Altered glucocorticoid regulation of the immune response in the chronic fatigue syndrome

Abstract:

It is increasingly recognized that glucocortiocoids (GCs) can have subtle modulatory effects in immunoregulation rather than having generalized immunosuppressive effects. GCs suppress Th1 cells and cellular immunity, but may favor Th2 responses and humoral immunity. The chronic fatigue syndrome (CFS) appears to be associated with a disturbed HPA-axis. Moreover, CFS patients show several immunological changes suggestive of decreased cellular immunity. It is postulated herein that in CFS patients a decreased Th1/Th2 balance may be the result of selective effects of GC on the IL-10/IL-12 regulatory circuit.

 

Source: Visser JT, De Kloet ER, Nagelkerken L. Altered glucocorticoid regulation of the immune response in the chronic fatigue syndrome. Ann N Y Acad Sci. 2000;917:868-75. http://www.ncbi.nlm.nih.gov/pubmed/11268418

 

Chronic fatigue syndrome and fibromyalgia: clinical assessment and treatment

Abstract:

Chronic fatigue syndrome (CFS) and fibromyalgia (FM) are closely related illnesses of uncertain etiology. This article reviews the research literature on these biobehavioral conditions, with an emphasis on explanatory models, clinical evaluation of comorbid psychiatric disorders, assessment of stress factors, pharmacologic and alternative therapies, and cognitive-behavioral treatment studies. Furthermore, clinical protocols suitable for professional practice are presented based on an integration of the authors’ clinical observations with published data. The article concludes with the recognition that mental health professionals can offer substantial help to these patients.

Copyright 2001 John Wiley & Sons, Inc.

 

Source: Friedberg F, Jason LA. Chronic fatigue syndrome and fibromyalgia: clinical assessment and treatment.  Clin Psychol. 2001 Apr;57(4):433-55. http://www.ncbi.nlm.nih.gov/pubmed/11255201

 

Fibromyalgia, chronic fatigue syndrome, and myofascial pain syndrome

Abstract:

The prevalence of chronic widespread pain in the general population in Israel was comparable with reports from the USA, UK, and Canada. Comorbidity with fibromyalgia (FM) resulted in somatic hyperalgesia in patients with irritable bowel syndrome. One sixth of the subjects with chronic widespread pain in the general population were also found to have a mental disorder.

Mechanisms involved in referred pain, temporal summation, muscle hyperalgesia, and muscle pain at rest were attenuated by the N-methyl-D-aspartate (NMDA) antagonist, ketamine, in FM patients. Delayed corticotropin release, after interleukin-6 administration, in FM was shown to be consistent with a defect in hypothalamic corticotropin-releasing hormone neural function. The basal autonomic state of FM patients was characterized by increased sympathetic and decreased parasympathetic systems tones.

The severity of functional impairment as assessed by the Medical Outcome Survey Short Form (SF-36) discriminated between patients with widespread pain alone and FM patients. Chronic fatigue syndrome (CFS) occurred in about 0.42% of a random community-based sample of 28,673 adults in Chicago, Illinois.

A significant clinical overlap between CFS and FM was reported. Cytokine dysregulation was not found to be a singular or dominant factor in the pathogenesis of CFS. A favorable outcome of CFS in children was reported; two thirds recovered and resumed normal activities. No major therapeutic trials in FM and CFS were reported over the past year.

 

Source: Buskila D. Fibromyalgia, chronic fatigue syndrome, and myofascial pain syndrome. Curr Opin Rheumatol. 2001 Mar;13(2):117-27. http://www.ncbi.nlm.nih.gov/pubmed/11224736

 

Neuropsychological functioning in chronic fatigue syndrome: a review

Abstract:

OBJECTIVE: In this paper we review critically the current status of neurocognitive studies in patients with chronic fatigue syndrome (CFS).

METHOD: CFS literature was monitored as part of a large research project which involved several neuropsychological and psychopathological studies. The literature survey was the result of several consecutive searches on Medline and PsycInfo databases.

RESULTS: The neurocognitive studies are reviewed in terms of scientifically accepted aspects of attention and memory. In addition, we review possible explanations for cognitive dysfunction in CFS. This is preceded with a discussion of the methodological limitations that are considered to explain inconsistencies across neuropsychological studies in CFS.

CONCLUSION: The current research shows that slowed processing speed, impaired working memory and poor learning of information are the most prominent features of cognitive dysfunctioning in patients with CFS. Furthermore, to this date no specific pattern of cerebral abnormalities has been found that uniquely characterizes CFS patients. There is no overwhelming evidence that fatigue is related to cognitive performance in CFS, and researchers agree that their performance on neuropsychological tasks is unlikely to be accounted solely by the severity of the depression and anxiety.

 

Source: Michiels V, Cluydts R. Neuropsychological functioning in chronic fatigue syndrome: a review. Acta Psychiatr Scand. 2001 Feb;103(2):84-93. http://www.ncbi.nlm.nih.gov/pubmed/11167310

 

Sleep and circadian rhythm disorders in fibromyalgia

Abstract:

Fibromyalgia (FM) is a syndrome of generalized muscle pain that is also associated with equally distressing symptoms of sleep disturbance and fatigue. FM shows clinical overlap with other stress-associated disorders, including chronic fatigue syndrome (CFS) and depression. All of these conditions have the features of disrupted sleep patterns and dysregulated biologic circadian rhythms, such as stress hormone secretion. This review focuses on the role of sleep and circadian rhythm disorders in FM and, in the absence of any specific treatment for FM, presents a pragmatic therapeutic approach aimed at identifying and treating comorbid sleep and depressive disorders, optimizing sleep habits, and judicious use of pharmacologic agents.

 

Source: Korszun A. Sleep and circadian rhythm disorders in fibromyalgia. Curr Rheumatol Rep. 2000 Apr;2(2):124-30. http://www.ncbi.nlm.nih.gov/pubmed/11123049

 

Sympathetic nervous system function in fibromyalgia

Abstract:

This review focuses on studies of the sympathetic nervous system in fibromyalgia (FM). First, a brief review of the sympathetic system, and its relationship to the human stress response, is outlined. Then various studies of functional assessment of sympathetic function in FM are highlighted. Certain methods of assessment (eg, heart rate variability, biochemical, and psychophysical responses to various stressors) that we believe to be of specific importance for future research are discussed in greater detail. Finally, findings on autonomic function in related disorders–specifically, chronic fatigue syndrome, irritable bowel syndrome, and migraine–will be briefly presented.

 

Source: Petzke F, Clauw DJ. Sympathetic nervous system function in fibromyalgia. Curr Rheumatol Rep. 2000 Apr;2(2):116-23. http://www.ncbi.nlm.nih.gov/pubmed/11123048

 

The sympathetic nerve–an integrative interface between two supersystems: the brain and the immune system

Abstract:

The brain and the immune system are the two major adaptive systems of the body. During an immune response the brain and the immune system “talk to each other” and this process is essential for maintaining homeostasis. Two major pathway systems are involved in this cross-talk: the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS). This overview focuses on the role of SNS in neuroimmune interactions, an area that has received much less attention than the role of HPA axis.

Evidence accumulated over the last 20 years suggests that norepinephrine (NE) fulfills the criteria for neurotransmitter/neuromodulator in lymphoid organs. Thus, primary and secondary lymphoid organs receive extensive sympathetic/noradrenergic innervation. Under stimulation, NE is released from the sympathetic nerve terminals in these organs, and the target immune cells express adrenoreceptors.

Through stimulation of these receptors, locally released NE, or circulating catecholamines such as epinephrine, affect lymphocyte traffic, circulation, and proliferation, and modulate cytokine production and the functional activity of different lymphoid cells. Although there exists substantial sympathetic innervation in the bone marrow, and particularly in the thymus and mucosal tissues, our knowledge about the effect of the sympathetic neural input on hematopoiesis, thymocyte development, and mucosal immunity is extremely modest.

In addition, recent evidence is discussed that NE and epinephrine, through stimulation of the beta(2)-adrenoreceptor-cAMP-protein kinase A pathway, inhibit the production of type 1/proinflammatory cytokines, such as interleukin (IL-12), tumor necrosis factor-alpha, and interferon-gamma by antigen-presenting cells and T helper (Th) 1 cells, whereas they stimulate the production of type 2/anti-inflammatory cytokines such as IL-10 and transforming growth factor-beta.

Through this mechanism, systemically, endogenous catecholamines may cause a selective suppression of Th1 responses and cellular immunity, and a Th2 shift toward dominance of humoral immunity. On the other hand, in certain local responses, and under certain conditions, catecholamines may actually boost regional immune responses, through induction of IL-1, tumor necrosis factor-alpha, and primarily IL-8 production.

Thus, the activation of SNS during an immune response might be aimed to localize the inflammatory response, through induction of neutrophil accumulation and stimulation of more specific humoral immune responses, although systemically it may suppress Th1 responses, and, thus protect the organism from the detrimental effects of proinflammatory cytokines and other products of activated macrophages.

The above-mentioned immunomodulatory effects of catecholamines and the role of SNS are also discussed in the context of their clinical implication in certain infections, major injury and sepsis, autoimmunity, chronic pain and fatigue syndromes, and tumor growth.

Finally, the pharmacological manipulation of the sympathetic-immune interface is reviewed with focus on new therapeutic strategies using selective alpha(2)- and beta(2)-adrenoreceptor agonists and antagonists and inhibitors of phosphodiesterase type IV in the treatment of experimental models of autoimmune diseases, fibromyalgia, and chronic fatigue syndrome.

 

Source: Elenkov IJ, Wilder RL, Chrousos GP, Vizi ES. The sympathetic nerve–an integrative interface between two supersystems: the brain and the immune system. Pharmacol Rev. 2000 Dec;52(4):595-638. http://pharmrev.aspetjournals.org/content/52/4/595.long (Full article)

 

Feminist perspectives on the social construction of chronic fatigue syndrome

Abstract:

We contrast Western medical views of chronic fatigue syndrome (CFS) etiology, diagnosis, and treatment with views maintained by a predominantly female CFS population. We argue that the failure of Western medicine to demonstrate a viral etiology for CFS led to a paradigmatic shift in research perspectives, which then embraced psychiatric and sociocultural explanations for CFS. As a result, CFS was delegitimized as a biomedical phenomenon within medical, academic, governmental, and public arenas.

We compare alternative social constructions of CFS with issues pertaining to multiple sclerosis (MS), an illness that similarly predominates among women. Patient perspectives suggest that the history of medical attitudes toward CFS may eventually parallel the transformations that occurred in relation to MS. In particular, the discovery of biological markers for CFS may lay to rest the categorization of CFS as largely within the psychiatric realm.

 

Source: Richman JA, Jason LA, Taylor RR, Jahn SC. Feminist perspectives on the social construction of chronic fatigue syndrome. Health Care Women Int. 2000 Apr-May;21(3):173-85. http://www.ncbi.nlm.nih.gov/pubmed/11111464

 

Controversies in neurological infectious diseases

Abstract:

The past several years have seen major advances in our understanding of neurological infectious diseases, their diagnosis, and their treatment. Along with these advances, however, new information about infectious agents and new therapeutic options have also introduced both uncertainty and controversy in the approach and management of patients with diseases of the central nervous system. Here, we discuss six such areas: the long-term efficacy of HAART therapy in treatment of HIV infection; the role of viral infection in chronic fatigue syndrome; Rasmussen’s encephalitis as an infectious or autoimmune disease; the spectrum of neurological diseases caused by rickettsial infection; the role of Mycoplasma pneumoniae in human central nervous system disease; and the possible association of Chlamydia pneumoniae and human herpesvirus 6 with multiple sclerosis.

 

Source: Greenlee JE, Rose JW. Controversies in neurological infectious diseases. Semin Neurol. 2000;20(3):375-86. http://www.ncbi.nlm.nih.gov/pubmed/11051301

 

Chronic fatigue syndrome and Australian psychiatry: lessons from the UK experience

Abstract:

OBJECTIVE: The aim of this paper is to outline the opportunities and dangers the chronic fatigue syndrome (CFS) issue presents to Australian psychiatry.

METHOD: The scientific literature of the last 50 years on CFS in adults was reviewed and samples of recent media portrayals of CFS in the UK and Australia were collected. The author has worked in both the UK and Australia managing adult CFS patients in specialist outpatient consultation-liaison (C-L) psychiatry settings.

RESULTS: Chronic fatigue syndrome has been at the heart of an acrimonious debate in the UK, both within the medical profession and in the wider community. UK psychiatry has been drawn into the debate, at times being the target of strong and potentially damaging criticism, yet UK psychiatry, especially the C-L subspecialty, has played a crucial role in clarifying appropriate research questions and in devising management strategies. The issue has served to enhance and broaden psychiatry’s perceived research and clinical role at the important medicine-psychiatry interface in that country.

CONCLUSIONS: Handled properly, the CFS issue offers Australian psychiatry, especially C-L psychiatry, an opportunity to make a useful contribution to patient care in a clinically difficult and contentious area, while at the same time serving to help broaden psychiatry’s scope in the Australian medical landscape.

 

Source: Couper J. Chronic fatigue syndrome and Australian psychiatry: lessons from the UK experience. Aust N Z J Psychiatry. 2000 Oct;34(5):762-9. http://www.ncbi.nlm.nih.gov/pubmed/11037362