Загальне підвищення чутливості: біопсихологічне пояснення хронічного болю у хворих на фіброміалгію і хронічний синдром втоми

The syndromes may overlap, but despite the similarities between the two syndromes, there are also differences. For example, immunological dysregulations such as the abnormal 2-5A synthetase/RNase L pathway [16] have been revealed in CFS but have never been detected in FM patients. Furthermore, there is not yet any good evidence for similar pain mechanisms in CFS and FM. Some authors already found evidence suggesting differences in pain processing. For example, patterns of functional brain activity in patients with FM are quite different from those in patients with CFS.

Patients with CFS, relative to controls, showed significantly lower blood perfusion in the brain stem [17, 18]. Patients with FM exhibited significantly lower rCBF levels, during rest, in the thalamus and the caudate nucleus [19]. Furthermore, Substance P has been found to be elevated in CSF of FM patients [20] and not in patients with CFS [21]. Therefore, the knowledge on pain in FM cannot be applied on CFS patients without further study. Based on the similarities and differences between the two syndromes, further research on pain in CFS is advised to get an image of pain processing in the two diseases.

The goal of this article is to provide a rational basis for future investigations. First, the concept of central sensitisa-tion as a cause of chronic pain will be explained. This theoretical background will then be applied to FM and an overview of the evidence for central sensitization in FM will follow. Finally, based on the theoretical background and the findings in FM, the hypothesis concerning central sensitization in CFS will be unfolded, supported with the present knowledge on CFS.

Chronic widespread pain can be the consequence of central sensitization. Central sensitization is known as an increased central neuronal responsiveness and causes hyperalgesia, allodynia, and referred pain and hyperalgesia across multiple spinal segments, leading to chronic widespread pain. Possible triggers for sensitization of the spinal cord have extensively been discussed, such as wind-up or temporal summation, dysregulated descending inhibitory pathways, and upregulated facilitatory modulation. Wind-up or temporal summation is the result of repetitive noxious stimuli, leading to an increase in electrical discharges in the dorsal horn. Inhibitory modulation can be impaired by abnormalities in the central nervous system and the facilitatory pain pathways can be stimulated by certain behavioral and cognitive factors.

This theoretical background can be applied to FM. In FM, studies already provided evidence for central sensitization as the cause of chronic pain. Temporal summation was found to be more facilitated, and the inhibitory pain modulation seemed impaired in FM patients. These findings can explain the chronic spontaneous pain in FM. Furthermore, some central abnormalities could be examined/objectified in FM: 1) hyperexcitability of the spinal cord, 2) decreased perfusion of pain-related brain structures, and 3) high levels of substance P in CSF. In addition, FM patients often present with pain hypervigilance, maladaptive coping strategies, and catastrophic thoughts, leading to cognitive central sensitization.

Based on the knowledge on central sensitization, on FM and on CFS, it is suggested that chronic widespread pain in CFS is the consequence of central sensitization. There are arguments and probable mechanisms that could explain this phenomenon in CFS. Also, in other chronic pain populations, central sensitization may play a key role. In fact, there are many similarities between CFS patients and other chronic pain populations such as patients with chronic low-back pain, whiplash, FM, etc. The psychosocial factors, for example, have been proved to contribute to pain perception in these different pain populations. But the specific nature of CFS such as the immunological abnormalities, elevated NO amounts, preceding infections etc., invites further research, in particular, on the possible contributory role of these abnormalities to pain processing in CFS.

In FM, many researches have been conducted to prove the theory of central sensitization. In CFS, however, it sticks to «supposing. « To give a scientific basis to the theory, the protocols applied in FM investigations could be used for patients with CFS. It would, for example, be interesting to test the efficacy of temporal summation in CFS. The inhibitory control of pain could be another point of interest. The influence of exercise on pain tolerance has already been studied in CFS [88], however, on a relatively small sample. On the contrary, spatial summation has, to our knowledge, never been investigated in CFS. Furthermore, the role of depression, hypervigilance, kinesiophobia, catastrophising, etc. on chronic pain in CFS requires further research. To obtain more direct and