Conceptual models of how pain is created influence medical practice, neuroscientific research, and philosophical ideas about pain and other neurological functions. Given the broad scope of pain experiences, realistic models of pain neurobiology must consider the correlation between pain and tissue damage and how it is strongly affected by neurological disease, emotionally compelling circumstances, and by complex cognitive processes. Recent discoveries have made it clear that both sensory and affective systems are strongly modulated by activity in other sensory pathways and by affective and cognitive processes originating in the brain. As a result, pain should then be conceived as emerging from the conjoint activity of both sensory and affective neural systems, each becoming a target for pain treatment. Historically, pain has been conceived as emerging either from an undefined pattern of neural activity or from anatomically and physiologically unique structures in the nervous system. Observations made during the early and mid- 20th century showed that pain and pain-like behaviors normally require not only sensory detectors of noxious events (called nociceptors) but also brain affective (hedonic) mechanisms that generate emotional experience and expression. In Chasing Pain, pain specialists and neuroscientists will find a thoughtful discussion of the neuroscientific and clinical evidence that has led to contemporary concepts of pain neurobiology and how pain might emerge from neuronal activity. Written in a concise and annotated format, Doctor Kenneth Casey reveals that while contemporary research has greatly enriched our model of pain neurobiology, several important and therapeutically challenging clinical conditions remain poorly understood.
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Kenneth L. Casey, MD is Professor Emeritus of Neurology and Molecular and Integrative Physiology at the University of Michigan in Ann Arbor, Michigan.
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