Predictors of chronic "postviral" fatigue

doi:10.1016/S0140-6736(94)92833-9

The Lancet

Volume 344, Issue 8926, 24 September 1994, Pages 864-868

https://doi.org/10.1016/S0140-6736(94)92833-9 Get rights and content

Abstract

Summary

We set out to determine the relation between a general practitioner (GP) diagnosis of viral illness and development of chronic fatigue 6 months later. 618 subjects who attended GPs clinics in London, south, and southwest England and who received a diagnosis of viral illness were followed prospectively and fatigue was assessed by questionnaire after 6 months.

At presentation, GPs recorded fatigue in 62·6% of subjects, usually since the onset of symptoms. 502 (81·2%) subjects completed the 6-month questionnaire, of whom 88 (17·5%) met criteria for chronic fatigue and 65 (12·9%) had no reported fatigue before the viral illness. Compared with a similar group of non-postviral GP attenders, the risk ratio for chronic fatigue in the present cohort was 1·45 (95% Cl 1·14-2·04). Infective symptoms did not predict fatigue 6 months later. Psychiatric morbidity, belief in vulnerability to viruses, and attributional style at initial presentation were all associated with self-designated postviral fatigue. Logistic regression showed that somatic attributional style, less definite diagnosis by the GP, and sick certification were the only significant predictors of chronic fatigue after viral infection when other factors were controlled for.

Chronic severe fatigue 6 months after GP-diagnosed viral illness is related to symptom-attributional style and doctor behaviour, rather than to features of the viral illness. Some subjects with apparent postviral fatigue had complained of tiredness before their presentation with a viral illness.

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Petersen et al. [37] reported that pre-infectious fatigue was associated with sub-acute fatigue. In terms of chronic fatigue, pre-morbid fatigue was a risk factor in a higher quality, large community study [39] but not a smaller, primary-care study [31]. More general, pre-existing (chronic) health problems were associated with both chronic fatigue [36], and long-term fatigue [40].
Fatigue is a prevalent and debilitating symptom, preceded by an acute infectious episode in some patients. This systematic review aimed to identify risk factors for the development of persistent fatigue after an acute infection, to develop an evidence-based working model of post-infectious fatigue.
Electronic databases (Medline, PsycINFO and EMBASE) were searched, from inception to March 2016, for studies which investigated biopsychosocial risk factors of on-going fatigue after an acute infection. Inclusion criteria were: prospective design; biological, psychological or social risk factors; standardised measure of post-infectious fatigue (self-report scales or clinical diagnosis). Studies were excluded if the sample had a pre-existing medical condition, infection was conceptualised as ‘vaccination’ or they were intervention trials. A narrative synthesis was performed.
Eighty-one full texts were screened, of which seventeen were included in the review. Over half included glandular fever populations. Other infections included dengue fever, ‘general’/‘viral’ and Q-fever. Risk factors were summarised under biological, social, behavioural, cognitive and emotional subthemes. Patients' cognitive and behavioural responses to the acute illness, and pre-infection or baseline distress and fatigue were the most consistent risk factors for post-infectious fatigue.
An empirical summary model is provided, highlighting the risk factors most consistently associated with persistent fatigue. The components of the model, the possible interaction of risk factors and implications for understanding the fatigue trajectory and informing preventative treatments are discussed.
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There is still a lack of large, well-characterized cohort studies with CFS/ME as endpoint. Studies in general practice suggest that prolonged fatigue is not specifically related to features of common viral illnesses [36,37]. By following subjects with either acute Epstein–Barr virus infection, Q fever or Ross river virus infection in a rural region of Australia, it was found that 11% had prolonged illness with disabling fatigue [20].
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is associated to infections and it has been suggested that vaccination can trigger the disease. However, little is known about the specific association between clinically manifest influenza/influenza vaccine and CFS/ME. As part of a registry surveillance of adverse effects after mass vaccination in Norway during the 2009 influenza A (H1N1) pandemic, we had the opportunity to estimate and contrast the risk of CFS/ME after infection and vaccination.
Using the unique personal identification number assigned to everybody who is registered as resident in Norway, we followed the complete Norwegian population as of October 1, 2009, through national registries of vaccination, communicable diseases, primary health, and specialist health care until December 31, 2012. Hazard ratios (HRs) of CFS/ME, as diagnosed in the specialist health care services (diagnostic code G93.3 in the International Classification of Diseases, Version 10), after influenza infection and/or vaccination were estimated using Cox proportional-hazards regression.
The incidence rate of CFS/ME was 2.08 per 100,000 person-months at risk. The adjusted HR of CFS/ME after pandemic vaccination was 0.97 (95% confidence interval [CI]: 0.91–1.04), while it was 2.04 (95% CI: 1.78–2.33) after being diagnosed with influenza infection during the peak pandemic period.
Pandemic influenza A (H1N1) infection was associated with a more than two-fold increased risk of CFS/ME. We found no indication of increased risk of CFS/ME after vaccination. Our findings are consistent with a model whereby symptomatic infection, rather than antigenic stimulation may trigger CFS/ME.
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Research on hypochondriasis and other somatoform disorders (SFD) has provided evidence that patients with SFD tend to attribute their symptoms to organic dysfunctions or disease. However, recent studies appear to discredit this. There is no systematic evidence on whether patients with SFD predominantly rely on somatic attributions, despite calls to include somatic attributions as a positive criterion of somatic symptom disorder (SSD) in the upcoming Diagnostic and Statistical Manual of Mental Disorders (DSM-5).
This study is a systematic review of quantitative studies which assess the descriptive and predictive validity of somatic attribution in SFD. The literature search was restricted to studies with patients who met the DSM-IV criteria for SFD.
Somatic attribution style in SFD has acceptable descriptive but insufficient predictive validity. This confirms that the overlap between somatic and psychological attributions is often substantial. Attribution style can discriminate between SFD patients with and without comorbidity.
A somatic attribution style does not qualify as a positive criterion in SSD. However, there is an urgent need for further research on causal illness perceptions in the full spectrum of medically unexplained symptoms in order to confirm this result. Given its high prevalence, research on psychological attribution style is warranted. Re-attribution does not provide a framework sophisticated enough to address the needs of patients in primary care.
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More recently, prospective studies investigated whether acute viral infections could predict the onset of CFS. Two of the earlier studies showed that common viral infections, such as upper respiratory tract infections, were not associated with the subsequent development of either chronic fatigue or CFS, and concluded that viruses did not play a role in the onset of CFS (Cope et al., 1994; Wessely et al., 1995). Subsequent studies, however, showed that certain more severe infections played a role in the onset of CFS including infectious mononucleosis (glandular fever) (White et al., 2001; Moss-Morris and Spence, 2006), hepatitis (Berelowitz et al., 1995), viral meningitis (Hotopf et al., 1996), Q fever (Wildman et al., 2002), and Ross River virus (Hickie et al., 2006).
Chronic fatigue syndrome (CFS) is an illness characterized by disabling fatigue of at least 6 months. The aetiology of the condition has been hotly debated. In this chapter the evidence for CFS as a post viral condition and/or a neurological condition is reviewed. Although there is evidence that CFS is triggered by certain viruses in some patients and that neurobiological changes such as hypocortisolism are associated with the syndrome, neither mechanism is sufficient to explain the extent of the symptoms or disability experienced by patients. It is unlikely that CFS can be understood through one aetiological mechanisms. Rather it is a complex illness which is best explained in terms of a multifactorial cognitive behavioural model. This model proposes that CFS is precipitated by life events and/or viral illness in vulnerable individuals, such as those who are genetically predisposed, prone to distress, high achievement, and over or under activity. A self perpetuating cycle where physiological changes, illness beliefs, reduced and inconsistent activity, sleep disturbance, medical uncertainty and lack of guidance interact to maintain symptoms. Treatments based on this model including cognitive behavioural therapy and graded exercise therapy are effective at significantly reducing fatigue and disability in CFS. This chapter provides a description of these approaches and details of the trials conducted in the area.

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Cinical PracticePredictors of chronic "postviral" fatigue

Abstract

J Psychosomatic Res

Post-viral fatigue syndrome: time for a new approach

BMJ

The chronic fatigue syndrome ("ME"): signs of a new approach

Br J Hosp Med

Chronic fatigue in general practice attenders

Psychol Med

Fatigue syndromes: a comparison of chronic "postviral" fatigue with neuromuscular and affective disorders

J Neurol Neurosurg Psychiatry

A comparative psychiatric assessment of patients with chronic fatigue syndrome and neuromuscular disease

Psychol Med

Psychiatric illness in patients with chronic fatigue and rheumatoid arthritis

J Gen Intern Med

The post viral fatigue syndrome and psychiatry

Br Med Bull

Chronic fatigue syndrome

Antibody to coxsackie B virus in diagnosing postviral fatigue syndrome

BMJ

Human quadriceps strength and fatiguability in patients with post viral fatigue

J Neurol Neurosurg Psychiatry

Enteroviral RNA sequences detected by polymerase chain reaction in muscle of patients with postviral fatigue syndrome

BMJ

Studies on enterovirus in patients with chronic fatigue syndrome

Clin Infect Dis

Search for retrovirus in chronic fatigue syndrome

J Clin Pathol

Cinical Practice
Predictors of chronic "postviral" fatigue