Abstract
During the course of a psychophysical study of fibromyalgia syndrome (FMS), one of the subjects with a long history of headache and facial pain displayed an extraordinarily severe thermal allodynia. Her stimulus-response function for ratings of cutaneous heat pain revealed a sensitivity clearly beyond that of normal controls and most FMS subjects. Specially designed psychophysical methods showed that heat sensitivity sometimes increased dramatically within a series of stimuli. Prior exposure to moderate heat pain served as a trigger for allodynic ratings of series of normally neutral thermal stimulation. These observations document a case of breakthrough pain sensitivity with implications for mechanisms of FMS pain.
Highlights
Fibromyalgia syndrome (FMS) is characterized by widespread hyperalgesia and allodynia for mechanical and thermal stimuli of deep and superficial tissues [1]
Normal subjects and typical FMS patients temporally summate when presented with a pulse durations (PDs) of 0.7 sec and an interstimulus interval (ISI) of 2.5 second, but 49◦C or higher temperatures are required
The FMS patient sensitized during stimulation at ISIs far beyond the longest that will maintain temporal summation of pain for a normal subject tested at a higher temperature [9]
Summary
Fibromyalgia syndrome (FMS) is characterized by widespread hyperalgesia and allodynia for mechanical and thermal stimuli of deep and superficial tissues [1]. The magnitude, distribution, and frequency of the clinical pain and the responses to experimental stimuli vary widely [2, 3] suggesting to some: (1) that FMS represents the upper portion of the normal distribution of pain sensitivity [4], (2) that individuals with FMS are predisposed by their genetic makeup and psychological history to exhibit exaggerated pain effect (catastrophize) [4, 5] and (3) that chronic FMS represents a psychological pain state According to these suppositions, the widespread hypersensitivity characteristic of FMS would be associated with excessive activation of cortical levels involved in affective interpretation of pain [6, 7], without abnormal processing within pain pathways extending from the periphery to the initial stages of cortical somatosensory processing.
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