Abstract
Despite clear advancements in our understanding of the genesis of central pain (CP) [1,2], four notions continue to stand out in the neuropathic pain literature that—we will argue—must be thoroughly revised, if not discarded. We will refer to them as Pain Myths. In light of the supposed failures of cortectomies or thalamotomies to relieve phantom percepts and pain, Melzack [3] proposed that the anatomical substrate of the physical self is a network of neurons that extends throughout widespread areas of the brain ( Neuromatrix ). The repeated cyclical processing and synthesis of nerve impulses in the neuromatrix imparts a characteristic pattern ( neurosignature ) produced by the pattern of synaptic connections in the entire neuromatrix. Neuromodules of the matrix are dedicated to process specialized sensory events, which impress subsignatures on the larger one. This active neuromatrix, when deprived of modulating inputs, produces an abnormal signature pattern that subserves the different qualities of, e.g., neuropathic pain. Ever since 1991, many investigators concluded that the neurosignature of pain is dependent on a core neuromodule of four cortical areas: primary somatosensory cortex (SI), secondary somatosensory cortex (SII), insula and anterior cingulate cortex (ACC), the so-called pain matrix (e.g., [4]). A review of imaging studies concluded that “ acute physiological pain and neuropathic pain have distinct although overlapping brain activation patterns, but there is no unique “pain matrix” or “allodynia network” ” [5]. Importantly, conclusive evidence [6] has emerged that this so-called pain matrix is actually a multimodal network related to the detection of and reaction to salient sensory inputs, regardless of whether these sensory events are conveyed by nociceptive pathways or are perceived as painful: “ the neural activity recorded in the so-called ‘pain matrix’ cannot be considered as a direct correlate of the conscious perception of a somatosensory stimulus as painful ” [7] …
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