1. 1. Can you please explain the theoretical underpinnings of the CMT approach? Briefly, by what mechanisms may it achieve improvement in a patient’s pain with movement?

In essence, CMT emphasizes the importance of consideration of the starting position for passive or active mobilization treatment and advocates a clinical reasoning process that incorporates changes in the starting position as part of progression and regression of treatment (Edwards, 1999; McCarthy, 2010). This approach appears to be most efficacious with patients who have a ‘nociceptive pattern’ to their dysfunction, a directional sensitivity to movement, commonly referred to as a ‘mechanical presentation’. Typically, a mechanical presentation involves a combination of movements that reproduce local and referred pain and an opposite set of movements that reduce symptoms. Similar to most manual therapy approaches, it is generally not as useful when other pain types are dominant, such as peripheral neuropathic or nociplastic pain (McCarthy, 2010).

The CMT approach advocates the positioning of patients in severe pain in the opposite position to that in which they experience their symptoms. Here, the use of passively applied or patient-generated movement can be effective in decreasing pain, theoretically through afferent mechanoreceptor stimulation that evokes a (sympathetico-excitatory) rapid-responding, descending inhibitory pain mechanism. Thus, the perception of nociceptive pain can be rapidly reduced in this way; however, the analgesic effect of this approach will tend to plateau with repetition as the patient habituates to the repetitive stimulus. At this juncture, treatment progression involving a graded exposure to the provocative direction of movement is required. This is produced by altering the starting position in which treatment occurs to habituate or desensitize the patient to the painful or sensitive movement. In essence, the patient undergoing CMT is thus guided through a process of graded exposure to the specific directions of movement that are sensitized.

Conversely, in cases in which the pain is not severe the starting position used with CMT tends to be toward the end of the range of motion rather than being in a more midline or neutral position. In this manner, CMT deliberately aims to provoke the patient’s symptoms, theoretically by eliciting afferent signals from high-threshold mechanoreceptors (type III/IV). These receptors normally remain silent unless significant tension is applied to them but can fire with lower levels of stimulation when sensitized by local inflammation (Pickar, 2002). The descending inhibitory pain mechanism moderated by the dorsal periaqueductal gray area of the brainstem is particularly sensitive to this type of mechanical afferent stimulation, which can be evoked with deep pressure and strong stretches (Kaufman et al., 2002).

The box diagram in Fig. 26.1 shows an example of classical CMT treatment progression. This diagram depicts the combination of movements that reproduces the symptoms (prime combination) and also the direction of movement in which the patient is most sensitive (prime movement). Around the outer boundary of the box is the direction that treatment could be progressed to provide a graded exposure to the sensitive movements. The anticlockwise direction of progression around the box ensures that the most sensitive movement is introduced toward the end of the progression, when the patient is less sensitive (i.e. not in severe pain). Thus, phase 1 of the CMT approach requires the patient to be positioned away from the pain and involves evocation of the descending inhibitory pain mechanism. Phase 2 involves habituation to sensitive movement, with a gradual increase in stimulus via changes in the starting position for treatment. Finally, phase 3 employs mobilization treatment to facilitate motion into the range of impaired movement, thereby stimulating and lengthening passive tissues that may be causing impairment. This, supported by the provision of a home stretch programme, will continue tissue remodelling over many weeks. With a non-severe clinical presentation, assessment and treatment would simply occur in the prime combination.

1. 2. What were your initial thoughts regarding the source of Rohan’s symptoms, the persistence of the problem and his short-term response to previous treatment?

The initial impression formed was that Rohan had developed some direction-specific sensitivity to movement, leading to localized pain in the right, mid-thoracic spinal region. It was clear that particular movements changed the symptoms in a reliable, repeatable manner. The sensitized patterns of movement matched patterns of motion that typically create tension in certain tissues of the vertebral column and potentially provided information on which to base the direction and location of applied passive-movement treatment. Previously, local passive movements had been applied to the sensitized area, resulting in short-term reductions in pain typical of those reported in the literature following the application of therapeutic movement and exercise (Koes et al., 1991; Martinez-Segura et al., 2012; O’Leary et al., 2007). Despite these repeated episodes of pain reduction, there had been no permanent reduction in the directional sensitivity to movement. This suggested that the movement impairment(s) remained and that normal motion had not yet been regained or, alternatively, that the resolution of the impairment(s) had been temporary and that the functional demands of playing were continuing to induce sensitivity.

In addition to providing a mechano-sensory afferent stimulus to evoke descending pain inhibition, therapeutic movement can be delivered in a localized manner that provides an upgrading of exposure in the sensitized direction. The impression formed of previous manual treatment was that essentially the same techniques, performed in a neutral spinal position, were repeated at each session and that there was no provision of graded exposure to movement in the specific direction of sensitivity. Combined movement theory affords a framework to introduce this approach to physical examination and management. This suggested that a biomechanical analysis of the sensitized patterns of movement would at least provide a guide for a treatment approach to influencing the perception of pain.

1. 3. Psychosocial factors are often an important part of a patient’s presentation where pain persists and function is impacted. Can you comment on your psychosocial considerations in this case?

During the course of the initial interview of the patient, careful consideration of the psychosocial context of Rohan’s presentation was undertaken. It is common for athletes to have psychological barriers to returning to play, ranging from hypervigilance to team politics (Clement et al., 2013); however, these were not evident during the interview. A sense of anxiety regarding ‘the diagnosis’ was evident, to some degree, but the patient felt that this had reduced since the return of his normal MRI scan results. Moreover, Rohan’s view was that his problem was of a mechanical nature, and thus it was considered that approaching management from a mechanical paradigm would be well accepted by him and likely meet his expectations.

1. 4. What are your thoughts about the described allodynia and why this might occur? How might manual therapy be of benefit?

Persistent nociceptive afferent stimulation of the pain neuromatrix will commonly lead to alterations in neurotransmitter levels, responsiveness of first- and second-order neurones, inhibitory pain mechanisms and processing within the pain neuromatrix and immune system (Iannetti and Mouraux, 2010). The duration of his persistent symptoms would have been sufficient for these physiological adaptations to have occurred, albeit the region of allodynia had apparently not expanded to beyond a few centimetres from the midline.

There is some evidence to suggest manual therapy can reduce the degree of temporal summation (or wind-up) in the dorsal horn of the spinal cord (Bialosky et al., 2009) and thus might have a role in preventing the development of clinical symptoms of chronic pain, such as allodynia or hyperpathia (typically considered features of peripheral neuropathic and nociplastic pain states [Bialosky et al., 2009]). However, with severe chronic pain states, where these features are already present, ongoing pain can reduce the level of the inhibitory neurotransmitter gamma-aminobutyric acid and lead to a relatively overactive hypothalamus–pituitary–adrenal (HPA) axis (Pickar, 2002). Manual therapy’s influence on the HPA axis is overwhelmingly sympathetico-excitatory (Kovanur Sampath et al., 2015), and thus caution is needed in using manual therapy in such cases because further stimulating an amplified system can be counterproductive.