In many countries of the world, there is now a dual epidemic of tuberculosis and HIV disease. HIV specifically eliminates the tissue macrophages and CD4 lymphocytes, the very cells that provide immunity against tuberculosis. Tuberculosis is one of the more virulent opportunistic infections and it therefore appears fairly early in HIV disease. For the same reasons, bone and joint tuberculosis is becoming much more common. The disturbances of the lymphocyte count, ESR and antigen skin tests associated with HIV, now often make tuberculosis difficult to distinguish from other inflammatory lesions. The only change in the pattern of disease that we have so far registered is an increased incidence of disease affecting the lumbar spine. HIV-positive patients respond poorly to chemotherapy and are subject to drug sensitivity reactions. Major surgery is fraught with infectious complications and should be avoided. Once Pott's paraplegia has developed, the demise of the HIV-positive patient is rapid.

Six different mosquito-borne viruses (Chikungunya, O'nyong-nyong, Mayaro, Ross River, Sindbis and Barmah Forest) have been associated with arthritis in humans. These viruses are prevalent in the tropics and subtropics and they produce similar symptoms, consisting of fever, joint pains and rash. The symptoms are usually of short duration, around 1 week; complete recovery is the rule apart from exceptional cases of Chik infection. Precise diagnosis requires a serological service which is not available in many parts of the tropics these days. Treatment is symptomatic and there is no vaccine currently available. With an increasing number of visitors to the tropics being exposed to potential infection and with rapid air transport it is possible that visitors may return home during the viraemic incubation stage, infect the local mosquito populations and then develop clinical disease.

Reactive arthritis is common in HIV-positive patients and may be mistaken for septic arthritis. We feel that the association is probably, in part, due to the increased incidence of diarrhoeal diseases in HIV-infected patients rather than a specific effect of HIV on the synovium. Disabling, chronic, sero-negative polyarthritis is common in the later stages of HIV infection and further palliative therapeutic strategies are urgently needed.

HIV disease has reached epidemic proportions in Africa over the last decade and is severely stretching the health services of the many poor countries of the region. Increased sepsis during fracture surgery and the late infection of implants impels us to rethink many standard methods of treatment. Musculoskeletal infections, including tropical pyomyositis and long bone haematogenous osteomyelitis, are now common manifestations of advanced HIV disease in adults. Despite their severe infections, such patients may survive for more than 5 years and certainly cannot be written off as terminally ill. Treatment is often prolonged and, in the case of osteomyelitis, may necessitate amputation. These patients now occupy many of the available orthopaedic beds.

The incidence of RF and RHD in the tropics remains high, with a high proportion of children suffering from carditis with the first attack. Severe, incapacitating haemodynamic disturbances occur early. Many patients are seen with established RHD at their first visit, and the default rate is high. Poverty, overcrowding, poor transport facilities, understaffed and overburdened clinics, and poor follow-up add to the problem. A genetic predisposition to develop RHD appears to be important in certain countries like India, Egypt and Turkey, but no work to show this has been done in black Africa. Secondary prophylaxis remains the most practical means of controlling the disease in the tropics. Compliance with long-term prophylaxis depends on organized and concerted efforts of physicians, other health personnel, parents, teachers, and the community.

It has been recognized that the remarkable decline in infant mortality and the extension in human lifespan involving both developing and developed countries alike, has been influenced by social and economic developments and public health orientated measures (such as clean water and sewerage) rather more than by developments in medical research. However, the identification of important disease risk factors for a number of common conditions such as smoking, solar exposure, dietary fat and alcohol has led to further reductions in disease prevalence and mortality, at least in some countries. The varied success of strategies to reduce the mortality from circulatory, nutritional and diseases due to infection has had the predictable result of leaving communities more exposed to the chronic non-communicable diseases, especially those affecting the elderly. The COPCORD community-based studies, carried out largely in tropical Asia/Pacific countries, have indicated that the burden of musculoskeletal conditions as far as pain and disability, as well as from an economic point of view, are substantial and WHO has called for increased research and educational activities into the causes and consequences of chronic disease and in particular rheumatic diseases. To the problems of an increasing ageing population can be added the rapid growth of urban populations, new occupational stresses, lifestyle changes and a number of other factors (WHO, 1984). The common community-based rheumatic diseases are not RA or SLE that dominate admissions to hospital arthritis clinics. Pain and disability are most often caused by osteoarthritis, especially knee OA, and various soft tissue rheumatic problems producing neck, back, shoulder and elbow pain. Viral and reactive arthritis cannot be ignored and the complications from osteoporosis (although not normally considered a rheumatic condition), are a significant threat to ageing populations worldwide. It is clear that for many of these conditions, certain risk factors have been identified and that preventative strategies are becoming available although far more detailed research is still required (Wigley, 1993). Community education is an essential part of prevention and treatment and the ILAR-sponsored publication Aches and Pains--Living with Arthritis and Rheumatism (Hampton, 1992) is available in at least 10 different languages and fills an important need. Education helps to influence not only knowledge but also skills and attitudes.(ABSTRACT TRUNCATED AT 400 WORDS)

Over the past two decades in Latin America, there has been a slow but definite upsurge in studies on the epidemiology of RD but, thus far, the data on the distribution and determinants of RD in the population are limited, and knowledge of time trends and geographical differences in disease risk are lacking. It is still not clear what proportion of disabilities are due to RD. The impact of RD on communities in developing countries is believed to be substantial, due to the cost of treatment and rehabilitation, and loss of earnings. There are important gaps in our knowledge, leaving unanswered such questions as the cost of treatment and rehabilitation, and loss of earnings. There are important gaps in our knowledge, leaving unanswered such questions as the cost to society of RD and the potential impact of RD prevention on the overall burden of disability. It is also important to point out, however, that from the relatively simple descriptive studies which dominated the RD literature a few years ago, we are now witnessing a shift towards increasing sophistication in study design and incorporation of multicentre collaboration. The rheumatologists and epidemiologists in LA who have managed to continue their work merit admiration. Even with unavoidable omissions, this summary demonstrates that the epidemiology of RD is alive and well in LA, where it has managed to continue to function under extremely difficult conditions. Yet, few methodologists appear to have directed their attention to the unique challenges of conducting studies in a resource-poor environment.(ABSTRACT TRUNCATED AT 250 WORDS)

A firm theoretical basis for patient education in rheumatic disease care has been built up over the past 10 to 15 years. Education in self-management has enabled patients to control symptoms and become partners in care with their health providers. Education for fibromyalgia patients has come to the foreground during the last 5 years as health professionals have come to understand the syndrome better and recognize the role that stress plays in the exacerbation of symptoms. A few controlled trials of various strategies, such as aerobic conditioning and cognitive-behavioural techniques, have been reported recently. All have shown significant benefits to patients with fibromyalgia. Only one controlled trial has studied the effects of a self-management education programme alone. The results of this programme were positive. Self-efficacy and life quality were enhanced. This programme and an uncontrolled programme that integrated many strategies have shown some of the first positive long-term indications that patients who are treated intensively for even a short time can continue to improve as they practice self-management techniques. There is still a need for further documentation of non-drug treatment strategies and especially further research into who is helped by which strategies, the optimal length of time for a programme, and the need for ongoing treatment.

Many different interventions have been studied in the therapy of fibromyalgia syndrome (Tables 1 and 2). While most have been effective, in general these trials have been short term. Furthermore, important or substantial improvement, when it has been assessed, occurs in only small proportions of patients. Long-term, comparative trials of both efficacy and toxicity are necessary. Trials such as these require large numbers of patients (compared with placebo-controlled trials, which are generally impractical in long-duration trials due to the large numbers of dropouts in the placebo arm) and therefore are expensive and difficult to accomplish. Two other approaches offer potential solutions to the problem of adequate long-term comparative trials: (a) N-of-1 trials and (b) meta-analysis. N-of-1 trials have the advantage of random assignment, double-blinding and multiple potential comparisons in the same patient. Meta-analysis involves combining the results of studies, which individually may have conflicting results and lack adequate statistical power, to reach an overall result with sufficient statistical power to make meaningful conclusions, especially with respect to comparative efficacy. Peluso and colleagues (1993) have performed a recent meta-analysis of available therapies in fibromyalgia syndrome and found that the effect-size (a standardized measure of the efficacy of a given therapy) of several non-medication therapies such as electroacupuncture exceeded that of traditional medication therapies. Unfortunately, lack of uniformity in the use of outcome measures across included trials and the small numbers of comparable non-medication trials makes definitive conclusions regarding relative efficacy of therapies difficult. Nevertheless, application of meta-analytic methods such as these should facilitate future comparisons of different interventions. Ideally, future clinical trials in fibromyalgia syndrome should employ the same outcome measures to permit application of these methods. Few trials have assessed improvement in functional status. Functional status measures such as the HAQ (Fries et al., 1980), the Fibromyalgia Impact Questionnaire (Burckhardt et al, 1991) or similar instruments should be employed in future studies of therapy in fibromyalgia. Given that individual modalities appear to confer relatively modest benefit on average. Combination approaches are reasonable, although randomized, blinded trials to assess these approaches are methodologically complex. Several preliminary studies which have addressed this approach appear promising (see Chapter 12; Goldenberg et al, 1993). Finally, no studies have yet assessed the comparative cost-efficacy of available treatments. Controlled trials which address the cost-efficacy of commonly employed, but unproven treatments such as physiotherapy chiropractic manipulation and injection techniques are urgently needed.

In summary, we have presented the physical medicine and rehabilitation medicine approaches for treating patients with fibromyalgia and the myofascial pain syndromes. The importance of approaching these patients from a holistic and multidisciplinary standpoint has been stressed, paying attention to the physical, emotional, spiritual and behavioural components of the presentation. Although fibromyalgia and the myofascial pain syndromes are two distinct conditions, they often overlap, and when they do the myofascial component should be treated first. However, the clinician should remember that pain, tissue dysfunction and disability from pain are all separate issues and should be treated as such. Treatment in all cases should be individualized and comprehensive. It is imperative to make the patient an active participant in his care and to establish mutually agreed upon goals at the outset of treatment. It is important to establish an adequate and appropriate home exercise programme to supplement formal treatment. A good home exercise programme should stress both stretching and strengthening. Formal treatment programmes should not be geared to pain relief alone but rather to restoration of function, and return to functioning lifestyles. The clinician has available a wide array of modalities and tools to control pain, but the major goal of all treatment programmes is to restore individuals to functional lifestyles and to promote both physical and emotional flexibility, balance and 'wellness'. It is often necessary to involve the family unit as an inherent and critical part of the treatment team, particularly with the patient who continues to be dysfunctional despite apparently appropriate treatment. Although treatment always starts at the tissue level, a good treatment programme must always be holistic in nature and treat the tissues, the patient as a whole, and his or her environmental stressors and contingencies as well.

MFP is a regional muscle pain disorder characterized by localized muscle tenderness and pain and is the most common cause of persistent regional pain. The affected muscles may also display an increased fatiguability, stiffness, subjective weakness, pain on movement and slightly restricted range of motion that is unrelated to joint restriction. MFP is frequently overlooked as a diagnosis because it is often accompanied by signs and symptoms in addition to pain, coincidental pathological conditions, and behavioural and psychosocial problems. Chronic pain characteristics often precede or follow the development of MFP. Evaluation of MFP includes locating the trigger points and muscles involved as well as recognition of the contributing factors. Management of the syndrome naturally follows with muscle exercises, therapy to the trigger points, and reduction of all the contributing factors. The short-term goal is to restore the muscle to normal length and posture and full joint range of motion with exercises and trigger point therapy. The long-term goals include reducing the symptoms and their negative effects while helping the patient return to normal function without the need for future health care. The difficulty in managing MFP lies in the critical need to match the level of complexity of the management programme with the complexity of the patient's situation. Failure to address the entire problem, through a team approach if needed, may lead to failure to resolve the pain and perpetuation of a chronic pain syndrome.

A review of the evidence from diurnal physiological, seasonal environmental and prospective studies of social-behavioural functions suggest that a chronobiological theoretical model provides a comprehensive basis for the dynamics of central nervous system mechanisms, the assessment and the management of patients with fibromyalgia. The chronobiological model stresses the importance of temporal variation and the factors that influence and govern recurrent patterns of biological functions and behaviour that determine health and illness. Finally, the theory allows for an integrated study of brain, behaviour and somatic functions over time and emphasizes that such a comprehensive approach is core to any therapeutic intervention.

Since the first comprehensive description of the symptoms of FMS by Yunus et al (1981), numerous investigations have confirmed that FMS is a clinical entity. However, the aetiology of the syndrome is still not fully elucidated. It seems, however, logical to place the origin of the disorder in the muscle. Muscle pain, especially at the muscle-tendon junctions, fatigue and stiffness are the first symptoms. A malfunction of energy metabolism has been detected in part of the muscle fibres. However, it has to be considered that the muscle is not an isolated entity. Its activity is controlled by segmentally arranged motor units of the ventral horn of the spinal cord in response to proprioceptive afferent signals arising in the muscle spindles or in other sensory elements including nociceptors. Together with supraspinal descending inputs, the spinal motor neurone pool is the common final pathway for segmental and suprasegmental inputs, making the motor system extremely powerful for adaptive adjustments but also vulnerable if deficits occur in either of these input levels. A second, recently discovered abnormality seen in FMS is a lowered serotonin level in peripheral and most likely also central structures. The underlying mechanism seems to be defective absorption of the precursor amino acid tryptophan from the gut. Serotonin is involved centrally in the regulation of the sleep pattern, and at the spinal level it acts as a 'gain setter' of motoneurone excitability and suppresses signal transmission of noxious stimuli in dorsal horn neurones. Either of these two disturbances, muscle energy depletion or serotonin deficiency, could by itself evoke many of the symptoms of FMS, and their combined appearance will perpetuate the disease. Depressed levels of somatomedin C, caused by a deficit of stage 4 sleep-dependent release of GH, might represent an additional factor in preventing proper development or repair of myoskeletal structures. Malabsorption of certain amino acids, possibly due to a genetic disorder of gut transport mechanisms, may constitute an additional deleterious factor. The abnormalities found in the HPA and HPT axis may be seen as an attempt of the organism to restore homeostasis. The stimulus eliciting this counter-regulatory reaction may be pain or other afferent signals which normally do not reach the central nervous system. It is doubtful whether the unspecific activation of the HPA axis in a non-inflammatory disease is beneficial.(ABSTRACT TRUNCATED AT 400 WORDS)

The clinical phenomenon of the MTrP is accessible to any clinician who takes the time to learn to palpate skeletal muscle gently and carefully, and who is willing to learn the functional anatomy necessary to understand the regional spread of MTrPs through functional muscle units (Travell and Simons, 1992). Yet despite the years of clinical study of MPS, the pathophysiology of the central feature, the trigger point, has remained elusive. Many investigators have contributed to the general understanding of the mechanisms of pain perception, but we owe a particular debt of gratitude to Dr Seigfried Mense of Heidelberg for his pursuit of the study of pain originating in muscle lesions. However, Dr Mense would be the first to caution us against the direct transference of the results obtained with an inflammatory lesion produced in the experimental animal to the pain of MTrPs in the clinic patient. Notwithstanding that, researchers in the field of pain have given us an understanding of the basis for the hyperalgesia, allodynia and the previously difficult-to-understand finding of referred pain zones that we see daily in our patients. Finally, the interesting initial observations of Hubbard and Berkoff (1993), suggesting that the muscle spindle may be associated with the trigger point, open yet another door in our understanding of the nature of MPS.

It may be concluded that both peripheral and central mechanisms may operate in the pathophysiology of both impaired muscle function and pain in FM. These mechanisms may in part be attributable to physical deconditioning and disuse of muscle secondary to the characteristic pain and fatigue so often seen in FM. Most likely the initiation of this condition is multifactorial and the combination of peripheral and central factors that constitute a vicious circle may perpetuate the condition into a chronic state.

The conclusion is that no one single mechanism can explain FMS and is thus in that sense a compromise. FMS in some patients may start in the muscle, in other patients in the brain. The combination of peripheral and central factors is the key to the pathogenesis of FMS as long as FMS is defined as a pain syndrome.