Evidence, mechanisms, and clinical implications of central hypersensitivity in chronic pain after whiplash injury

Objectives: To provide insights into the mechanisms underlying central hypersensitivity, review the evidence on central hypersensitivity in chronic pain after whiplash injury, highlight reflections on the clinical relevance of central hypersensitivity, and offer a perspective of treatment of central hypersensitivity. Methods: A review of animal and human studies focusing on the mechanisms of postinjury central sensitization, an analysis of psychophysical investigations on central hypersensitivity in patients with chronic pain after whiplash injury, and a review of possible treatment modalities. Results: Animal data show that tissue damage produces plasticity changes at different neuronal structures that are responsible for amplification of nociception and exaggerated pain responses. Some of these changes are potentially irreversible. There is consistent psychophysical evidence for hypersensitivity of the central nervous system to sensory stimulation in chronic pain after whiplash injury. Tissue damage, detected or not by the available diagnostic methods, is probably the main determinant of central hypersensitivity. Psychologic distress could contribute to central hypersensitivity via imbalance of supraspinal and descending modulatory mechanisms. Although specific treatment strategies are limited, they are largely unexplored. Implications: Central hypersensitivity may explain exaggerated pain in the presence of minimal nociceptive input arising from minimally damaged tissues. This could account for pain and disability in the absence of objective signs of tissue damage in patients with whiplash. Central hypersensitivity may provide a common neurobiological framework for the integration of peripheral and supraspinal mechanisms in the pathophysiology of chronic pain after whiplash. Therapy studies are needed.