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Textbook of pain

John J Bonica, +2 more
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The article was published on 1999-01-01 and is currently open access. It has received 2623 citations till now.

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Journal ArticleDOI

The Cloned Capsaicin Receptor Integrates Multiple Pain-Producing Stimuli

Makoto Tominaga, +8 more
- 01 Sep 1998 - 
TL;DR: It is shown that protons decrease the temperature threshold for VR1 activation such that even moderately acidic conditions (pH < or = 5.9) activate VR1 at room temperature, and VR1 can be viewed as a molecular integrator of chemical and physical stimuli that elicit pain.
Journal ArticleDOI

The Biopsychosocial Approach to Chronic Pain: Scientific Advances and Future Directions

Robert J. Gatchel, +4 more
- 01 Jan 2007 - 
TL;DR: A review of the basic neuroscience processes of pain (the bio part of biopsychosocial, as well as the psychosocial factors, is presented) and on the development of new technologies, such as brain imaging, that provide new insights into brain-pain mechanisms.
Journal ArticleDOI

Molecular mechanisms of nociception

David Julius, +1 more
- 13 Sep 2001 - 
TL;DR: Efforts to determine how primary sensory neurons detect pain-producing stimuli of a thermal, mechanical or chemical nature have revealed new signalling mechanisms and brought us closer to understanding the molecular events that facilitate transitions from acute to persistent pain.
Journal ArticleDOI

Identification of a cold receptor reveals a general role for TRP channels in thermosensation

David D. McKemy, +2 more
- 07 Mar 2002 - 
TL;DR: These findings, together with the previous identification of the heat-sensitive channels VR1 and VRL-1, demonstrate that TRP channels detect temperatures over a wide range and are the principal sensors of thermal stimuli in the mammalian peripheral nervous system.
Journal ArticleDOI

Neuropathic pain: aetiology, symptoms, mechanisms, and management

Clifford J. Woolf, +1 more
- 05 Jun 1999 - 
TL;DR: This work highlights current theories about peripheral neuropathic pain and shows that progress in management is contingent on targeting treatment not at the aetiological factors or the symptoms but at the mechanisms that operate to produce the symptoms.