Pasty

1) Layman's description: // High velocity low amplitude (HVLA): // is a widely used manual therapy technique involving a short sharp thrust to a specific joint in an effort to increase its mobility and reduce pain. Careful application of leverages enables a rapid separation of the two opposing joint surfaces, depressurising it and often generating an audible ‘pop’ or ‘click’.
 * ETHICS:**[[file:ETHICS - LaymansTerms .doc]]
 * GLOSSARY: **

// Motor evoked potential (MEP): // is a targeted electrical impulse generated within the brain that travels via nerves down the spinal cord and out into the muscles, identical to the nerve impulses we voluntarily generate to contract our muscles. The size of the MEP is indicative of the level of excitability of the central nervous system. If the nervous system is in an increased state of excitability, the MEP’s produced will be larger, whereas if the nervous system is inhibited, the MEP’s will be smaller. It can be stimulated using transcranial magnetic stimulation.

// Transcranial magnetic stimulation ( //// TMS //// ): // is a pain-free non-invasive method of stimulating specific regions of the brain. Weak electric currents are created within the grey matter of the brain by placing a coil over the scalp. This coil, when turned on, carries a large electrical current within it, which generates an electromagnetic field around it. This causes a small focal electrical impulse being generated in the brain tissue – MEP. --- There have been many theories as to what effects HVLA has on various systems of the body, both locally and distally, including its effect on neurological processing and central nervous system excitability (Picker, J. 2002). Our proposed research project aims to investigate the effects of high velocity low amplitude (HVLA) thrust techniques on the nervous system. More specifically, our study will use Transcranial Magnetic Stimulation (TMS) to produce Motor Evoked Potentials (MEP’s) in the gastrocnemius muscle, which we shall measure before and after the intervention (HVLA technique applied to the Lumbosacral junction). The study is based upon previous research by Dishman et al 2002. We hope to provide clear results regarding the effect on central motor excitability as influenced by HVLA technique applied to the lumbosacral junction. The reason for manipulating this joint is because the lumbosacral level of the spinal cord provides innervations to the gastrocnemius muscle, as such we will be able to view what changes occur in a segmentally related tissue.

Currently, conflicting evidence regarding the neurophysiologic effects of HVLA and therefore muscle activity exists. Two studies have shown an increase in motor neuronal activity following spinal HVLA techniques, (Dishman et al 2002, Dishman et al 2008).Conversely, another study by the same author reported a decrease in motor neuronal activity (Dishman et al 2000). Both sets of results have theories as to how they may provide a resultant decrease in related musculature tone. More definitive research would obviously lend weight to one of these theories.

Our research project will be conducted as a controlled cross-over design where participants will be undergo both the control and experimental intervention, tested one week apart. The order of the treatment intervention will be randomised.

Firstly, participants will undergo TMS to map out and localise the area of the brain that generates maximal MEP’s in the gastrocnemius muscle. They will be seated, and a snug cap with premarked points of reference on it will be placed on their head. Once located, these coordinates will be recorded and returned to after the intervention has been applied. We will take 10 MEP’s 4-5seconds apart to give us an average baseline measurement, then participants will be relocated to a treatment table and an intervention randomly applied (either HVLA thrust, or control group of just sidelying with no contact). Immediately after the intervention, MEP’s will be measured at 20sec intervals for the first 2 minutes, then again at 5 minutes, and 10 minutes. Participants will then return one week later for the alternative intervention.

Our participants for this study will be drawn from the student population at Victoria University. Volunteers will be recruited via posters placed around the teaching clinics and university campuses at both the City Flinders and Footscray Park Campus. Volunteers will be invited to contact the principal researcher to indicate their interest to participate in the study and discuss what will be required of them. These volunteers will be sent Information to Participants sheets and will sign Consent forms if they are willing to participate. We hope to gain valid data from at least 21 participants to ensure our study has enough statistical power. Participants will be eligible if they are healthy of either gender without low back pain, aged between 18 and 50yrs old. --- // TMS //// : // The patient will be seated in a comfortable chair, with the special cap containing the electric coil placed against your head. This coil, when turned on, carries a large electrical current which generates an electromagnetic field surrounding it. This magnetic field induces a small electrical current in the neural tissues underneath the skull next to the coil. This electrical current then travels down the nerves and out into the periphery as MEPs. They will first undergo mapping for the gastrocnemius area of the brain. As everyone’s brain is different, the practitioner will have to identify the exact point at which there is maximal MEP production into the gastrocnemius muscle. The machine will be turned on and they will hear clicking sounds and possibly feel some tapping on their forehead. The mapping will be completed within 30 minutes. Once mapped, the patient will have MEPs measured before and after the application of either the HVLA or control intervention, and the results compared.
 * TECHNIQUES: **

// HVLA: // A right sided L5-S1 side-posture HVLA manipulation will be administered. The patient is placed in a side-lying position, with hips in approximately 20 degrees of flexion. The lower left leg is left straight, with the upper right leg slightly flexed. The upper body is rotated to the right until the level of L5-S1. The clinician then manually contacts the tissues overlying the zygapophyseal joint, reinforcing both the lower and upper body rotation. Ensuring that the participant is relaxed and once tissue tension was maximised, a HVLA force is applied. The thrust is applied in the direction of the apophyseal joint plane, commonly in the direction of a line along the long axis of the patient's right femur (Gibbons & Tehan, 2008).

The control intervention involves the operator assisting the participant into a side posture; however no truncal torque will be applied and no manual contact will be made with the spine.

**PROPOSAL:** Pasty's part: 1) Neurophysiology of HVLA - research demonstrating neurophys changes and mechanisms. Word doc as of 9/6/10




 * a) Central effects**

HVLA has been reported to cause numerous neurophysiological effects at both the spinal cord and cortical levels. One of the proposed central effects is called facilitation or sensitisation. This refers to the increased excitability or responsiveness of dorsal horn neurons to an afferent input. An alteration between vertebral segments may produce a biomechanical overload leading to the alteration of signalling from mechanically or chemically sensitive neurons in paraspinal tissues. These changes in afferent input are believed to alter neural integration either by directly affecting reflex activity and/or by affecting central neural integration within motor and neuronal pools [Pickar].

Denslow et al were one of the first groups to investigate this phenomenon, and their findings suggested that motoneurons could be held in a facilitated state because of sensory bombardment from segmentally related dysfunctional musculature. It has been shown that central facilitation increases the receptive field of central neurons and allows innocuous mechanical stimuli access to central pain pathways [Woolf]. Essentially this means that sub-threshold stimuli may become painful as a result of increased central sensitisation. As discussed in the other sections of this proposal, spinal manipulation is believed to be able to overcome this facilitation by making biomechanical changes to the joint [Pickar], and/or by creating a barrage of afferent inputs into the spinal cord from muscle spindle and small-diameter afferents, ultimately silencing motoneurons. [Korr].

Melzack and Wall’s [#] Gate Control Theory dsecribes the dorsal horn of the spinal cord as having a gate-like mechanism which not only relays sensory messages but also modulates them. Nociceptive afferents from small diameter Aγ and C fibres tend to open this gate, and non-nociceptive large diameter Aβ fibres (from joint capsule mechanoreceptor, secondary muscle spindle afferents, and cutaneous mechanoreceptors) tend to close the gate to the central transmission of pain. This modulation takes place in the lamina of the dorsal horn. Simplistically, Aβ afferents enter lamina II and V, stimulating an inhibitory interneuron in lamina II (which connects to lamina V); Aγ and C fibres enter lamina V. Consequently, the central transmission of pain is a balance between the influences of these opposing stimuli. [Potter, Kandel] HVLAT may modulate the pain gate mechanism in the dorsal horn by producing a barrage of non-nociceptive input from large diameter myelinated Aβ afferents from muscle spindles and facet joint mechanoreceptors to inhibit nociceptive C fibres [Besson & Chaouch].


 * b) Cortical/motoneuronal effects**

__Dishman et al__ recently published an article which questioned some of their own previous research findings. In this subsequent paper, the authors stated that the H-reflex technique is susceptible to the effects of pre-synaptic inhibition of the afferent arm of the reflex pathway. So, by using transcranial magnetic stimulation to directly measure the effect of corticospinal inputs on the alpha motor neuron pool, they were able to perform an experiment which showed a transient (20–60 s) increase in motor alpha neuron excitability post manipulation. This paper lends further support to the theory that spinal manipulation produces a brief activation of the motor alpha neuron leading to brief muscle contraction.

Descending pathways also influence pain perception. Stimulation of the Periaqueductal gray produces analgesia via the descending PAG pathways[Morgan MM]. Stimulation of the dorsal PAG (dPAG) in the brain produces selective analgesia to mechano-nociception, whereas temperature nociception is modulated via the ventral PAG (vPAG). It is also known that sympatho-excitation results from stimulation of the dPAG, in contrast to sympatho-inhibition which occurs as a result of stimulating vPAG[Morgan MM]. Activation of the descending dPAG is a possible mechanism for the antinociceptive effects of spinal manipulation. __Sterling__ //__et al__// measured changes in pain and sympathetic outflow by comparing a C5/6 HVLA to a sham intervention (manual contact but with no movement). The authors demonstrated HVLA produced mechanical hypoalgesia, measured by an increase in pain pressure threshold, and increased sympathetic outflow, measured by decreased blood flow, decreased skin temperature, and increased skin conductance. However, there was no alteration to thermal pain thresholds. Given such selective mechanical anti-nociception and sympathoexcitation, this supports the theory that the mechanism of effect is due to activation of the dPAG descending pain mechanism. Vincenzino //et al// conducted a similar experiment on subjects with epicondylitis and showed again that cervical spine HVLA lead to selective analgesia to mechanical stimulus and sympatho-excitation, adding further weight to the argument that spinal manipulation may influence the perception of pain by activation of the descending dPAG. This does not prove conclusively that there is definitely direct activation of dPAG, only that the effects of HVLA are give similar findings to what you would expect with stimulation of the dPAG, hence there is a plausible link between the two, and it is inferred that HVLA may lead to stimulation of the dPAG.

Pickar JG, Neurophysiological effects of spinal manipulation. //The Spine Journal 2// 2002 357–371. Denslow JS, Korr IM, Krems AD. Quantitative studies of chronic facilitation in human motoneuron pools. Am J Physiol 1947;150: 229–38. Woolf CJ. The dorsal horn: state-dependent sensory processing and the generation of pain. In: Wall PD, Melzack R, editors. Textbook of pain, 3rd ed. Edinburgh: Churchill Livingstone, 1994:101–12. Korr IM. Proprioceptors and somatic dysfunction. J Am Osteopath Assoc 1975;74:638–50. Melzack R, Wall PD. Pain mechanisms: a new theory. Science 1965;150:971–9. Besson J-M, Chaouch A. Peripheral and spinal mechanisms of nociception. Physiol Rev 1987;67(1):67–186. Kandel ER, Schwartz JH, Jessell TM. //Principles of Neural Science//, 4th edn. London: McGraw-Hill, 2000 Potter L, McCarthy C, Oldham J. Physiological effects of spinal manipulation: A review of proposed theories. Physical Therapy Reviews 2005; 10:163-170. Dishman JD, Ball KA, Burke J. Central motor excitability changes after spinal manipulation: a transcranial magnetic stimulation study. //J Manipul Physiol Therap// 2002;**25**:1–10 Morgan MM. Differences in antinociception evoked from dorsal and ventral regions of the caudal periaqueductal gray matter. In: Depaulis A, Bandlier R. (eds) //The Midbrain Periaqueductal Gray Matter//. New York: Plenum, 1991;139–50 Sterling M, Jull G, Wright A. Cervical mobilisation: concurrent effects on pain, sympathetic nervous system activity and motor activity. //Manual Therapy// 2001;**6**:72–81 Vincenzino B, Collins D, Wright A. An investigation of the interrelationship between manipulative therapy-induced hypoalgesia and sympathoexcitation. //J Manipul Physiol Therap// 1998;**21**:448–53
 * References:**

"Korr’s theory of the facilitated segment was that an increase in gamma motor neuron activity reflexly increased the alpha motor neuron, and led to hypertonicity. Korr proposed that HVLAT increased joint mobility by producing a barrage of impulses which silenced the facilitated gamma motor neurons. This theory is contentious, as there is no clear evidence that there is facilitation of the alpha motor neuron."

"Dishman et al.32 later questioned some of their own previous work. In this subsequent paper, the authors stated that the H-reflex technique is susceptible to the effects of pre-synaptic inhibition of the afferent arm of the reflex pathway. So, by choosing a technique that directly measured the effect of corticospinal inputs on the alpha motor neuron pool (transcranial magnetic stimulation), they were able to perform an experiment which showed a transient (20–60 s) increase in motor alpha neuron excitability post manipulation. This paper lends further support to the theory that spinal manipulation produces a brief activation of the motor alpha neuron leading to brief muscle contraction."

"Melzack and Wall’s45 theory of the pain gate mechanism. They described the dorsal horn of the spinal cord as having a gate-like mechanism which modulates the central transmission of afferent nociceptive input. Nociceptive afferents from small diameter Aγ and C fibres tend to open this gate, and non-nociceptive large diameter Aβ fibres (from joint capsule mechanoreceptor, secondary muscle spindle afferents, and cutaneous mechanoreceptors) tend to close the gate to the central transmission of pain. This modulation takes place in the lamina of the dorsal horn. Simplistically, Aβ afferents enter lamina II and V, stimulating an inhibitory interneuron in lamina II (which connects to lamina V); Aγ and C fibres enter lamina V. Consequently, the central transmission of pain is a balance between the influences of these opposing stimuli.44 HVLAT may modulate the pain gate mechanism in the dorsal horn by producing a barrage of non-nociceptive input from large diameter myelinated Aβ afferents from muscle spindles and facet joint mechanoreceptors." -http://hvlaandtms.wikispaces.com/file/view/Potter+2005+Physiological+effects+SM.pdf

" The current study findings __suggest__ that the initial changes that occur after spinal manipulation occur at the cortical level . This is in agreement with previous research.22 The peripheral N9 peak, representing the afferent volley in the brachial plexus,54-56 was maintained stable in this experiment. The changes observed in this study therefore most likely reflect central changes. However, although the P14 and N18 SEP components, known to originate at the level of the brainstem,23,55,57-60 did not show any changes in this study, the design of the study limits the ability to rule out the possibility that subcortical changes did occur. It is generally agreed that although 500 sweeps (and the current study averaged 800 sweeps per trial) are sufficient to record reliable peripheral Erbs and cortical SEP potentials, far-field potentials such as subcortical P14-N18 do generally require a higher number of averaged sweeps.24,25 The possibility for subcortical SEP changes after spinal manipulation does therefore need further investigation." **Quote from** ALTERED CENTRAL INTEGRATION OF DUAL SOMATOSENSORY INPUT AFTER CERVICAL SPINE MANIPULATION - Heidi Haavik Taylor et al. Study investigated somatosensory evoked potentials (SEP) from the median and ulnar nerves (stimulate median and ulnar nerves and then measure potentials at cortical level) after Cx manipulation of a **dysfunctional** Cx segment. The study suggests that cervical spine manipulation it likely to alter cortical integration of dual somatosensory input - supposedly cephalad to the brainstem. - effect on motor systems?

1) “persistent alterations in normal sensory input from a functional spinal unit increases the excitability of neuronal cells or circuits in the spinal cord [25,36,76]." “alpha-motoneurons could be held in a facilitated state because of sensory bombardment from segmentally related paraspinal structures. The motor reflex thresholds also correlated with pain thresholds, further suggesting that some sensory pathways were also sensitized or facilitated in the abnormal segment” ---__Facilitated segment__ – increased sensory input increases segmental excitability. HVLA decreases this facilitation (FIND REFERENCE)  2) “non-noxious mechanical inputs themselves can also have therapeutic effect. The gate control theory of Melzack and Wall [81] drew attention to the active role of the dorsal horn of the spinal cord. The dorsal horn is not simply a passive relay station for sensory messages but can modulate the messages as well. Numerous studies inspired by Melzack and Wall’s theory clearly demonstrate that non-noxious mechanical inputs travelling by means of the large, myelinated A fiber neurons can inhibit the response of dorsal horn neurons to nociceptive stimuli from C fibers” ---__Gate Control theory__ – increased mechanoreceptor input into the spinal cord from alpha fibres can inhibit the segmental nociceptive response for C fibres. 3) Central effects: cortical / motoneuronal excitability. “The current data indicates that the central motor system, in total, is facilitated.” Unable to determine whether it is the motor cortex being excited which then increases excitability of the motoneuron pool, or whether SMT activates spinal interneuron pathways which increase the excitability level of the motoneuron pool.

Extracts from articles: "A biomechanical alteration between vertebral segments hypothetically produces a biomechanical overload the effects of which may alter the signaling properties of mechanically or chemically sensitive neurons in paraspinal tissues. These changes in sensory input are thought to modify neural integration either by directly affecting reflex activity and/or by affecting central neural integration within motor, nociceptive and possibly autonomic neuronal pools."

"Their findings lead to one of the predominant rationales for the clinical use of spinal manipulation, namely, the premise that persistent alterations in normal sensory input from a functional spinal unit increases the excitability of neuronal cells or circuits in the spinal cord [25,36,76]."

"The patterns they observed suggested that alpha-motoneurons could be held in a facilitated state because of sensory bombardment from segmentally related paraspinal structures. The motor reflex thresholds also correlated with pain thresholds, further suggesting that some sensory pathways were also sensitized or facilitated in the abnormal segment"

"Subthreshold mechanical stimuli may initiate pain, because central neurons have become sensitized. Removal of these subthreshold stimuli should be clinically beneficial. One mechanism underlying the clinical effects of spinal manipulation may be the removal of subthreshold stimuli induced by changes in joint movement or joint play (see previous section: Neurophysiological and biomechanical mechanisms underlying the effects of spinal manipulation). In addition, nonnoxious mechanical inputs themselves can also have therapeutic effect. The gate control theory of Melzack and Wall [81] drew attention to the active role of the dorsal horn of the spinal cord. The dorsal horn is not simply a passive relay station for sensory messages but can modulate the messages as well. Numerous studies inspired by Melzack and Wall’s theory clearly demonstrate that nonnoxious mechanical inputs travelling by means of the large, myelinated A fiber neurons can inhibit the response of dorsal horn neurons to nociceptive stimuli from C fibers" -http://hvlaandtms.wikispaces.com/file/view/Neurophysiological+effects+of+spinal+manipulation.pdf

"Recent reports indicate that an excitatory reflexive discharge of paraspinal muscles occurs as a consequence of spinal manipulative therapy. 19  This result has been attributed to a reflexive primary afferent discharge of various receptors, such as joint mechanoreceptors and muscle spindles. 19 Some investigators have reported inhibitory effects on the motoneuron pool as a consequence of spinal manipulation,9,10,25 whereas others report excitatory effects on the human motor system.19,31,32 Thus, a paradox has developed in the investigation of the mechanism that spinal manipulation may exert on the excitability of the motoneuron pool. This apparent paradox is further promoted by the fact that most of the individual mechanoreceptors in spinal and paraspinal structures3,13 produce excitatory discharges when stimulated.30 "

- [|Spinal Reflex Attenuation Associated with Spinal Manipulation. J Donald Dishman, 2000.] Will our study offer an insight into this apparent paradox of the inhibitory/excitatory effect of HVLA? How?

***Nick's input** - fucking hand typed from first prize article "One basic physiologic response to SMT is a transient decrease in motoneuron activity as assessed by the hoffmann reflex (H - Reflex) technique....However, these H-Reflex findings of motorneurone inhibition appear to be in frank contrast to other investigations in which SMT has been reported to produce a reflex activation of paraspinal musculature. In addition, mechanical strain of the ligament-muscular system of the spine evokes reflex activation of paraspinal muscles in feline. Although these research findings appear **paradoxical** with respect to understanding the effects of SMT on the human motor system, **reflex activation of paraspinal muscles may trigger the subsequent reduction in motoneuron activity**. There is one case.....reflex activation of SMT-targeted thoracic musculature led to a subsequent alleviation of hypertonicity in one symtomatic patient with Tx back spasms. Mechanistically, SMT is equivalent to rapidly applying a mechanical strain to the trunk. Depression of Ia-motoneuron synapse after a previous activation of the stretch reflex arc is a well-documented neurophysiologic phenomenon known as postactivation-depression. Although postactivation depression appears to be limiated to the fibers activated by the conditioning procedure, there is sufficient evidencce to suggest heteronymous inhibition of motoneurons by altering Ia- afferent dicharge rates from postural, synergystic, and antagonistic muscles." ....more stuff

__the **Dishman 2002 first prize article** that we are modelling hypothesised as above. We need to look to more recent research for our answers.__

There is a **transient decrease** in **motoneuronal activity** after high-velocity, low-amplitude SM, as assessed by the response was encountered in experiments involving SM of both the cervical and lumbar spines, as well as the sacroiliac joint, and persists from 10 seconds to 15 minutes. 2-6 However, these H-reflex findings of motoneuron inhibition appear to be in **frank contrast to** other investigations in which SM has been reported to produce a **reflexive activation of** the ligament-muscular system of the spine evokes reflex activation of paraspinal muscles in the feline. 9,10 Although the above research findings in asymptomatic individuals appear **paradoxical** with respect to understanding the effects of SM on the human motor system, **reflex** hypothesis, reflex responses are associated with SM treatments, and observations from electromyographic (EMG) records of patients with local muscular hypotoni- cities indicate a reduction in hypertonicity after SM-induced reflex responses. 8 **Clearly, though, no consensus has been** ** <-still no proof even 2 years ago ** **reached as to whether SM leads to an overall excitation or** **inhibition of motoneuronal activity** .3-6,11
 * Hoffman reflex** (H-reflex). 1 This consistent and reproducible ** <-Hoffmann Reflex studies show transient decrease in motoneuronal activity post SM **
 * paraspinal musculature**. 7,8 In addition, mechanical strain of ** <-Other studies show reflex activation of paraspinal muscles post SM **
 * activation of paraspinal muscles may trigger the subsequent <- still a hypothesis **
 * reduction of motoneuronal activity**. In support of this


 * - from 2008 Dishman - MOTOR-EVOKED POTENTIALS RECORDED FROM LUMBAR ERECTOR SPINAE MUSCLES: A STUDY OF CORTICOSPINAL**
 * EXCITABILITY CHANGES ASSOCIATED WITH SPINAL MANIPULATION**

the argument persists even now, with Dishman2008 still no closer to finding the answer only 2 years ago....

TMS can create MEP which can be measured pre/post manipulation. The post-intervention EMG readings will be the same/higher/lower than previously (and hopefully the same over multiple patients). If there is an increased EMG response from TMS to the same area at the same intensity (with the same muscle activation levels) then we can assume that manipulation causes an excitatory effect on the motoneurone pool. If it is decreased, then we can assume there is an inhibitory effect. Currently, there is evidence to support both hypothesis. Which is correct? And what research do we base our hypothesis on?

Research: Accuracy of TMS - reliability, validity, ethics. Proposed HVLA theories - what evidence is out there to support the different proposed reflex outcomes?