Most practitioners continue to take post-graduate courses or attend professional conferences to improve their knowledge pertaining to clinical theory and research (propositional) as well as their technical skills (non-propositional or craft); however, Rivett & Jones (2004) note that there is a tendency in both courses and conferences to neglect an essential component of daily clinical practice – clinical reasoning. How should the practitioner integrate into clinical practice the newly learned scientific and theoretical knowledge? Who is it appropriate for and when is the new skill appropriate to use? Clinical practice is, and always will be, a blend of science and ‘art’ with a healthy dose of logic and reasoning. Clinical expertise comes from reasoning, reflection, skill acquisition and the continual life-long pursuit of knowledge (propositional (declarative) and non-propositional (procedural and personal)) (Figure 7.1) (Jensen et al. 2007). This takes time, discipline and often mentorship and professional affiliation with both individuals and groups.

Figure 7.1 • Five components for the development of clinical expertise.

Adapted from Jensen et al. (2007) Expertise in Physical Therapy Practice, second ed. Saunders.

Recently, for best practice, there is increasing pressure for practitioners to become evidence-based when making all clinical decisions. However, it appears that this term, evidence-based practice, means different things to different people. What is evidence-based practice and what is its history?

Evidence-based practice: Where did it come from? Where is it going?

The term ‘evidence-based’ was first used in 1990 by David Eddy and ‘evidence-based medicine’ by Guyatt et al. in 1992. The methodologies used to determine ‘best evidence’ were largely established by the Canadian McMaster University research group led by David Sackett and Gordon Guyatt. Professor Archie Cochrane, a Scottish epidemiologist, has been credited with increasing the acceptance of the principles behind evidence-based practice (Cochrane 1972). Cochrane’s work was honoured through the naming of centres of evidence-based medical research, Cochrane Centers, and an international organization, the Cochrane Collaboration. Since the early 1990s there has been an explosion of research evidence, and accessibility to this evidence has been facilitated for those involved in research or formal study through easy internet access to full-text articles in indexed journals. Unfortunately, access to full-text articles is still limited, or expensive, for clinicians not affiliated with research centres or universities.

Evidence-based medicine categorizes and ranks the different types of clinical evidence. The terms ‘levels of evidence’ or ‘strength of evidence’ refer to the protocols for ranking the evidence based on the strength of the study to be free from various biases. The highest level of evidence for therapeutic interventions is a systematic review, or meta-analysis, including only randomized, double-blind, placebo-controlled trials that involve a homogeneous patient population and condition. Expert opinion has little value as evidence and is ranked the lowest due to the placebo effect, the biases inherent in both the observation, and reporting of the cases and difficulties in discerning who is really an expert.

Evidence-based practice (EBP) embraces all disciplines of health care (not just medicine) and has become synonymous with best practice, but what does the term really mean? To some, it appears that EBP means that a clinician can only use assessment tests and treatment techniques/protocols that have been validated through the scientific process with high-ranking studies as valued by the ‘levels of evidence’. This is difficult to adhere to for many reasons, one being that there is not enough evidence at this time. Indeed, could there ever be enough scientific evidence for every situation met in clinical practice? Sackett and colleagues define EBP as ‘the integration of best research evidence, with clinical expertise and patient values’ (Sackett et al. 2000) (Figure 7.2). They note that:

External clinical evidence can inform, but can never replace individual clinical expertise, and it is this expertise that decides whether the external evidence applies to the patient at all, and if so, how it should be integrated into a clinical decision.

Figure 7.2 • The three components of evidence-based practice as defined by Sackett et al. (2000)

Clinical expertise, as noted above, comprises both propositional (declarative) and non-propositional (procedural, craft and personal) knowledge; in other words, knowing what, and how, to do the right thing at the right time (clinical reasoning and skill). The type of knowledge gained from scientific studies contributes to building only one kind of knowledge. In EBP according to Sackett et al.’s definition, clinical expertise plays an equal role alongside the research evidence. A third component of EBP is the patient’s values and goals, which come from the person for whom all of the research and expertise is intended to help.

Recently, the term ‘evidence-informed’ has surfaced, the intent being to suggest that since there is not enough research evidence for every situation met in clinical practice, the clinician should be informed of what is known and make their clinical decisions accordingly. However, if we adopt Sackett et al.’s definition of EBP, there is no need to modify the term since clinical expertise (reasoning and skill) is considered part of the definition of best practice.

Understanding pain: What do we need to know?

Understanding the neurophysiology of pain mechanisms is essential knowledge for treating patients with pelvic pain. Since the proposal of the gate control theory of pain by Melzack and Wall in 1965, significant advances in pain research and therapy have occurred. It is not our intent to provide an in-depth coverage of this topic here, but instead to highlight key features and establish a common language to be used throughout this chapter. See Chapter 3 for a full discussion of pain mechanisms in general, and as these relate to chronic pelvic pain.

What causes pain? Searching for the pain driver

The search for ‘the pain driver’ in peripheral tissues began when Descartes, in the 17th century, proposed that specific pathways existed from the peripheral tissues to the passive brain to transmit information notifying the brain of tissue injury. The premise that injury of the tissues (ligaments, connective tissue, bones, nerves, organs, etc.) is the cause of pain is the basis of the pathoanatomical or biomedical model of pain, and has prevailed in the assessment and treatment of pain until quite recently. This model has led to research and increased understanding about nociception, including the stimuli that can cause it (mechanical, thermal and chemical), which peripheral tissues can be painful and the pain patterns they generate. Clinicians believed that if the tissues could heal or be fixed (by whatever means, including by anaesthetic injection, anti-inflammatory medication, or removal of the offending tissue), then nociception would stop, the pain would go away, and the patient would recover function.

It is now well recognized that the pathoanatomical model is limited in several ways. Pelvic pain commonly exists in the absence of any findings on diagnostic tests (X-ray, CT scan, blood tests, nerve conduction tests, etc.), and damaged tissues can be identified in people who experience no pain (Nachemson 1999, Waddell 2004). Tissues heal and yet the pain experience persists. Furthermore, a focus on only treating ‘the painful tissue’ neglects to consider that other systems or structures, which may be dysfunctional but painfree, could be the underlying cause of excessive mechanical stresses on the painful structures, or the cause of decreased blood flow or nutritional supply. In order to resolve the pain, the painfree but impaired structures or systems need to be treated for long-term resolution. Identification of what tissue hurts does not provide insight as to why it hurts. Finally, significant developments in neuroscience have changed our understanding of what pain is, and have required us to reframe and change our thinking.

We now understand that at any time in one patient there are many ‘pain drivers’ that do not exist solely in the peripheral tissues. Rather than looking for one source of pain, we need to consider that multiple mechanisms are at play in the experience of pain in all our patients. These mechanisms can be broadly separated into peripherally mediated (nociception and peripheral neurogenic pain) or centrally mediated (related to processing in the central nervous system (CNS)) (Butler 2000), and will be discussed in more detail later in this section.

Classifying pain

Timelines and mechanism of injury

Patients are commonly classified according to the timeline or duration of their pain experience, and the cause or mechanism of their injury. In general, problems are considered to be acute if they are within the first 6 weeks to 3 months (depending on the type of tissue injured) after an initiating incident (Brukner & Khan 2002, Magee et al. 2007). Tissue injury results in a known sequence of events aimed at protecting and repairing the damaged structures. These stages of tissue healing occur in three overlapping stages that have been given multiple names but refer to the same processes:

1. Acute inflammatory stage;

2. Subacute or proliferation stage;

3. Chronic or maturation and remodelling stage.

The term chronic is often used to indicate the persistence of pain beyond the normal timeline for tissue healing (Bonica 1953, Merskey & Bogduk 1994), as opposed to a stage of the tissue-healing process. In the Classification of Chronic Pain (Merskey & Bogduk 1994) published by the International Association for the Study of Pain, it is noted that the normal time of healing ‘may be less than one month, or more often, more than six months. With nonmalignant pain, three months is the most convenient point of division between acute and chronic pain, but for research purposes six months will often be preferred.’ Chronic pain is also further outlined as ‘a persistent pain that is not amenable, as a rule to treatments based upon specific remedies, or to the routine methods of pain control such as non-narcotic analgesics’ (Merskey & Bogduk 1994).

More recently, the term persistent low back pain has emerged in the literature, to indicate pain that continues past the expected timeframe for tissue healing. Others are suggesting that acute episodes of low back pain would be better termed recurrent episodes in a chronic problem as the underlying mechanisms contributing to recurrent low back pain are likely to be different from a first-time traumatic episode of low back pain, and recurrence of pain after an acute episode is a common problem (Pengel et al. 2003).

Acute pain, especially when related to a specific initiating incident, is commonly perceived as being relatively straightforward in terms of what pain mechanisms are at play. These are generally accepted to be types of peripherally mediated pain (nociceptive or peripheral neurogenic) related to tissue damage and the resultant inflammatory processes are aimed at restoring homeostasis in the body. However, is any pain experience truly simple? Consider the following report:

A builder aged 29 came to the accident and emergency department having jumped down on to a 15 cm nail. As the smallest movement of the nail was painful he was sedated with fentanyl and midazolam. The nail was then pulled out from below. When his boot was removed a miraculous cure appeared to have taken place. Despite entering proximal to the steel toecap the nail had penetrated between the toes; the foot was entirely uninjured.

(Fisher et al. 1995)

The initial logical hypothesis in this case was that acute trauma to the foot was causing severe nociceptive input from the damaged tissues. However, as physical examination revealed completely intact tissues, this cannot explain the patient’s pain experience. Clearly other pain mechanisms were at play, despite the timeline (acute onset) and mode of onset (traumatic) of the pain.

Empirical evidence now exists to explain these kinds of stories. A consistent factor that has emerged from the pain sciences is that the meaning of the pain experience, and especially the threat value of the experience, is significant. In other words, does the pain signify something harmful or not? While some may continue to function and keep going in spite of pain, others are completely debilitated by the mere thought of the sensation. There is increasing evidence to support that an individual’s experience of pain is significantly influenced by the way they think and feel about the situation as a whole, regardless of the severity of tissue injury. The story above illustrates these influences; his pain experience is an example of 100% centrally mediated pain, driven by his beliefs (cognitive dimension) and emotional state (affective dimension) related to the event (having a nail driven through his boot). It is clear that we cannot separate the tissues from the person to which they belong; we are integrated beings and our experience of our body (whether positive or negative) is the result of complex interactions and processes occurring in the brain.

Thus, although the mechanism of onset and timeframes related to the pain experience are important to know, we must take care that this information does not lead us to assume that certain timelines necessitate certain pain mechanisms. Acute pain can be largely driven by central mechanisms. Persistent pain can also be largely driven by peripheral mechanisms. That is, persistent or chronic pain states may have central components, but these are not necessarily the dominant mechanism for every patient simply because the pain experience has persisted for a long period of time. While evidence supports that ‘the relationship between pain and the state of the tissues becomes less predictable as pain persists (Moseley 2007), we need to remember that the pain experience is uniquely individual. Regardless of whether the pain is a newly occurring event or a persistent experience, it is a multidimensional experience, and thus any person presenting with pain should be evaluated with a framework in mind that allows for the consideration of all these factors. As Butler (2000, p. 53) notes:

Overlap of mechanisms is the key feature because the boundaries are often fuzzy. There will be differing contributions of mechanisms to the injury state over time, person and injury.

Classification by pain mechanisms

So what are the different biological mechanisms that drive the pain experience? Pain mechanisms can be further categorized (Gifford 1998, Butler 2000) as they relate to:

1. Input into the nervous system;

2. Processing in the nervous system;

3. Output from the nervous and other systems.

The brain receives continuous information from the body and the environment (input mechanisms or all sensory pathways) that is assessed and interpreted (processing at both conscious and unconscious levels) prior to producing a response (output mechanisms). Some of this incoming information is nociceptive. There are many factors that determine an individual’s behaviour and pain experience (physical, cognitive, emotional) in response to nociceptive input, including:

• Contextual factors of the immediate circumstance (i.e. how dangerous is this sensation in the light of environmental and internal factors?); as well as

• Past experiences and personal knowledge that collectively contribute to the individual’s beliefs, attitudes, emotions and physical responses.

Input mechanisms as they pertain to pain include all the sensory information reaching the CNS from the body internally and externally. This includes nociceptive pain from tissues including bones, ligaments, tendons, muscles, connective tissue, viscera, etc. (Gifford 1998, Butler 2000, Wright 2002) and peripheral neurogenic pain from neural tissue outside of the CNS. Processing occurs in the dorsal root ganglion and in the CNS. In the brain, an individual’s thoughts and feelings (cognitions + emotions = perception) are integrated and can influence the output mechanisms, which include:

1. Somatic or motor (altered posture, altered motor control);

2. Autonomic (increased sympathetic response for ‘fight or flight’);

3. Neuroendocrine (increased stress, heightened emotions, hormonal changes);

4. Neuroimmune.

Thinking within the context of stress biology creates a broader framework for understanding pain. Gifford (1998), in proposing the Mature Organism Model (Figure 7.3), notes that

… the sensation of pain is seen as a perceptual component of the stress response whose prime adaptive purpose is to alter our behaviour in order to enhance the processes of recovery and chances of survival. Stress biology and the stress response broadly considers the systems and responses concerned with maintaining homeostasis.

(Gifford 1998)

Figure 7.3 • The Mature Organism Model of Gifford (1998).

Adapted from Rivett & Jones (2004). Improving clinical reasoning in manual therapy. In: Jones, M.A., Rivett, D. (Eds.), Clinical reasoning for manual therapists, Churchill Livingstone; and Gifford (1998) Physiotherapy 84:27.

It has been proposed that continued activation of the stress-regulation systems and excessive or prolonged cortisol output has a destructive effect on peripheral tissues such as muscle, bone and nerve tissue, thereby perpetuating a vicious cycle of stress, pain and tissue injury (Melzack 2005).

In his Neuromatrix Theory of Pain, Ronald Melzack (2001, 2005) highlights the need to assess and treat the whole person, not just the painful parts.

The body is felt as a unity, with different qualities at different times. … [Together all outputs] produce a continuous message that represents the whole body [which he also describes] as a flow of awareness.

(Melzack 2001, 2005)

Melzack’s model has four components (2001, 2005):

1. The body-self neuromatrix – an anatomical substrate in the brain of the body-self;

2. Cyclical processing and synthesis of nerve impulses which produces a neurosignature;

3. The flow of neurosignatures is projected back to areas of the brain, the sentient neural hub, which converts them into the flow of awareness;

4. Activation of an action neuromatrix occurs to provide the pattern of movements to bring about the desired goal.

The neuromatrix, distributed throughout many areas of the brain, comprises a widespread network of neurons which generates patterns, processes information that flows through it, and ultimately produces the pattern that is felt as a whole body. The stream of neurosignature output with constantly varying patterns riding on the main signature pattern produces the feelings of the whole body with constantly changing qualities…. The final, integrated neurosignature pattern for the body-self ultimately produces awareness and action.

(Melzack 2005)

Figure 7.4 is a modification of Melzack’s representation of the body-self neuromatrix to illustrate the sensorial, cognitive and emotional dimensions of pain. Perhaps the best summary for this section highlighting the broad view we need to take when considering pain comes from this leader in the study of pain himself, Ronald Melzack (2001):

We have traveled a long way from the psychosocial concept that seeks a simple one-to-one relationship between injury and pain. We now have a theoretical framework in which a genetically determined template for the body-self is modulated by the powerful stress system and the cognitive functions of the brain, in addition to the traditional sensory inputs. The neuromatrix theory of pain – which places genetic contributions and the neural-hormonal mechanisms of stress on a level of equal importance with the neural mechanisms of sensory transmission – has important implications for research and therapy. The expansion of the field of pain to include endocrinology and immunology may lead to insights and new research strategies that will reveal the underlying mechanisms of chronic pain and give rise to new therapies to relieve the tragedy of unrelenting suffering.

Figure 7.4 • An adaptation of Melzack’s Body-Self Neuromatrix (Melzack 2001, 2005). HPA, hypothalamic–pituitary–adrenal

It is very clear that as clinicians we need to be aware of all the possible mechanisms that can create pain and to challenge ourselves to have an open mind as we seek to understand each individual’s unique pain experience in order to determine which mechanisms are primary and specifically related to their problem in all stages of their rehabilitation process.

Classification and clinical prediction rules: Are we searching for the holy grail?

Given the multidimensional nature of pain, it is not surprising that using pain presentation (location, duration, onset) as the sole means to classify patients and determine best treatment has been ineffective. Fritz and colleagues report that despite over 1000 randomized clinical trials investigating the effectiveness of interventions for the management of low back pain, ‘the evidence remains contradictory and inconclusive’ (Fritz et al. 2007). One key reason believed to contribute to this state of the evidence is the lack of classification of low back pain patients into subgroups, not only for studying treatment efficacy, but also for determining aetiological and prognostic factors (Leboeuf-Yde et al. 1997, Riddle 1998, Gombatto et al. 2007).

Sahrmann in the late 1980s noted:

As we all know, general diagnoses such as low back pain or hip pain do not often relate to the cause or to the underlying nature of the condition.

(Sahrmann 1988)

As clinicians have long recognized, it is now widely accepted that patients with pain do not form homogeneous populations, but consist of multiple subgroups with different combinations of underlying impairments (physical and psychosocial), and these subgroups require different treatment approaches for best outcomes. Furthermore, given that multiple factors contribute to pain, it is also unrealistic to expect that one single type of treatment modality will resolve a patient’s presenting pain and functional limitations. Thus, the pursuit of valid ways to identify subgroups of patients with pain has become an increasingly prominent theme in the literature over the last three decades.

The classification for lumbopelvic pain has evolved since the pathoanatomically based classification of MacNab (1977) with a variety of patient characteristics proposed for use in creating homogeneous subgroups (McKenzie 1981, Kirkaldy-Willis 1983, Bernard & Kirkaldy-Willis 1987, Coste et al. 1992, Delitto et al. 1995, Sahrmann 2001, O’sullivan 2005, Reeves et al. 2005, Fritz et al. 2007, O’sullivan & Beales 2007) (Table 7.1).

Table 7.1 Multiple proposals for the classification of patients

Model/system	Description	Diagnostic/classification determinants
Pathoanatomical (McNab 1977, Kirkaldy-Willis & Hill 1979, Kirkaldy-Willis 1983, Nachemson 1999)	Focuses on structural changes which occur as a consequence of inflammation, infection, metabolic disorders, trauma and/or disease (pathology-based)	Radiological diagnosis, blood work
Mechanical diagnosis and therapy (The McKenzie Method) (McKenzie 1981)	Directional preference and centralization or peripheralization of pain with repeated movements. Four subgroups: • derangement syndrome • dysfunction syndrome • posture syndrome • other	Rapidly reversible symptoms with repeated movements in a specific direction
Peripheral pain generator model (Laslett & Williams 1994, Laslett et al. 2005)	Attempts to identify the painful peripheral pain-generating structure with the main therapeutic intervention being to block or denervate the nociceptive source	Diagnostic blocks of various peripheral structures seeking to relieve pain
Neurophysiological pain model (Butler 2000)	Generation and maintenance of pain both peripherally and/or centrally mediated (central and/or peripheral sensitization of neural networks)	Subjective examination (confirmed/negated by features of the objective examination)
Psychosocial model (Waddell 2004)	Cognitive and emotional factors such as negative thinking, fear-avoidance behaviours and hypervigilance	Subjective examination
Treatment-based Classification System (Delitto et al. 1995) updated criteria (Fritz et al. 2007)	Intended for patients with acute/acute exacerbation of low back pain (LBP). Patients placed into treatment categories based on patterns of signs and symptoms: • manipulation • specific exercise (flexion, extension, lateral-shift patterns) • stabilization • traction	Subjective examination, objective examination features based on clinical experience and propositional knowledge. Specific exercise grouping based primarily on centralization/peripheralization principles (McKenzie 1981). Updated criteria include disability questionnaire data and is based on CPRs and scientific research. Traction group removed in updated classification
Movement System Impairment System (Sahrmann 2001)	Based on the kinesiopathic model of movement; musculoskeletal pain develops as a result of repeated movements and postural alignments in the same direction across daily activities, causing repeated loading and microtrauma. LBP subgroups: • lumbar flexion • lumbar extension • lumbar rotation • lumbar rotation with flexion • lumbar rotation with extension	Subjective and objective examination aimed to identify the direction of movement and alignment that is related to LBP. Symptoms are monitored in response to standardized movement and alignment tests, along with observation of timing of relative motion of body segments, and the response to modification of alignment/movement

O’sullivan (2005) noted that a limitation of many classification systems is that often only a single dimension (pathoanatomical, psychosocial, neurophysiological, motor control, signs and symptoms, etc.) is used to create subgroups. Classification systems will be most useful in clinical practice if variables across multiple domains are used to create subgroups.

Features that have been incorporated into different systems include (note this is not intended to be an exhaustive list):

• Presence or absence of identifiable underlying pathology (pathoanatomical, peripheral pain generator models);

• Pain presentation (central, unilateral, with or without radiation of symptoms to the lower extremity) (signs and symptoms models);

• Underlying pain mechanisms/neurophysiology;

• Response of pain to movement (centralization or peripheralization) (signs and symptoms models) (movement impairment models);

• Physical impairments such as loss or increase of mobility, altered motor control, altered posture/spinal alignment, and the relationship of symptom provocation to these impairments (motor control models, signs and symptoms models, movement impairment models);

• Response to specific treatments (manipulation, stabilization exercises, specific exercises, traction); and

• Psychosocial and cognitive features such as fear avoidance, coping strategies and beliefs (biopsychosocial models).

In recent years, the development of clinical prediction rules (CPRs) has emerged as another way to classify patients. CPRs are derived statistically with the aim of identifying the combinations of clinical examination findings that can predict a condition or outcome. Thus, they are proposed to be a useful tool to assist in clinical decision-making by improving the accuracy of diagnosis, prognosis or prediction of response to specific treatment protocols (Beattie & Nelson 2006, Cook 2008, Fritz 2009). Development of CPRs in physiotherapy has mainly focused on the response to treatment protocols (Fritz 2009) in order to identify subgroups of patients most likely to respond to a specific treatment approach. It is important to note that, at this time, CPRs are still in their infancy of development and validation, and are not yet at the appropriate stage to be widely applied in clinical practice (Cook 2008).

It has been suggested that CPRs will best impact physiotherapy practice where there is complexity in the clinical decision-making process, and that ‘an appeal of CPRs is their potential to make [the] subgrouping process more evidence based and less reliant on unfounded theories and tradition’ (Fritz 2009). However, the use of CPRs should be balanced with the knowledge that:

Clinical prediction rules provide probabilities of a given diagnosis or prognosis but do not necessarily recommend decisions. Clinical prediction rules can be of great value to assist clinical decision-making but should not be used indiscriminately. They are not a replacement for clinical judgment and should complement rather than supplant clinical opinion and intuition.

(Beattie & Nelson 2006)

Research on specific subgroups and development of classification systems will definitely provide a much better understanding of the specific impairments, mechanisms and psychosocial features that characterize subgroups and their response to treatment. As Melzack wrote about the evolution of the gate control theory of pain:

As historians of science have pointed out, good theories are instrumental in producing facts that eventually require a new theory to incorporate them.

(Melzack 2001)

However, it is important to recognize that there are limitations on how information gained from classification systems, CPRs, clinical trials, and indeed the findings of any scientific study, can be translated and applied to the reality of clinical practice. Firstly, statistical averages tell us about the average response of the group defined by the characteristics used in design of the study. Individual responses may be to a greater or lesser degree than the average, or even in the opposite direction of the reported response. Indeed, practising clinicians are well aware of the many patients they have seen who do not fit the data from clinical trials or other studies. These clinical cases provide valuable insight and can generate questions for further research. Secondly, while the data provide relatively unbiased information, the interpretation and conclusions made from the data, and published alongside the data, are subject to bias just as much as clinical opinion is subject to bias. It is also important to recognize that a lack of data or science does not invalidate a technique or approach, nor does it mean that approaches that have been studied are necessarily superior. In clinical practice, application of any classification system/CPR requires care to ensure that it does not create a rigid, narrow mindset. Placing the patient ‘in a box’ could prevent the clinician from considering other options for treatment that may be greatly beneficial. Neglecting to provide these other options could then result in sub-optimal outcomes.

Consider the one domain of underlying pain mechanism as a way to create subgroups.

Butler (2000) notes that:

The word “division” can be instant trouble because these mechanisms all occur in a continuum. All pain states probably involve all mechanisms, however in some, a dominance of one mechanism may become obvious. Pain mechanisms are not diseases or specific injuries. They simply represent a process or biological state.

In their classification of pelvic pain disorders, O’sullivan & Beales (2007) categorize non-specific pelvic pain disorders into two groups: one that has centrally mediated pain, and one that has peripherally mediated pain. Although the group of centrally mediated pain is further classified into those with non-dominant psychosocial factors and those with dominant psychosocial factors, the treatment protocol for the subgroup of centrally mediated pelvic girdle pain is medical management (central nervous system modulation), psychological (cognitive-behavioural therapy), and functional capacity rehabilitation. Specific interventions directed at identified physical impairments in the periphery are not recommended, and yet it is highly unlikely that many patients will have 100% centrally mediated pain. In the authors’ experience, even in patients with a strong contributor of central sensitization to their pain experience, careful assessment often reveals specific meaningful tasks that relate to a consistent reproduction of symptoms. It is reasonable to suggest that even if peripheral mechanisms only contribute 20% to the complete picture, addressing that 20% in addition to the other approaches will provide the greatest chance for the best outcome. Furthermore, it is likely that by addressing the physical impairments, psychosocial variables will also be impacted, further advancing the goals of treating drivers of central sensitization. It is also crucial to recognize that our patients change as a result of their changing life circumstances and our interactions with them (both physical and personal). Thus, during the course of treatment continual re-evaluation is necessary to adapt the treatment programme accordingly. Sticking to a rigid plan based on an initial placement into a subgroup may result in the provision of sub-optimal care.

Finally, in our quest for better classification schemes and science to support and test our clinical approaches, it is important to remember that at the end of the day no matter how detailed and well defined our classification schemes, the person presenting to the clinician is a unique individual

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