Tuesday, September 20th
Plenary Lecture | Virtual Program
Plenary Room Level 800
John J. Bonica Award Lecture: “Central Sensitization: Clinical Utility of a Physiological Concept for ICD-11 and Nociplastic Pain”
The physiological concept of „central sensitization“ refers to a leftward shift of the stimulus-response functions of nociceptive neurons in the central nervous system, with lowered response thresholds, enhanced suprathreshold responses, new or enlarged receptive fields and increased spontaneous activity. We currently know three distinct types of central sensitization: spinal, brainstem and thalamo-cortical. Use-dependent synaptic plasticity in the spinal cord induces mechanical hyperalgesia or allodynia in adjacent uninjured tissue. Dysregulation of descending brainstem controls leads to widespread or regional pain and hypersensitivity. Comorbid anxiety or depression may be considered as indicators of central sensitization in thalamo-cortical circuits. The new International Statistical Classification of Diseases and Related Health Problems (ICD-11) distinguishes chronic primary pain conditions (“pain as a disease”) and six classes of chronic secondary pain conditions (“pain as a symptom”). Use-dependent synaptic plasticity in the spinal cord contributes to all of them. Evidence for dysregulated brainstem controls has been found in many chronic primary pain conditions. The relationship between sensitization of brain circuits and comorbidities of chronic pain deserves further study. The new concept of “nociplastic pain” does not yet distinguish between these subtypes, which may contribute to its lack of broad acceptance in the pain research and management communities.