This is a summary of Chapter III of “The Sensitive Nervous System” by David Butler. Intro When we discuss peripheral issues, we are not only talking about the pathoanatomical source, but pathobiological processes dominating the clinical picture. There are several instances in which the pathoanatomical model falls short: Phantom limb pain. Why pain persists post-healing. Why similar injuries heal faster in certain people. Why 10-14% of the world’s population have an ongoing pain state. Tissues do get injured, but we must not forget the nervous system’s intricate link to injury. When tissues are hurt, they repair but are unlikely to ever be the same again. To protect against further threat, the CNS has the ability to increase nerve sensitivity. This change happens only if the person decides consciously or subconsciously that there is a need for it, and does not occur in everyone. There are two ways in which this sensitivity develops; Primary sensitivity: Increased sensitivity to input at the injury site. Secondary sensitivity: Increased sensitivity to uninjured tissues around the injury. All pain is neurogenic, operates in a continuum, and has many components. Nociception (NOC) NOC is tissue pain that occurs at a neuron’s end that is excited by mechanical, thermal, or chemical stimuli. It does not always match up with tissue health status. A normal nerve ending has a very high firing threshold, and nearly 1/3 will never fire. These are called silent nociceptors. Looking at a chemical process such as inflammation shows us how these nerves fire.
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