Fibromyalgia, chronic fatigue syndrome, and myofascial pain

Abstract:

The prevalence of fibromyalgia in the general population was found to be 2% and increased with age. Multiple traumatic factors, including sexual and physical abuse, may be important initiating events. The most important pathophysiologic studies in fibromyalgia included evidence of altered blood flow to the brain and hypothalamic-pituitary-adrenal dysfunction. The prevalence of chronic fatigue syndrome is much less than that of fibromyalgia. Epidemiologic studies demonstrated that chronic fatigue and symptoms of fibromyalgia are distributed as continuous variables in the general population. No association between chronic fatigue and initial infections was seen in primary care practices.

 

Source: Goldenberg DL. Fibromyalgia, chronic fatigue syndrome, and myofascial pain. Curr Opin Rheumatol. 1996 Mar;8(2):113-23. http://www.ncbi.nlm.nih.gov/pubmed/8732795

 

The use of transfer factors in chronic fatigue syndrome: prospects and problems

Abstract:

Chronic fatigue syndrome (CFS) is a heterogeneous disorder characterized by severe prolonged unexplained fatigue and a variety of associated symptoms such as arthralgias, myalgias, cognitive dysfunction, and severe sleep disturbances.

Many patients initially present with an acute onset of apparent infectious origin with either an upper respiratory or gastrointestinal illness, fever, chills, tender lymphadenopathy, and malaise suggestive of a flu-like illness. In some cases, specific viral infections can be identified at the outset, particularly herpes viruses such as Epstein-Barr virus (EBV), human herpes virus-6 (HHV-6), and cytomegalovirus (CMV).

Transfer factors (TF) with specific activity against these herpes viruses has been documented. With some studies suggesting that persistent viral activity may play a role in perpetuation of CFS symptoms, there appears to be a rationale for the use of TF in patients with CFS and recent reports have suggested that transfer factor may play a beneficial role in this disorder.

This report focuses on the heterogeneity of CFS, the necessity for randomized coded studies, the importance of patient selection and sub-classification in clinical trials, and the need to utilize specific end-points for determining efficacy of treatment.

 

Source: Levine PH. The use of transfer factors in chronic fatigue syndrome: prospects and problems. Biotherapy. 1996;9(1-3):77-9. http://www.ncbi.nlm.nih.gov/pubmed/8993762

 

Use of exercise for treatment of chronic fatigue syndrome

Abstract:

Chronic fatigue syndrome (CFS) is a condition that results in moderate to severe disability, the primary feature of which is fatigue of unknown origin. There is a lot of interest in classifying, characterising and treating patients with CFS. Currently, the two major theories of a medical cause of CFS are viral infection and immune dysregulation.

Patients report critical reductions in levels of physical activity, and many experience ‘relapses’ of severe symptoms following even moderate levels of exertion. Despite this, most studies report CFS patients to have normal muscle strength and either normal or slightly reduced muscle endurance.

Histological and metabolic studies report mixed results: CFS patients have either no impairment or mild impairment of mitochondria and oxidative metabolism compared with sedentary controls.

Current treatments for CFS are symptom-based, with psychological, pharmacological and rehabilitation treatments providing some relief but no cure. Immunological and nutritional treatments have been tried but have not provided reproducible benefits. Exercise training programmes are thought to be beneficial (if ‘relapses’ can be avoided), although few controlled studies have been performed.

CFS is a long-lasting disorder that can slowly improve with time, but often does not. Further studies are needed to better understand the multiple factors that can cause chronic fatigue illness, as well as the effect that exercise training has on the symptoms of CFS.

 

Source: McCully KK, Sisto SA, Natelson BH. Use of exercise for treatment of chronic fatigue syndrome. Sports Med. 1996 Jan;21(1):35-48. http://www.ncbi.nlm.nih.gov/pubmed/8771284

 

Corticotropin releasing hormone in the pathophysiology of melancholic and atypical depression and in the mechanism of action of antidepressant drugs

Abstract:

Hypercortisolism in depression seems to preferentially reflect activation of hypothalamic CRH secretion. Although it has been postulated that this hypercortisolism is an epiphenomenon of the pain and stress of major depression, our data showing preferential participation of AVP in the hypercortisolism of chronic inflammatory disease suggest specificity for the pathophysiology of hypercortisolism in depression.

Our findings that imipramine causes a down-regulation of the HPA axis in experimental animals and healthy controls support an intrinsic role for CRH in the pathophysiology of melancholia and in the mechanism of action of psychotropic agents. Our data suggest that hypercortisolism is not the only form of HPA dysregulation in major depression.

In a series of studies, commencing in patients with Cushing’s disease, and extending to hyperimmune fatigue states such as chronic fatigue syndrome and examples of atypical depression such as seasonal affective disorder, we have advanced data suggesting hypofunction of hypothalamic CRH neurons. These data raise the question that the hyperphagia, hypersomnia, and fatigue associated with syndromes of atypical depression could reflect a central deficiency of a potent arousal-producing anorexogenic neuropeptide.

In the light of data presented elsewhere in this symposium regarding the role of a hypofunctioning hypothalamic CRH neuron in susceptibility to inflammatory disease, these data also raise the question of a common pathophysiological mechanism in syndromes associated both with inflammatory manifestations and atypical depressive symptoms. This concept of hypofunctioning of hypothalamic CRH neurons in these disorders also raises the question of novel forms of neuropharmacological intervention in both inflammatory diseases and atypical depressive syndromes.

 

Source: Gold PW, Licinio J, Wong ML, Chrousos GP. Corticotropin releasing hormone in the pathophysiology of melancholic and atypical depression and in the mechanism of action of antidepressant drugs. Ann N Y Acad Sci. 1995 Dec 29;771:716-29. http://www.ncbi.nlm.nih.gov/pubmed/8597444

 

Chronic fatigue syndrome–a review of the literature

Abstract:

Chronic fatigue syndrome is a clinical condition characterized by abnormal fatigue, subfebrile body temperature, sore throat, lymphadenopathy, arthralgia, myalgia and neuropsychiatric symptoms. Typically, the syndrome develops after a flu-like illness and is markedly exacerbated by exercise. The etiology is unknown and there is no single diagnostic test. The patients may have cognitive dysfunction, immunological and endocrinological abnormalities and abnormal mitochondria. Magnetic resonance imaging scans may show increased uptake of signals in the brain, and single photon emission computerized tomography reveals regional hypoperfusion of the brain. The author discusses similarities and distinctions between the syndrome and depression.

 

Source: Hamre HJ. Chronic fatigue syndrome–a review of the literature. Tidsskr Nor Laegeforen. 1995 Oct 10;115(24):3042-5. [Article in Norwegian] http://www.ncbi.nlm.nih.gov/pubmed/7570537

 

Postviral fatigue syndrome

Abstract:

The post-viral fatigue syndrome occurs sporadically and in local outbreaks (Los Angeles, Akureyri, Royal Free Hospital). The clinical picture is marked by long-lasting muscular fatigue directly following an acute infection. Other conditions associated with pronounced fatigue must be excluded. The diagnostic criteria set up by Centers for Disease Control (CDC) are the ones most commonly used. Aetiology and pathogenesis are unknown. Coxsackie B-virus seems to be associated with some cases at least. Immunological and endocrinological aberration, morphological changes in mitochondria and reduced cerebral blood perfusion have been demonstrated in some patients. There is no specific therapy. It is important for the patient that the symptoms be accepted by the doctor and society in general.

Comment in: [Chronic fatigue syndrome]. [Tidsskr Nor Laegeforen. 1995]

 

Source: Haukenes G, Aarli JA. Postviral fatigue syndrome. Tidsskr Nor Laegeforen. 1995 Oct 10;115(24):3017-22. [Article in Norwegian] http://www.ncbi.nlm.nih.gov/pubmed/7570529

 

Chronic fatigue syndrome (myalgic encephalopathy)

Abstract:

Chronic fatigue syndrome is associated with many misconceptions. In this review, we attempt to summarize various pathogenic hypotheses for this disease and discuss new lines of insight into causes and treatments of this baffling and most frustrating condition.

 

Source: Plioplys S, Plioplys AV. Chronic fatigue syndrome (myalgic encephalopathy). South Med J. 1995 Oct;88(10):993-1000. http://www.ncbi.nlm.nih.gov/pubmed/7481975

Chronic fatigue syndrome: current perspectives on evaluation and management

Abstract:

OBJECTIVE: To describe clinical and laboratory guidelines for assessment and management of patients presenting with chronic fatigue syndrome(CFS).

DATA SOURCES: Relevant international consensus diagnostic criteria and research literature on the epidemiology, pathophysiology, concurrent medical and psychological disturbance and clinical management of CFS.

CONCLUSIONS: Medical and psychiatric morbidity should be carefully assessed and actively treated, while unnecessary laboratory investigations and extravagant treatment regimens should be avoided. No single infective agent has been demonstrated as the cause of CFS, and immunopathological hypotheses remain speculative. The aetiological role of psychological factors is debated, but they do predict prolonged illness. The rate of spontaneous recovery appears to be high. Effective clinical management requires a multidisciplinary approach, with consideration of the medical, psychological and social factors influencing recovery.

Comment in: Chronic fatigue syndrome: is total body potassium important? [Med J Aust. 1996]

 

Source: Hickie IB, Lloyd AR, Wakefield D. Chronic fatigue syndrome: current perspectives on evaluation and management. Med J Aust. 1995 Sep 18;163(6):314-8. http://www.ncbi.nlm.nih.gov/pubmed/7565238

 

Can the chronic fatigue syndrome be defined by distinct clinical features?

Abstract:

To determine whether patients diagnosed as having chronic fatigue syndrome (CFS) constitute a clinically homogeneous class, multivariate statistical analyses were used to derive symptom patterns and potential patient subclasses in 565 patients. The notion that patients currently diagnosed as having CFS constitute a single homogeneous class was rejected.

An alternative set of clinical subgroups was derived. The validity of these subgroups was assessed by sociodemographic, psychiatric, immunological and illness behaviour variables. A two-class statistical solution was considered most coherent, with patients from the smaller class (27% of the sample) having clinical characteristics suggestive of somatoform disorders. The larger class (73% of sample) presented a more limited combination of fatigue and neuropsychological symptoms, and only moderate disability but remained heterogeneous clinically. The two patient groups differed with regard to duration of illness, spontaneous recovery, severity of current psychological morbidity, utilization of medical services and CD8 T cell subset counts. The distribution of symptoms among patients was not unimodal, supporting the notion that differences between the proposed subclasses were not due simply to differences in symptom severity.

This study demonstrated clinical heterogeneity among patients currently diagnosed as CFS, suggesting aetiological heterogeneity. In the absence of discriminative clinical features, current consensus criteria do not necessarily reduce the heterogeneity of patients recruited to CFS research studies.

 

Source: Hickie I, Lloyd A, Hadzi-Pavlovic D, Parker G, Bird K, Wakefield D. Can the chronic fatigue syndrome be defined by distinct clinical features? Psychol Med. 1995 Sep;25(5):925-35. http://www.ncbi.nlm.nih.gov/pubmed/8588011

 

Fibromyalgia, chronic fatigue syndrome, and myofascial pain syndrome

Abstract:

Two important studies in which nuclear magnetic resonance spectroscopy was used convincingly demonstrated that muscle is not the primary pathologic factor in fibromyalgia. There were further studies reporting that fibromyalgia-chronic fatigue syndrome may follow well treated Lyme disease or mimic Lyme disease. The longest therapeutic trial to date in fibromyalgia demonstrated an initial modest effect of tricyclic medications, but at 6 months that efficacy was no longer evident. Investigation in both fibromyalgia and chronic fatigue syndrome now focuses on the central nervous system. The use of new technology, eg, neurohormonal assays and imaging such as single-photon emission computed tomography scan, may be important in understanding these elusive conditions.

 

Source: Goldenberg DL. Fibromyalgia, chronic fatigue syndrome, and myofascial pain syndrome. Curr Opin Rheumatol. 1995 Mar;7(2):127-35. http://www.ncbi.nlm.nih.gov/pubmed/7766493