{'fraction_non_alphanumeric': 0.03578422645540324, 'fraction_numerical': 0.010147765711233755, 'mean_word_length': 5.398633257403189, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Listen to the Story: Chronic Fatigue Syndrome Patients Do Not Live in a Vacuum

Thus, effort and stress intolerance, i.e. a loss of physical and mental resilience [10, 12] , seems to delineate the illness, rather than a CFS/myalgic encephalomyelitis dichotomy, and deserves more emphasis when revising diagnostic criteria. With regard to research, further retroviral studies in larger samples will hopefully contribute to unraveling the etiological mystery of CFS. On the other hand, clinical experience and several studies suggest that although infections are common triggers of CFS, the majority of patients also reports preceding – proximal and distal – chronic ‘stressors’, the nature of which may be physical, mental or (very often) a combination of both [14] . For example, a protracted infection precipitated CFS in a patient during a severe conflict at work, adding to the chronic burden of a handicapped child. Or a women who grew up with a violent, alcoholic father developed CFS following a whiplash injury while being stalked by her ex-partner. Again, by fully appreciating the narrative of a patient’s illness, the abovementioned dichotomy [6, 11] may prove to be futile. Consistent with this view, patients attending a ‘psychologically’ and ‘biomedically’ oriented CFS center, respectively, showed no major differences in psychopathology [15] . Contextual information may also be useful to elucidate the pathophysiological basis of CFS. Most CFS patients strongly oppose the suggestion that they are ‘only fatigued’ since they regularly experience flu-like malaise, generalized pain and an overwhelming tendency to withdraw from the environment, especially when exceeding their limits. This abnormal ‘sickness response’ has been related to deficient glucocorticoid signaling, contributing to low-grade immune activation, which may lead to an excessive production of proinflammatory cytokines and sensitization of central pain mechanisms [12] . Although these dysregulations are subtle and considered by some authors to be secondary (e.g. related to inactivity or sleep disturbance), the typical coping style of CFS patients suggests that stress system failure may be the primum movens. Indeed, many patients reported that when faced with adverse life circumstances, they neglected bodily signs of overload until their body eventually ‘gave up’ [16] . Some added that becoming ill felt like a ‘switch’ from emotional misery to physical exhaustion and pain (e.g. after leaving an abusive partner). In this context, it is tempting to hypothesize that CFS patients may pay the price for their perseverance, which would mean that following an extended period of functioning ‘in overdrive’ – and based on some preexistent vulnerability – their stress system may lose its adaptability, including the dysfunctional hypothalamic-pituitary-adrenal axis becoming unable to ‘contain’ the immune system [10, 12] . Clearly, the story of the CFS patient may invite researchers to move away from monocausal and dualistic etiopathogenetic thinking, and to engage in multidisciplinary studies based on psychosomatic assessment [17] and inspired by modern psychoneurobiological stress Despite intensive research during the past decades, chronic fatigue syndrome (CFS) remains a poorly understood illness. The recent discovery of the XMRV (xenotropic murine leukemia virus-related virus) [1] and similar retroviruses [2] in blood samples of CFS patients has revived speculations about an infectious etiology. Nonetheless, these intriguing results have not been unambiguously confirmed [3, 4] . The ensuing debate focuses on methodological and technical issues regarding retrovirus detection [5] as well as case ascertainment [6] . Contradictory findings have even led to the decision to keep a key publication on hold [7] . Not unexpectedly, antiviral drugs have created new hope for a cure [8] . In our opinion, the enduring controversy surrounding CFS may, at least in part, be caused by the neglect of contextual factors, or in other words, the patient’s ‘story’. We argue that taking these factors into account may not only facilitate the diagnostic delineation of the illness, but may also have heuristic value and optimize treatment. From a diagnostic point of view, the widely used CDC (Centers for Disease Control and Prevention) criteria for CFS, requiring at least 4 additional symptoms next to chronic fatigue [9] , have been criticized for being overinclusive and underestimating the importance of postexertional malaise [6, 10] . Therefore, some assert that the CDC criteria may fail to detect patients with ‘myalgic encephalomyelitis’, considered to be a ‘neurological’ illness and distinguished from chronic fatigue with a ‘psychiatric’ background [6, 11] . However, such an alleged dichotomy would be superfluous if clinicians did not only ‘count symptoms’ to diagnose CFS, but also paid attention to contextual factors. First, by carefully listening to patients’ symptom descriptions, a typical configuration of key features emerges: abnormal physical/mental fatigue and fatigability; hypersensitivity to pain and various sensory and emotional stimuli, and impaired recovery after effort, manifesting as postexertional malaise. Second, CFS patients often describe their illness onset in terms of a ‘crash’ [12] while emphasizing that they do not lack drive or motivation, in contrast to the depression that some of them have experienced earlier. Understandably, they feel ‘betrayed by their body’ [13] . Received: August 20, 2010 Accepted after revision: September 3, 2010 Published online: January 4, 2011