Illness behavior and dysfunction: review of concepts and application to chronic pain

The purpose of this presentation is to review the elements that comprise the concept of illness behavior including elaboration of a more formal theoretical and operational model for illness behavior and then discuss the application of the illness behavior model to chronic pain, especially chronic orofacial pain. The model of illness behavior presented emphasizes four critical areas of conceptual interest, namely, (1) monitoring of somatic signals; (2) cognitive processes whereby bodily symptoms are interpreted; (3) attaching meaning to symptoms in the context of emotional state and concurrent environmental events; and (4) the ethnocultural influences that pervade meaning and shape coping responses. Our model of illness behavior was generalized from a closely related model developed to guide research when the specific illness behavior of interest was dysfunctional chronic pain behavior. We also include a time dimension in our chronic pain model. Dysfunctional chronic pain is understood to be the most important undesirable consequence associated with suffering a persistent pain condition. Dysfunctional chronic pain is a subset of illness behaviors inconsistent with medically documented findings, while the complaints of pain are prominent. Changes occur in emotional status, most typically reported as mood and behavioral changes associated with depression, such as demoralization, helplessness, and social isolation. Excesses in medical care, hospitalizations for surgery, and abuse of medications are further characteristics of dysfunctional chronic pain.     

Hypoprothrombinemic hemorrhage due to cholestyramine therapy.

Somatization is the tendency to experience and communicate psychologic distress in the form of somatic symptoms that the patient misinterprets as signifying serious physical illness. Patients with persistent somatization relentlessly seek medical diagnosis and treatment despite repeated reassurance that physical illness is either absent or insufficient to account for their symptoms and disability. Such abnormal illness behaviour leads to overuse of health care facilities and contributes to the high cost of health care. Somatization may occur transiently in response to stressful life events or it may be persistent and result in chronic partial or total disability. Diagnostic and therapeutic guidelines that may help physicians identify and manage such patients more effectively are discussed.     

Violent behaviour among people with schizophrenia: a framework for investigations of causes, and effective treatment, and prevention

Robust evidence has accumulated showing that individuals who develop schizophrenia are at elevated risk when compared to the general population to engage in violence towards others. This violence impacts negatively on victims as well as perpetrators and poses a significant financial burden to society. It is posited that among violent offenders with schizophrenia there are three distinct types defined by the age of onset of antisocial and violent behaviour. The early starters display a pattern of antisocial behaviour that emerges in childhood or early adolescence, well before illness onset, and that remains stable across the lifespan. The largest group of violent offenders with schizophrenia show no antisocial behaviour prior to the onset of the illness and then repeatedly engage in aggressive behaviour towards others. A small group of individuals who display a chronic course of schizophrenia show no aggressive behaviour for one or two decades after illness onset and then engage in serious violence, often killing, those who care for them. We hypothesize that both the developmental processes and the proximal factors, such as symptoms of psychosis and drug misuse, associated with violent behaviour differ for the three types of offenders with schizophrenia, as do their needs for treatment.     

Peripheral Nerve Injury Is Associated with Chronic,Reversible Changes in Global DNA Methylation in the Mouse Prefrontal Cortex

Changes in brain structure and cortical function are associated with many chronic pain conditions including low back pain and fibromyalgia. The magnitude of these changes correlates with the duration and/or the intensity of chronic pain. Most studies report changes in common areas involved in pain modulation, including the prefrontal cortex (PFC), and pain-related pathological changes in the PFC can be reversed with effective treatment. While the mechanisms underlying these changes are unknown, they must be dynamically regulated. Epigenetic modulation of gene expression in response to experience and environment is reversible and dynamic. Epigenetic modulation by DNA methylation is associated with abnormal behavior and pathological gene expression in the central nervous system. DNA methylation might also be involved in mediating the pathologies associated with chronic pain in the brain. We therefore tested a) whether alterations in DNA methylation are found in the brain long after chronic neuropathic pain is induced in the periphery using the spared nerve injury modal and b) whether these injury-associated changes are reversible by interventions that reverse the pathologies associated with chronic pain. Six months following peripheral nerve injury, abnormal sensory thresholds and increased anxiety were accompanied by decreased global methylation in the PFC and the amygdala but not in the visual cortex or the thalamus. Environmental enrichment attenuated nerve injury-induced hypersensitivity and reversed the changes in global PFC methylation. Furthermore, global PFC methylation correlated with mechanical and thermal sensitivity in neuropathic mice. In summary, induction of chronic pain by peripheral nerve injury is associated with epigenetic changes in the brain. These changes are detected long after the original injury, at a long distance from the site of injury and are reversible with environmental manipulation. Changes in brain structure and cortical function that are associated with chronic pain conditions may therefore be mediated by epigenetic mechanisms.     

P2X7受体在病理性疼痛中的研究进展

病理性疼痛主要包括组织损伤或炎症引起的炎症痛、神经系统损伤或疾病引起的神经病理性疼痛和恶性肿瘤及治疗引起的癌症痛三大类。病理性疼痛对常规的镇痛药物反应不理想,迫切需要寻找新的对病理性疼痛更有效和更特异的治疗手段。P2X7受体作为离子通道型嘌呤能受体,在炎症痛、神经病理性疼痛和癌症痛中都具有重要作用。靶向P2X7受体的新药物将为病理性疼痛的治疗带来新的希望。该文综述了P2X7受体在三类病理性疼痛中的研究进展。     

Democratic organization of the thalamocortical neural ensembles in nociceptive signal processing

Acute pain is a warning protective sensation for any impending harm. However, chronic pain syndromes are often resistant diseases that may consume large amount of health care costs. It has been suggested by recent studies that pain perception may be formed in central neural networks via large-scale coding processes, which involves sensory, affective, and cognitive dimensions. Many central areas are involved in these processes, including structures from the spinal cord, the brain stem, the limbic system, to the cortices. Thus, chronic painful diseases may be the result of some abnormal coding within this network. A thorough investigation of coding mechanism of pain within the central neuromatrix will bring us great insight into the mechanisms responsible for the development of chronic pain, hence leading to novel therapeutic interventions for pain management.     

Chronic myelogenous leukemia simulating chronic granulomatous disease.

A 5-year illness of a child, characterized by recurrent bacterial infections and abnormal results of nitroblue tetrazolium dye reduction tests, was suggestive of chronic granulomatous disease but the illness terminated in overt myeloid leukemia. During this progression studies of leukocyte structure and metabolic activity revealed abnormalities that suggested the existence of a "preleukemic" state.     

The pain-adaptation model: a discussion of the relationship between chronic musculoskeletal pain and motor activity

Articles describing motor function in five chronic musculoskeletal pain conditions (temporomandibular disorders, muscle tension headache, fibromyalgia, chronic lower back pain, and postexercise muscle soreness) were reviewed. It was concluded that the data do not support the commonly held view that the pain of these conditions is maintained by some form of tonic muscular hyperactivity. Instead, it seems clear that in these conditions the activity of agonist muscles is often reduced by pain, even when this does not arise from the muscle itself. On the other hand, pain causes small increases in the level of activity of the antagonist. As a consequence of these changes, force production and the range and velocity of movement of the affected body part are often reduced. To explain how such changes in the behaviour come about, we propose a neurophysiological model based on the phasic modulation of excitatory and inhibitory interneurons supplied by high-threshold sensory afferents. We suggest that the "dysfunction" that is characteristic of several types of chronic musculoskeletal pain is a normal protective adaptation and is not a cause of pain.     

Treatment of the chronic pain patient.

A small percentage of patients with persistent pain are sufficiently angry, demanding, and manipulative to require the negotiation of an explicit treatment and/or management contract. The very few studies in this field suggest that pain is both a function of and a stimulus to abnormal illness behavior, thus requiring special attention to therapeutic "ground rules." Treatment requires an unequivocal assertion by the patient that he wishes to get better and is willing to work at doing so; the specification of clearcut goals and the means of working towards them ("pacing behavior"); and the possible use of electrical neurostimulation and/or weak analgesics for pain control. Explicit understanding of mutual expectations and the patient's and doctor's "rights" is also helpful in fostering goodwill and desirable results.     

Mentally abnormal prisoners on remand: I—Rejected or accepted by the NHS?

Increasing numbers of mentally abnormal offenders are sentenced to prison. The decision to treat or imprison them is influenced by the attitudes of consultant psychiatrists and their staff. The process whereby those decisions were made and the willingness of consultants to offer treatment were investigated. A retrospective survey of all (362) mentally abnormal men remanded to Winchester prison for psychiatric reports over the five years 1979-83 showed that one in five were rejected for treatment by the NHS consultant psychiatrist responsible for their care. Those with mental handicaps, organic brain damage, or a chronic psychotic illness rendering them unable to cope independently in the community were the most likely to be rejected. They posed the least threat to the community in terms of their criminal behaviour yet were more likely to be sentenced to imprisonment. Such subjects were commonly described by consultants as too disturbed or potentially dangerous to be admitted to hospital or as criminals and unsuitable for treatment. Consultants in mental hospitals were most likely and those in district general hospitals and academic units least likely to accept prisoners.The fact that many mentally ill and mentally handicapped patients can receive adequate care and treatment only on reception into prison raises serious questions about the adequacy of current management policies and the range of facilities provided by regional health authorities.     

Psychological assessment of factors affecting pain

Use of traditional stimulus-response models of pain leads to differentiation between organic and psychogenic pain, which is often not helpful, if not dangerous, in treating chronic pain. Pain does not simply reflect bodily damage but also complex psychological malfunctioning. Viewing chronic pain as an obsessional state may often help in treating the entire patient and prevent the physician from being obsessed with the patient''s obsession. Psychological assessment of pain should focus on the role of psychological processes in the multifactorial causation of the illness causing the pain, notably their role in illness-proneness in general. Also, iatrogenic psychological distress, associatively precipitated psychological conflict and illness-perpetuating psychological processes should be looked for. A serious obstacle to progress with pain problems is not lack of hard data but conceptual confusion. Before medicine can meaningfully assess psychological factors in pain problems it must first learn to perceive psychological disturbances in medical and surgical patients.     

Specific subunits of voltage-gated sodium channel underlying the subthreshold membrane potential oscillations: Potential therapeutic targets for neuropathic pain

The treatment of neuropathic pain remains a major challenge to pain clinicians. Certain nociceptive and non-nociceptive dorsal root ganglion (DRG) neurons may develop abnormal spontaneous activities following peripheral nerve injury, which is believed to be a major contributor to chronic pain. Subthreshold membrane potential oscillation (SMPO) observed in injured DRG neurons was reported to be involved in the generation of abnormal spontaneous activity. Tetrodotoxin-sensitive sodium (Na⁺) channels were testified to be involved in the generation of SMPO, but their specific subunits have not been clarified. We hypothesize that the subunits of voltage-gated sodium channel, Na_v1.3 and Na_v1.6, are involved in the generation of SMPO. An attempt to test this hypothesis may lead to a new therapeutic strategy for neuropathic pain.     

Do glial cells control pain?

Management of chronic pain is a real challenge, and current treatments that focus on blocking neurotransmission in the pain pathway have resulted in limited success. Activation of glial cells has been widely implicated in neuroinflammation in the CNS, leading to neurodegeneration in conditions such as Alzheimer's disease and multiple sclerosis. The inflammatory mediators released by activated glial cells, such as tumor necrosis factor-a and interleukin-1b not only cause neurodegeneration in these disease conditions, but also cause abnormal pain by acting on spinal cord dorsal horn neurons in injury conditions. Pain can also be potentiated by growth factors such as brain-derived growth factor and basic fibroblast growth factor, which are produced by glia to protect neurons. Thus, glial cells can powerfully control pain when they are activated to produce various pain mediators. We review accumulating evidence that supports an important role for microglial cells in the spinal cord for pain control under injury conditions (e.g. nerve injury). We also discuss possible signaling mechanisms, in particular mitogen-activated protein kinase pathways that are crucial for glial-mediated control of pain.Investigating signaling mechanisms in microglia might lead to more effective management of devastating chronic pain.     

Change in the nociceptive reactions caused by dental pulp stimulation during excitation of the midbrain]

It was demonstrated in chronic experiments on cats that stimulation of certain midbrain regions decreased or fully depressed the pain reaction evoked by dental pulp stimulation. The antinociceptive effect depending on the parameters of the brain stimulation was shown in differential change of the separate motor and vegetative and emotional - behaviour components, forming a general pain reaction. A poststimulation analgesia was revealed and the dynamic of restoration of different pain manifestations after the cessation of brain stimulation was traced. Possible mechanism of the realization of the antinociceptive effect are discussed.     

Analgesia in phasic and tonic pain tests in a pharmacological model of autotomy

Self-mutilation or self-injurious behaviour is a well known behavioural disorder in humans. The proposition that this behaviour in animals is a response to chronic pain of peripheral nerve injury has been met with controversy. In the present study a pharmacological model, which produces no sensory or motor loss was used to study how autotomy is related to pain. In a group of rats autotomy was induced by amphetamine in phenoxybenzamine and reserpine treated animals. The pain tests, both phasic and tonic were then performed. The results of this study showed that a total analgesia was produced in both phasic and tonic pain tests, in animals that exhibited autotomy. Injection of naloxone in these animals prevented autotomy. A correlation between autotomy and no pain is suggested in this pharmacological model of autotomy.     

Drug Addiction,Psychotic Illness and Brain Self-Stimulation: Effective Treatment and Explanatory Hypothesis

Similarities between drug addiction and psychotic illness suggested that drug addicts could be treated with intensive ECT and phenothiazine drugs, a therapeutic approach effective in more serious psychotic illnesses.The use of this intensive treatment method is described in six drug addicts. Successful results were achieved in four patients who have been followed up for two to five years. The treatment program, the preliminary investigations and the follow-up procedures are described.Particular reference is made to the brain self-stimulation studies of Olds and others in animals, and those of Heath in man. A hypothesis is advanced to explain the various aspects of the clinical picture in both psychotic illness and drug addiction.The intensive method of treatment should be considered for drug addicts whose prognosis is otherwise poor. Further investigations along the lines of the proposed hypothesis might be profitable in other types of abnormal and maladaptive behaviour.     

Social withdrawal behaviour in infant: clinical and research interest

The social withdrawal behaviour concept is presented, along with its historical background and its links to infant depression. Sustained social withdrawal behaviour in infancy is observed either with attachment disorders, in autism, sensory impairment, intense and chronic pain, or in interaction disorders and as effects of maternal depression on the infant. The alarm distress baby scale (ADBB) is a 8 item-assessment scale. It has been built to help screening early withdrawal behaviour, making use for example of the routine physical examination in a Well Baby clinic. Current clinical and research application and validations of the scale are presented.     

Reduction of the behavioral response to a viscero-peritoneal nociceptive stimulation during the development of experimental polyarthritis in the rat

Writhing behaviour induced by a viscero-peritoneal nociceptive stimulus (i.p. acetic acid) has been investigated during the development of arthritis experimentally induced in rats by s. c. injection of Mycobacterium butyricum; experiments were carried out at various (1-9 weeks) post-inoculation periods. In the most severe phase (2-5 weeks post-inoculation), when arthritis-induced hyperaesthesia was most pronounced, writhing behaviour was strongly reduced (80%). In the following period, the progressive decrease of hyperaesthesia was contemporaneous with a recovery of the writhing behaviour. We conclude that, in this chronic pain model, the behavioural reaction to a viscero-peritoneal nociceptive stimulus is impaired. Such heterotopic inhibitory processes could be relevant to some paradoxical clinical observations such as the masking of a pain by the experience of pain at another locus (i. e. counter-irritation phenomenon).     

Explanatory models of medically unexplained symptoms: a qualitative analysis of the literature

Background Medically unexplained symptoms (MUS) are common in primary health care. Both patients and doctors are burdened with the symptoms that negatively affect patients' quality of life. General practitioners (GPs) often face difficulties when giving patients legitimate and convincing explanations for their symptoms. This explanation is important for reassuring patients and for maintaining a good doctor-patient communication and relationship.Objective To provide an overview of explanatory models for MUS.Study design We performed a systematic search of reviews in PsycINFO and PubMed about explanatory models of MUS. We performed a qualitative analysis of the data according to the principles of constant comparative analysis to identify specific explanatory models.Results We distinguished nine specific explanatory models of MUS in the literature: somatosensory amplification, sensitisation, sensitivity, immune system sensitisation, endocrine dysregulation, signal filter model, illness behaviour model, autonomous nervous system dysfunction and abnormal proprioception. The nine different explanatory models focus on different domains, including somatic causes, perception, illness behaviour and predisposition. We also found one meta-model, which incorporates these four domains: the cognitive behavioural therapy model.Conclusion Although GPs often face difficulties when providing explanations to patients with MUS, there are multiple explanatory models in the scientific literature that may be of use in daily medical practice.     

Giving an Account of One’s Pain in the Anthropological Interview

In this paper, I analyze the illness stories narrated by a mother and her 13-year-old son as part of an ethnographic study of child chronic pain sufferers and their families. In examining some of the moral, relational and communicative challenges of giving an account of one’s pain, I focus on what is left out of some accounts of illness and suffering and explore some possible reasons for these elisions. Drawing on recent work by Judith Butler (Giving an Account of Oneself, 2005), I investigate how the pragmatic context of interviews can introduce a form of symbolic violence to narrative accounts. Specifically, I use the term “genre of complaint” to highlight how anthropological research interviews in biomedical settings invoke certain typified forms of suffering that call for the rectification of perceived injustices. Interview narratives articulated in the genre of complaint privilege specific types of pain and suffering and cast others into the background. Giving an account of one’s pain is thus a strategic and selective process, creating interruptions and silences as much as moments of clarity. Therefore, I argue that medical anthropologists ought to attend more closely to the institutional structures and relations that shape the production of illness narratives in interview encounters.