Pain and neuroplasticity

The traditional specificity theory of pain perception holds that pain invol ves a direct transmission system from somatic receptors to the brain. The a mount of pain perceived, moreover, is assumed to be directly proportional t o the extent of injury. Recent research, however, indicates far more comple x mechanisms. Clinical and experimental evidence shows that noxious stimuli may sensitize central neural structures involved in pain perception. Salie nt clinical examples of these effects include amputees with pains in a phan tom limb that are similar or identical to those felt in the limb before it was amputated, and patients after surgery who have benefited from pre-empti ve analgesia, which blocks the surgery-induced afferent barrage and/or its central consequences. Experimental evidence of these changes is illustrated by the development of sensitization, wind-up or expansion of receptive fie lds of CNS neurons, as well as by the enhancement of flexion reflexes and t he persistence of pain or hyperalgesia after inputs from injured tissues ar e blocked. It is clear from the material presented that the perception of p ain does not simply involve a moment-to-moment analysis of afferent noxious input, but rather involves a dynamic process that is influenced by the eff ects of past experiences. Sensory stimuli act on neural systems that have b een modified by past inputs, and the behavioural output is significantly in fluenced by the "memory" of these prior events. An increased understanding of the central changes induced by peripheral injury or noxious stimulation should lead to new and improved clinical treatment for the relief and preve ntion of pathological pain.