Chronic fatigue syndrome: Harvey and Wessely's

Background In a recently published paper, Harvey and Wessely put forward a 'biopsychosocial' explanatory model for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), which is proposed to be applicable to (chronic) fatigue even when apparent medical causes are present. Methods Here, we review the model proposed by Harvey and Wessely, which is the rationale for behaviourally oriented interventions, such as cognitive behaviour therapy (CBT) and graded exercise therapy (GET), and compare this model with a biological model, in which inflammatory, immune, oxidative and nitrosative (IOandNS) pathways are key elements. Discussion Although human and animal studies have established that the pathophysiology of ME/CFS includes IOandNS pathways, these abnormalities are not included in the model proposed by Harvey and Wessely. Activation of IOandNS pathways is known to induce fatigue and somatic (FandS) symptoms and can be induced or maintained by viral and bacterial infections, physical and psychosocial stressors, or organic disorders such as (auto)immune disorders. Studies have shown that ME/CFS and major depression are both clinical manifestations of shared IOandNS pathways, and that both disorders can be discriminated by specific symptoms and unshared or differentiating pathways. Interventions with CBT/GET are potentially harmful for many patients with ME/CFS, since the underlying pathophysiological abnormalities may be intensified by physical stressors. Conclusions In contrast to Harvey and Wessely's (bio)psychosocial model for ME/CFS a bio(psychosocial) model based upon IOandNS abnormalities is likely more appropriate to this complex disorder. In clinical practice, we suggest physicians should also explore the IOandNS pathophysiology by applying laboratory tests that examine the pathways involved.