Tag: 1992

Epstein-Barr virus serology in the chronic fatigue syndrome

Abstract:

The antibody profiles against Epstein-Barr virus were studied in 136 patients presenting with chronic fatigue syndromes. These profiles were compared with a panel of sera from blood donors. The patients exhibited higher titres in a combined assay for antibodies to the Restricted (R) and Diffuse (D) components of the Early Antigen complex than controls (P less than 0.001) but titres against these antigens were not useful on an individual patient basis. The patients who displayed elevated titres of antibodies to Early Antigens did not differ clinically from those displaying titres in the control range. Four of nine patients who had increased antibodies to Early Antigens also had evidence of active enterovirus infection.

 

Source: Woodward CG, Cox RA. Epstein-Barr virus serology in the chronic fatigue syndrome. J Infect. 1992 Mar;24(2):133-9. http://www.ncbi.nlm.nih.gov/pubmed/1314860

 

Neuropsychological and psychiatric abnormalities in myalgic encephalomyelitis: a preliminary report

Abstract:

Ten patients attending one general medical hospital clinic who fulfilled operational criteria for the diagnosis of myalgic encephalomyelitis (ME) and with a history longer than three months, underwent a series of standardized neuropsychological and psychiatric tests. Nine were able to complete the tests and were individually matched with a normal control group for age, sex, educational background and premorbid intelligence. The ME subjects showed inferior performance to the controls on two tests of verbal memory. Their personality scores displayed less extraversion and less psychoticism. This is the first report of objective neuropsychological abnormalities in patients with ME, suggesting a discrete deterioration of short-term memory. The findings may also suggest a concurrent psychiatric component of the condition, but the direction of causality remains to be clarified.

 

Source: Riccio M, Thompson C, Wilson B, Morgan DJ, Lant AF. Neuropsychological and psychiatric abnormalities in myalgic encephalomyelitis: a preliminary report. Br J Clin Psychol. 1992 Feb;31 ( Pt 1):111-20. http://www.ncbi.nlm.nih.gov/pubmed/1559114

 

A chronic illness characterized by fatigue, neurologic and immunologic disorders, and active human herpesvirus type 6 infection

Abstract:

OBJECTIVE: To conduct neurologic, immunologic, and virologic studies in patients with a chronic debilitating illness of acute onset.

DESIGN: Cohort study with comparison to matched, healthy control subjects.

PATIENTS: We studied 259 patients who sought care in one medical practice; 29% of the patients were regularly bedridden or shut-in.

MAIN OUTCOME MEASURES: Detailed medical history, physical examination, conventional hematologic and chemistry testing, magnetic resonance imaging (MRI) studies, lymphocyte phenotyping studies, and assays for active infection of patients’ lymphocytes with human herpesvirus type 6 (HHV-6).

MAIN RESULTS: Patients had a higher mean (+/- SD) CD4/CD8 T-cell ratio than matched healthy controls (3.16 +/- 1.5 compared with 2.3 +/- 1.0, respectively; P less than 0.003). Magnetic resonance scans of the brain showed punctate, subcortical areas of high signal intensity consistent with edema or demyelination in 78% of patients (95% CI, 72% to 86%) and in 21% of controls (CI, 11% to 36%) (P less than 10(-9)). Primary cell culture of lymphocytes showed active replication of HHV-6 in 79 of 113 patients (70%; CI, 61% to 78%) and in 8 of 40 controls (20%; CI, 9% to 36%) (P less than 10(-8], a finding confirmed by assays using monoclonal antibodies specific for HHV-6 proteins and by polymerase chain reaction assays specific for HHV-6 DNA.

CONCLUSIONS: Neurologic symptoms, MRI findings, and lymphocyte phenotyping studies suggest that the patients may have been experiencing a chronic, immunologically mediated inflammatory process of the central nervous system. The active replication of HHV-6 most likely represents reactivation of latent infection, perhaps due to immunologic dysfunction. Our study did not directly address whether HHV-6, a lymphotropic and gliotropic virus, plays a role in producing the symptoms or the immunologic and neurologic dysfunction seen in this illness. Whether the findings in our patients, who came from a relatively small geographic area, will be generalizable to other patients with a similar syndrome remains to be seen.

Comment in:

The chronic fatigue syndrome controversy. [Ann Intern Med. 1992]

The chronic fatigue syndrome controversy. [Ann Intern Med. 1992]

 

Source: Buchwald D, Cheney PR, Peterson DL, Henry B, Wormsley SB, Geiger A, Ablashi DV, Salahuddin SZ, Saxinger C, Biddle R, et al. A chronic illness characterized by fatigue, neurologic and immunologic disorders, and active human herpesvirus type 6 infection. Ann Intern Med. 1992 Jan 15;116(2):103-13. http://www.ncbi.nlm.nih.gov/pubmed/1309285

 

Cell-mediated immunity in patients with chronic fatigue syndrome, healthy control subjects and patients with major depression

Abstract:

The chronic fatigue syndrome (CFS) is characterized by severe persistent fatigue and neuropsychiatric symptoms. It has been proposed that the abnormalities in cell-mediated immunity which have been documented in patients with CFS may be attributable to a clinical depression, prevalent in patients with this disorder.

Cell-mediated immune status was evaluated in patients with carefully defined CFS and compared with that of matched subjects with major depression (non-melancholic, non-psychotic) as well as healthy control subjects.

Patients with CFS demonstrated impaired lymphocyte responses to phytohaemagglutinin (PHA) stimulation, and reduced or absent delayed-type hypersensitivity (DTH) skin responses when compared either with subjects with major depression or with healthy control subjects (P less than 0.05 for each analysis).

Although depression is common in patients with CFS, the disturbances of cell-mediated immunity in this disorder differ in prevalence and magnitude from those associated with major depression. These observations strengthen the likelihood of a direct relationship between abnormal cell-mediated immunity and the etiology of CFS.

 

Source: Lloyd A, Hickie I, Hickie C, Dwyer J, Wakefield D. Cell-mediated immunity in patients with chronic fatigue syndrome, healthy control subjects and patients with major depression. Clin Exp Immunol. 1992 Jan;87(1):76-9. http://www.ncbi.nlm.nih.gov/pubmed/1733640

Note : You can read the full article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1554231/

 

Hypothesis: cytokines may be activated to cause depressive illness and chronic fatigue syndrome

Abstract:

Abnormalities in the regulation of the hypothalamo-pituitary-adrenal (HPA) axis are a well recognised feature of endogenous depression. The mechanism underlying this phenomenon remains obscure although there is strong evidence suggesting excessive CRH activity at the level of the hypothalamus.

We propose a novel hypothesis in which we suggest that the aetiological antecent to CRH hyperactivity is cytokine activation in the brain. It is now well established both that interleukins -1 and -6 are produced in a number of central loci and that cytokines are potent stimulators of the HPA axis.

Hence, we suggest that activation of IL-1 and IL-6 by specific mechanisms (such as neurotropic viral infection) in combination with the consequent CRH-41 stimulation, may (via their known biological effects) underly many of the features found in major depression and other related disorders, particularly where chronic fatigue is a prominent part of the symptom complex.

This theory has considerable heuristic value and suggests a number of experimental stratagems which may employed in order to confirm or reject it.

 

Source: Ur E, White PD, Grossman A. Hypothesis: cytokines may be activated to cause depressive illness and chronic fatigue syndrome. Eur Arch Psychiatry Clin Neurosci. 1992;241(5):317-22. http://www.ncbi.nlm.nih.gov/pubmed/1606197

 

Immune responsiveness in chronic fatigue syndrome

Comment on: Immune responsiveness in chronic fatigue syndrome. [Postgrad Med J. 1991]

 

Sir, The paper by Milton and colleagues (1) challenges the hypothesis that patients with postviral fatigue syndrome (myalgic encephalomyelitis) have a persisting viral infection along with consequent immune dysregulation. The protocol employed in the study suggests that their conclusions may not be valid.

Firstly, the 31 patients were selected from a group attending a ‘muscle clinic’ who complained of ‘unexplained chronic fatigue’. Of these only 15 had a clear history of a precipitating viral illness – a key diagnostic feature of postviral fatigue syndrome. Secondly, although other research groups have also demonstrated that raised levels of Coxsackie B virus IgG and IgM antibodies are not diagnostic of the syndrome, (2) these findings cannot be used to exclude the possibility of persisting viral infection within either muscle or the central nervous system.

As far as muscle is concerned, Gow and colleagues( 3) have recently detected enteroviral RNA sequences in muscle biopsies of 53% of patients with a well-defined postviral fatigue syndrome compared to 15% in a control group, and Archard et al. (4) have shown that this persisting enterovirus is poorly replicating.

Demonstrating the presence of persisting virus within the central nervous system is obviously far more difficult without autopsy material. However, Daugherty et al. (5) in America have published the results of MRI scans and cognitive function tests on 20 patients (with age and sex matched healthy controls) showing abnormalities consistent with an organic brain syndrome similar to that seen in patients who are positive for human immunodeficiency virus.

You can read the rest of this letter here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2399327/pdf/postmedj00061-0069a.pdf

 

Source: Shepherd C. Immune responsiveness in chronic fatigue syndrome. Postgrad Med J. 1992 Jan;68(795):66-7. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2399327/

 

Conversation piece

Dr E.G. Dowsett is Honorary Consultant Microbiologist, Basildon and Thurrock Health Authority and is the President of the Myalgic Encephalomyelitis Society.

 

DR P.D. WELSBY: I, and indeed many general physicians, are often asked to see patients whose main complaint is ‘tiredness all the time (TATT)’. From my previous experience also of general practice it seems that there is a wide continuous spectrum of debility ranging from a few days or weeks, but sometimes, distressingly, lasting for years. Such illnesses may or may not follow symptoms of an infection. Does the Myalgic Encephalomyelitis (ME) Society differentiate between post-viral debility, postinfectious (often an undefined infection) fatigue syndrome, chronic fatigue syndrome and ME? If so, how, and should it make any difference to medical management?

DR E.G. DOWSETT: One of the most striking features of ME is that the patient is not tired all the time! Extreme and sudden variability of energy levels both within and between episodes of illness differentiate this syndrome from other diseases associated with fatigue. One can only deplore the current fashion in the United States as well as the United Kingdom to redefine and rename a disability which has been clearly described in the literature for at least 100 years.’ There is nothing to be said in favour of the American acronym CFIDS (chronic fatigue immune deficiency syndrome) with its connotation of a primary immune dysfunction. The term ‘chronic fatigue syndrome’ recently adopted in this country also is nonspecific and non-descriptive because most of the definition is based on a vast number of exclusions (some of which, for example, endocrine disturbance, are actually found in ME). ‘Post-viral fatigue syndrome’, another British name, describes one essential feature (the association of the illness with viral infection) but gives the impression that the infection was antecedent rather than, as we now know, persistent. I prefer to use the more specific term ‘myalgic encephalomyelitis’ as it emphasizes the essential encephalitic component of the illness, the muscle pain, and the close clinical and epidemiological similarity to poliomyelitis.

You can read the rest of this interview here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2399326/pdf/postmedj00061-0066.pdf

 

Source: E. G. Dowsett. Conversation piece. Interview by P. D. Welsby.Postgrad Med J. 1992 Jan; 68(795): 63–65. PMCID: PMC2399326 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2399326/

 

Chronic fatigue syndrome

Comment on: Chronic fatigue syndrome. [J Neurol Neurosurg Psychiatry. 1991]

 

As neurologists in a country where the chronic fatigue syndrome (CFS) has almost no recognized official existence, we often feel bewildered by the papers on the subject we read in the Anglo-Saxon literature. We wonder whether the clinical experience of some of their authors is so different from ours that they do not consider that their approach may result in a disservice to their patients. The JNNP has followed a sensitive line culminating in Wessely’s excellent editorial. We still, however, feel that his kid-glove handling of the subject reflects the controversy that surrounds it in the UK.

Avoiding the futile organic versus functional debate, in our neurology department we refer to many of the problems we see in our practice as the “chronic vigilance syndromes”: specific patterns of enhanced attention centred on particular bodily structures and functions. Naturally, the commonest in a neurologist’s outpatient clinic are the “cephalic vigilance syndromes” in their two main forms: the painful, with its several varieties of chronic headaches, and the operational one with its subjective unsteadiness, concentration problems and various odd turns. “Thoracic vigilance” patients are often referred to cardiologists or pneumologists but a fair number also come to us, especially if they have hyperventilation symptoms such as dizziness and paraesthesiae. Among the different types of patients with fatigue we are also familiar with the occasional “neuro-muscular vigilance” patient whose symptoms parallel your CFS cases. We have the noncontrolled impression that in our environment such patients often have a premorbid preoccupation with their locomotor system.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC488951/pdf/jnnpsyc00486-0096a.pdf

 

Source: Digon A, Goicoechea A, Moraza MJ. Chronic fatigue syndrome. J Neurol Neurosurg Psychiatry. 1992 Jan;55(1):85. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC488951/

 

Chronic fatigue syndrome and women: can therapy help?

Abstract:

This article presents current research on chronic fatigue syndrome, which currently afflicts mostly females between the ages of 25 and 55. Because depression is a common symptom of chronic fatigue syndrome, mental health practitioners are often involved with the victims and must formulate an appropriate treatment strategy that considers the physiological, intrapsychic, interpersonal, and environmental aspects of the client. This article includes case material focusing on a woman who was medically diagnosed with the Epstein-Barr virus and was in psychotherapy with the author. The difficulty of managing the interplay of the real health problems and the emotional issues presented by the client is highlighted.

Comment in:

“Chronic fatigue syndrome and women: can therapy help?”. [Soc Work. 1992]

“Chronic fatigue syndrome and women: can therapy help?”. [Soc Work. 1992]

“Chronic fatigue syndrome and women: can therapy help?”. [Soc Work. 1992]

Source: Burke SG. Chronic fatigue syndrome and women: can therapy help? Soc Work. 1992 Jan;37(1):35-9.  http://www.ncbi.nlm.nih.gov/pubmed/1542805

 

Chronic fatigue syndromes in clinical practice

Abstract:

Chronic fatigue is a common and difficult challenge in clinical practice. The majority of patients with this chief complaint have treatable mood or anxiety disorders, complicated by a tendency toward somatization. A minority of patients suffer from sleep disorders, endocrinologic abnormalities, or chronic inflammatory conditions. Prolonged recovery after viral infections is only rarely the cause of chronic fatigue. Specific pharmacologic interventions and cognitive-behavioral therapy are effective in an environment that is sensitive to the patient’s interpretation of symptoms and avoids unproven medical investigations and therapies.

 

Source: Manu P, Lane TJ, Matthews DA. Chronic fatigue syndromes in clinical practice. Psychother Psychosom. 1992;58(2):60-8. http://www.ncbi.nlm.nih.gov/pubmed/1484921