1. 1. Based on this initial information from your patient history, what were your early hypotheses and associated reasoning regarding (a) dominant ‘pain type’ (nociceptive, neuropathic, nociplastic) and (b) possible ‘sources of symptoms’ if you believed a nociceptive pain type might have been present?

There were no features suggestive of a neuropathic pain (Tampin 2014). However, Sabrina’s symptoms had become chronic, and her persistent pain and disability supported the presence of changes in her pain-modulating system (Chimenti et al. 2018). Her slow recovery during the 9 months after her first whiplash trauma might have been partially related to the painful exercises she had been given. Repeated evocation of pain might have created a sensitization of the pain-modulating system and even a ‘pain memory’ (Zusman, 2003). The localized nature of her suboccipital pain and consistent pattern of aggravation related to posture and movement supported a possible nociceptive component that may also have contributed to her ongoing symptoms (Giamberardino, 2003).

Sabrina had resigned herself to living with her symptoms, and her belief was that nobody could help her (but she was not happy with this situation and, accordingly, sought our assistance). This negative outlook could adversely affect her pain modulation because inappropriate emotions and cognitions can influence the descending pain-inhibitory mechanisms (Nijs et al., 2009). Her reserved attitude suggested she did not want to discuss this and limited further questioning.

Specific structural sources of neck pain (nociception), such as the intervertebral disc or the zygapophyseal joint, cannot be clinically diagnosed (Bogduk and McGuirk, 2006). Furthermore, we do not have musculoskeletal treatment techniques specific to different spinal structures (Zusman, 2013). Consequently, as musculoskeletal clinicians, we should first look for dysfunctions in posture and movement as indicating possible sources of nociception (Jones and Rivett, 2004). Once a posture/movement dysfunction has been found, the clinician can then attempt to differentiate if it is caused or influenced by connective (joint), muscular or neural tissues, as the treatment techniques are different for these three tissues (Kaltenborn, 2012).

From a mechanical point of view, Sabrina’s story pointed more to a hypermobility presentation than a hypomobility problem. If she had significant symptomatic restrictions in movement, they would be expected to evoke pain at the end of her cervical movements when tissues become tightened, stimulating mechanoreceptors and nociceptors. This pattern was not reflected in her reported behaviour of symptoms. Furthermore, the development of hypomobility requires a period of immobilization or of non-usage or a specific pathology such as ankylosing spondylitis, none of which were apparent in Sabrina’s history. The variability of Sabrina’s symptoms and the alleviation of her neck pain possibly through the movement associated with her moderate running were more consistent with a pattern of hypermobility. Intensive movements in a large range of motion or prolonged immobile postures in lying, sitting or standing usually aggravate hypermobility symptoms (Niere and Torney, 2004; Olson and Joder, 2001). This seems to fit with Sabrina’s story.

The systematic physical examination will show whether Sabrina’s symptoms are related to the neck and, if so, to which region or segment of the cervical spine. Although the information from the subjective examination supports a typical pattern of cervical hypermobility and a sensitized pain-modulating system, at this stage of the examination, specific hypotheses regarding potential nociceptive sources for her three major symptoms are not considered. Instead, a systematic structured physical examination for cervical problems is followed in order to generate specific hypotheses regarding the most likely tissues involved (e.g. connective tissue (joint), muscle, neural).

1. 2. What were your thoughts regarding ‘precautions or contraindications to the patient’s physical examination and initial treatment’?

The subjective examination did not reveal any ‘red flags’ suggestive of serious pathology or an acute and severe compression of the nervous system requiring medical intervention. Sabrina reported only two (dizziness and nausea) of the classic 5 D and 3 N symptoms associated with cervical arterial dysfunction (the others being diplopia, drop attacks, dysarthria, dysphagia; numbness, nystagmus). She also denied ataxia as the ninth ‘classic sign’ (Kerry and Taylor, 2006). This screening, however, is insufficient on its own to rule out this condition (Kerry and Taylor, 2006). Sabrina’s dizziness, nausea and tunnel-vision symptoms represented a precaution and would need to be carefully monitored during the physical examination and treatment. Further screening would also need to be carried out in the physical examination prior to any orthopaedic manual therapy, including manipulation, mobilization and exercise (Rushton et al., 2014). In addition, the high irritability of her symptoms also warranted caution during the physical examination and treatment to avoid excessive aggravation.

At this point, without any evidence of serious pathology, Sabrina seemed to have what is called a ‘simple mechanical dysfunction’ (Waddell, 1998) with a possible sensitization of the pain-modulating system, including a ‘pain memory’.

As discussed in Chapters 1 and 2, it is important to hypothesize about ‘pain type’ because this influences the interpretation of physical findings, management decisions and prognosis. However, as highlighted here, even when features of a nociplastic pain type are present (e.g. sensitization of pain modulating system and pain memory) this does not discount a nociceptive component contributing to symptoms and sensitization. Physical examination will provide further clarification, as will initial treatments and re-assessments.

Clinical reasoning regarding potential ‘sources of symptoms’ (i.e. specific structures/tissues involved and pathology) is relevant to nociceptive- and/or neuropathic-dominant presentations and needs to be balanced with impairment-focussed reasoning. Although the validity of the clinical examination to differentiate specific sources of nociception and pathology is usually limited, these can still be hypothesized on the basis of common clinical patterns (involving area, behaviour and history of symptoms and later physical findings). We know pathology in general does not typically correlate well with the clinical presentation (i.e. pathology can be asymptomatic; pathology can have varied clinical presentations; symptoms can exist without overt pathology) – hence the importance of impairment-focussed assessment and management. However, despite these limitations, pathology should still be hypothesized because potential serious and sinister pathology has implications for safety (e.g. specific physical testing or referral for further investigation as with, for example, subjective features of craniovertebral instability, cervical arterial dysfunction, or neurological involvement). Potential ‘sources of symptoms’ and ‘pathology’ hypothesized from the subjective examination can then be correlated with symptomatic and asymptomatic impairments in posture, mobility, palpation and muscle control/strength from the physical examination to generate further hypotheses regarding joint, muscle, soft tissue, neural and vascular impairments that may require treatment.

1. 3. Please discuss how your reasoning regarding dominant ‘pain type’ and possible ‘sources of symptoms’ from the subjective examination has been supported or not supported by your physical examination findings.

Fig. 23.2 presents an overview of the categories of problems considered and Sabrina’s positive findings. Her physical examination revealed impairments in the mid- and upper cervical spine, which might activate the nociceptive system and/or stimulate the sensitized pain-modulating system. The major one was hypomobility at C2–C3 that was correlated with Sabrina’s neck pain. In this segment, the gliding of the right inferior articular process of C2 in a dorsal–caudal direction seemed limited, possibly due to an articular capsular restriction. Furthermore, muscle activation in this segment seemed to be reduced, perhaps due to inhibition by nociception/pain (Lund et al., 1991; Arendt-Nielsen and Graven-Nielsen, 2008; Arendt-Nielsen and Falla, 2009).

Because Sabrina could not reproduce her headache and associated symptoms in any specific movement or position, it was not possible to correlate them through the specific symptom localization tests to selected segments of the cervical spine. Therefore, it was unclear at this stage whether these impairments were related to her symptoms or not.

Theoretically, many structures can provoke headache and neck pain:

• • The zygapophyseal joint of C2–C3 is often a structural cause of neck pain with headache, as confirmed by local anaesthesia in patients with idiopathic neck pain (Bogduk and Marsland, 1988) and with neck pain after whiplash injury (Lord et al., 1996).
  
• • Headache activated by segment C2–C3 is often associated with headache and irradiating pain from segment C0–C1 (Watson and Drummond, 2012, 2014).
  
• • The intervertebral discs from C2–C3 down to C6–C7 can cause cervicogenic headache and neck pain, as confirmed by discography (Slipman et al., 2005).

Thus, theoretically and based on the examination findings, possible involvement of dysfunction in the segments C2–C3, C0–C1 and C5–C6 had some support.

The differentiation between migraine, tension-type, cervicogenic or other types of headache is not an aim of our examination. Clinical tests for impairments, such as movement restrictions from C0 to C4 and motor control/strength impairments in the cranio-cervical flexion (CCF) test, allow differentiation of cervicogenic headache from migraine and tension-type headache with 100% sensitivity and 94% specificity (Jull et al., 2007). However, migraine and tension-type headaches can also be positively influenced by manual therapy of the cervical spine, similar to cervicogenic headache (Watson, 2014). Consequently, the usefulness of headache type differentiation can be questioned. All of Sabrina’s physical impairments listed previously might therefore suggest musculoskeletal manual techniques could positively influence her symptoms.

However, because Sabrina’s symptoms cannot be evoked with most physical assessments, it is unlikely she only has a simple nociceptive pain problem. A nociplastic pain type is further supported and might explain why afferent activity from these common impairments provokes the significant symptoms Sabrina has been suffering. This sensitization might affect her pain-modulating system, resulting in persistent pain, as well as her neurovegetative system, producing sensations of dizziness, nausea and tunnel vision. The contribution of each of Sabrina’s impairments will be assessed further through a systematic process of manual trial treatments.

1. 4. Based on both the subjective and physical examination findings, do you have any hypotheses regarding possible ‘contributing factors’ to the development and/or maintenance of Sabrina’s symptoms and disability?

Clinical reasoning is not an exact science, and hence judgements are best considered as hypotheses. The complexity of interpreting patient information is evident in, for example, the influence judgements regarding dominant pain type have on judgements regarding potential sources of symptoms. As discussed in Chapter 1, nociplastic pain can create local false-positive provocation of symptoms suggestive of tissue nociception/pathology. As such, a challenge of interpreting physical findings is ensuring they are analyzed within the broader picture of the patient’s full presentation and hypothesized dominant pain type. Whether the physical impairments should be treated initially as per the trial treatment planned here or whether other interventions more broadly addressing the pain-modulating system should be addressed first will elicit ongoing discussion and debate. However, from a reasoning perspective, what we feel is essential is that, as occurs here, whichever path clinicians take, they view their judgements regarding pain type and sources of symptoms as hypotheses and carefully monitor the effects of any intervention (passive, active, educational) on the patient’s disability and symptoms, including the patient’s activity and participation restrictions and capabilities, the patient’s perspectives on his or her experience and key physical impairments.

1. 5. Would you please briefly explain your use of a ‘trial treatment’ in the context of Sabrina’s case?

The summary of Sabrina’s positive findings highlighted in Fig. 23.1 is categorized according to pain, inflammation and movement/posture dysfunction. The question is which finding in which category should be addressed first to most efficiently establish their relevance to her symptoms. Treatment directed to mechanical dysfunction has the potential to provide a relatively quick answer, whereas treatment directed to sensitization of the pain-modulating system in the form of progressive movement training would take considerably longer (e.g. several weeks). Because of the high irritability of Sabrina’s symptoms, the mechanical treatment needed to be gentle and progressed slowly. A curious finding was the change in the direction of the hypomobility at C2–C3 from the right to the left side. This points more to a functional limitation instead of a structural restriction such as capsular tightness.

Traction of the zygapophyseal joint was chosen as a trial treatment because it is an effective technique for neck pain (Schomacher, 2009).

1. 6. You indicated that the trial treatments directed at posture/movement dysfunction would be used to assess the contribution of these physical findings and the involvement of local tissue nociception in Sabrina’s presentation. Would you please discuss how these trial treatments and the associated re-assessments have informed that reasoning?

Nociceptive afferent activity from the segments of the upper cervical spine arrive at the trigemino-cervical nucleus, where they might cause symptoms like headache, dizziness and nausea (Bogduk, 2004). This short-term relief indicated that the segment C0–C1 might provide an area where treatment could positively influence Sabrina’s symptoms. However, her reaction to the treatment that evening and next day would need to be assessed prior to making such a decision.

Traditional manual therapy may have interpreted upper cervical segmental hypomobility, associated with examination-elicited provocation of local pain, as sufficient evidence that the tissues of that segment are responsible for the pain (i.e. nociception). Although this is still reasonable when the pain type is nociceptive dominant, the greater the likelihood of nociplastic pain the more likely the segmental provocation of pain represents an allodynic mechanosensitivity, particularly if the hypomobility is minor and variable. As noted in the previous commentary, the debate about the place for manual therapy (even as trial treatments) versus hands-off interventions for chronic pain presentations is inevitable and important given our growing understanding of pain science (see Chapter 2) but also considering our lack of sufficient research to understand the benefits of differing and combined interventions for different pain types. All therapies will have CNS influences, and this is reflected in the previous interpretation that ‘the segment C0–C1 might provide an area to positively influence Sabrina’s symptoms’, as opposed to claiming C0–C1 is the source of her pain and as such requires mobilization. Although there is growing evidence for pain neuroscience education and cognition-targeted exercise in the management of chronic nociplastic pain (Louw et al., 2018; Moseley and Butler, 2017; Nijs et al., 2014), manual therapy may also prove to be an additional adjunct to the desensitization of symptoms, provided it too is cognition-targeted and combined with appropriate education and activity promotion strategies.