19 results
Contributors
-
- By Cecil S. Ash, Paul Barach, Ulrike Buehner, M. Ross Bullock, Leonardo Canale, Henry G. Chou, Jeffrey A. Claridge, John J. Como, Armagan Dagal, Martin Dauber, James S. Davis, Shalini Dhir, François Donati, Roman Dudaryk, Richard P. Dutton, Talmage D. Egan, Yashar Eshraghi, John R. Fisgus, Jeff Gadsden, Sugantha Ganapathy, Mark A. Gerhardt, Inderjit Gill, Joseph F. Golob, Glenn P. Gravlee, Marcello Guglielmi, Jana Hambley, Peter Hebbard, Elena J. Holak, Khadil Hosein, Ken Johnson, Matthew A. Joy, George W. Kanellakos, Olga Kaslow, Arthur M. Lam, Vanetta Levesque, Jessica Anne Lovich-Sapola, M. Jocelyn Loy, Peter F. Mahoney, Donn Marciniak, Maureen McCunn, Craig C. McFarland, Maroun J. Mhanna, Timothy Moore, Cynthia Nguyen, Maxim Novikov, E. Orestes O’Brien, Ketan P. Parekh, Claire L. Park, Michael J. A. Parr, Elie Rizkala, Steven Roth, Alistair Royse, Colin Royse, Kasia Petelenz Rubin, David Ryan, Claire Sandstrom, Carl I. Schulman, Rishad Shaikh, Ranjita Sharma, Jeffrey H. Silverstein, Peter Slinger, Charles E. Smith, Christopher Smith, Paul Soeding, Rakesh V. Sondekoppam, P. David Soran, Eldar Søreide, Elizabeth A. Steele, Kristian Strand, Dennis M. Super, Kutaiba Tabbaa, Nicholas T. Tarmey, Joshua M. Tobin, Kalpana Tyagaraj, Heather A. Vallier, Sandra Werner, Earl Willis Weyers, William C. Wilson, Shoji Yokobori, Charles J. Yowler
- Edited by Charles E. Smith
-
- Book:
- Trauma Anesthesia
- Published online:
- 05 April 2015
- Print publication:
- 09 April 2015, pp vii-x
-
- Chapter
- Export citation
Contributors
-
- By Phillip L. Ackerman, Soon Ang, Susan M. Barnett, G. David Batty, Anna S. Beninger, Jillian Brass, Meghan M. Burke, Nancy Cantor, Priyanka B. Carr, David R. Caruso, Stephen J. Ceci, Lillia Cherkasskiy, Joanna Christodoulou, Andrew R. A. Conway, Christine E. Daley, Janet E. Davidson, Jim Davies, Katie Davis, Ian J. Deary, Colin G. DeYoung, Ron Dumont, Carol S. Dweck, Linn Van Dyne, Pascale M. J. Engel de Abreu, Joseph F. Fagan, David Henry Feldman, Kurt W. Fischer, Marisa H. Fisher, James R. Flynn, Liane Gabora, Howard Gardner, Glenn Geher, Sarah J. Getz, Judith Glück, Ashok K. Goel, Megan M. Griffin, Elena L. Grigorenko, Richard J. Haier, Diane F. Halpern, Christopher Hertzog, Robert M. Hodapp, Earl Hunt, Alan S. Kaufman, James C. Kaufman, Scott Barry Kaufman, Iris A. Kemp, John F. Kihlstrom, Joni M. Lakin, Christina S. Lee, David F. Lohman, N. J. Mackintosh, Brooke Macnamara, Samuel D. Mandelman, John D. Mayer, Richard E. Mayer, Martha J. Morelock, Ted Nettelbeck, Raymond S. Nickerson, Weihua Niu, Anthony J. Onwuegbuzie, Jonathan A. Plucker, Sally M. Reis, Joseph S. Renzulli, Heiner Rindermann, L. Todd Rose, Anne Russon, Peter Salovey, Scott Seider, Ellen L. Short, Keith E. Stanovich, Ursula M. Staudinger, Robert J. Sternberg, Carli A. Straight, Lisa A. Suzuki, Mei Ling Tan, Maggie E. Toplak, Susana Urbina, Richard K. Wagner, Richard F. West, Wendy M. Williams, John O. Willis, Thomas R. Zentall
- Edited by Robert J. Sternberg, Oklahoma State University, Scott Barry Kaufman, New York University
-
- Book:
- The Cambridge Handbook of Intelligence
- Published online:
- 05 June 2012
- Print publication:
- 30 May 2011, pp xi-xiv
-
- Chapter
- Export citation
8 - Functional imaging of chronic pain
- Frederick A. Lenz, Kenneth L. Casey, Edward G. Jones, University of California, Davis, William D. Willis, University of Texas Medical Branch, Galveston
-
- Book:
- The Human Pain System
- Published online:
- 05 October 2010
- Print publication:
- 21 January 2010, pp 540-589
-
- Chapter
- Export citation
-
Summary
Introduction
In Chapter 5, we discussed the normal responses to a variety of noxious stimuli and their modulation by peripheral and central neural mechanisms. This review showed that noxious stimuli preferentially and most commonly activate a set of interconnected structures, namely the insula and secondary (SII) somatosensory cortices, anterior cingulate gyrus and thalamus. Several additional structures are also activated during normal acute pain although somewhat less frequently: the primary (SI) somatosensory cortex, components of the striatum, the cerebellum, premotor cortex, dorsolateral and orbitofrontal regions of the prefrontal cortex, and the medial midbrain in the region of the periaqueductal gray matter.
In this chapter we review the evidence that chronically painful conditions, whether of peripheral or central origin, may alter the nociceptive processing that normally follows the application of noxious or innocuous stimuli (see Chapter 7). In clinical practice and in the interpretation of the results of pain research, the assumption is often made that the perceptual abnormalities sometimes associated with chronic pain states are attributable only to changes occurring at the peripheral or spinal level. Although this assumption may be correct in most instances, functional imaging studies provide evidence to the contrary in some cases. We cannot assume that, in pathological or chronically painful conditions, information ascending through the spinothalamic tract will be processed by the same mechanisms used for acute pain; this has important clinical implications for the management of chronic pain.
The term “chronic pain” is seldom defined.
7 - Peripheral and central mechanisms and manifestations of chronic pain and sensitization
- Frederick A. Lenz, Kenneth L. Casey, Edward G. Jones, University of California, Davis, William D. Willis, University of Texas Medical Branch, Galveston
-
- Book:
- The Human Pain System
- Published online:
- 05 October 2010
- Print publication:
- 21 January 2010, pp 453-539
-
- Chapter
- Export citation
-
Summary
Neuropathic pain is pain following a disease or injury to the nervous system, and can be categorized by the location of the causative injury. Chronic pain following injury of the peripheral nervous system, distal to the oligodendroglial cell – Schwann cell junction, can be termed deafferentation pain or peripheral neuropathic pain. Chronic pain “associated with lesions of the CNS” is termed central pain syndrome (Merskey, 1986; Bonica, 1991). There are many situations in which there is injury of both the peripheral and central nervous system, particularly with injuries of the conus medullaris. In this chapter we will consider primate neuropathic pain states, beginning with peripheral neuropathic or deafferentation syndromes, and concluding with central pain syndromes.
In general terms, both central and peripheral chronic pain syndromes have similar characteristics. These include evidence of sensory loss, ongoing pain and pain evoked by stimuli that are not normally painful (allodynia or hyperalgesia). The sensory loss and hypersensitivity are demonstrated by quantitative sensory testing (QST). In addition, a number of primate models have been developed which mimic the sensory abnormalities in patients with neuropathic pain.
Clinical characteristics of peripheral neuropathic pain
The cause of most neuropathies is based on the medical history, supported by laboratory investigations (Casey et al., 1996b). Diabetes is the most common cause of painful neuropathy. Generally, a progressive course suggests an inherited, metabolic or recurrent toxic etiology.
2 - Organization of the central pain pathways
- Frederick A. Lenz, Kenneth L. Casey, Edward G. Jones, University of California, Davis, William D. Willis, University of Texas Medical Branch, Galveston
-
- Book:
- The Human Pain System
- Published online:
- 05 October 2010
- Print publication:
- 21 January 2010, pp 64-195
-
- Chapter
- Export citation
-
Summary
Inputs from nociceptors
The nature of nociceptors
Nociceptors are sensory receptors that respond to stimuli that are damaging or potentially damaging to tissues (Sherrington,1906). The thresholds for activation of many nociceptors can be reached when stimuli of only moderate or non-damaging intensities are applied, but responses continue to increase as stimulus intensity is progressively increased to a level that produces overt damage. By contrast, other nociceptors respond only to intense stimuli and some may not respond at all, even to the strongest mechanical stimuli, unless they are first sensitized (Lynn and Carpenter, 1982; Meyer et al., 1991; Kress et al., 1992; Davis et al., 1993; Treede et al., 1998). The last mentioned have been called “silent nociceptors” (Schaible and Schmidt, 1985, 1988a, 1988b; Schmidt et al., 1995, 2000). Overall, if we include receptors responding to innocuous warming and cooling of the skin, there may be as many as six receptor classes specific for cooling, warming, noxious heat or cold, destructive mechanical or mixed noxious stimuli in humans and other animals.
Types of nociceptors
Nociceptors can be subdivided according to the tissue in which they are found, the size or conduction velocity of the afferent fiber supplying them and the type of stimulus that activates them. Most experimental studies of nociceptors have been performed on common laboratory animals, especially rodents and cats. Some of the most informative, however, have been made during recordings from peripheral nerves of monkeys or human subjects (reviewed in Willis and Coggeshall, 2004).
9 - Functional implications of spinal and forebrain procedures for the treatment of chronic pain
- Frederick A. Lenz, Kenneth L. Casey, Edward G. Jones, University of California, Davis, William D. Willis, University of Texas Medical Branch, Galveston
-
- Book:
- The Human Pain System
- Published online:
- 05 October 2010
- Print publication:
- 21 January 2010, pp 590-623
-
- Chapter
- Export citation
-
Summary
The clinical descriptions of cordotomy played a major role in elucidating the function and the anatomy of the human spinothalamic tract (STT) (Chapter 1). There are a number of other examples of surgical interventions which have informed our understanding of the pain system. In particular, the pain-related role of the cingulate gyrus is suggested by imaging studies and by the effect of cingulotomy on experimental pain (Rainville et al., 1997; Gildenberg, 2004). Similarly the role of the motor cortex in these systems has suggested the effects of stimulation on activity throughout the pain system (Brown and Barbaro, 2003; Brown, 2004; Peyron et al., 2007). The purpose of this chapter is to examine these surgical interventions in terms of the anatomy and function of structures involved in these interventions. The inclusion of procedures in this chapter is arbitrary and many other such procedures which might have been included have been excluded.
Cordotomy and myelotomy
Percutaneous cordotomy produces relief of pain by interrupting the transmission of signals in the STT from below the level of intervention (Tasker, 1988; Tasker, 2004). The anterolateral quadrant of the spinal cord has long been recognized as the location of the STT (Chapter 1). Recent findings indicate that the dorsal column system also has an important role in visceral nociception (Nauta et al., 1997; Willis et al., 1999). The STT terminates in the primate thalamus, brainstem and other structures such as the hypothalamus and amygdala whereas the dorsal column system terminates in the dorsal column nuclei (Newman et al., 1996).
5 - Functional brain imaging of acute pain in healthy humans
- Frederick A. Lenz, Kenneth L. Casey, Edward G. Jones, University of California, Davis, William D. Willis, University of Texas Medical Branch, Galveston
-
- Book:
- The Human Pain System
- Published online:
- 05 October 2010
- Print publication:
- 21 January 2010, pp 329-422
-
- Chapter
- Export citation
-
Summary
Introduction
Before the introduction of computerized tomographic (CT) brain imaging, studying human brain mechanisms of pain was largely limited to clinical reports and the post-mortem analysis of brain lesions. Although this approach provided important information and established the background for current investigations, these studies were usually limited by clinical descriptions of each patient's condition. Somatosensory psychophysics seldom included studies of pain and even then it was not possible to relate these observations to brain function or physiology. Because the living brain was invisible (except in the neurosurgery operating suite), research on pain mechanisms focused almost exclusively on the peripheral nervous system.
Brain CT scans introduced the opportunity to apply quantitative sensory testing to the study of living patients with visible, localized brain lesions and to begin to test hypotheses about functional localization and brain mechanisms of pain. The introduction of functional imaging by positron emission tomography (PET) and magnetic resonance imaging (MRI; fMRI) launched a new investigational paradigm into the study of pain mechanisms. Now it is possible to go well beyond the lesion analysis method and to relate human experience, in this case using somatosensory psychophysics, directly to a surrogate measure of activity in groups of neurons at the level of visible, localized brain structure. Since the early 1990s, the number and technical sophistication of functional brain imaging studies, including those related to pain, has increased at a rate that makes it almost impossible to incorporate the results into a conceptual framework.
Contents
- Frederick A. Lenz, Kenneth L. Casey, Edward G. Jones, University of California, Davis, William D. Willis, University of Texas Medical Branch, Galveston
-
- Book:
- The Human Pain System
- Published online:
- 05 October 2010
- Print publication:
- 21 January 2010, pp v-vi
-
- Chapter
- Export citation
6 - Pain modulatory systems
- Frederick A. Lenz, Kenneth L. Casey, Edward G. Jones, University of California, Davis, William D. Willis, University of Texas Medical Branch, Galveston
-
- Book:
- The Human Pain System
- Published online:
- 05 October 2010
- Print publication:
- 21 January 2010, pp 423-452
-
- Chapter
- Export citation
-
Summary
Introduction
It is well known that much of the sensory input to the central nervous system can be modulated by centrifugally organized control systems that originate in the central nervous system (Head and Holmes, 1911; Hagbarth, 1960). The control mechanisms can be excitatory or inhibitory processes that may occur in the periphery or within the central nervous system. Inhibition can be at pre- and/or postsynaptic sites (Fig. 6.1(I)). Presynaptic inhibition at the first central synapse of a sensory pathway has the potential advantage of being able to reduce sensory input prior to wide dissemination of that sensory input within the central nervous system through the activation of interneuronal networks and multiple ascending pathways, for example, in the spinal cord (Schmidt, 1973; see Chapter 3).
Pre- and postsynaptic inhibition can have somewhat different effects on the stimulus-response curves of second-order sensory neurons, as shown in Fig. 6.1(II). Postsynaptic inhibition involves inhibitory postsynaptic potentials that sum with excitatory postsynaptic potentials (Fig. 6.1(IIA)). If there is a linear summation, the stimulus-response curve will be shifted to the right in a parallel fashion (Carstens et al., 1980). However, if the IPSP is generated in a membrane area near that in which the EPSP is generated, the excitatory current may be shunted and the slope of the stimulus-response curve reduced, causing a reduction in the gain of synaptic transmission (Fig. 6.1(IIB)). A similar reduction in gain can be produced by presynaptic inhibition.
1 - Discovery of the anterolateral system and its role as a pain pathway
- Frederick A. Lenz, Kenneth L. Casey, Edward G. Jones, University of California, Davis, William D. Willis, University of Texas Medical Branch, Galveston
-
- Book:
- The Human Pain System
- Published online:
- 05 October 2010
- Print publication:
- 21 January 2010, pp 1-63
-
- Chapter
- Export citation
-
Summary
Introduction
On January 19 1911, persuaded by his colleague, the neurologist William Spiller, a Philadelphia surgeon named Edward Martin made a small transverse cut in the spinal cord of a patient suffering from severe pain caused by a tumor affecting the lower end of the spinal column. The cut, made with a thin cataract knife, was no more than 2 mm deep or wide and entered the cord some 3 mm ventral to the entry of a dorsal root in the middle thoracic region. The patient experienced much relief from what had until then been intractable pain (Spiller and Martin,1912). The operation of “chordotomie” or section of the anterolateral tracts of the spinal cord had been introduced in 1910 by Schüller in work on monkeys in which he was exploring the possibility of using the operation for the alleviation of spastic paralysis and tabetic crises in humans. Spiller argued for the procedure on the basis of clinico-pathological observations that appeared to implicate the anterolateral tracts as pathways for conduction of impulses related to pain and temperature through the spinal cord (Müller, 1871; Gowers, 1879; Spiller, 1905; Petrén, 1910). Reports of other successful cases quickly followed (Beer, 1913; Foerster, 1913) and soon, at the hands of Foerster (1913, 1927; Foerster and Gagel, 1932) in Germany and Frazier (1920) in the United States, cordotomy was to become for a time the surgical method of choice in dealing with intractable pain.
4 - Physiology of supraspinal pain-related structures
- Frederick A. Lenz, Kenneth L. Casey, Edward G. Jones, University of California, Davis, William D. Willis, University of Texas Medical Branch, Galveston
-
- Book:
- The Human Pain System
- Published online:
- 05 October 2010
- Print publication:
- 21 January 2010, pp 237-328
-
- Chapter
- Export citation
-
Summary
Introduction
It is well understood that there are different components to the sensation of pain (Melzack and Casey,1968). The sensory-discriminative aspect of pain refers to the location, intensity and quality of the sensory experience of pain. The affective-motivational aspect of pain refers to the unpleasantness of the pain and how likely it is that it will motivate the animal to escape the pain. We refer to these different components of the pain sensation throughout this review as we examine the possibility that these different components are mediated by different structures in the brain.
The spinothalamic tract (STT) is the spinal tract projecting toward the brain which is most often associated with the sensation of pain (Price and Dubner, 1977; Willis, 1985; Price et al., 2003). Cells of origin of the STT can be divided into those which respond to low-threshold stimuli (LT cells), those which respond to stimuli across the intensive continuum into the noxious range (wide dynamic range, WDR), and those that respond only to noxious stimuli (nociceptive specific, NS). Evidence that any structure mediates the sensory aspect of pain is grouped into four lines: that the structure is connected to other structures known to demonstrate pain-related activity; that neural elements in that structure respond to noxious stimuli; that stimulation of that structure produces pain; and that interventions which interfere with the function of that structure interfere with the sensation of pain evoked by noxious stimuli (Price and Dubner, 1977).
The Human Pain System
- Experimental and Clinical Perspectives
- Frederick A. Lenz, Kenneth L. Casey, Edward G. Jones, William D. Willis
-
- Published online:
- 05 October 2010
- Print publication:
- 21 January 2010
-
Pain is a subject of significant scientific and clinical interest. This has resulted both from realistic rodent models, and the publication of imaging, psychological and pharmacological studies in humans. Investigators studying rodents refer to anatomical and physiological studies in non-human primates to make their results relevant to humans. Psychophysical and pharmacological studies in humans are interpreted in terms of anatomical and physiological studies in animals; primarily evidence from rodents and cats. There are significant differences in pain mechanisms between these species and primates. Over 20 years of imaging studies have demonstrated the activation of human cortical and subcortical structures in response to painful stimuli. Interpretation of these results relies upon an understanding of the anatomy and physiology of these structures in primates. Jones, Lenz, Casey and Willis review the anatomy and physiology of nociception in monkeys and humans, and provide a firm basis for interpreting studies in humans.
3 - Physiology of cells of origin of spinal cord and brainstem projections
- Frederick A. Lenz, Kenneth L. Casey, Edward G. Jones, University of California, Davis, William D. Willis, University of Texas Medical Branch, Galveston
-
- Book:
- The Human Pain System
- Published online:
- 05 October 2010
- Print publication:
- 21 January 2010, pp 196-236
-
- Chapter
- Export citation
-
Summary
Introduction
As discussed in Chapter 2, several of the sensory pathways that ascend from the spinal cord or brainstem to higher levels of the monkey central nervous system have a nociceptive component and thus may contribute to pain sensation. Spinal cord projections with nociceptive components that ascend to the brain in the anterolateral quadrant of the spinal cord include the spinothalamic, spinoreticular, spinomesencephalic and spinohypothalamic tracts; nociceptive projections that ascend in the dorsolateral or dorsal funiculus are the spinocervical tract and the postsynaptic dorsal column pathway (see Willis and Coggeshall, 2004). Brainstem projections include the trigeminothalamic tract (Price et al., 1976).
To investigate the physiology of an individual spinal cord or brainstem neuron that belongs to one of the ascending nociceptive pathways, it is important to “identify” the neuron by showing that the axon of the individual neuron under investigation actually projects to the appropriate target (Willis and Coggeshall, 2004). Recordings from a neuron unidentified in terms of its projection can be misleading, since many unidentified neurons are likely to be interneurons, and these could be excitatory or inhibitory and might or might not influence the activity of sensory projection neurons. For instance, many spinal cord interneurons belong to neural circuits that function to control motor output (Jankowska et al., 1981; Rudomin et al., 1987).
Identification of a projection neuron is typically accomplished by demonstrating that the neuron can be activated antidromically in response to electrical stimulation in a region in which the axon of that projection neuron synapses (Trevino et al., 1973; Bryan et al., 1974; Haber et al., 1982; see Willis and Coggeshall, 2004).
Index
- Frederick A. Lenz, Kenneth L. Casey, Edward G. Jones, University of California, Davis, William D. Willis, University of Texas Medical Branch, Galveston
-
- Book:
- The Human Pain System
- Published online:
- 05 October 2010
- Print publication:
- 21 January 2010, pp 624-638
-
- Chapter
- Export citation
Frontmatter
- Frederick A. Lenz, Kenneth L. Casey, Edward G. Jones, University of California, Davis, William D. Willis, University of Texas Medical Branch, Galveston
-
- Book:
- The Human Pain System
- Published online:
- 05 October 2010
- Print publication:
- 21 January 2010, pp i-iv
-
- Chapter
- Export citation
Preface
- Frederick A. Lenz, Kenneth L. Casey, Edward G. Jones, University of California, Davis, William D. Willis, University of Texas Medical Branch, Galveston
-
- Book:
- The Human Pain System
- Published online:
- 05 October 2010
- Print publication:
- 21 January 2010, pp vii-x
-
- Chapter
- Export citation
-
Summary
Unless suffering from one of those rare forms of hereditary indifference to pain, no human is without the experience of pain. Yet humans have always had difficulty in conveying a unified concept of pain since it can include subjective states ranging from mere unpleasantness to extreme physical agony, or to the feeling of sadness and desolation accompanying an episode of major depression. Plato and Aristotle did not regard pain as an elemental sensation like touch or vision but rather saw pain and pleasure as contrasting elements vying with one another for the maintenance of internal wellbeing of the individual by operating on the soul, which was thought to be located in the liver or heart. For Aristotle, pain arose from ripples in the heart and blood vessels, not from the activity of the reasoning brain. Perhaps we can still see crude echoes of the Aristotelian position in modern suggestions that pain is no more than a disruption of bodily homeostasis, akin to that associated with dysautonomia and other visceral disturbances.
It is to Galen, writing more than 450 years after Aristotle, that we owe the recognition that sensory impressions, including those leading to pain, are carried by nerves to the brain and Galen described carrying out cordotomies in animals in order to demonstrate the key role of the spinal cord in the conduction of painful impressions to the brain.
Responses of neurons in the rat ventral posterior lateral thalamic nucleus to noxious visceral and cutaneous stimuli
- JIRI PALECEK, WILLIAM D. WILLIS
-
- Journal:
- Thalamus & Related Systems / Volume 3 / Issue 1 / March 2005
- Published online by Cambridge University Press:
- 13 October 2005, pp. 25-32
- Print publication:
- March 2005
-
- Article
- Export citation
-
Visceral nociceptive responses to distention of the ureter, and responses to innocuous and noxious mechanical stimulation of the skin were recorded from neurons in the ventral posterior lateral nucleus of the thalamus in anesthetized rats. The ventral posterior lateral (VPL) neurons were classified by their responses to cutaneous stimuli as either low-threshold or wide-dynamic-range neurons. No high-threshold neurons were found in the population of VPL neurons sampled. Some VPL neurons that responded to distention of the ureter appeared to lack a cutaneous receptive field. The majority of VPL neurons that responded to noxious visceral stimulation of the ureter were classified as low-threshold neurons, based on their responses to cutaneous stimuli. Transection of the DC at an upper cervical level dramatically reduced the responses of VPL neurons to ureter distention and to innocuous mechanical stimulation of the skin, but the responses to noxious mechanical stimulation of the skin remained intact. Ureter distention and mechanical stimulation of the skin might activate dorsal horn neurons, including postsynaptic dorsal-column pathway (PSDC) neurons and spinothalamic tract (STT) cells. We conclude that both the DC pathway and the STT are likely to contribute to the visceral and somatic responses of some VPL neurons.
Looking Backward, Looking Forward: MLA Members Speak
- April Alliston, Elizabeth Ammons, Jean Arnold, Nina Baym, Sandra L. Beckett, Peter G. Beidler, Roger A. Berger, Sandra Bermann, J.J. Wilson, Troy Boone, Alison Booth, Wayne C. Booth, James Phelan, Marie Borroff, Ihab Hassan, Ulrich Weisstein, Zack Bowen, Jill Campbell, Dan Campion, Jay Caplan, Maurice Charney, Beverly Lyon Clark, Robert A. Colby, Thomas C. Coleman III, Nicole Cooley, Richard Dellamora, Morris Dickstein, Terrell Dixon, Emory Elliott, Caryl Emerson, Ann W. Engar, Lars Engle, Kai Hammermeister, N. N. Feltes, Mary Anne Ferguson, Annie Finch, Shelley Fisher Fishkin, Jerry Aline Flieger, Norman Friedman, Rosemarie Garland-Thomson, Sandra M. Gilbert, Laurie Grobman, George Guida, Liselotte Gumpel, R. K. Gupta, Florence Howe, Cathy L. Jrade, Richard A. Kaye, Calhoun Winton, Murray Krieger, Robert Langbaum, Richard A. Lanham, Marilee Lindemann, Paul Michael Lützeler, Thomas J. Lynn, Juliet Flower MacCannell, Michelle A. Massé, Irving Massey, Georges May, Christian W. Hallstein, Gita May, Lucy McDiarmid, Ellen Messer-Davidow, Koritha Mitchell, Robin Smiles, Kenyatta Albeny, George Monteiro, Joel Myerson, Alan Nadel, Ashton Nichols, Jeffrey Nishimura, Neal Oxenhandler, David Palumbo-Liu, Vincent P. Pecora, David Porter, Nancy Potter, Ronald C. Rosbottom, Elias L. Rivers, Gerhard F. Strasser, J. L. Styan, Marianna De Marco Torgovnick, Gary Totten, David van Leer, Asha Varadharajan, Orrin N. C. Wang, Sharon Willis, Louise E. Wright, Donald A. Yates, Takayuki Yokota-Murakami, Richard E. Zeikowitz, Angelika Bammer, Dale Bauer, Karl Beckson, Betsy A. Bowen, Stacey Donohue, Sheila Emerson, Gwendolyn Audrey Foster, Jay L. Halio, Karl Kroeber, Terence Hawkes, William B. Hunter, Mary Jambus, Willard F. King, Nancy K. Miller, Jody Norton, Ann Pellegrini, S. P. Rosenbaum, Lorie Roth, Robert Scholes, Joanne Shattock, Rosemary T. VanArsdel, Alfred Bendixen, Alarma Kathleen Brown, Michael J. Kiskis, Debra A. Castillo, Rey Chow, John F. Crossen, Robert F. Fleissner, Regenia Gagnier, Nicholas Howe, M. Thomas Inge, Frank Mehring, Hyungji Park, Jahan Ramazani, Kenneth M. Roemer, Deborah D. Rogers, A. LaVonne Brown Ruoff, Regina M. Schwartz, John T. Shawcross, Brenda R. Silver, Andrew von Hendy, Virginia Wright Wexman, Britta Zangen, A. Owen Aldridge, Paula R. Backscheider, Roland Bartel, E. M. Forster, Milton Birnbaum, Jonathan Bishop, Crystal Downing, Frank H. Ellis, Roberto Forns-Broggi, James R. Giles, Mary E. Giles, Susan Blair Green, Madelyn Gutwirth, Constance B. Hieatt, Titi Adepitan, Edgar C. Knowlton, Jr., Emanuel Mussman, Sally Todd Nelson, Robert O. Preyer, David Diego Rodriguez, Guy Stern, James Thorpe, Robert J. Wilson, Rebecca S. Beal, Joyce Simutis, Betsy Bowden, Sara Cooper, Wheeler Winston Dixon, Tarek el Ariss, Richard Jewell, John W. Kronik, Wendy Martin, Stuart Y. McDougal, Hugo Méndez-Ramírez, Ivy Schweitzer, Armand E. Singer, G. Thomas Tanselle, Tom Bishop, Mary Ann Caws, Marcel Gutwirth, Christophe Ippolito, Lawrence D. Kritzman, James Longenbach, Tim McCracken, Wolfe S. Molitor, Diane Quantic, Gregory Rabassa, Ellen M. Tsagaris, Anthony C. Yu, Betty Jean Craige, Wendell V. Harris, J. Hillis Miller, Jesse G. Swan, Helene Zimmer-Loew, Peter Berek, James Chandler, Hanna K. Charney, Philip Cohen, Judith Fetterley, Herbert Lindenberger, Julia Reinhard Lupton, Maximillian E. Novak, Richard Ohmann, Marjorie Perloff, Mark Reynolds, James Sledd, Harriet Turner, Marie Umeh, Flavia Aloya, Regina Barreca, Konrad Bieber, Ellis Hanson, William J. Hyde, Holly A. Laird, David Leverenz, Allen Michie, J. Wesley Miller, Marvin Rosenberg, Daniel R. Schwarz, Elizabeth Welt Trahan, Jean Fagan Yellin
-
- Journal:
- PMLA / Publications of the Modern Language Association of America / Volume 115 / Issue 7 / December 2000
- Published online by Cambridge University Press:
- 23 October 2020, pp. 1986-2078
- Print publication:
- December 2000
-
- Article
- Export citation
Central sensitization following intradermal injection of capsaicin
- William D. Willis
-
- Journal:
- Behavioral and Brain Sciences / Volume 20 / Issue 3 / September 1997
- Published online by Cambridge University Press:
- 01 September 1997, p. 471
-
- Article
- Export citation
-
Intradermal capsaicin in humans causes pain, primary hyperalgesia, and secondary mechanical hyperalgesia and allodynia. Parallel changes occur in the responses of primate spinothalamic tract cells and in rat behavior. Neurotransmitters that trigger secondary mechanical hyperalgesia and allodynia include excitatory amino acids and substance P. Secondary mechanical allodynia is actively maintained by central mechanisms. Our group has investigated mechanisms of central sensitization of nociceptive neurons by examining the responses to intradermal injection of capsaicin. These experiments are pertinent to issues raised by
coderre & katz (sect. 2).