Chronic pain: a consequence of dysregulated protective action

Abstract

Introduction:

Pain is considered to be one of a number of idiosyncratic, context-dependent ‘protective actions’ projected into the conscious domain by the central nervous system (CNS), as a result of a series of complex interactions in response to perceived threat. A model is described which proposes chronic pain and a variety of long-term, systemic functional neurological conditions to be a consequence of significant dysregulation of these protection systems.

The Model:

Previous research has demonstrated that a cognitive–behavioural model, first described in 1995 by Surawy et al., for chronic fatigue has been successful in predicting the transition from acute to chronic states in a number of conditions. This model includes predisposing, precipitating and perpetuating biopsychosocial factors. This article discusses the potential role of these factors in affecting descending inhibition in the CNS, significantly altering its ability to modulate the threat detection system. The development of ‘central sensitisation’ is considered in this context.

Conclusion:

This model proposes that chronic pain, chronic fatigue and other so-called functional neurological phenomena can, perhaps, be more helpfully seen as the actions of a dysregulated neurological protection system, rather than symptoms of an untreatable and deteriorating medical condition. Recommendations are made for the development of appropriate therapeutic interventions indicated by this model.

Introduction

Chronic pain is a complex, varied and potentially debilitating phenomenon, associated with biological, physiological, psychological, emotional, social and environmental factors and there is a comprehensive literature describing this.^1–6 Pain continues to reveal itself to be the product of a series of complex interactions between multiple systems, as predicted by Wall⁷ in 1994. Studies indicate that chronic pain is a particularly idiosyncratic, complex, context-dependent, emergent experience.^8,9 This article presents a model of chronic pain that draws particular attention to some psychological and behavioural aspects, but maintains a systemic focus and places emphasis on the need for a biopsychosocial framework. As indicated by the collaboration that resulted in the Gate Control Theory,¹⁰ a truly comprehensive model of (chronic) pain is only likely to emerge from a significant multidisciplinary research effort that is yet to come.

Psychological interventions for chronic pain have shown promise; however, more recent systematic reviews of published studies^11–13 revealed only limited success beyond some short-term gains. The reviews indicate a need to clarify the mechanisms involved in the development and maintenance of chronic pain and to identify targets for interventions that may lead to more sustainable outcomes.

Central to the model presented in this article is the concept of a human central nervous system (CNS) that has evolved to detect and manage threat.¹⁴ The proposal builds on the idea that complex biopsychosocial regulation systems, both under and beneath conscious control, in the middle and higher brain, produce degrees of descending inhibition over the powerful threat detection systems in the spinal cord and brain stem.^14–16 This process is here referred to as ‘modulation’ over the constant flow of information about the environment and body status, including nociception. The interaction of these processes will, at times, result in the projection of sensations such as pain, thirst, hunger, fatigue or anxiety into consciousness, in order to draw attention to potential or actual threat to the body integrity and prompting a behavioural response. In this context, chronic pain is hypothesised to be the consequence of a significant impairment in the wider systems recruited into the process of modulation, resulting in a dysregulated system.

The term ‘protective action’ is used to refer to the output into the conscious domain, which, it is proposed here, can take a number of forms. Which manifestation this protective action takes is likely to depend on the individual and the context they live in. Thus, pain, anxiety, fatigue and systemic effects which mimic neurological phenomena such as seizures or the kind of idiosyncratic total shut down of ‘Resignation Syndrome’, only seen in child refugee populations in Sweden,¹⁷ are all proposed here as potential, context-dependent protective actions.

Observations

Chronic pain is not a well-defined, uniform condition, but clinical experience suggested that the histories and profiles of many people with chronic pain seen in a number of specialist pain clinics appeared to have a ‘goodness of fit’ with the predisposing, triggering and maintenance factors proposed by Surawy et al.¹⁸ for chronic fatigue syndrome (CFS). Van Houdenhove et al.¹⁹ have suggested ‘over-activity’ as a behavioural propensity of people with chronic pain, but previous systematic research on this characteristic was inconclusive.²⁰ However, increasing numbers of people seen in specialist pain services across the United Kingdom, with both widespread chronic pain and fatigue, often labelled as fibromyalgia syndrome (FMS), suggested the exploration of the CFS model and possible relevance to chronic pain.

The model

Figure 1 shows a representation of the suggested biopsychosocial modulation of the threat detection system, as if it was acting on a metaphorical balance switch in a circuit. The switch is not envisaged as a binary ‘on or off’ mechanism, but a graduated analogue system, like a potentiometer controlling gain or volume, with the level of output depending on the proximity of the contacts.

Figure 1.

A regulated system.

This model assumes constant input from a threat detection system that is always ‘on’; however, when modulation regulates it effectively, the ‘contact’ at the other end of the metaphorical balance switch is left open, not completing the ‘circuit’ and not producing protective action. Should the input of the threat detection system increase, resulting from a change of state, such as through injury, where increases in nociceptive and inflammatory activity may amplify this input, overcoming the modulation, then the balance switch will tip, moving the ‘contacts’ closer together, releasing appropriate degrees of protective action, which might be experienced as pain in the periphery. As normal healing takes place and the inflammation and nociceptive activity reduce, the proximity of the contacts in the metaphorical circuit move apart and the protective action or pain reduces.

The disabling impact of the protective action may be greater if, in addition to the increased input from the threat system, modulation is reduced by the temporary removal of some other proposed factors affected by the protective action, such as sleep and the ability to relax (see Figure 2). However, if enough components of the suggested modulation system, such as the ability to express emotion and manage activity effectively, are present in the system, there is likely to be a gradual restoration of equilibrium. In the case of an acute injury where healing occurs, as the threat reduces, a virtuous circle ensures the reinstatement of biopsychosocial inhibitory factors which may have a role in the modulation system, such as physical fitness and a sense of achievement, which in combination restore the system to its previous regulated and balanced state as illustrated in Figure 1.

Figure 2.

A regulated system comes under increased threat.

The challenge for many years has been to create a model that might explain the development of chronic pain. In some cases following surgery or an acute injury, when the trauma has resolved, rather than pain or other symptoms reducing, as expected, some people experience a transition to a chronic state. In others, there may be no obvious triggering lesion, but symptoms develop and become chronic or long term. Previous studies^21,22 have suggested that psychological processes may influence this transition, but it is also likely that other biological, social, cultural and environmental factors play a part.^3,6

In the model presented here, it follows that most people only experience the protective actions temporarily, when an increase in threat overrides the modulation system and the ‘balance’ tips to close the contacts. Framed in the paradigm of this model, the chronic pain question arises: why in some cases does the system not return to normal regulation and switch off the protective action?

The proposal is that some individuals may have vulnerable modulation systems, which can transition into a much more weakened state, where restoration becomes increasingly difficult and protective action can become constantly invoked. This is not inevitable, but, for example, where the normal responses (rest and a gradual return to normal function) to protective actions such as pain and fatigue do not occur, people are perhaps at a higher risk of experiencing chronic or persistent protective action. This will depend on the coincidence of particular combinations of triggering biological, social, psychological and environmental factors.

A system vulnerable to chronicity

Figure 3 illustrates this idea of potential vulnerability, through the absence of some, as yet to be formally defined, aspects of the modulation system outlined in Figure 1, creating a shift in the normal balance of the system, leaving it more biased towards the possibility of producing protective action and reducing the possibility of a return to equilibrium, following triggering events.

Figure 3.

A system vulnerable to chronicity.

To examine this idea of vulnerability and its consequences in more detail, Surawy et al.’s¹⁸ cognitive behavioural model, originally developed for chronic fatigue, is considered. This model was derived from the observations of the characteristics of patients attending a clinic with CFS. The model proposed by Surawy et al. and developed by Moss-Morris et al.²³ includes predisposing, precipitating and perpetuating factors. It has been shown to predict CFS following an acute condition, glandular fever²³ and other chronic conditions such as irritable bowel syndrome (IBS)²⁴ from campylobacter infection and postconcussional syndrome following mild head injury.²⁵ More recently, Brooks et al.²⁶ suggested that the model should be considered for other conditions.

In generic terms, the Surawy model proposes the following:

• Predisposing factors, which can include premorbid behavioural propensities towards goal-oriented ‘striving’ or ‘action-proneness’ and a dependence on the external validation of self-esteem by others. This is frequently combined with a negative attitude towards expressing emotion or vulnerability, leading to a tendency to ‘bottle up’ feelings. A perfectionist drive resulting in unachievably high personal standards, both at work and in personal behaviour, is also suggested as a predisposing tendency.

• Precipitating events, which in a pain context may (or may not) involve an injury or development of an acute condition such as a repetitive strain injury, non-specific low back or abdominal pain. Other precipitating factors include an experience of prolonged stress, such as from a relationship breakdown, illness in the family or caring for an elderly relative. At work, a culture of long hours, bullying or being set unreasonable targets may also play a part in precipitating events.

• Perpetuating factors, which reflect the predisposing vulnerabilities, such as a propensity towards ‘all-or-nothing’ behaviour²⁷ or ‘boom and bust’ attempts to return to normal high levels of activity. Such attempts are typically followed by an exacerbation of symptoms, resulting in avoidance of activity and concerns about a worsening physical condition.

To explore these a little further, vulnerabilities such as a ‘perfectionist’ drive often result from earlier adaptations to difficult environments¹⁸ but are also likely to accompany high levels of self-criticism and low self-esteem, producing a pattern of long-term self-neglect. Over a longer timescale, these propensities tend to manifest in poor levels of self-care, the expenditure of significant amounts of energy in looking after others and driving ever harder in the quest for external approval.

From a psychological perspective, although low mood and depression have received attention over the years in pain research, they have been shown to have little direct correlation with pain²⁸ and its role in the aetiology of chronic pain has been largely unproven. More recently, anxiety has been identified^29,30 as having a potentially more important role in chronic pain than previously considered. Although a causal role cannot be assumed, if such predisposing tendencies as perfectionism, increased self-criticism and reduced self-esteem are significant, this may suggest that anxiety is an important area for future investigation.

Raised levels of stress have long been associated with chronic pain and fatigue and would seem to be particularly associated with the precipitating factors suggested by Surawy et al., potentially having a role in amplifying the level of threat in the model proposed here. In many areas, biological processes such as a dysregulation of stress signal sensitivity in immune cells have been identified³¹ although the exact mechanisms regarding cause and effect remain unclear.

In terms of perpetuating factors, a loss of fitness and physical deconditioning through increasing levels of ‘fear-avoidance’³² are common. Sleep disruption, accumulating side effects from medication, increased frustration, low mood and a medicalised preoccupation with symptoms are often present and over time financial, relationship, employment, social and even housing difficulties can occur. These can all create a number of self-perpetuating vicious circles, resulting in increased disability for the person and impacting on their family and health and social care services, often fostering beliefs that the symptoms emanate from an untreatable physical condition.^33,34

Moss-Morris et al.²³ provide an elegant summary of the Surawy model in action, in their discussion of the development of CFS following an acute viral infection such as glandular fever. This is paraphrased here to illustrate the potential transition from acute to chronic pain:

When predisposed people are faced with precipitating factors which affect their ability to perform, such as a combination of excessive stress (at work, from home stress or life events) and the onset of pain, their initial reaction is to press on and keep coping. This behaviour leads to the experience of ongoing symptoms, which may be more closely related to their behaviour of ‘pushing too hard’ than to any initial injury. However, in making sense of the situation, people perhaps understandably attribute the ongoing symptoms to an injury, rather than their behaviour. The common response to a physical illness is rest. However, reduced activity conflicts with achievement orientation and may result in boom and bust behaviour or activity cycling (bursts of high levels of activity when they feel better, followed by the need to rest and recover) in an attempt to meet unrealistic expectations.

Spence et al.²⁷ identified this ‘all-or-nothing behaviour’ as a highly predictive construct for the development of CFS and, from clinical experience, is a behavioural propensity observed in many people with long-term health conditions, including chronic pain. In terms of perpetuating factors, these periodic attempts at recovery, still executed in terms of ‘all-or-nothing’ activity, inevitably exacerbate physical symptoms and fail to achieve goals. The most acceptable interpretation of this for the individual is that they have a serious medical condition, rather than an unhelpful set of behavioural propensities. Unfortunately, medical investigation, including imaging, will often reveal abnormalities, often within the normal range³⁵ but to which symptoms can easily be attributed, a condition diagnosed and expectations of treatment or progressive levels of disability established.

To return to the model presented here, Figure 4 shows the impact of increased threat in a vulnerable system, where the experience of protective action such as pain is likely to remove proposed components of the modulation system, such as a sense of achievement and fitness, weakening a previously vulnerable modulation system still further. In a non-vulnerable system, this shift would be predicted as temporary, with regulation being restored, as increases in the input of the threat detection system (such as from nociception and inflammation) reduce.

Figure 4.

A vulnerable system comes under increased threat.

A vulnerable system is defined as one where some of the components of the modulating system are absent prior to the triggering events, suggesting the presence of the behavioural propensities suggested by Surawy. If precipitating events have a significant impact, that is, interfere with the ‘all-or-nothing’ striving and normal patterns of overachieving behaviour, then such predisposed individuals, being thwarted in their goals, are likely to try and override the messages embodied in the protective action (such as using medication and treatments) and overexert themselves, rather than undertake the more adaptive behavioural responses of rest and a graduated return to normal activity.

Over time, this approach is likely to become more difficult to maintain and the increased levels of frustration interact with the protective actions such as pain and fatigue, making them even more difficult to manage³³ and creating vicious circles where the overall sense of ‘threat’ increases and restoration of modulation is less likely to occur. The system may begin to transition to a state of dysregulation, with the chronic or long-term production of protective action.

Central sensitisation³⁶ is a term used to describe changes in the CNS that relate to pain hypersensitivity and reflects the chronic pain experience. The idea of a dysregulated threat management system, with increasingly reduced biopsychosocial modulation, may offer a partial explanation for the development of this phenomenon, where benign input becomes interpreted as a potential threat. As time progresses, sensitivity is likely to increase, as modulation reduces and perceived threat increases. As components such as sleep become more disrupted and medication side effects and levels of stress increase, the system is likely to become more consistently off balance, with a background of constant protective action and increases in response to the most minor input (see Figure 5).

Figure 5.

A system becomes dysregulated.

Discussion

In summary, the proposal is that predisposing factors, as suggested by Surawy’s 1995 model, create vulnerability in the modulation of the threat detection system through reduced inhibition. Particular combinations of precipitating events can result in a further significant reduction in modulation, which can leave the threat detection system at risk of dysregulation. A dysregulated system is likely to respond to a whole range of benign inputs as potential threats and thus constantly create protective action. This may partly account for triggering the phenomenon ‘central sensitisation’, where people with chronic pain begin to experience constant protective action such as pain (and or fatigue) with increases in response to small amounts of activity or particular movements, as their dysregulated system is no longer able to modulate input resulting from harmless activities and treats them as potentially threatening.

Over time, this constant experience of protective action is likely to be interpreted by the individual as the symptoms of a deteriorating or progressive medical condition, which is understandable, but adds to the overall sense of ‘threat’, reinforced by negative biopsychosocial and environmental consequences that further consolidate the situation as shown in Figure 5.

With regard to targets for intervention that might lead to more sustainable outcomes, this model would suggest that the origins of the vulnerability or predisposing factors should be explored.^14,37 For the individual, understanding and gaining mastery over patterns likely to have their origins in their ‘childhood story’³⁸ is likely to be an essential part of their long-term learning, in order to restore some elements of modulation into their dysregulated systems. Clearly, there will be a number of people in any chronic pain population whose vulnerabilities may be influenced by significant emotional trauma, who will require more in-depth psychological and emotional support.³⁹ However, for the majority of people with chronic pain, who have not experienced identifiable trauma, any such predisposing factors may be more implicit than explicit. The key behavioural patterns or propensities discussed here can be adaptive in certain contexts and therefore can remain hidden, often only being clearly revealed in ‘high-stakes’ situations such as when distressed family members demand help. As the type of behaviour suggested here is not usually considered by the individual to be relevant to their pain problem, it is also unlikely to be considered, unless prompted by an investigating clinician. Cognitive–behavioural psychology is an important framework for intervention.^11,12,13 However, facilitating sustainable changes in behaviour, mood and confidence to self-manage chronic pain remains a challenge. In terms of addressing some of the perpetuating factors suggested by Surawy’s model, incorporating elements of a self-compassionate approach in pain management programmes^40,41 would seem appropriate.

While this reflects observations of a particular population, that is, those accessing specialist pain services, in contemporary clinical practice, it is now common to observe people having undertaken multiple rehabilitation programmes, often in different centres, receiving repetitive coaching in the same behaviours, such as applied relaxation or pacing and planning of activity. The model would suggest that if the predisposing behavioural propensities are not addressed, people are likely to return to their familiar patterns of behaviour, post programme. For example, as resting conflicts with a perfectionist drive, if these propensities remain unchallenged, despite rising or constant levels of pain, they are likely to ‘press on’, perhaps taking increasing amounts of medication to help them fulfil their goals. Where this continues, despite continuing pain, it is possible that the protective action system also subsequently invokes fatigue. Where pain often has only partial success, fatigue (or a combination of pain and fatigue) will win. There is some qualitative evidence to suggest that fatigue or perhaps the combination of pain and fatigue is more difficult to manage^33,34 and hence Van Houdenhove’s conclusion: ‘The exhausted fighter eventually capitulates’.⁴²

Conclusion

Chronic pain, fatigue and other functional neurological phenomena can perhaps therefore be considered, not as physical or psychological abnormalities, the attack of mysterious pathogens or even an autoimmune reaction, but as the constant protective actions of a dysregulated neurological protection system that, in a desperate struggle for self-preservation, is trying to shut down an organism that finds it extremely difficult to alter its established behavioural patterns.