Central sensitization: neurophysiological mechanisms

Since its discovery, the concept central sensitization has become increasingly popular. However, in the scientific literature central sensitization is defined and operationalized in many different ways, which seriously hampers scientific progression. The original description of central sensitization that derives from animal studies referred to a phenomenon of increased spinal excitability induced after peripheral noxious input and was thought to mediate increases in pain perception present after injury (i.e. the spread of hyperalgesia and allodynia restricted to a limited number of spinal segments). The exact spinal mechanisms underlying these forms of hyperalgesia and allodynia are yet unknown, although our understanding is rapidly growing, for example. The results of recent studies clearly indicate that hyperalgesia and allodynia do not depend on one single mechanism, but can be triggered by a range of mechanisms. More recent interpretations of central sensitization, in particular those used in the clinical domain, are broader than the original concept; central sensitization refers to a general state of central nervous system hypersensitivity that explains a variety of symptoms, including pain and non-pain symptoms (e.g. increased sensitivity to bright light, sounds and odors). We have recently argued that when central sensitization is interpreted too broadly, the chance of finding evidence of central sensitization increases. Consequently, the presence of central sensitization is established in many patients but also the heterogeneity of underlying processes/mechanisms increases. The biopsychosocial model considers that different interacting processes/mechanisms can contribute to a patient’s clinical presentation. Grouping different processes/mechanisms under the same umbrella (central sensitization) does not seem to contribute to a mechanism-based approach and may not improve – and may even hamper – pain management.