Chronic pain and medullary descending facilitation.

By F. Porreca, M. Ossipov, G. Gebhart. Trends in Neurosciences, 2002

975 citations recorded by the source corpus.

Subfields: Pediatrics, Perinatology and Child Health, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/f90c22e26afb65b0b5b76c54d6a7d6357eb843be

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Pediatrics, Perinatology and Child Health

1. Katja Wiech
2. Jürgen Sandkühler
3. Irene Tracey
4. Clifford J. Woolf

In Pharmacology

1. Jürgen Sandkühler
2. Clifford J. Woolf
3. R. Ji
4. M. Suter
5. J. Scholz
6. R. Kuner
7. Irene Tracey
8. Katja Wiech

In Physiology

1. Clifford J. Woolf
2. R. Ji
3. Jürgen Sandkühler
4. M. Suter
5. R. Kuner
6. J. Scholz
7. Irene Tracey
8. R. Burstein

Citations in the corpus

• The Amygdala and Persistent Pain (2004, background): “…and endogenous pain control, the CeA is well positioned to play a key role in the emotional-affective pain response and pain modulation (Bernard and others 1996; Heinricher and McGaraughty 1999; Millan 1999; Fields 2000; Rhudy and Meagher 2000; Bourgeais and others 2001; Gauriau and Bernard 2002).”
• Pain: Moving from Symptom Control toward Mechanism-Specific Pharmacologic Management (2004, background): “Relatively little is known about the normal role of descending facilitatory influences, but indications exist that these positive controls are activated or augmented after both inflammation and peripheral nerve injury and in this way contribute to the general increase in sensory transmission (41).”
• Can we conquer pain? (2002, background): “Such plasticity or modifiability of the sensory system essentially characterizes clinical pain syndrome”
• Migraine pathophysiology: anatomy of the trigeminovascular pathway and associated neurological symptoms, CSD, sensitization and modulation of pain (2013, background): “In theory, dysfunctional brainstem areas including the PAG could either enhance activity of neurons that facilitate trigeminovascular pain transmission or suppress activity of neurons that inhibit trigeminovascular pain transmission in the spinal and medullary dorsal horn [102] to generate migraine-”
• State-dependent opioid control of pain (2004, background): “Bidirectional control of pain transmission One of the more striking and informative discoveries about the pain-modulating circuit is that it can facilitate as well as inhibit nociceptive transmissio”
• Pathophysiology of Migraine: A Disorder of Sensory Processing. (2017, background): “Brain stem modulation can have both a facilitatory effect, contributing to chronic pain (270) and an inhibitory influence, through supraspinal and spinal stimulation, on spinal nociceptive processing (271, 666, 703).”
• p38 MAPK, microglial signaling, and neuropathic pain (2007, background): “to spinal neuron hypersensitivity and neuropathic pain [10,11].”
• Descending control of nociception: Specificity, recruitment and plasticity. (2009, background): “A shift in the balance ON- and OFF-cell populations such that ON-cells predominate for extended periods likely underlies the pro-nociceptive influence that this region develops during chronic inflammatory and nerve injury states (Heinricher et al., 2003; Porreca et al., 2002).”
• Central mechanisms of pathological pain (2010, background): “Converging lines of evidence from anatomical, electrophysiological and pharmacological studies show that the axis of the periaqueductal gray (PAG) and rostroventral medulla (RVM) can inhibit or facilitate sensory processing in the spinal dorsal hor”
• Models and mechanisms of hyperalgesia and allodynia. (2009, background): “The roles of ON- and OFF-cells have been reviewed (177, 327, 417).”
• The cerebral signature for pain perception and its modulation. (2007, background): “There are descending pathways that facilitate pain transmission, however, and it is thought that sustained activation of these circuits may underlie some states of chronic pain (see later; Gebhart, 2004; Porreca et al., 2002; Suzuki et al., 2004).”
• The influence of negative emotions on pain: Behavioral effects and neural mechanisms (2009, positive): “This is supported by a wealth of animal studies showing that sustained activation in facilitatory descending pathways may underlie some states of chronic pain (Gebhart, 2004; Porreca et al., 2002; Suzuki et al., 2004).”
• Cellular and Molecular Mechanisms of Pain (2009, neutral): “Such facilitation is especially prominent in the setting of injury and appears to counteract the feedback inhibitory controls that concurrently arise from various brainstem loci (Porreca et al., 2002).”