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Abstract
Neuropathic pain is triggered by lesions to the somatosensory nervous system that
alter its structure and function so that pain occurs spontaneously and responses to
noxious and innocuous stimuli are pathologically amplified. The pain is an expression
of maladaptive plasticity within the nociceptive system, a series of changes that
constitute a neural disease state. Multiple alterations distributed widely across
the nervous system contribute to complex pain phenotypes. These alterations include
ectopic generation of action potentials, facilitation and disinhibition of synaptic
transmission, loss of synaptic connectivity and formation of new synaptic circuits,
and neuroimmune interactions. Although neural lesions are necessary, they are not
sufficient to generate neuropathic pain; genetic polymorphisms, gender, and age all
influence the risk of developing persistent pain. Treatment needs to move from merely
suppressing symptoms to a disease-modifying strategy aimed at both preventing maladaptive
plasticity and reducing intrinsic risk.
[1
]Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts
General Hospital and Harvard Medical School, Boston, Massachusetts 02129; email: ,
,