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Tactile sensory abnormalities, such as tactile hypoesthesia and mechanical allodynia, are frequently present in patients with chronic pain. A growing body of evidence indicates that hyperesthetic phenomena, like mechanical allodynia, are at least in part due to altered processing by neurons in the CNS. We propose that the hyperesthesia is associated with a functional tactile hypoesthesia that is similarly mediated by altered processing by CNS neurons, and that this association is characterized by a particular topography that may be related to the receptive field organization of somatosensory CNS neurons. Moreover, we propose that the hyperesthetic–hypoesthetic association is dynamically modulated in tandem by pain input.