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The neurochemistry of central pain: evidence from clinical studies,hypothesis and therapeutic implications
Affiliation:1. Equine Department, VetAgro-Sup, University of Lyon, Marcy l''Étoile, France;2. USC1233, VAS-INRA RS2GP, VetAgro Sup, University of Lyon, Marcy l''Étoile, France;3. Laboratoire Carmen, INSERM U1060, INRA U1235, INSA Lyon, Université Claude Bernard Lyon 1, 69621 Villeurbanne Cedex, France;1. King''s College London, Institute of Psychiatry, Psychology and Neuroscience, Psychological Medicine, London SE5 8AF, UK;2. King''s College London, Institute of Psychiatry, Psychology and Neuroscience, Psychology Department, London SE5 8AF, UK;3. Ilia State University, 3/5 Cholokashvili Street, Tbilisi 0162, Georgia
Abstract:Recent evidence suggests that central pain, i.e., pain due to central nervous system damage, may be due to a deranged neurotransmission between the sensory thalamus and sensory cortical areas. Central pain can be controlled either by opposing glutamate neurotransmission or potentiating GABAergic transmission. It is speculated that a relative hypofunction of the GABAergic inhibition both at thalamic and cortical levels leads to a sectorial excitatory hypertonus in those same areas. A blend of the two should mark each patient. A pharmacological dissection approach is provided that should optimize the treatment, up to now globally poor, of central pain.
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