Learning pain-related fear: Neural mechanisms mediating rapid differential conditioning, extinction and reinstatement processes in human visceral pain

This article is Part II of a review of the neuronal circuits, neural mechanisms, and neuromodulators that seem to be involved in anxiety and fear states. Part I focused on the specific brain structures, including the roles of the amygdala, locus coeruleus, hippocampus, and various cortical regions and the neural mechanisms of fear conditioning, extinction, and behavioral sensitization in mediating the signs and symptoms of anxiety and fear. Part II attempts to develop a better understanding of neurochemical mediation of traumatic remembrance and the neurobiological consequences of stress, particularly when experienced early in life. Finally, the data is synthesized to provide a basis for understanding the pathophysiology of anxiety disorders, such as Panic disorder and Posttraumatic Stress Disorder. NEUROSCIENTIST 4:122–132, 1998

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Faculty Opinions recommendation of Neural mechanisms mediating positive and negative treatment expectations in visceral pain: a functional magnetic resonance imaging study on placebo and nocebo effects in healthy volunteers.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.718158947.793486927 ◽

2013 ◽

Author(s):

Douglas Drossman ◽

Eva Szigethy

Keyword(s):

Magnetic Resonance Imaging ◽

Magnetic Resonance ◽

Visceral Pain ◽

Imaging Study ◽

Neural Mechanisms ◽

Magnetic Resonance Imaging Study ◽

Functional Magnetic Resonance ◽

Resonance Imaging ◽

Treatment Expectations ◽

Nocebo Effects

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Neural Mechanisms Mediating Placebo Analgesia in Visceral Pain: An FMRI Study in Placebo Responders and Non-Responders

Gastroenterology ◽

10.1016/s0016-5085(11)60228-x ◽

2011 ◽

Vol 140 (5) ◽

pp. S-56 ◽

Cited By ~ 1

Author(s):

Sigrid Elsenbruch ◽

Vassilios Kotsis ◽

Sven Benson ◽

Daniel Reidick ◽

Christina Rosenberger ◽

...

Keyword(s):

Visceral Pain ◽

Neural Mechanisms ◽

Placebo Analgesia ◽

Fmri Study

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Differential conditioning extinction, and secondary reinforcement.

Journal of Experimental Psychology ◽

10.1037/h0021625 ◽

1965 ◽

Vol 69 (1) ◽

pp. 67-74 ◽

Cited By ~ 5

Author(s):

Roger W. Black

Keyword(s):

Differential Conditioning ◽

Secondary Reinforcement ◽

Conditioning Extinction

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Neural mechanisms mediating positive and negative treatment expectations in visceral pain: A functional magnetic resonance imaging study on placebo and nocebo effects in healthy volunteers

Pain ◽

10.1016/j.pain.2013.07.013 ◽

2013 ◽

Vol 154 (11) ◽

pp. 2372-2380 ◽

Cited By ~ 60

Author(s):

Julia Schmid ◽

Nina Theysohn ◽

Florian Ga ◽

Sven Benson ◽

Carolin Gramsch ◽

...

Keyword(s):

Magnetic Resonance Imaging ◽

Magnetic Resonance ◽

Visceral Pain ◽

Imaging Study ◽

Neural Mechanisms ◽

Magnetic Resonance Imaging Study ◽

Functional Magnetic Resonance ◽

Resonance Imaging ◽

Treatment Expectations ◽

Nocebo Effects

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Central neural mechanisms mediating human visceral hypersensitivity

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.2001.281.5.g1196 ◽

2001 ◽

Vol 281 (5) ◽

pp. G1196-G1202 ◽

Cited By ~ 118

Author(s):

Sanchoy Sarkar ◽

Anthony R. Hobson ◽

Paul L. Furlong ◽

Clifford J. Woolf ◽

David G. Thompson ◽

...

Keyword(s):

Central Sensitization ◽

Pain Threshold ◽

Visceral Pain ◽

Functional Gastrointestinal Disorders ◽

Neural Mechanisms ◽

Visceral Hypersensitivity ◽

Afferent Pathway ◽

Healthy Human ◽

Pain Pathway ◽

Stimulation Of

Although visceral hypersensitivity is thought to be important in generating symptoms in functional gastrointestinal disorders, the neural mechanisms involved are poorly understood. We recently showed that central sensitization (hyperexcitability of spinal cord sensory neurones) may play an important role. In this study, we demonstrate that after a 30-min infusion of 0.15 M HCl acid into the healthy human distal esophagus, we see a reduction in the pain threshold to electrical stimulation of the non-acid-exposed proximal esophagus (9.6 ± 2.4 mA) and a concurrent reduction in the latency of the N1 and P2 components of the esophageal evoked potentials (EEP) from this region (10.4 ± 2.3 and 15.8 ± 5.3 ms, respectively). This reduced EEP latency indicates a central increase in afferent pathway velocity and therefore suggests that hyperexcitability within the central visceral pain pathway contributes to the hypersensitivity within the proximal, non-acid-exposed esophagus (secondary hyperalgesia/allodynia). These findings provide the first electrophysiological evidence that central sensitization contributes to human visceral hypersensitivity.

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