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Open AccessJournal ArticleDOI

Transition from acute to chronic postsurgical pain: risk factors and protective factors

TLDR
It is argued that a focus on the transition from acute to chronic pain may reveal important cues that will help to predict who will go on to develop chronic pain and who will not and how to identify the risk factors and protective factors that predict the course of recovery.
Abstract
Most patients who undergo surgery recover uneventfully and resume their normal daily activities within weeks. Nevertheless, chronic postsurgical pain develops in an alarming proportion of patients. The prevailing approach of focusing on established chronic pain implicitly assumes that information generated during the acute injury phase is not important to the subsequent development of chronic pain. However, a rarely appreciated fact is that every chronic pain was once acute. Here, we argue that a focus on the transition from acute to chronic pain may reveal important cues that will help us to predict who will go on to develop chronic pain and who will not. Unlike other injuries, surgery presents a unique set of circumstances in which the precise timing of the physical insult and ensuing pain are known in advance. This provides an opportunity, before surgery, to identify the risk factors and protective factors that predict the course of recovery. In this paper, the epidemiology of chronic postsurgical pain...

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Citations
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Journal ArticleDOI

Causes and prevention of chronic postsurgical pain.

TL;DR: Surgical incision invariably causes some measure of nerve damage and inflammatory response that, in most cases, heals quickly without long-term negative consequence, but a subset of patients go on to develop lasting neuropathic pain that is difficult to treat and, in many cases, impossible to treat.
Journal ArticleDOI

Variations in potassium channel genes are associated with distinct trajectories of persistent breast pain after breast cancer surgery.

TL;DR: Findings suggest that variations in potassium channel genes are associated with both mild and severe persistent breast pain after breast cancer surgery, and provide intriguing preliminary information on potential therapeutic targets.
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Short-Term Sleep Disturbance–Induced Stress Does not Affect Basal Pain Perception, but Does Delay Postsurgical Pain Recovery

TL;DR: It is reported that pre- or postexposure to rapid eye movement sleep disturbance (REMSD) for 6 hours daily for 3 consecutive days did not alter basal responses to mechanical, heat, and cold stimuli, but did delay recovery in incision-induced reductions in paw withdrawal threshold to mechanical stimulation and paw withdrawal latencies to heat andcold stimuli.
Journal ArticleDOI

The pathophysiology, incidence, impact, and treatment of opioid-induced nausea and vomiting

TL;DR: The underlying mechanisms, clinical implications, and treatment strategies of OINV are discussed, which can lead to complications including electrolyte imbalances, malnutrition, and volume depletion, and can also negatively affect quality of life and postoperative recovery.
References
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Journal ArticleDOI

Measuring the thickness of the human cerebral cortex from magnetic resonance images

TL;DR: An automated method for accurately measuring the thickness of the cerebral cortex across the entire brain and for generating cross-subject statistics in a coordinate system based on cortical anatomy is presented.
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A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man.

TL;DR: A peripheral mononeuropathy was produced in adult rats by placing loosely constrictive ligatures around the common sciatic nerve and the postoperative behavior of these rats indicated that hyperalgesia, allodynia and, possibly, spontaneous pain were produced.
Journal ArticleDOI

Neuronal plasticity: increasing the gain in pain.

TL;DR: Here, a conceptual framework for the contribution of plasticity in primary sensory and dorsal horn neurons to the pathogenesis of pain is developed, identifying distinct forms of Plasticity, which are term activation, modulation, and modification, that by increasing gain, elicit pain hypersensitivity.
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