PHRM 211 Lecture Notes - Lecture 11: Postherpetic Neuralgia, Neuropathic Pain, Paresthesia
Document Summary
Pathophysiology of acute and chronic pain (part 2) Definition: pain due to peripheral and central mechanisms as a result of disease or injury to a peripheral nerve. After some time, cut ends sprout new axons which start to generate spontaneous action potentials. Sensitivity to adrenaline increases, sympathetic stimulation releases na. Na induces powerful shower of afferent discharges that travel toward cns. Dysesthesia : unpleasant , abnormal sensation (e. g. burning, itching, shock, pins and needles) Paresthesia : an abnormal sensation (e. g. tingling, pricking, numbness, limb falling asleep ) Cns sensitization of nmda receptors long term potentiation. Damage to peripheral nerve: neuroma generates ectopic spike activity. Neuroma enhanced by sympathetic activity, na amplifies afferent signal strength. Glutamate and substance p released in larger amounts from central terminals. Windup of wdr stt neurons, via nmda receptors. Short-lived does not last longer than a few minutes! Likely an intrinsic property of spinal nociceptive neurons. May play permissive role in "central sensitization"
