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Although the term "(quasi) phantom head pain" was coined by Sicuteri [4], the hypothesis of "pain memory" (a well-known mechanism for the development of phantom limb pain) has been suggested only quite recently in a few case reports of headache disorders.
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The authors suggested the possibility of "pain memory" hypothesis for the delayed response to indomethacin.
Recently, Marmura et al. [6] suggested the possibility of "pain memory" hypothesis for interictal pain in cluster headache (CH).
Studies with functional neuroimaging support the hypothesis of central pain augmentation in FMS.
This idea was based on the principle of the neutral zone and the neutral zone hypothesis of back pain.
The first 'worse pain' subgroup may have some characteristics similar to those of Cluster 4 our study, and would support the hypothesis of longer pain duration being a feature of Cluster 4.
Any of these changes would be consistent with the hypothesis that augmentation of pain and sensory processing is found in FM.
These results supported our hypothesis of reduced hip pain and symptoms and improved hip function after arthroscopic treatment of FAI.
The absence of reproducible peripheral pathology has supported the hypothesis of abnormal central pain sensitisation/processing, with both psychological and biological theories invoked.
These results support the threat value of pain hypothesis and suggest the necessity for the inclusion of own- versus other-related information in future empathy for pain research.
Our results support the hypothesis that central mechanisms of pain processing in the medial pain system, favourable cognitive/affective factors even during the anticipation of pain, may play an important role for pain processing in patients with FMS.
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CEO of Professional Science Editing for Scientists @ prosciediting.com