A case for studying the psychological aspects of pain is made through a discussion of the problems resulting from investigations of the so-called rheumatoid personality. Following a review of the current theory about pain mechanisms, proposals are made about the best ways of measuring pain in the rheumatological disorders. Later sections tackle issues about the many meanings of pain. Discussion particularly focuses on expectations about pain, on lay beliefs about the rheumatic diseases and on beliefs about pain control. Recommendations are made about the ways in which some of these psychological features might profitably be incorporated into the management of clinical pain.

RA patients may develop a coping style early in the illness and utilize their favourite strategies when confronted with the stressor of illness. Little distinction was found between specific illness stressors, i.e. pain vs. disability, or whether a strategy had been successfully used before. In the face of a new illness, strategies may be tried out over a period of time, as the stressor is one for which everyday coping strategies are no longer appropriate or sufficient. As one health psychologist has written, 'Individuals' coping responses are often spontaneous; that is, people do what comes naturally to them and what has worked in the past. But sometimes these efforts will not be enough. The stressor may be so novel, so chronic, or so elusive that people's own efforts may be unsuccessful in reducing stress' (Taylor, 1985, p 213).

Organized educational programmes and individual educational counselling are primary means by which health care providers equip rheumatic disease patients with the skills and knowledge necessary to monitor and manage variable symptoms. Many outpatients educational programmes were evaluated in the 1980s. In brief, well designed programmes are generally effective in improving knowledge and compliance with a regimen, and in reducing pain, depression, and disability. However, most persons with arthritis never use such programmes. Greater emphasis is needed on education of patients at the time of the clinical encounter, where the greatest opportunity lies for reaching the greatest number. Researchers have examined the dynamics of the doctor-patient interaction during the clinical encounter. Results show that: better information sharing leads to improved patient satisfaction, compliance, and health outcomes; information sharing could be greatly improved; and doctors and patients can be trained to improve information sharing, resulting in improved outcomes. A review of attribution and decision-making theory and the empirical literature on doctor-patient communication suggests a number of techniques that could be usefully incorporated into the management of each patient. These include: (1) encouraging patients to write down their concerns before each visit; (2) addressing each concern specifically, however briefly; (3) asking patients what they think has caused their problems; (4) tailoring treatments to patients' goals and preferences as possible; (5) explaining the purpose, dosage, common side-effects and inconveniences, and how to judge the efficacy of each treatment, including length of trial; (6) checking patients' understanding; (7) anticipating problems in compliance with treatment plans, and discussing methods to cope with common problems; (8) writing down the diagnosis and treatment plan to help patients remember; (9) giving out written materials that are now widely available; (10) reinforcing patients' confidence in their ability to manage their regimen; (11) using ancillary personnel in patient education; and (12) referring patients to organized programmes in the community.

Ankylosing spondylitis is an inflammatory disease involving entheses and joints, especially those in and around the spine. The most widespread involvement of the respiratory system by this disease occurs when this pathological process gives rise to chest wall pain, diminished chest wall movement and a dorsal stoop. As healing of the inflammatory process takes place, calcification occurs which leads to rigidity of these structures, with consequent loss of chest expansion which is exacerbated by the increasingly kyphotic spinal posture and intercostal muscle inefficiency. Fortunately diaphragmatic function is unimpaired and compensates well, so that there are only minor restrictive changes found in tests of respiratory function. Treatment is by mobilizing physiotherapy coupled with a home exercise programme encouraging mobility and improved cardiovascular fitness. As with many physical treatment methods, good quality controlled studies of efficacy are rare. The role of medication is to ease symptoms and hence enable exercise. Apical fibrobullous lung disease is found in a small proportion of AS patients. The initial changes are mainly fibrotic, with bullae becoming more important as the condition progresses. The disease may progress to major cavitation, which is prone to infection, especially with aspergillae. No methods exist which can either prevent the development of fibrobullous disease or halt its progression, although this may happen spontaneously. The main effects of therapy are aimed at the diagnosis and treatment of superinfection. Treatment of established aspergillosis, especially when aspergilloma formation has taken place, is unsatisfactory and carries substantial risks of morbidity and death. Non-apical pleural involvement, including pleural effusion, is very rare. The most common cause of breathlessness in AS patients is cardiac involvement by the disease.

Scleroderma (SSc) is a disease characterized by skin fibrosis but it is the end-organ effect of microvascular injury and fibrosis that is important prognostically. Pulmonary involvement in SSc patients, either of parenchymal fibrosis and/or pulmonary hypertension, is a major cause of morbidity and mortality. Interstitial lung disease occurs more commonly in patients with diffuse SSc and is associated with a loss of lung volume, as well as a defect of gas exchange. Parenchymal fibrosis may also cause pulmonary hypertension. Isolated pulmonary hypertension occurs exclusively in patients with limited SSc and is detectable by a reduced DCO. The early identification of either manifestation is difficult. Patients may have minimal symptoms, unremarkable physical findings, normal chest radiographs and/or minimally abnormal pulmonary function tests at a time when significant lung pathology is present. It is essential to attempt to identify pulmonary disease early, at a potentially reversible stage. Multiple therapeutic endeavours have yielded only short-term or minimal benefits in symptoms and pulmonary function, and thus a major alteration in SSc pulmonary prognosis has not been achieved. Further study of the pathogenesis of this disease manifestation will be helpful in its earlier identification and intervention.

Significant abnormalities in pulmonary function are encountered in about 24% of patients with primary Sjögren's syndrome. The most common cause of dyspnoea is interstitial fibrosis, with a prevalence of around 8%, but a number of other pathologies may be encountered in the lungs of these patients (Table 1). Lymphoproliferative disorders are relatively uncommon, but these apparently benign lesions may harbour malignant potential. Interstitial fibrosis and the lymphoproliferative disorders may be responsive to corticosteroids or cytotoxic agents, and it is therefore important to establish an accurate diagnosis at an early stage. On the basis of our experience we would recommend the investigative strategy outlined below. Patients should be screened for significant lung disease by taking a careful history of respiratory symptoms followed by standard pulmonary function testing (including measurement of carbon monoxide diffusing capacity) and chest radiography. High resolution computed tomography is a non-invasive technique that should prove superior to chest radiography in the detection of early cases of interstitial fibrosis. When the disease is patchy it may be useful in identifying areas of maximal involvement for subsequent biopsy. Bronchoalveolar lavage is a sensitive tool in the non-smoker, but lacks the specificity to command a significant role in the investigation of pulmonary pathology in these patients. One exception to this may be in the investigation of the clonality of lymphocytes which may allow early and specific diagnosis of lymphomatous proliferation. The application of techniques such as the polymerase chain reaction may assist in the investigation of the role of the Epstein-Barr virus in the causation of lymphoproliferative lesions. In most patients with significant symptoms and abnormalities of pulmonary function a tissue diagnosis will be required, either by transbronchial biopsy or by open lung biopsy. Both bronchial and interstitial lung tissue should be obtained where possible. Histological confirmation is probably mandatory when there is a recent history of parotid enlargement, weight loss or the appearance of a monoclonal gammopathy. Advances in our understanding of the mechanisms of the MALT system may provide the key to unlocking some of the mysteries of 'autoimmune' diseases such as Sjögren's syndrome. The response of lymphoproliferative disorders to immunosuppressive therapy provides hope that if the diagnosis of sicca syndrome can be made earlier lymphocyte induced tissue damage may be halted or reversed.

Systemic lupus erythematosus (SLE) is the most common of the connective tissue disorders and can involve virtually any organ in the body. It is associated with pleuropulmonary manifestations in well over 50% of cases. Pleuritis with or without pleural effusion is the most common manifestation and can be particularly troublesome to manage but is rarely life-threatening. More serious manifestations in the lung include acute lupus pneumonitis with or without alveolar haemorrhage, chronic lupus pneumonitis and pulmonary hypertension. These all contribute significantly to overall mortality in SLE. The association between SLE and the antiphospholipid syndrome, leading to venous thrombosis and pulmonary embolism, is well recognized. Up to 20% of all cases of SLE present in childhood and many of these have pulmonary features at presentation or during the course of their illness. Sepsis is one of the main causes of death in SLE and pulmonary sepsis in these often immunocompromised patients contributes a significant proportion. Several drugs can produce a clinical syndrome that has many of the clinical and immunological features of SLE. Pleuritis may be seen in up to half of these cases of drug induced SLE. The development of SLE and conditions such as sarcoidosis or asbestosis in the same patient may represent a simple coincidence but there is some evidence for a closer association between these disorders.

No more than 100 patients with respiratory involvement in Behçet's disease have been described in the literature. Haemoptysis, cough, dyspnoea and pleuritic chest pain are the main symptoms. Vasculitis and thrombosis of the great pulmonary vessels is the underlying condition in the majority of patients. Aneurysmal formation and rupture is possible and constitutes the most life-threatening aspect of the disease. Behçet's syndrome should be considered in the differential diagnosis of haemoptysis and veno-occlusive disease, especially where large vessels are involved. Early detection and treatment is mandatory to save the patient's life. Other pleuropulmonary manifestations described, such as fibrosing alveolitis and pleural disease, occur less frequently in Behçet's disease, and carry a better prognosis.

In summary, it appears that factors such as smoking and the presence of secondary Sjögren's syndrome might be important in predisposing the rheumatoid patient to the development of lung disease. Genetic factors may moderate or magnify these risks. At a cellular level, specific macrophage colonies within the lung may interact with a subgroup of CD4 T lymphocytes to produce unopposed B-cell activation, leading to local IgM production and the formation of immune complexes. This can damage lung both directly by cytolysis and indirectly by granulocyte recruitment through the release of neutrophil chemotaxins. Early in the evolution of these processes, steroids appear able to reduce lymphocyte numbers and prevent lung damage occurring, presumably by immunological mechanisms, while later they may reduce granulocyte numbers and activity, halting further progression of lung disease in some patients, perhaps by a direct anti-inflammatory effect. Confirmation of these mechanisms and the development of more specific therapeutic tools is probably dependent on studies which examine lung tissue directly by biopsy and may be aided by the application of more sensitive imaging techniques.

Drug-induced lung disease during treatment with antirheumatic drugs should be considered in all patients receiving these agents who develop new pulmonary symptoms. When a potential drug-related reaction is identified, the possible offending agents should be discontinued, appropriate respiratory support initiated, and a thorough investigation for other causes of respiratory disease launched to exclude infection or other pulmonary processes. Lung biopsy may be needed to define the disorder completely. In patients with acute pneumonitis, the use of corticosteroids should be considered. Although significant morbidity and even mortality may occur with drug-induced pulmonary events, proper and prompt evaluation and treatment of these disorders can often result in complete resolution of the pulmonary disease.