Tag: comment

Postviral fatigue syndrome

Comment on: Possible upregulation of hypothalamic 5-hydroxytryptamine receptors in patients with postviral fatigue syndrome. [BMJ. 1992]

 

EDITOR, -A M 0 Bakheit and colleagues recently reported’ a possible upregulation of hypothalamic 5-hydroxytryptamine receptors in patients with the postviral fatigue syndrome, giving some evidence for hypothalamic functional abnormalities in these patients, which are different from others with depression. There is a growing body of evidence which claims that this clinical condition is organic and cannot be simply perceived as a somatisation disorder in patients with predisposition to psychiatric disease.”

We reviewed and quantitatively analysed with Ceretec and single photon emission tomography the brain perfusion of 14 patients fulfilling the Oxford criteria for diagnosis of myalgic encephalomyelitis. They had all had disease for more than six months (more than half the time) manifested with generalised malaise and myalgia, as well as significant physical and intellectual disability. None had any medical condition known to produce fatigue or had recently or in the past had psychiatric disease. When compared with a group of 24 nondepressed age and sex matched controls (normal volunteers) there was significant reduction of the perfusion to several areas of the brain cortex but particularly the brain stem (table).

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1882397/pdf/bmj00077-0053b.pdf

 

Source: Costa DC, Brostoff J, Douli V, Ell PJ. Postviral fatigue syndrome. BMJ. 1992 Jun 13;304(6841):1567. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1882397/

 

Postviral fatigue syndrome

Comment on: Possible upregulation of hypothalamic 5-hydroxytryptamine receptors in patients with postviral fatigue syndrome. [BMJ. 1992]

 

EDITOR,-A M 0 Bakheit and colleagues report enhanced release of prolactin after administration of buspirone in patients with the postviral fatigue syndrome compared with controls and patients with depression. Their report would have been improved if they had described more fully the differences between the two groups of patients. As they point out, depression can be difficult to distinguish clinically from the postviral fatigue syndrome.

The authors used the criteria of the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised to define depressive illness, but to qualify for this diagnosis a patient need complain of only four symptoms such as fatigue, hypersomnia, retardation, and loss of concentration in addition to depressed mood. The criteria they used for the postviral fatigue syndrome included depression, fatigue, reversed sleep pattern, and constipation alternating with diarrhoea. It would be surprising if there was not a substantial overlap between the two groups and if one of the main factors affecting diagnosis was not whether the patient presented first to a psychiatrist or a neurologist.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1882437/pdf/bmj00077-0052e.pdf

 

Source: Curtis D, Bullock T. Postviral fatigue syndrome. BMJ. 1992 Jun 13;304(6841):1566-7. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1882437/

 

Postviral fatigue syndrome

Comment on: Possible upregulation of hypothalamic 5-hydroxytryptamine receptors in patients with postviral fatigue syndrome. [BMJ. 1992]

 

EDITOR,-A M 0 Bakheit and colleagues suggest that the buspirone challenge test may be useful in distinguishing between a “primary depressive illness” and the postviral fatigue syndrome. It is difficult to assess the truth of this from the data presented in their paper. To know the usefulness of this test the numbers of controls and patients scored above or below an appropriately chosen cut off point of serum prolactin concentration needs to be known. Unfortunately, the authors present the prolactin concentrations as mean values. If the aim of the test is to exclude major depression then a cut off which produces few false negative results should be chosen. Were the high mean values in the postviral fatigue group due to one or two extreme outliers? It is noteworthy that the standard deviations in the patients were much higher in the controls at baseline assessment. Why was this?

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1882426/pdf/bmj00077-0052c.pdf

 

Source: Hatcher S. Postviral fatigue syndrome. BMJ. 1992 Jun 13;304(6841):1566; author reply 1567. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1882426/

 

Postviral fatigue syndrome

Comment on: Possible upregulation of hypothalamic 5-hydroxytryptamine receptors in patients with postviral fatigue syndrome. [BMJ. 1992]

 

EDITOR,-A M 0 Bakheit and colleagues report an enhanced prolactin response to buspirone in patients with postviral fatigue syndrome and suggest this may be due to upregulation of hypothalamic 5-hydroxytryptamine receptors. They fail to mention the considerable evidence indicating that the drug is a moderately potent dopamine antagonist, a pharmacological action which suggests an alternative explanation for their data.

They administered a single 60 mg dose of buspirone-in excess of the daily maximum of 45 mg recommended by the British National Formulary-so antidopaminergic effects may well have been significant in their studies. The fact that the prolactin releasing effect of buspirone can be blocked by the drug metergoline does not prove 5-hydroxytryptamine receptor specificity. Indeed, metergoline is used commonly as an alternative dopamine agonist to bromocriptine in managing hyperprolactinaemia. Thus enhanced prolactin release after buspirone in postviral fatigue syndrome may reflect, at least in part, inhibition of increased hypothalamic dopaminergic tone on the  It would be interesting to study the same groups of patients using a specific D2 dopamine antagonist (such as domperidone) to see whether this is the case.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1882431/pdf/bmj00077-0052d.pdf

 

Source: Bevan JS. Postviral fatigue syndrome. BMJ. 1992 Jun 13;304(6841):1566; author reply 1567. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1882431/

 

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

Comment in: Chronic fatigue syndrome. [Br J Gen Pract. 1992]

Comment on: Antidepressant therapy in the chronic fatigue syndrome. [Br J Gen Pract. 1991]

 

Sir, The adoption of the term chronic fatigue syndrome for conditions like myalgic encephalomyelitis and effort syndrome in the paper by Lynch and colleagues (August Journal, p.339) is difficult to understand. The differences between these disorders are so marked, that an umbrella term is destined to be both confusing and misleading.

The emphasis on the term fatigue is unfortunate for many reasons. First; research has shown that only a tiny proportion of people with unexplained fatigue fulfil the standard diagnostic criteria for myalgic encephalomyelitis. (1) Secondly, Lynch and colleagues’ definition of chronic fatigue syndrome is too broad to distinguish people with myalgic encephalomyelitis from those who are feeling run down or depressed or suffering from the more common and less severe post-viral syndrome. Thirdly, the term trivializes the illness. Everyone gets tired now and then and most people find it hard to understand how some may be disabled by it. In our view, the name suggests something which is tolerable and volitional, requiring little more than adequate rest and a positive attitude. What the term fails to communicate is that the fatigue reported by people with myalgic encephalomyelitis is severe and debilitating; that it is unlike anything most of them have experienced before and that it is often associated with an intense influenza-like malaise. (2’3) We therefore agree with English that as far as myalgic encephalomyelitis is concerned, ‘fatigue is the most pathetically inadequate term’. (2)

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1371802/pdf/brjgenprac00062-0041.pdf

 

Source: Goudsmit EM, Macintyre A, Sullivan M. Chronic fatigue syndrome. Br J Gen Pract. 1991 Nov;41(352):479-80. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1371802/

 

Chronic fatigue syndrome

Comment on:

Antidepressant therapy in the chronic fatigue syndrome. [Br J Gen Pract. 1991]

General practitioners’ experience of the chronic fatigue syndrome. [Br J Gen Pract. 1991]

 

Sir, I read with interest the papers on the chronic fatigue syndrome (August Journal, p.324, 339). This syndrome has become an important diagnosis in both general practice and psychiatry. With the awareness of such a diagnostic entity, more patients are being recognized and managed (although the aetiology still remains unknown).

Depression as an inherent feature of chronic fatigue syndrome remains a controversial issue and great care is needed in treating these patients as ‘depressed’. Subjectively, many patients with the chronic fatigue syndrome describe their mood state as depressed, probably because of lack of any other socially approved metaphor. For a practitioner, however, it is important to make an objective assessment about the significance of this expression in terms of the range and reactivity of affect and the disproportion of depressive presentation in the context of the patient’s life situation and experiences. If depression is significant, the diagnosis of chronic fatigue syndrome becomes secondary to that of depressive disorder as fatigue may be a feature of depression. However, if chronic fatigue syndrome remains the primary diagnosis, one must remember that antidepressant drugs are neither euphoriants nor stimulants and that there is no empirical evidence for the benefit of antidepressant treatment in this syndrome, although there is a recommendation for it to be tried as an alternatp mode of treatment.

 

Source: Arya DK. Chronic fatigue syndrome. Br J Gen Pract. 1991 Nov;41(352):480. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1371803/

 

Chronic fatigue syndrome

Comment on: General practitioners’ experience of the chronic fatigue syndrome. [Br J Gen Pract. 1991]

 

Sir, Ho-Yen and McNamara give an interesting account of general practitioners’ experience of the chronic fatigue syndrome (August Journal, p.324). However, many of the conclusions which they draw are not supported by their study.

The problem lies in the method by which cases were identified. It seems unlikely that the doctors who responded to the questionnaire would have screened every patient on their practice lists for the condition. Even to screen only those patients who attended the surgery would have been a massive undertaking. There is no evidence that the practices involved kept a case register for this illness. I presume therefore that the cases reported were identified from memory by the doctors who responded to the survey. Thus, for patients who meet the criteria for this illness to be identified as a ‘case’ they must: decide that they are ill, decide to visit the doctor, be correctly identified as a case by the general practitioner and leave such an impression on the doctor’s mind as to be easily recalled later. It is very unlikely that, having passed through such a selection procedure, the cases identified would represent either the true number or display the typical characteristics of patients with this condition in the general population.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1371804/pdf/brjgenprac00062-0042b.pdf

 

Source: Plummer WP. Chronic fatigue syndrome. Br J Gen Pract. 1991 Nov;41(352):480. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1371804/

 

Myalgic encephalomyelitis

Comment on: Myalgic encephalomyelitis. [J R Soc Med. 1991]

 

The exchange of views between Drs Wessely and Wilson in the correspondence columns of the March issue of the Journal (March 1991 JRSM, p 182) highlights the divergence of opinion concerning the nature of myalgic encephalomyelitis (ME).

Recognition of ME as a significant health problem in New Zealand dates from an outbreak of ‘Tapanui ‘flu’ in a small country town in 1983. As it seemed possible that the wide range of symptoms could be indicative of impaired capillary blood flow, we studied the filtrability of blood samples from members of ME support groups. We found that subjects who were acutely unwell had prolonged blood filtration times which returned towards normal in the chronic state.

More recently it has been shown that ME symptoms are associated with increased percentages of nondiscocytic erythrocytes and the percentage of such cells showed an inverse correlation with wellbeing. The significance of altered red cell shape in the pathogenesis of ME has been discussed and it has been found that an injection of vitamin B12 improved wellbeing within 24 h. The loss of symptoms was associated with reduced percentages of nondiscocytes in about 50% of subjects. Those who failed to perceive a beneficial response from the B12 showed no change in red cell shape. Further studies at varying degrees of completion confirm and extend the published observations.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1295578/pdf/jrsocmed00119-0075a.pdf

 

Source: Simpson LO. Myalgic encephalomyelitis. J R Soc Med. 1991 Oct;84(10):633. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1295578/

 

Intravenous immunoglobulin and myalgic encephalomyelitis

Comment on: Intravenous immunoglobulins. [BMJ. 1991]

 

SIR, In his editorial on intravenous immunoglobulin Dr A D B Webster calls for multicentre trials to assess the possible efficacy of this product in various conditions including mvalgic encephalomyelitis. Two such placebo controlled trials have been completed. Unfortunately, the results are conflicting. American investigators treated their patients with 1 g/kg every month for six months. There were no obvious benefits when the treated patients were compared with controls given placebo. An Australian trial used an even higher dose of 2 g/kg over three months. Here there were significant benefits in both physical and psychological wellbeing in the treatment group.

You can read the rest of this comment here:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1670935/pdf/bmj00145-0062d.pdf

 

Source: Shepherd C. Intravenous immunoglobulin and myalgic encephalomyelitis. BMJ. 1991 Sep 21;303(6804):716. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1670935/