ognizant Communication Corporation

Reviews in Analgesia, Vol. 10, pp. 1-9
1542-961X/08 $90.00 + .00
E-ISSN 1555-3876
Copyright © 2008 Cognizant Comm. Corp.
Printed in the USA. All rights reserved.

Department of Anesthesiology and Pain Medicine, School of Medicine, The Catholic University of Korea, Seoul, Korea

Botulinum toxin type A (BoNT-A) has been used to treat many disorders related to excessive muscle contraction. Recent clinical reports suggest that BoNT-A is effective at treating the neuropathic pains associated with multiple sclerosis, postherpetic neuralgia, peripheral neuropathy and the severe tingling caused by herniation of cervical vertebrae. In addition, the peripheral application of BoNT-A was found to have an antiallodynic effect in a rat neuropathic model. Although its precise mechanism of pain relief is not completely understood, BoNT-A may reduce the activities of various substances that sensitize nociceptors. Moreover, the use of BoNT-A as a novel analgesic is providing hope to patients with intractable chronic pain, especially neuropathic pain.

Key words: Botulinum toxin type A; Neuropathic pain

Address correspondence to Dr. Dong Eon Moon, Department of Anesthesiology and Pain Medicine, School of Medicine, The Catholic University of Korea, Kangnam St. Mary’s Hospital, 505 Banpo-Dong, Seocho-Gu, Seoul, Korea 137-040. Tel: 82-2-590-1545, 1537; Fax: 82-2-537-1951; E-mail: demoon@catholic.ac.kr

Clinical Psychological Science, Maastricht University, Maastricht, The Netherlands

According to the biopsychosocial model of chronic pain and disability, the experience of pain is the result of a dynamic interaction between physiological, psychological, and social factors. Fear-avoidance beliefs have been identified as being among the most prominent psychological factors influencing the development and persistence of chronic pain. This article reviews the evidence that personality traits contribute to the process of pain chronification by making people more vulnerable to respond to physical threat in an anxious and avoidant manner. We will consider three potential vulnerability factors: negative affectivity, anxiety sensitivity, and injury/illness sensitivity. For all three factors evidence has been found that they may indeed contribute to maladaptive ways of dealing with pain. Recently researchers have also begun to consider the role of resilience factors that may protect people against maladaptive cognitive and behavioral reactions to acute and chronic pain. We will review the evidence for three of these potential resilience factors: optimism, hope, and (generalized) self-efficacy. It is concluded that there is at least some evidence pointing towards a role of these three factors in chronic pain and disability, but the evidence for trait characteristics acting as resilience factors in chronic pain is less compelling than that for traits acting as vulnerability factors.

Key words: Vulnerability factors; Resilience factors; Personality traits; Chronic pain; Disability

Address correspondence to Madelon L. Peters, Clinical Psychological Science, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands. Tel: 31 43 3881603; Fax: 31 43 3884155; E-mail: Madelon.Peters@dep.unimaas.nl

Department of Applied Chemistry, Dongduk Women’s University, Seoul 136-714, Korea

Artemin is a glial cell line-derived neurotrophic factor (GDNF) that supports survival of sensory neurons. The GDNF family ligands signal through a receptor complex consisting of a ligand binding component and RET receptor tyrosine kinase. A recent study showed that systemic artemin prevents and reverses neuropathic pain and normalizes spinal nerve ligation (SNL)-induced morphological changes. It was suggested that artemin plays a role in inducing neurite outgrowth in the early stages of neuron development. However, the mature DRG neurons showed some response to artemin, suggesting that they exhibited a developmental shift to the ligand as prenatal DRG neurons. A set of genes involved in regulation of actin dynamics, including Wiskott-Aldrich syndrome protein (WASP) interacting protein, cofilin, and dynamin, were downregulated by artemin, suggesting a previously undefined role in the regulation of synaptic vesicle movement by artemin. DNA methylation provides a mechanism for artemin-dependent genetic regulation responsible for axonal growth.

Key words: Artemin; Receptor; Systemic treatment; Neurite growth

Address correspondence to Seyeon Park, Ph.D., Department of Applied Chemistry, Dongduk Women’s University, 23-1 Wolgok-dong, Sungbuk-ku, Seoul 136-714, Korea. Tel: 82-2-940-4514; Fax: 82-2-940-4193; E-mail: sypark21@dongduk.ac.kr or seypark21@hotmail.com

¹Department of Medicine, University of Florida Colleges of Medicine, Gainesville, FL, USA
²North Florida/South Georgia VA Medical System, USA

During the last decade, research focusing primarily on alterations in the peripheral and central nervous system has improved our understanding of the pathophysiological mechanisms of chronic visceral pain. These studies have demonstrated significant physiological changes following injury to the viscera in the firing patterns of both primary afferent neurons that transmit nociceptive information from the viscera and in central neurons that process the nociceptive information. A number of receptors, neurotransmitters, cytokines, and second messenger systems in these neurons have been implicated in the enhancement of visceral nociception. N-methyl-D-aspartic acid (NMDA) receptors play an important role in chronic visceral pain and hypersensitivity that is present in the setting of colonic inflammation. NMDA receptors are found in the peripheral nervous system as well as the central terminal of primary afferent neurons and have been shown to play an important role in regulating the release of nociceptive neurotransmitters. Recent work has demonstrated the presence of NMDA receptors in the enteric nervous system. In this article, we will discuss more recent evidence of the role of NMDA receptors in visceral pain associated with colitis.

Key words: NMDA receptor; Colitis; Visceral pain; Visceral hypersensitivity

Address correspondence to G. Nicholas Verne, M.D., at his current address: Professor and Chief, Division of Gastroenterology, Hepatology, and Nutrition, Ohio State University, 395 West 12th Avenue, 288A Office Tower, Columbus, OH 43210, USA. E-mail: Nicholas.Verne@osumc.edu

¹Department of Anesthesiology, School of Medicine, University of California Irvine, Irvine, CA 92697, USA
²Department of Pharmacology, School of Medicine, University of California Irvine, Irvine, CA 92697, USA

The combination of microarray technologies with well-defined animal models provides unparalleled detection power to gain insights into gene expression profiles in sensory pathways responding to pain-inducing pathological conditions in a high throughput manner. This, in turn, provides critical information for further identification and characterization of differentially regulated genes and pathways that may play pivotal roles in pain processing and analgesia sensitivity. Appropriate experimental design with additional variants from animal models would allow the detection of factors and underlying pathways related to pain susceptibility and analgesic sensitivity. Clinical application of these technologies certainly improves our understanding in mechanisms of pain and analgesic actions, leading to advancements in diagnosis and prognosis as well as patient care qualities. In this review, the advantages and limitations of microarray technologies are reviewed; strategic applications of these technologies in recent preclinical and clinical researches related to mechanisms of pain and analgesic actions are summarized.

Key words: Microarray technologies; Gene expression profiles; Sensory pathways; Analgesic actions

Address correspondence to Dr. Z. David Luo, Department of Anesthesiology, University of California, Irvine Medical Center, Bldg 53, Room 227, 101 The City Drive South, Orange, CA 92868, USA. Tel: 714-456-7962; Fax: 714-456-7903; E-mail: zluo@uci.edu