[Mechanisms of endogenous pain modulation illustrated by placebo analgesia : functional imaging findings].
Standard
[Mechanisms of endogenous pain modulation illustrated by placebo analgesia : functional imaging findings]. / Bingel, Ulrike.
In: SCHMERZ, Vol. 24, No. 2, 2, 2010, p. 122-129.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - [Mechanisms of endogenous pain modulation illustrated by placebo analgesia : functional imaging findings].
AU - Bingel, Ulrike
PY - 2010
Y1 - 2010
N2 - Nociceptive information processing and related pain perception are subject to substantial pro- and antinociceptive modulation. Research on the involved circuitry and the implemented mechanisms is a major focus of contemporary neuroscientific studies in the field of pain and will provide new insights into the prevention and treatment of chronic pain states. Placebo analgesia is a powerful clinical example of the cognitive modulation of pain perception. In placebo analgesia the administration of an inert substance will produce an analgesic effect if the subject is convinced that the substance is a potent analgesic. Recent neuroimaging studies have started to characterize the neural circuitry supporting the placebo analgesic effect. The converging evidence from these studies supports the concept that during placebo analgesia cingulo-frontal regions interact with subcortical structures involved in endogenous antinociception to produce the placebo-induced reduction in pain perception. The subject's report of reduced pain during placebo analgesia coincides with decreased activity in the classic pain areas. This indicates that the altered pain experience during placebo analgesia results from active inhibition of nociceptive input. This cognitively triggered endogenous modulation of pain involves, at least in part, the endogenous opioid system. Most recently, functional magnetic resonance imaging data of the human spinal cord revealed that these mechanisms involve the inhibition of nociceptive processing at the level of the dorsal horn of the spinal cord. Here we discuss recent advances in pain imaging research focusing on cognitively triggered endogenous pain control mechanisms and respective implications for future research strategies.
AB - Nociceptive information processing and related pain perception are subject to substantial pro- and antinociceptive modulation. Research on the involved circuitry and the implemented mechanisms is a major focus of contemporary neuroscientific studies in the field of pain and will provide new insights into the prevention and treatment of chronic pain states. Placebo analgesia is a powerful clinical example of the cognitive modulation of pain perception. In placebo analgesia the administration of an inert substance will produce an analgesic effect if the subject is convinced that the substance is a potent analgesic. Recent neuroimaging studies have started to characterize the neural circuitry supporting the placebo analgesic effect. The converging evidence from these studies supports the concept that during placebo analgesia cingulo-frontal regions interact with subcortical structures involved in endogenous antinociception to produce the placebo-induced reduction in pain perception. The subject's report of reduced pain during placebo analgesia coincides with decreased activity in the classic pain areas. This indicates that the altered pain experience during placebo analgesia results from active inhibition of nociceptive input. This cognitively triggered endogenous modulation of pain involves, at least in part, the endogenous opioid system. Most recently, functional magnetic resonance imaging data of the human spinal cord revealed that these mechanisms involve the inhibition of nociceptive processing at the level of the dorsal horn of the spinal cord. Here we discuss recent advances in pain imaging research focusing on cognitively triggered endogenous pain control mechanisms and respective implications for future research strategies.
KW - Humans
KW - Magnetic Resonance Imaging
KW - Image Processing, Computer-Assisted
KW - Neural Inhibition physiology
KW - Brain Mapping
KW - Positron-Emission Tomography
KW - Brain physiopathology
KW - Analgesia
KW - Awareness physiology
KW - Ganglia, Spinal physiopathology
KW - Neural Pathways physiology
KW - Nociceptors physiology
KW - Opioid Peptides physiology
KW - Oxygen Consumption
KW - Pain drug therapy
KW - Pain Threshold physiology
KW - Placebo Effect
KW - Spinal Cord physiopathology
KW - Humans
KW - Magnetic Resonance Imaging
KW - Image Processing, Computer-Assisted
KW - Neural Inhibition physiology
KW - Brain Mapping
KW - Positron-Emission Tomography
KW - Brain physiopathology
KW - Analgesia
KW - Awareness physiology
KW - Ganglia, Spinal physiopathology
KW - Neural Pathways physiology
KW - Nociceptors physiology
KW - Opioid Peptides physiology
KW - Oxygen Consumption
KW - Pain drug therapy
KW - Pain Threshold physiology
KW - Placebo Effect
KW - Spinal Cord physiopathology
M3 - SCORING: Zeitschriftenaufsatz
VL - 24
SP - 122
EP - 129
JO - SCHMERZ
JF - SCHMERZ
SN - 0932-433X
IS - 2
M1 - 2
ER -
