Tag: review

Human herpesvirus-7 (HHV-7)

Abstract:

HHV-7 first isolated in 1990 from a healthy individual, is a ubiquitous agent. The second independent isolation of HHV-7 from a chronic fatigue syndrome patient was reported in 1992. The seroepidemiology of HHV-7 suggested that its prevalence rate in the U.S.A. population is > 85%; however, in Japan a low prevalence rate has been reported. HHV-7 can be more readily isolated from the saliva than HHV-6. The primary infection of HHV-7 appears later in life than HHV-6. No disease has been reported that is etiologically linked to HHV-7. HHV-7 is more closely related to HHV-6 and the human cytomegalovirus than other members of the human herpesvirus family.

 

Source: Ablashi DV, Berneman ZN, Kramarsky B, Asano Y, Choudhury S, Pearson GR. Human herpesvirus-7 (HHV-7). In Vivo. 1994 Jul-Aug;8(4):549-54. http://www.ncbi.nlm.nih.gov/pubmed/7893982

 

Clinical correlates of infection with human herpesvirus-6

Abstract:

Human herpesvirus-6 is a lymphotropic virus which infects susceptible individuals during the first year of life and usually causes life-long latency. In a variable percentage primary infections are followed by a short acute disease, exanthema subitum. Older individuals may suffer from infectious mononucleosis-like illnesses or from Kikuchi-Fujimoto’s disease. In addition, there is a fairly wide spectrum of lymphoid and hematopoietic diseases or autoimmune disorders, which are associated with elevated titers of HHV-6 antibody, and from which replicating virus may be isolated. Such diseases include atypical polyclonal lymphoproliferation, Hodgkin’s disease, chronic fatigue syndrome and systemic lupus erythematosus. The present article reviews the current knowledge of such associations.

 

Source: Krueger GR, Klueppelberg U, Hoffmann A, Ablashi DV. Clinical correlates of infection with human herpesvirus-6. In Vivo. 1994 Jul-Aug;8(4):457-85. http://www.ncbi.nlm.nih.gov/pubmed/7893974

 

Neuropsychiatric status of patients with chronic fatigue syndrome: an overview

Abstract:

Chronic fatigue syndrome (CFS) is an illness that results in debilitating fatigue as well as rheumatological, infectious, and neuropsychiatric symptoms. The present paper is a brief overview of the neuropsychological and psychiatric research on CFS. Studies from our laboratory contrasting CFS with patients with multiple sclerosis, depression, and healthy controls are detailed. Our hypothesis of neuropsychological impairments in CFS is discussed.

 

Source: Deluca J, Johnson SK, Natelson BH. Neuropsychiatric status of patients with chronic fatigue syndrome: an overview. Toxicol Ind Health. 1994 Jul-Oct;10(4-5):513-22. http://www.ncbi.nlm.nih.gov/pubmed/7778111

 

The treatment of chronic fatigue syndrome: science and speculation

Abstract:

The chronic fatigue syndrome (CFS) is a heterogeneous disorder characterized by fatigue, neuropsychiatric symptoms, and various other somatic complaints. Treatment studies to date reflect both the diversity of medical disciplines involved in the management of patients with CFS and the multiple pathophysiologic mechanisms proposed.

There have been few attempts to study integrated treatment programs, and although several controlled studies have been reported, no treatment has been shown clearly to result in long-term benefit in the majority of patients. Good clinical care integrating medical and psychologic concepts, together with symptomatic management, may prevent significant secondary impairment in the majority of patients.

Future treatment studies should examine differential response rates for possible subtypes of the disorder (eg, documented viral onset, concurrent clinical depression), evaluate the extent of any synergistic effects between therapies (ie, medical and psychologic), and employ a wide range of biologic and psychologic parameters as markers of treatment response.

 

Source: Wilson A, Hickie I, Lloyd A, Wakefield D. The treatment of chronic fatigue syndrome: science and speculation. Am J Med. 1994 Jun;96(6):544-50. http://www.ncbi.nlm.nih.gov/pubmed/8017453

 

Fibromyalgia, chronic fatigue syndrome, and myofascial pain syndrome

Abstract:

No major pathophysiologic or therapeutic findings have appeared over the past year regarding fibromyalgia, chronic fatigue syndrome, and myofascial pain syndrome, three poorly understood, controversial, and overlapping syndromes. The frequent prevalence of these disorders in association with Lyme disease and other medical and psychiatric illness was emphasized. New studies demonstrated the potential role for central nervous system activation in fibromyalgia and chronic fatigue syndrome.

 

Source: Goldenberg DL. Fibromyalgia, chronic fatigue syndrome, and myofascial pain syndrome. Curr Opin Rheumatol. 1994 Mar;6(2):223-33. http://www.ncbi.nlm.nih.gov/pubmed/8024971

 

A comparative review of systemic and neurological symptomatology in 12 outbreaks collectively described as chronic fatigue syndrome, epidemic neuromyasthenia, and myalgic encephalomyelitis

Abstract:

Outbreaks of illnesses of unknown etiology typified by a chronic relapsing course of constitutional symptoms and nervous system involvement have collectively been referred to as chronic fatigue syndrome, epidemic neuromyasthenia, and myalgic encephalomyelitis. To examine heterogeneity of clinical presentation, a comparative review was undertaken for 12 well-documented outbreaks reported since 1934.

A systemic syndrome characterized by excessive fatigue, myalgias, headache, low-grade fever, and other constitutional symptoms was common to cases in all outbreaks. However, marked heterogeneity in the range of neurological features was apparent.

On the basis of predominant neurological manifestations, outbreaks could be grouped into four levels of increasing neurological involvement: affective neuropsychological changes (level I); prominent cutaneous sensory symptoms with both affective and cognitive neuropsychological changes (level II); marked objective paresis with cutaneous sensory as well as affective and cognitive neuropsychological changes (level III); and cutaneous sensory, affective and cognitive neuropsychological, posterior column, cranial nerve, and mixed upper and lower motor neuron changes (level IV). Groups with the most prominent objective neurological findings (levels III and IV) comprised exclusively outbreaks reported between the 1930s and 1950s. All but one outbreak in groups with less prominent neurological findings (levels I and II) were reported between the 1960s and 1980s; a range of neurological features was observed for these groups.

Because a complete neurological examination is not emphasized as part of the diagnostic workup in current outbreaks, it is possible that less obvious neurological findings may be overlooked. Careful evaluation of neurological features in epidemic and endemic cases of what is now called chronic fatigue syndrome may be one approach to distinguishing subtypes of what has been described in the past as a nosological entity.

 

Source: Briggs NC, Levine PH. A comparative review of systemic and neurological symptomatology in 12 outbreaks collectively described as chronic fatigue syndrome, epidemic neuromyasthenia, and myalgic encephalomyelitis. Clin Infect Dis. 1994 Jan;18 Suppl 1:S32-42. http://www.ncbi.nlm.nih.gov/pubmed/8148451

 

Viral studies of chronic fatigue syndrome

Abstract:

Chronic fatigue syndrome (CFS) has many characteristics suggesting persistent fatigue following a viral illness. At least nine different RNA and DNA viruses have been considered to be associated with this disease, but none of these viruses has been found to be the etiologic agent. Immunologic studies have demonstrated activated CD8+ cells and reduced function of natural killer cells suggesting a host response to an infection that has led to persistent immune disorders. Some of the symptoms of CFS may be due to cytokines produced by this hyperactive immune response to a virus that is still present in the host or that has been eliminate but leaves abnormal immunologic sequelae. These possibilities offer directions for future studies of CFS and therapeutic approaches to this condition.

 

Source: Levy JA. Viral studies of chronic fatigue syndrome. Clin Infect Dis. 1994 Jan;18 Suppl 1:S117-20. http://www.ncbi.nlm.nih.gov/pubmed/8148437

 

The chronic fatigue syndrome

Abstract:

CFIDS (chronic fatigue and immune disfunction syndrome) is also known as CFS (chronic fatigue syndrome), CEBV (chronic Epstein-Barr virus), M.E. (myalgic encephalomyelitis), yuppie flu and by other names.

It is a complex illness characterized by incapacitating fatigue (experienced as exhaustion and extremely poor stamina), neurological problems and a constellation of symptoms that can resemble many disorders, including; mononucleosis, multiple sclerosis, fibromyalgia, AIDS-related complex (ARC) and autoimmune diseases such as lupus. These symptoms tend to wax and wane, but any often severely debilitating and may last for many months or years. All sections of the population (including children) are at risk, but women under 45 seem to be most susceptible.

The investigators suggest that CFIDS results from dysfunction of the immune system. The exact nature of this dysfunction is not yet well defined, but it can generally be viewed as an unregulated or overactive state which is responsible for most of the symptoms. There is also evidence of some immune suppression in CFIDS. None of the treatments is consistently satisfactory, but some may be helpful: psychotherapy, physiotherapy, exercise programs, acupunctures, small doses of antidepressants, etc.

 

Source: Artsimovich NG, Chugunov VS, Kornev AV, Ivanova TM, Chugunov AV, Oprishchenko MA. The chronic fatigue syndrome. Zh Nevrol Psikhiatr Im S S Korsakova. 1994;94(5):47-50. [Article in Russian] http://www.ncbi.nlm.nih.gov/pubmed/7900453

 

Pathogenic tracks in fatigue syndromes

Abstract:

This review analyses the recent literature devoted to two related fatigue syndromes: chronic fatigue syndrome (CFS) and acute onset postviral fatigue syndrome (PVFS). The articles are grouped into five pathogenic tracks: infectious agents, immune system, skeletic muscle, hypothalamo-pituitary-adrenal (HPA) axis and psychiatric factors.

Although a particular infectious agent is unlikely to be responsible for all CFS cases, evidence is shown that host-parasite relationships are modified in a large proportion of patients with chronic fatigue. Antibody titres against infectious agents are often elevated and replication of several viruses could be increased.

Chronic activation of the immune system is also observed and could be due to the reactivation of persistent or latent infectious agents such as herpes viruses (i.e. HHV-6) or enteroviruses. It could also be favorised by an impaired negative feedback of the HPA axis on the immune system.

A model is proposed where the abnormalities of the HPA axis are primary events and are mainly responsible for a chronic activation of the immune system which in turn induces an increased replication of several viruses under the control of cellular transcription factors. These replicating viruses together with cytokines such as TNF-alpha would secondarily induce functional disorders of muscle and several aspects of asthenia itself.

 

Source: Moutschen M, Triffaux JM, Demonty J, Legros JJ, Lefèbvre PJ. Pathogenic tracks in fatigue syndromes. Acta Clin Belg. 1994;49(6):274-89. http://www.ncbi.nlm.nih.gov/pubmed/7871934

 

Treatment of the chronic fatigue syndrome. A review and practical guide

Abstract:

The chronic fatigue syndrome (CFS) was formally defined in 1988 to describe a syndrome of severe and disabling fatigue of uncertain aetiology associated with a variable number of somatic and/or psychological symptoms. CFS has been reported in most industrialised countries and is most prevalent in women aged between 20 and 50 years.

Despite occasional claims to the contrary, the aetiology of CFS remains elusive. Although abnormalities in tests of immune function and cerebral imaging have been described in variable numbers of CFS patients, such findings have been inconsistent and cannot be relied upon, either to establish or exclude the diagnosis. Thus, diagnosis rests on fulfillment of the Centers for Disease Control case definition which was revised in 1992. This case definition remains somewhat controversial, largely due to its subjectiveness.

The mainstay of treatment is establishing the diagnosis and educating the patient about the illness. An empathetic clinician can stop further consultations elsewhere (‘doctor shopping’) and subsequent excessive investigations, which frequently occur in such patients.

Most patients should undertake a trial of antidepressant therapy, even if major depression is not present. The choice of antidepressant drug should tailor the tolerability profile to relief of particular CFS symptoms, such as insomnia or hypersomnia. Failure to improve within 12 weeks warrants an alternative antidepressant agent of another class. Many other drugs have been reported anecdotally to be beneficial, but no therapy has been demonstrated to be reproducibly useful in double-blind, placebo-controlled clinical trials with an adequate duration of follow-up.

 

Source: Blondel-Hill E, Shafran SD. Treatment of the chronic fatigue syndrome. A review and practical guide. Drugs. 1993 Oct;46(4):639-51. http://www.ncbi.nlm.nih.gov/pubmed/7506650