The mechanisms underlying the various forms of neuropathic pain are explored by leading experts in the field. The reviews provide state-of-the-art knowledge in pain research from the molecular and cellular level up to imaging of pain in the human cortex and to the perception of pain. In a truly interdisciplinary approach pain researchers and pain therapists give insights into the latest developments in the field. Some symptoms of neuropathic pain can now be understood at the molecular level, e.g. by modifications in the subunit composition of sodium channels or by the molecular properties of the vanilloid receptor. Synaptic mechanisms similar to those involved in learning and memory formation have now been discovered in pain pathways and real-time images of brain activity in human patients give novel insights into the differential processing of sensory-discriminative versus emotional-aversive aspects of pain.
This volume also documents another remarkable achievement in pain research during the past decade: The development of a common language and the assimilation of scientific concepts across disciplines. When reading the contributions, it becomes clear that new concepts and ideas developed in one arena of pain research have had impact on concepts and hypotheses important to other fields of pain research. Much of the foundation on which future pain research will rest is described in this volume. Numerous cross-references between the chapters and a detailed subject index make this book highly accessible to the reader.

Table of Contents

List of contributors. Foreword. I. Molecular causes of chronic pain. 1. Sodium channels and the molecular pathophysiology of pain (T.R. Cummins, S.D. Dib-Hajj, J.A. Black and S.G. Waxman, West Haven, CT, USA). 2. Chemical mediators of pain due to tissue damage and ischemia (S.P. Eckert, S.P. Cook and E.W. McCleskey, Portland OR, USA). Nociceptor excitation by thermal sensitization - a hypothesis (P.W. Reeh and G. Pethö Erlangen, Germany and Pecs, Hungary). 4. Protein kinase subtypes involved in injury - induced nociception (A.B. Malmberg, Palo Alto, CA, USA). II. Synaptic mechanisms of hyperalgesia and allodynia. 5. Synaptic transmission and plasticity in the superficial dorsal horn (K.A. Moore, H. Baba and C.J. Woolf, Charleston, MA, USA). 6. Synaptic mechanisms of hyperalgesia (J. Sandkühler, J. Benrath, C. Brechtel, R. Ruscheweyh and B. Heinke, Heidelberg, Germany). 7. Silent glutamatergic synapses and long-term facilitation in spinal dorsal horn neurons (M. Zhuo, St. Louis, MO, USA). 8. Spinal dorsal horn synaptic plasticity: involvement of group I metabotropic glutamate receptors (G. Gerber, D.-H. Youn, C.H. Hsu and RandiĆ Ames, IA, USA). III. Long-term changes in the spinal nociceptive system. 9. The functional anatomy of lamina I and its role in post-stroke central pain (A.D. Graig, Phoenix, AZ, USA). 10. Long-term potentiation in single wide dynamic range neurons induced by noxious stimulation in intact and spinalized rats (F. Svendsen, K. Hole and A. Tølsen Bergen,Norway). 11. The role of spinal nitric oxide in the control of spontaneous pain following nociceptive input (U. Hoheisel and S. Mense, Heidelberg, Germany). 12. The role of high threshold calcium channels in spinal neuron hyperexcitability induced by knee inflammation (H.-G. Schaible, J. Nebe, V. Neugebauer, A. Ebersberger and H. Vanegas, Jena, Germany). 13. Neuroplasticity in the spinal cord of monoarthritic rats: from


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© 2000
Elsevier Science
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@from:P.J. Siddall @qu:...This is a high quality book which is an excellent resource for anyone who has an interest in pain medicine and neuroscience. It brings together the latest authoritative thinking on a defining concept in the way that we approach pain. ...I would highly recommend its purchase by libraries which serve either clinicians or scientists in this field. @source:Anaesthesia and Intensive Care