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Journal ArticleDOI

Neuronal plasticity and pain

Ronald Dubner
- 01 Jan 1990 - 
- Vol. 41
TLDR
This presentation will review some of the recent findings on physiological and neurochemical changes in the spinal dorsal horn associated with tissue damage and nerve injury.
Abstract
A frequent response to peripheral tissue damage or nerve injury is the appearance of constant pain, pain produced by innocuous stimulation, and increased sensitivity to noxious stimuli. The underlying pathophysiological mechanisms of these clinical features are poorly understood. Although peripheral neural mechanisms, such as nociceptor sensitization associated with tissue damage and neuroma formation following nerve injury, are contributors to the pathophysiology, recent studies indicate that changes in neuronal activity in the central nervous system also play an important role. This presentation will review some of the recent findings on physiological and neurochemical changes in the spinal dorsal horn associated with tissue damage and nerve injury.

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Citations
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TL;DR: This paper is a critical analysis of clinical studies on the effects of pre-emptive analgesia on acute postoperative pain.
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Local anesthesia for inguinal hernia repair step-by-step procedure.

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Abnormal endogenous pain modulation is a shared characteristic of many chronic pain conditions.

TL;DR: Considerable indirect evidence seems to indicate that not only increased pain facilitation but also ineffective pain inhibition represents a predisposition for chronic pain.
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Facilitation of the withdrawal reflex by repeated transcutaneous electrical stimulation: an experimental study on central integration in humans.

TL;DR: It is demonstrated clearly that a stimulus that is perceived as a localised, repetitive tactile tap can be integrated and cause severe pain, and suggests that pathologically generated sparse nociceptive afferent activity causes strong pain by central integration.