Persistent Pain in Lesions of the Peripheral and Central Nervous System

Harris, Wilfred

doi:10.1177/003591572201500802

Cited by 17 publications

(16 citation statements)

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“…In 1921, Wilfred Harris described his clinical experience treating patients with presumed injuries to peripheral nerves. He described pain in these patients as episodic with pain episodes provoked by acute exacerbation (Harris, 1921). Hence, from some of the earliest descriptions of pain as a disease, the notion of priming followed by sub-threshold provocation of long-lived pain episodes has been apparent.…”

Section: Clinical Implications Of Pain Memorymentioning

confidence: 99%

Commonalities Between Pain and Memory Mechanisms and Their Meaning for Understanding Chronic Pain

Price

Inyang

2015

Progress in Molecular Biology and Translational Science

130

108

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Pain sensing neurons in the periphery (called nociceptors) and the central neurons that receive their projections show remarkable plasticity following injury. This plasticity results in amplification of pain signaling that is now understood to be crucial for the recovery and survival of organisms following injury. These same plasticity mechanisms may drive a transition to a non-adaptive chronic pain state if they fail to resolve following the termination of the healing process. Remarkable advances have been achieved in the past two decades in understanding the molecular mechanisms that underlie pain plasticity following injury. The mechanisms bear a striking resemblance to molecular mechanisms involved in learning and memory processes in other brain regions, including the hippocampus and cerebral cortex. Here those mechanisms, their commonalities and subtle differences, will be highlighted and their role in causing chronic pain will be discussed. Arising from these data is the striking argument that chronic pain is a disease of the nervous system, which distinguishes this phenomena from acute pain that is frequently a symptom alerting the organism to injury. This argument has important implications for the development of disease modifying therapeutics.

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Section: Clinical Implications Of Pain Memorymentioning

confidence: 99%

Commonalities Between Pain and Memory Mechanisms and Their Meaning for Understanding Chronic Pain

Price

Inyang

2015

Progress in Molecular Biology and Translational Science

130

108

View full text Add to dashboard Cite

show abstract

“…In 1921, Wilfred Harris described his clinical experience treating patients with presumed injuries to peripheral nerves. He described pain in these patients as episodic with pain episodes provoked by acute exacerbation (Harris 1921). Hence, from some of the earliest descriptions of pain as a disease, the notion of priming followed by subthreshold provocation of long-lived pain episodes has been apparent.…”

Section: Why Use Hyperalgesic Priming Models?mentioning

confidence: 99%

The Pharmacology of Nociceptor Priming

Kandasamy

Price

2015

Handbook of Experimental Pharmacology

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Nociceptors and neurons in the central nervous system (CNS) that receive nociceptive input show remarkable plasticity in response to injury. This plasticity is thought to underlie the development of chronic pain states. Hence, further understanding of the molecular mechanisms driving and maintaining this plasticity has the potential to lead to novel therapeutic approaches for the treatment of chronic pain states. An important concept in pain plasticity is the presence and persistence of “hyperalgesic priming.” This priming arises from an initial injury and results in a remarkable susceptibility to normally subthreshold noxious inputs causing a prolonged pain state in primed animals. Here we describe our current understanding of how this priming is manifested through changes in signaling in the primary nociceptor as well as through memory like alterations at CNS synapses. Moreover, we discuss how commonly utilized analgesics, such as opioids, enhance priming therefore potentially contributing to the development of persistent pain states. Finally we highlight where these priming models draw parallels to common human chronic pain conditions. Collectively, these advances in our understanding of pain plasticity reveal a variety of targets for therapeutic intervention with the potential to reverse rather than palliate chronic pain states.

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“…The name 'periodic migrainous neuralgia' was first given in 1921 to a syndrome consisting of severe recurrent attacks of a knife-like unilateral pain in or around the eye (Harris, 1921). The pain is often intense and is sometimes designated as burning, pressing, or boring.…”

mentioning

confidence: 99%