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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.
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
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.
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 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).
Motor Learning and gaining of expertise through avoidance of injury
Clinical Examples
Clinical Reasoning Neck Example
Clinical Reasoning Back Example
LBP Treatment Progress
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Initially written June 1995, Last update : 16 October 2009
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Among one of the most widespread electrical wiring issues is regarding how to wire a switch. While using switches in your house is fairly quick, wiring 1 might not be that effortless for everybody. An ON-OFF switch is definitely quite simple to wire. There are actually different types of switches, but for this example, let's say that you are setting up a single-pole toggle switch, an exceptionally prevalent change (along with the simplest).
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text:
Slobozia (, , ) ist eine Stadt am Fluss Dnister im südlichen Transnistrien. Sie ist Verwaltungshauptstadt des nach ihr benannten Rajons und hat etwa 17.780 Einwohner (Stand: 1. Januar 2005), die sich überwiegend aus Moldauern und Russen zusammensetzen.

Die Ortschaft wurde erstmals Ende des 17. Jahrhunderts erwähnt und hat seit 2002 offiziellen Stadtstatus. Die heutige Stadt geht auf die ehemals selbstständigen Ortschaften Slobodseja Russkaja und Slobodseja Moldawskaja zurück, die 1972 zu einer einzelnen Gemeinde zusammengelegt wurden. Historisch war der nördliche Teil (Moldawskaja) hauptsächlich von ethnischen Moldauern bewohnt, während der südliche Teil (Russkaja) von Russen bewohnt war. Beide Siedlungen waren im Laufe des 20. Jahrhunderts zusammengewachsen und die Trennung nach ethnischen Gruppen verwischt. Das heutige Stadtzentrum mit Rathaus und den meisten Geschäften befindet sich im ehemals moldauischen Teil der Siedlung, aber auch der südliche, ehemals russische Stadtteil, verfügt über einen eigenen Ortskern.

Weblinks

Ort in Transnistrien
Ort am Dnister

redpajama_set_name: RedPajamaWikipedia


Kaspersky Security 10 is installed on iOS devices by means of MDM profiles.
Any Administration Server computer can function as an MDM server. The Administrator can manage MDM profiles of iOS device users.
During installation of the iOS MDM profile, Safe browser is installed by default. It can be managed through Kaspersky Security 10 for Mobile policies.
Change policies managing password properties, Microsoft Exchange connection settings, VPN connections, access to the camera, and other settings.
Lock the device, reset the password, and wipe the device.
Install or remove third-party applications and Apple Store applications.
Sign the iOS MDM profile.
Create a policy for the device.
Manage devices through Kaspersky Security 10 for Mobile.
Select Kaspersky Security Center 10 Administration Server and click Uninstall/Change.
In the Change or Uninstall the application step, select Change.
Select the check box Mobile devices support and click Next.
Go to Additional → Remote installation → Installation packages.
Select iOS MDM mobile device server and click Install the application.
Get and install an APN certificate.
You can locate one iOS MDM Mobile Device server on the computer with the Administration Server installed.
Right-click the Administration server and select Properties.
Install the Administration server certificate, or select Add certificate.
Select the certificate type and specify the path to the key file.
Click ОК to save the changes.
To make the profile trusted, sign it with a trusted root certificate. Adding a trusted sertificate is not a mandatory step for device management.
After the certificates needed for profile signing are installed, signed certificates will be applied to the device after they are added.
We recommend using a 2048-bit key from a third-party certificate authority such as Thawte or Symantec.
Run the plug-in installation, and wait until it is completed.
Send the invitation With iOS MDM profile with this configuration file. Specify the iOS MDM server.
InstallApple Configurator on the device running under OS X.
Create a configuration file with the policy according to the documentation.
Add the file with the .mobileconfig extension to the iOS MDM server.
If this requires changing the policy on the device, add the .mobileconfig file from Apple Configurator.
You can manage devices through the policy or from the Mobile devices section using commands.
Download the management plugin of Kaspersky Endpoint Security 10 for Mobile.
Create a policy for Kaspersky Endpoint Security 10 for Mobile.
Open th properties of the created policy and find the settings you want to use.
Go to General and select the Active policy check box.
Save the changes and click ОК.