et al 1991; Harvey et al 1994; Wall & Devor 1983). However, the effect of neurogenic inflammation of the ventral nerve root on sympathetic b -fibre and a -motor fibre activity is theoretically and clinically uncertain.

 

Spinal cord expansion of sensitised receptive fields.

Spinal cord sensitisation (hypersensitivity) of adjacent wide dynamic range (WDR) and nociceptive specific (NS) neurones may occur due to the direct synaptic connections between adjacent WDR neurones and between adjacent NS neurones (figure 5)(Price et al 1994). Spinal cord expansion of the sensitised (hypersensitive) receptive field has been demonstrated and is thought to be a compensatory mechanism for the dissipation of the afferent barrage of electrical stimulation from sensitised (hypersensitive) peripheral receptors (Coghill et al 1991; LaMotte et al 1991; Magal 1990; Mao et al 1992; Price et al 1994; Torebjoerk et al 1992; Vaccarino et al 1987) and from ectopic impulse generation from the DRG (Wall & Devor 1983). Evidence for central expansion of the neuronal receptive field comes from the findings that if the nerve of the new hypersensitive receptive field of the adjacent dorsal horn neurones is ligated no expansion of the sensitivity of the peripheral receptive field occurs (Attal et al 1994). This suggests that in the presence of inflammatory exudate around the nerve root/DRG/spinal nerve complex and/or the sinuvertebral nerve then an adjacent peripheral nerve (e.g. sinuvertebral nerve, median nerve, etc,) may be recruited for the projection of neurogenic inflammation into adjacent areas of the spinal canal and/or limb.

Figure 5: Central expansion of the hypersensitive receptive field.

 

The significance of treating the pain with manual therapy during peripheral and central expansion of the hypersensitive receptive fields.

Both people in pain and therapists may have varying difficulty in localising the source of symptoms. Significant expansion of the hypersensitive receptive field may be postulated to result in increased acuity to detect the locus of dysfunction through a "3 dimensional map" of areas of normal activity and those of primary and secondary hyperalgesia. Perhaps the analgesic effect of gentle stroking around a painful area may be an example of this mechanism? Hence, in the case of referred neurogenic pain non-noxious manual therapy directed at the site of pathology may enhance the modulation of electrical activity in type III and IV fibres through mechanical input to aid in the detection of the locus of dysfunction.

Alternatively, expansion of the hypersensitive receptive field may be postulated to result in decreased ability to detect the locus of dysfunction. A clinical example of such a scenario may be when referred limb pain is more intense then the spinal pain at the site of pathology (eg spinal nerve/dorsal root ganglion/nerve root irritation). In this example it is highly probably that distal limb pain can be more severe than proximal pain due to the high density of mechanoceptors in the hands and the feet and their resultant disproportionate representation in the somatosensory cortex. (Interested readers should refer to somatosensory homunculus for further details). Therefore, in the case of projected neurogenic limb pain it may be hypothesised that unloading the site of secondary neurogenic inflammation (with for example tape) may increase the awareness of the primary site of pathology. Regardless of the effect of central expansion of the hypersensitive receptive field, it is highly likely that determination of the precise source of symptoms is necessary for effective healing to take place.

Clinically, the subjective examination includes a body chart which describes the area of pain. Hence, pain in a dermatological distribution which may be accompanied by pins & needles and numbness should result in the practitioner using a different line of clinical reasoning then that for referred somatic pain. Therefore, inductive questioning should reflect the responses from deductive questioning (figures 6 & 7).

Figure 6 : Reasoning involved differentiating Somatic from Radicular pain

 

 

Decreased movement due to the effect of expansion of spinal cord neuronal and peripheral receptor hypersensitivity associated with spinal and limb pain.

Several experiments have been designed to differentiate the contribution of peripheral receptors and spinal cord neuronal plasticity in pain production. Expansion of the hypersensitive receptive field (Price et al 1992) together with the decreased activation threshold of low and high threshold mechanoceptors (Ferrell et al 1988; Koltzenburg et al 1994; Raja et al 1988; Schmidt et al 1994) and the five-fold increase in resting discharge of an articular nerve from an inflamed joint (Schmidt 1990) would mean that spinal cord neurones receive an unusually large barrage of nociceptive inflammation from inflamed deep tissue. These are the conditions thought to be required for intracellular changes in WDR neurones that would make them hyperresponsive (Dickenson & Sullivan 1990; 1987; Thompson & Woolf 1991; Urban & Randic 1984). Investigations demonstrate that if a source of ongoing nociceptor input continuously "refreshes" the hyperexcitable state of the dorsal horn neurones (Gracely et al 1992) then this may lead to the loss of function of the auto-inhibitory inter-neurones between the WDR and NS neurones (Alkon &Rasmussen 1988; Collingride & Singer 1990; Laird & Bennett 1993; Nishizuka 1989). Clinically, hyperexcitability of WDR neurones may result in motor abnormalities such as the marked and prolonged increase in the flexion withdrawal reflex, as exhibited in rats (Ferrell et al 1988; Woolf 1983; Woolf et al 1994). The rat will try to avoid contact of the inflamed paw with the ground (Woolf 1984; Woolf & McMahon 1985; Woolf & Wall 1986). A similar situation may arise in humans whereby joint movements are prevented by increased muscle activity so as to minimise the mechanical input onto inflamed mechanoceptors. Lack of movement may be postulated to effect blood flow with a resultant exacerbation of oedema and/or ischaemia. Furthermore, lack of movement may be postulated to result in decreased non-noxious mechanical input that may be required for the modulation of electrical activity in both WDR and NS neurones. Therefore, lack of movement is likely to result in pain.

Further, more potent neurotoxic effects on autoinhibitory interneurones may occur due to ectopic input onto WDR neurones from a nerve subject to constriction (Dubner 1991; Sugimoto et al 1990). Animal models using ligatures around the sciatic nerves demonstrate large increases in spontaneous discharges in large and small diameter myelinated afferents, whilst leaving small diameter unmyelinated afferents unaffected (Bennett & Xie 1988). Thus, inflammation within the nerve itself and at peripheral nerve terminals in the limb and/or around the nerve itself may contribute to decreased modulation of pain at the spinal cord level. Conceivably, therapeutic intervention which decreases the mechanical irritation, normalises blood flow and also activates the sympathetic nervous system's (SNS) neuromodulation of inflammation, muscle activity and blood flow may also activate WDR modulation of NS neurones and hence decrease pain.

 

The effect of manual therapy on muscle activity around the intervertebral foramen (IVF).

Manual therapy may be directed at reducing muscle spasm. It is conceivable that sustained techniques may have a direct effect on the stretch reflex of muscles. Alternatively, a sustained technique (e.g. traction) may decrease electrical activity in type III and IV fibres through normalisation of blood flow and decreased mechanical pressure generated by inflammation on soft tissue structures in and around the IVF. Indeed, only 30mmHg pressure is required to obliterate endoneurial venous return (Lundborg 1988). Finally, non-noxious input from gentle oscillatory pressures may generate sufficient WDR modulation of NS neurones to allow decreased muscle spasm and increased functional muscle activity to take place. Any decrease in pain should be followed by functional exercises to maintain soft tissue integrity. Further, examination of the neurological signs and symptoms, and the painful active movements should be examined to demonstrate the effects of treatment.

 

The dosage of manual therapy and the significance of the 'stage' of inflammation and 'irritability' on '24 hour behavior', 'current' and 'past history'.

The stage of the inflammation and the 'irritability' (Maitland 1986; 1991) may influence the treatment approaches under consideration. For example, in an 'irritable' dysfunction and/or during the acute stage of injury the non-neurogenic inflammatory process may be more beneficially affected by sustained mobilisation techniques or constant traction which are thought to relieve the pressure around the nerve tissue. If this hypothesis were clinically true, then neurological changes such as reduced muscle power, reduced reflexes and reduced sensation should improve if the correct technique (position and amount of force) are used. During the later stages of inflammation and/or in a 'non-irritable' dysfunction the clinical signs and symptoms may be more readily influenced by treatments (e.g. joint mobilisations, mobilisations of the SNS, taping) specifically directed at the neurogenic inflammation. Treatment directed at the neurogenic inflammation must ascertain the status of the receptor thresholds with the aim of treatment being a decrease of afferent electrical activity through an increase in the modulation of the receptor thresholds of the type III and IV mechanoceptors. The principles of these hypotheses involve the fact that if inflammation results in a decrease in the receptor thresholds and a decrease in the modulation of electrical activity in type III and IV fibres, then the reverse should be true as inflammation resolves. That is, receptor thresholds and modulation of afferent electrical activity should increase. The expected result is decreased pain and consequent increases in ranges of movement, normalisation of voluntary muscle power, sensory discrimination and reflexes. Improvement in the clinical status of the patient should simultaneously correlate with improvements in the 'irritability' and '24 hour behaviour' of the dysfunction. In this manner the practitioner must treat the pain and not just any pain of which the patient complains (figure 7).

If oscillatory mobilisation techniques are employed at a 'stage' too early during the inflammatory process (i.e. in a worsening condition [e.g. distal pain > proximal pain] and/or in an 'irritable' dysfunction and/or progressing ischaemic compromise of a nerve root/DRG/spinal nerve), then this may exacerbate muscle spasm directly due to a stretch reflex or indirectly due to activation of inflamed receptors and neural compromise. Summation of afferent electrical activity from inflamed receptors may result in pain and further 'splinting' of the joint. Under no circumstance should an examination process or technique be used that increases neural compromise. Hence specificity of dosage is crucial not only for optimal results but also for safety.

Importantly, the clinician will need to ascertain the expectations of treatment outcome in relation to the 'stage' and 'irritability' which may be questioned in the subjective examination through not only the '24 hour behaviour' but also through ascertaining the 'current' and 'past history' of the signs and symptoms. In this manner improvements or deterioration in the patient's condition may be monitored and attributed to either the consequences of the type and dosage of treatment or to the consequences of the natural progression of the pathology.

 

Descending inhibition in the modulation of pain.

It is quite likely that the sympathetic nervous system (SNS) is involved in very specific but very different ways depending on the stage of inflammation and the 'irritability' of the dysfunction. The peripheral modulation of inflammation by the SNS (discussed previously) may be quite distinct and more readily influenced by enhanced blood flow, reduced oedema and reduced muscle spasm due to movement of inflammatory exudate. However, in presence of reduced autoinhibitory interneurone modulation of pain (in the spinal cord by WDR neurones on NS neurones) then at least two potential sources of descending neuromodulation may be recruited. One source of descending inhibition involves pontine noradrenergic projections onto ventral and dorsal horn neurones involved with the modulation of pain (figure 8) (see Proudfit 1992 for review; Jaenig 1985; Morgan et al 1989; Nakagawa et al 1990; Post et al 1986; Ren et al 1990). Descending noradrenergic inhibition is considered to be an opioid-independent form of analgesia (Proudfit 1992) however, evidence exists which supports the view that m -opioid and a -2 noradrenergic receptors are functionally linked to pain modulation (Kalso et al 1993). Apart from animal investigations for descending sympathetic pain modulation, further evidence comes from clinical investigations where the sensory and affective aspects of ischaemic pain (Maixner et al 1990) and muscle spasm (Shindo et al 1994) correlate with SNS induced cardiovascular responses.

Figure 8 : Descending modulation of pain (adapted from Wall 1995)

 

Manual therapy and descending modulation of pain.

Investigations of grade III PA oscillatory mobilisation (Maitland 1986) of the cervical spine (C5/6) demonstrated an initial sympathoexcitatory effect which started very rapidly (within 15 seconds) after the commencement of treatment (Petersen et al 1993). Wright & Vicenzino (1995) attributed the modulation of the sympathoexcitatory effect on the dorsal periaqueductal grey (dPAG) via nucleus paragigantocellularis, using noradrenaline as the transmitter substance. A review (by the investigators) of the acupuncture literature suggested that this initial sympathoexcitatory effect might be followed by sympathoinhibition some 20-45 minutes later (Wright & Vicenzino 1995). This sympathoinhibition was postulated to be as a result of modulation by the ventral PAG (vPAG) via the nucleus raphe magnus (NRM) to the dorsal horn and intermediolateral horn (IML) of the spinal cord to effect analgesia and cardiovascular changes. The connection from the nucleus raphe pallidus and obscurus to the IML and anterior horn is thought to influence motor activity and autonomic function (Lovick 1991, cited by Wright & Vicenzino 1995). These preliminary results are interesting, as there are very few adequate studies that have investigated the neurophysiology of the analgesic effects of manual physiotherapy.

 

Sensorimotor "center-surround inhibition" of pain.

Apart from the SNS, another source of descending modulation of pain is considered to arise from the sensorimotor cortical regions involved with input on spinal cord and brainstem regions (Hsieh, Stahle-Backdahl, Hagermark, Stone-Elander, Rosenquist, Ingvar 1995; Wall 1995). Wall (1995) describes this system as setting a "sensory posture" whereby motor input exerts 'powerful' control over afferent spinal cord processing which 'focuses on action rather than perception' (p35) (also Galea & Darian-Smith 1995). Wall (1995) used positron emission tomography (PET) studies in patients with chronic pain to substantiate this claim whereas Galea & Darian-Smith (1995) used PET and anatomical dissection of primates. Further evidence for descending modulation comes from Gogas et al (1991) where supraspinal opioids were found to block the perception of pain through a 64% reduction in superficial laminae dorsal horn activity (usually associated with a predominance of nociceptive specific [NS] neurones (Lima et al 1994)) and an 85% reduction in ventral horn activity (usually associated with motor activity) (Schomburg & Steffens 1991). Investigations substantiated the finding that higher centers can act in an antinociceptive manner where a predominance of inhibition occurs at NS neurones but where excitation or inhibition occurs with equal frequency on wide dynamic range (WDR) neurones (Sandkuehler et al 1995). This appears to be a unique way of looking at pain perception where the cortical input is primary to a secondary ascending nociceptive stimulus. This arrangement is postulated to improve discrimination of NS neuronal activity and thereby possibly decrease pain (figure 9) (Bogduk 1993; Laird & Cervero 1990).

 

Figure 9 : Centre – Surround Inhibition (Bogduk 1993)

 

The focus on action with functional tape and motor control in the treatment of pain.

The clinical application of functional tape and specific motor control suggest a marked pain inhibitory effect beyond that which may be explained purely on biomechnical grounds. Since primary hyperalgesia in deep tissue may lead to secondary hyperalgesia in superficial structures then therapeutic intervention, which results in a decrease in secondary hyperalgesia, may be postulated to result in increased movement.

Evidence for descending inhibition comes from a recent study on the modulation of cutaneous nociception concluded that besides the brainstem, other higher regions may be responsible for the marked descending inhibition of nociception (Hsieh et al 1995; Morton, Siegel, Xiao, Zimmermann 1997). Specifically, the somatosensory-motor cortex has been postulated to be involved in movement dysfunction as a consequence to and as a consequence of pain. It is conceivable that the cutaneous feedback from tape and the decrease in noxious afferent input may increase the discriminatory role of descending inhibition. Further, the specificity of motor control may also increase the descending inhibition of nociception.

Evidence for the effect of pain on the specificity of motor control comes from investigations into low back pain. Altered patterns of abdominal muscle activation with arm or leg movements have been recorded in patients with chronic low back pain (O'Sullivan, Twomey, Allison, Sinclair, Miller, Knox 1997; Hodges and Richardson 1996; Hodges, Richardson, Jull 1996; Richardson and Jull 1995). Therefore, the role of specific exercise, specific functional tape, and specific feedback may be to modulate pain and improve muscular co-ordination.

Apart from tape and specific exercise, feedback may come in the form of demonstrating improvements in the signs and symptoms both to you and the patient. Demonstrating improvements in the symptoms may be possible only through a very discriminative subjective examination (figure 7). A discriminative subjective examination may use the Maitland (1986, 1991) approach as well as pain questionnaires such as McGill, Oswestry, etc. Further, the improvements in the clinical signs may occur through range of movement testing, pressure biofeedback, EMG biofeedback and the testing of neurological signs and neurological tension tests. Finally the ability of the manual therapist to discriminate the site of pathology in the spine has been demonstrated to be valid and reliable and to have high inter-examiner reliability (Jull, Zito, Trott, Potter, Shirley, Richardson 1997). This means that both the therapist and the patient are able to judge the effect of treatment technique and dosage on the current 'stage' of the dysfunction if an organised assessment and treatment procedure is implemented.

 

Conclusions: The need for a thorough subjective and physical examination to be able to make clinical decisions, to apply the correct technique and dosage, and to assess the expected treatment outcome.

The clinical implications of descending modulation of pain suggest that during the application of manual physiotherapy to the cervical spine a noticeable treatment effect may occur within 15 seconds of mobilisation. Furthermore, it would appear that if mobilisation does result in a focus by the patient on 'action', then it is imperative to re-examine the active movement (incl. combined active movement) which initially reproduced the patient's pain.

Since descending modulation involves a principle of "fine tuning" of the perception of pain, then the initial examination must be very discriminative as to the exact area and range of movement where pain occurs during active movements. Also the 'quality' and 'intensity' of pain and the 'relationship' between the pains must be noted since secondary mechanical hyperalgesia and spinal cord hypersensitisation may occur as a result of neurogenic inflammation.

Movement aberrations/inco-ordinations due to muscle spasm and/or due to muscle weakness, decreased reflexes and sensation should be noted and correlated with known anatomical innervations.

Meticulous recording of information may allow the practitioner to use their cognitive processing for analysis rather than for remembering. By implication, the questioning of the patient through the clinical reasoning process may be hypothesised to also aid the patients' cognitive processing and hence modulation of pain.

The information from the examination of active movements should correlate with the 'aggravating/easing factors' and '24 hour behaviour' of the pain as well as with 'stage', 'stability' and 'irritability' of the dysfunction. Only with a discriminative subjective examination will it be possible for the practitioner to focus their clinical reasoning skills in search of the pain (not any pain) during their physical examination. However the practitioner may never know the effect of treatment if the initial examination has left the practitioner with nothing on which the practitioner nor the patient can judge the expectations of treatment outcome (see Mechanical traction - clinical example of  neurophysiological and biomechanical pain modulation?) . Finally, visualisation, verbalisation and goal orientation have powerful influences on motor learning.  Improved motor performance reduces the likelihood of re-injury through increased awareness of the correct patterning of movements (see Motor Learning and Orienteering expertise ) .  This, in turn will improve the force closure required for stability around a joint (see Pelvic Girdle Pain - muscle energy techniques - Swiss Ball).

Many dysfunctions will improve with time, however the discriminatory practitioner should be able to predict treatment outcome and either minimises the period of pain and/or prevent an acute injury from becoming chronic by applying the optimal dosage of treatment.

Conceptualised and written by Martin Krause for lectures presented between 1997 and 1999.  Since this time an overwhelming body of evidence supports the neurogenic modulation of pain and inflammation in cortical, subcortical, cerebral, spinal cord, dorsal root ganglion, peripheral sympathetic nervous system and afferent somatic nervous system sites.  Undoubtedly, the cortical involvement highlights the importance of explanations and education of your patient during treatment.  Feedback, both visual and verbal, as well as realistic goal setting appear to be of paramount importance for involving the patient in their recuperation (Martin Krause 2004).

Clinical Examples

 

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Initially written June 1995, Last update : 16 October 2009


 

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  • Wed 01 Nov 2017

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  • 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 '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. 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 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 October 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

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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