Models and mechanisms of hyperalgesia and allodynia.

By Jürgen Sandkühler. Physiological Reviews, 2009

1,042 citations recorded by the source corpus.

Subfields: Behavioral Neuroscience, Cellular and Molecular Neuroscience, Physiology

View Paper: https://www.semanticscholar.org/paper/21bc23fdfde8cbc96379acf844450710fdd9c0fe

How researchers see this paper

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

In Behavioral Neuroscience

1. Michael R. Irwin
2. George M. Slavich
3. A. Todd
4. R. Kuner
5. Keith Bredemeier
6. A. Beck

In Cellular and Molecular Neuroscience

1. A. Todd
2. Niels Birbaumer
3. Michael R. Irwin
4. R. Baron
5. R. Kuner
6. George M. Slavich
7. M. Malcangio
8. Jonathan R. Wolpaw

In Physiology

1. A. Todd
2. Niels Birbaumer
3. Michael R. Irwin
4. L. Dvorakova
5. Rolf-Detlef Treede
6. I. Vetter
7. R. Baron
8. J. Deuis

Citations in the corpus

• From Stress to Inflammation and Major Depressive Disorder: A Social Signal Transduction Theory of Depression (2014, background): “Increasing evidence suggests that chronic pain is also associated with elevated levels of inflammation and that such inflammation drives hyperalgesia, or increased sensitivity to pain (Sandkühler, 2009; Sommer & Kress, 2004; Watkins & Maier, 2000).”
• Quantitative sensory testing in the German Research Network on Neuropathic Pain (DFNS): Somatosensory abnormalities in 1236 patients with different neuropathic pain syndromes (2010, background): “2%), suggesting a leftward shift of the stimulus–response–function [48,57].”
• Neuronal circuitry for pain processing in the dorsal horn (2010, background): “Several changes in the spinal cord that could underlie these phenomena have been proposed, and these have recently been reviewe”
• Central mechanisms of pathological pain (2010, background): “Diverse molecules modulate spinal pain processing by activating cell surface receptors in discrete spatial and temporal pattern”
• The role of glia in the spinal cord in neuropathic and inflammatory pain. (2015, background): “These changes increase excitability of CNS neurons and result in central sensitisation, which is fundamental for the generation of allodynia, secondary hyperalgesia and spontaneous pain (Kuner 2010; Latremoliere and Woolf 2009; Sandkuhler 2009).”
• Methods Used to Evaluate Pain Behaviors in Rodents (2017, background): “However, as animals cannot be said to be reporting pain, any reaction to such stimuli does not necessarily evidence experience of pain (Sandkühler, 2009).”