Stuart discusses the evidence behind mobilisations and their use in physiotherapy.
Mobilisations are commonly administered to increase joint range-of-movement (Wright & Sluka 2001). Mechanical models propose that tissues are stretched, scar tissue is broken down, and mechanical faults are corrected, although there is limited evidence for this ‘structural-anatomical-biomechanical’ basis for manual therapy (Zusman 2011). There is now a large body of literature highlighting the neurophysiological effects, including sympatho-excitatory and pain-relieving (hypoalgesic) (Vicenzino et al 1998, Wright 1995), of mobilisations, which has led authors to question which mechanism is the more prominent, although a combined effect may also be likely (Bialosky et al 2009).
Mobilisations initiate a chain of neurophysiological responses:
Peripheral hypoalgesic effects may be seen through a reduction of local inflammatory mediators following mobilisations, leading to decreased local nociceptive pain (Bialosky et al 2009). Teodorczyk-Injeyan et al (2006) noted a decrease in blood and serum level cytokines following joint mobilisations, something that was not seen in a control group. This may lead to a reduction in pain mediated by the peripheral nervous system, which in turn may decrease muscle inhibition and therefore improve function.
Spinal mechanisms are those that occur at the spinal cord. Malisza et al (2003), using functional MRI (fMRI), found decreased dorsal horn activation following mobilisation of the rat knee. These spinal mechanisms are associated with altered afferent discharge to the brain, altered motor-neuron activity, and possibly excitation of an inhibitory interneuron related to descending pathways, leading to altered muscle activity and hypoalgesia. That mobilisations are associated with hypoalgesia, altered motor-neuron pool activity, afferent discharge, and changes in muscle activity, further implicates spinal cord mediated effects (Bialosky et al 2009).
Supra-spinally mobilisations have been shown to stimulate areas of the brain known to be instrumental in the experience of pain. These areas include the Anterior Cingulate Cortex (ACC), Amygdyla, Periaqueductal Gray (PAG), and the Rostral Ventromedial Medulla (RVM). To be more specific it is the dorsal aspect of the PAG, the dPAG that appears to be affected. The dPAG and RVM, through descending inhibitory pathways, have been shown to selectively produce analgesia to mechano-nociception, and cause sympatho-excitation. The ventral periaqueductal gray (vPAG) in contrast produces sympatho-inhibition and modulation of temperature nociception (Morgan 1992).
Another proposed mechanism hypothesises the production of long-term depression (LTD) at the dorsal horn due to reductions in numbers of receptors, NMDA and AMPA, for excitatory neurotransmitters on the post-synaptic membrane, following prolonged manual therapy (Zusman 2011). This would produce a situation whereby less of the neurotransmitters, mostly Glutamate and Substance P, are taken up by the secondary neuron leading to decreased production of onward action potentials, and therefore afferent information. However this remains speculation at this stage.
Bialosky J.E, Bishop M.D, Price D.D, Robinson M.E, George S.Z. The mechanisms of manual therapy in the treatment of musculoskeletal pain: a comprehensive model. Manual Therapy 2009;14:531-538
Malisza K.L, Stroman P.W, Turner A, Gregorash L, Foniok T, Wright A. Functional MRI of the rat lumbar spinal cord involving painful stimulation and the effect of peripheral joint mobilization. Journal of Magnetic Resonance Imaging 2003;18:152-159
Morgan M.M. Differences in antinociception evoked from dorsal and ventral regions of the caudal periaqueductal gray matter. NATO ASI Series 1992;213(1):139-150.
Teodorczyyk-Injeyan J.A, Injeyan H.S, Ruegg R. Spinal manipulative therapy reduces inflammatory cytokines but not substance P production in normal subjects. Journal of Manipulative and Physiological Therapeutics 2006;29:14-21
Vincenzino B, Collins D, Benson H, Wright A. An investigation of the interrelationship between manipulative therapy-induced hypoalgesia and sympathoexcitation. Journal of Manipulative and Physiological Therapeutics 1998;21:448-53
Wright A. Hypoalgesia post-manipulative therapy: a review of a potential physiological mechanism. Manual Therapy 1995;1:11-16
Wright A, Sluka K.A. Nonpharmacological treatments for musculoskeletal pain. The Clinical Journal of Pain 2001;17:33-46
Zusman M. Mechanism of mobilization. Physical Therapy Reviews 2011;16(4);233-236