Fw: Suffering: the contributions of persistent pain

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Subject: Suffering: the contributions of persistent pain

Suffering: the contributions of persistent pain

C Chapman, Gavrin

Posted April 21, 2001

Department of Anesthesiology, Box 356540, School of Medicine, University of Washington, Seattle, WA 98195, USA (Prof C R Chapman PhD, J Gavrin MD)

Correspondence to: Prof C Chapman (e-mail:crc@...)

Basic definitions: pain and suffering How pain causes suffering Implications for care References

Pain is a perceived threat or damage to one's biological integrity. Suffering is the perception of serious threat or damage to the self, and it emerges when a discrepancy develops between what one expected of one's self and what one does or is. Some patients who experience sustained unrelieved pain suffer because pain changes who they are. At a physiological level, chronic pain promotes an extended and destructive stress response characterised by neuroendocrine dysregulation, fatigue, dysphoria, myalgia, and impaired mental and physical performance. This constellation of discomforts and functional limitations can foster negative thinking and create a vicious cycle of stress and disability. The idea that one's pain is uncontrollable in itself leads to stress. Patients suffer when this cycle renders them incapable of sustaining productive work, a normal family life, and supportive social interactions. Although patients suffer for many reasons, the physician can contribute substantially to the prevention or relief of suffering by controlling pain. Suffering is a nebulous concept for most physicians, and its relation to pain is unclear. This review offers a medically useful concept of suffering that distinguishes it from pain, accounts for the contributory relation of pain to suffering by describing pain as a stressor, and explores the implications of these ideas for the care of patients.

Basic definitions: pain and suffering

The standard definition for pain is that it is "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage".1 Viewed from an evolutionary perspective, pain is perceived threat or damage to one's biological integrity and has sensory and emotional features. The sensory awareness of tissue trauma represents information crucial for adaptation and survival. The emotional experience of tissue trauma represents the biological importance of the injury or condition to the individual.2 Most of the time pain serves us well in these respects, but when it persists relentlessly, it can contribute to disability and suffering.

The concepts of pain and suffering are frequently mixed and sometimes confused in the dialogue between patient and physician, especially since pain is commonly used as if it were synonymous with suffering. However, suffering and pain are distinct phenomena. Suffering is a broader state that encompasses more dimensions than pain and has many potential causes, of which pain is only one. Not all pain causes suffering, and not all suffering expressed as pain or, coexisting with pain, stems from pain. In lay terms, suffering connotes enduring something unpleasant and inconvenient, sustaining loss or damage, or experiencing a disability.

To understand a patient's suffering, we must recognise that patients are dynamic psychological and social entities. Cassell3 approached this issue with his proposition that physicians should see patients as people. He emphasised the complexity of identity, the unique personal history of the individual, and the sociocultural context of human existence. For Cassell, suffering is the consequence of perceived, impending destruction of the person or of some essential part of the person. We define suffering as perceived damage to the integrity of the self, which is a psychological construct that represents a subjective sense of identity.4 Broadly conceived, the self is what each of us consider to be "me" or experiences as "me". Viewed as a static entity, the self is complex and needs to be understood at multiple levels.5

Neurological self --At a neurological level, the self exists as a central representation of the body. Melzack6 called this self the body neuromatrix. Neurological studies of patients with phantom-limb sensation or those born without limbs reveal that the brain maintains a coherent internal representation of the body. When a person loses a hand, he or she experiences a phantom hand because the central representation of the hand remains intact. Thus, a "body self" exists, and this construct probably sustains many different dimensions of the sense of self. At a perceptual level, the self is a centre of experience for events, emotions, and ideas. It is a hypothetical point around which events and relationships seem to organise.

Agent self --At a behavioural level, the self is a goal-orientated agent that interacts with the material and social environment in pursuit of fulfilment of its needs. The agent self strives to define its relationship to others, sometimes by competition and at other times by cooperation. The defined relationship determines the extent of one's access to the resources needed to attain goals. These efforts define a social identity. One's personal belief in the effectiveness of one's self as agent is self-efficacy. This belief has an important role in adjusment to painful disease conditions.7

Cognitive self --At the cognitive level, a sense of self emerges as the product of more fundamental processes. The sense of self entails an awareness of the past and the future, and it imposes a coherent narrative on the historical record and future forecasts. The absence of these features becomes conspicuous in some patients after traumatic brain injury.8 Many patients with schizophrenia have an abnormal sense of self and a striking insensitivity to tissue trauma.9 In a healthy person, the sense of self is highly individual, but people vary substantially in degree of self-definition, openness to change, and vulnerability to emotional disorder.10,11

Dynamic self--Viewed as a dynamic entity, the sense of self emerges gradually in the course of early development and becomes more elaborate during the course of one's life. Relationship and social identity become increasingly important with older age; as we age, the sense of self evolves and adapts with varying degrees of success. Psychological research defines a transition from a sense of self based on physical attributes and activities to a sense of self based on wisdom and inward growth: a process termed successful ageing.12,13

Suffering, as threat or damage to the integrity of the self, entails a disparity between what one expects of one's self and what one does or is.10,14 A serious disruption in the psychosocial trajectory of a human life, such as the onset of uncontrolled pain, can cause such a disparity and thereby compel changes in the sense of self. Many patients grieve for the loss of self-esteem that they experience and need time to redefine who they are. Some individuals can communicate the sense of self by describing their life story as a narrative; those who suffer tend to express discontinuity and breakdown in personal narrative.

The psychosocial effect of a physiologically damaging event or condition varies between individuals. The development of painful arthritis in the fingers would have a minor impact for most middle-aged people, but could be devastating for a professional concert musician because it affects what he or she is and can hope to be in the future. For a given painful condition, vulnerability to suffering depends partly on who one is and what one does in society.

How pain causes suffering

Many physicians think of pain as a purely subjective, private experience; this view is correct but incomplete. Tissue trauma generates noxious signals, and figure 1 shows how excitation of nociceptors15 and sometimes neuropathic conditions16 can generate nociceptive afferent volleys. Peripheral and central mechanisms can exacerbate noxious signalling through sensitisation. Tissue trauma may cause nociception, neuropathy with abnormal neural firing patterns, or both. Inflammation and repetitive stimulation sensitise both peripheral nerves and cells of spinal transmission, and thus lower firing thresholds. Medullary structures exercise some degree of inhibitory modulation over centripetal noxious messages. Signals that follow thalamocortical pathways contribute to sensory awareness of tissue trauma (pain). Activity in spinohypothalamic pathways and pontine hypothalamic pathways acts as a stressor,17 and excite the paraventricular nucleus of the hypothalamus and thus initiate a complex, short-term adaptive neuroendocrine response (the stress response) in the hypothalamo-pituitary-adrenocortical (HPA) axis.18 If nociception or neuropathy persist, neuroendocrine dysregulation ensues. The debilitating consequences damage the sense of self.

Figure 1: Mechanisms and effects of stress in patients with chronic pain

A stressor is any experience, physiological or psychological, that disrupts homoeostasis. Stressors can be positive (adaptive, rewarding) or negative (threatening, harmful). Negative physiological stressors include traumatic injury, blood loss, toxic effects, starvation, and exposure to temperature extremes. Extensive work in animal models and in man shows that the settings in which the physiological responses occur can affect the magnitude and duration of the stress response.19 This work shows that psychological factors can determine whether an event is a stressor and that some psychological factors are inherent negative stressors. Negative psychological stressors include loss of control over one's circumstances, lack of predictability in the environment, and loss of feedback from the environment.20,21 Cognitions such as negative beliefs, expectations, and attributions, whether accurate or erroneous, can act as stressors. Thus, while noxious signalling can elicit the stress response in its own right, negative thinking can act as a secondary stressor. Psychological stressors may involve different stress circuits than physiological stressors and entail greater contribution from multisynaptic limbic forebrain areas;22 these areas may be critical for self-awareness.23

The stress response is an adaptive pattern of neural and endocrine activation and behavioural changes that is mediated via parvocellular neurons of the paraventricular nucleus and directed toward the restoration of homoeostasis.18,24 In most instances this pattern is a beneficial, short-term response to an acute negative stressor, but it can prove maladaptive when a stressor such as neuropathic signalling persists indefinitely. Maladaptive stress is a persistent and sometimes self-sustaining cascade of neural and endocrine responses that degrades physical and psychological well-being.20

The physiological manifestations of the stress response include extensive, and extended, sympathetic nervous-system arousal along with the secretion of glucocorticoids (primarily cortisol in human beings) and other neuroendocrine substances into systemic circulation via feedback-dependent mechanisms.25,26 This response prepares the body for emergency reaction and fosters survival in circumstances of immediate, time-limited threat, but becomes maladaptive when the stressor persists, partly because the actions of glucocorticoids are largely catabolic and tend to consume physiological resources. Moreover, excessive or dysregulated cortisol in systemic circulation can damage hippocampal neurons and accelerate some parts of brain ageing.20,21 The HPA axis involves negative feedback mechanisms through which cortisol can inhibit its own release, presumably because cortisol is potentially toxic.

The immune system also has a role in the stress response.27 Along with the identification and destruction of foreign substances, it may function as a sense organ that is diffusely distributed throughout the body, and communicates injury-related events and tissue pathology to the brain.28 The brain and immune system seem to form a bidirectional communication network.24,29 The key immune products are cytokines, such as interleukin-1 and interleukin-6, which macrophages and other immune cells release. Cytokines seem to act, not by functioning as blood-borne messengers, but by activation of the vagus nerve. Paraganglia surrounding vagal terminals have dense binding sites for interleukin-1, and they synapse on vagal fibres that terminate in the solitary nucleus. Thus, cytokines may excite (albeit indirectly) vagal afferents that terminate in one of the major control centres for the autonomic nervous system.

The brain controls the immune system via the actions of the sympathetic nervous system and the HPA axis, and it sometimes generates a sickness response. The pituitary releases peptides related to pro-opiomelan-ocortin such as adrenocorticotropin hormone and ß-endorphin. Because the cells and organs of the immune system express receptors for these hormones, they can respond to humoral messenger molecules of central origin. Through this mechanism a stressor can trigger a constellation of physiological changes and adaptive behaviours that a person experiences as sickness.29 The common manifestations of this response are familiar to anyone who has ever had the flu, fever, increased slow-wave sleep, increased leucocytosis, reduced expiration, diminished sexual interest, reduced activity, depressed mood, muscular soreness, and somewhat diminished cognitive abilities. Collectively, these responses conserve energy and foster its redirection to increased body temperature, which suppresses the reproduction of microbial organisms. Sickness tends to occur with both microbial infection and tissue trauma because an open wound normally invites infection. This response is clearly adaptive for short-term threat, but extended patterns of sickness response in a person not threatened with microbial invasion are counterproductive. Features of the sickness response are sometimes part of the maladaptive stress response in people with chronic pain.

The maladaptive stress response seems to have a contributory role in some psychiatric disorders. Roughly half of all patients with severe depression manifest hypersecretion of cortisol.30,31 Concentrations of cortisol in urine, plasma, and cerebrospinal fluid are frequently raised in patients with depression. Moreover, whereas healthy individuals secrete high concentrations of cortisol only at noon, people with depression tend to secrete high concentrations throughout the afternoon and evening. When patients get well again, cortisol secretion returns to the normal pattern. Patients with post-traumatic stress disorder have substantially raised catecholamine to cortisol ratios.32 These observations suggest that continual stress involves excessive neuroendocrine response and circadian dysregulation.

Studies of patients with depression,33,34 post-traumatic stress disorder,35,36 chronic pain,39-41 and other disorders27 suggest that the common behavioural markers of a maladaptive, sustained stress response are: fatigue; dysphoria with muscular aches and pains; disrupted or non-restorative sleep; somatic hypervigilance; reduced appetite and libido; impaired physical functioning; and impaired concentration. In addition to experiencing the stressor or stressor constellation (eg, persistent pain and negative thoughts about the pain and its impact on life), the person with persistent, unrelieved pain feels sick, exhausted, and impaired. Thus, in some respects, suffering resembles depression. However, suffering differs from depression in that it is: a broader, more inclusive concept than depression; not necessarily a psychopathological state; not necessarily associated with self-blame or self-deprecation; and more dependent on awareness of the future.

The right side of figure 1 shows the effect of the sustained stress response on a person who seeks to maintain a normal, productive life. In addition to dealing with pain as a source of distraction and discomfort, he or she must overcome fatigue, disabilities, and other features of illness. Individuals in this situation commonly identify the sensory experience of pain as the problem because it dominates their awarenesss; the pattern of dysphoria, fatigue, and disability is sometimes transparent to them. Although the sensory awareness of pain is the most salient issue to a patient with chronic pain, the disability that pain causes has a greater negative effect on his or her quality of life and sense of self.

Figure 2 shows the effect of chronic pain and its attendant disabilities on the productivity of a person in the workplace, at home, and in the community as a whole. The sense of self is an extension of past performance levels. "Who I am" as a capable productive person should be a function of who I have been in the past--before the pain. Now that I have unremitting pain, I can do less. As the task demands of everyday life increase, I can no longer match them. I am less than I once was and less than I should be. This disturbing disparity between what a person believes himself or herself to be and what the person is with chronic pain appears as the shaded area in figure 2. The disparity represents threat or damage to the integrity of the self, not only in the present but also in the future. This damage to the integrity of the self, which extends into the projected life trajectory, is the essence of suffering.

Figure 2: Effects of chronic pain on functional capability

After developing chronic pain, a person can no longer perform as usual in the workplace, community, or at home. The disparity between self-expectations and actual performance (shaded area) results in damage to the self.

Implications for care

Our concept of suffering resonates with the lay use of the term--the perception of damage to the self and grief over a loss in self-esteem. Although unrelieved pain can create an overwhelming degree of personal discomfort, its contribution to suffering is more insidious. At a physiological level, chronic pain is a stressor that promotes an extended and destructive stress response that involves neuroendocrine dysregulation, fatigue, dysphoria, myalgia, and impaired mental and physical performance. Such states can lead to a vicious cycle of stress and disability; indeed uncontrollable pain is in itself a stressor. Pain and related stressors can make it impossible for an individual to sustain productive work, normal family life, and supportive social interactions.

Pain is not a symptom that exists in isolation. Chronic pain, even when the pathophysiology is unknown, tends to create a cluster of related problems such as chronic fatigue, sleep disturbance, excessive rest and withdrawal from activity, compromised immune function, and mood disorder. In patients with progressive life-threatening diseases, pain can add greatly to the debilitating effects of the disease, foster hopelessness and fear, and reduce the ability of the patient to comply with interventions directed at the disease itself. Many patients suffer greatly from the toll that their disease exacts, and some find that the toxic or iatrogenic damage of antineoplastic or other aggressive interventions is in itself a cause of suffering. For such patients, unrelieved pain is a needless burden that can exacerbate pre-existing suffering. Patients who could otherwise cope emotionally and physically with the setbacks they encounter may fall into suffering and hopelessness because of uncontrolled pain.

An awareness of how pain contributes to suffering will enable physicians to prevent it. The physician should make every effort to prevent pain and to relieve pain promptly and effectively when it does occur. How patients think about their pain and whether the physician seems to care about the pain and its relief are also crucial factors. The fear that the pain of one's terminal illness will get out of control and lead to an agonising death is in itself a significant stressor. The sensitivity and reassurance of the physician on matters of present and future pain control is an important facet of care.

Support for preparation of this manuscript came from grants RO1 CA74249 and RO1 CA74269 and from the National Cancer Institute, National Institutes of Health, USA.

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