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Examination of the evidence that distinct excitatory amino acid receptors and intracellular messengers mediate thermal and mechanical hyperalgesia 不同兴奋性氨基酸受体和细胞内信使介导热痛觉和机械性痛觉过敏的证据检验
Pub Date : 1994-12-01 DOI: 10.1016/S1058-9139(05)80270-0
Terence J. Coderre
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引用次数: 4
Regional section news 地区新闻
Pub Date : 1994-12-01 DOI: 10.1016/S1058-9139(05)80280-3
Sridhar V. Vasudevan
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引用次数: 0
Secondary gain in pain medicine 止痛药的二次增益
Pub Date : 1994-12-01 DOI: 10.1016/S1058-9139(05)80275-X
Rollin M. Gallagher
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引用次数: 18
Acknowledgment 鸣谢
Pub Date : 1994-12-01 DOI: 10.1016/S1058-9139(05)80268-2
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引用次数: 0
Concept of secondary gain 二次增益的概念
Pub Date : 1994-12-01 DOI: 10.1016/S1058-9139(05)80276-1
Steven A. King
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引用次数: 13
Secondary gain concept 二次增益概念
Pub Date : 1994-12-01 DOI: 10.1016/S1058-9139(05)80274-8
David A. Fishbain

Secondary gain is claimed to be important to the generation and maintenance of disease or illness behavior. This concept is of major interest to the clinician dealing with the chronic pain patient, as these clinicians often encounter patients with whom secondary gain factors are suspected or inferred, or both. The author begins a critical examination of the concept of secondary gain. Primary, secondary, and tertiary gains and secondary losses are defined and described. Difficulties with and abuses of the secondary gain concept in chronic pain treatment are presented.

次生增益被认为对疾病或疾病行为的产生和维持很重要。这个概念是主要感兴趣的临床医生处理慢性疼痛患者,因为这些临床医生经常遇到的患者继发性增益因素被怀疑或推断,或两者兼而有之。作者开始了对二次增益概念的批判性检查。定义和描述了一级、二级和三级收益和二级损失。提出了慢性疼痛治疗中二次增益概念的困难和滥用。
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引用次数: 83
Hyperalgesia and amino acids 痛觉过敏和氨基酸
Pub Date : 1994-12-01 DOI: 10.1016/S1058-9139(05)80271-2
P.M. Dougherty , S. Mittman , L.S. Sorkin

The reader may have noted that we have tried to restrict our discussion to mechanisms of cutaneous hyperalgesia. We have taken the liberty to include some discussion of hyperalgesia produced by inflammation of deeper tissues and articular spaces since these conditions appear to share many mechanisms in common with cutaneous hyperalgesia. We have carefully avoided a discussion of the mechanisms underlying hyperalgesia produced by injury to viscera or nervous tissue because space constraints do not permit us to address the special issues that pertain to these conditions.

Dr. Meller's thesis outlines an interesting new perspective on the chemical mechanisms of hyperalgesia. Although the widely accepted preexisting intensity-based hypothesis may not yet account for all aspects of hyperalgesia, it does account for a large body of psychophysical data as well as experimental data that has been gathered from study of the dorsal horn alone. It is not at all clear that this previously established hypothesis has been refuted, or that Dr. Meller's alternate hypothesis better accounts for this same body of information. Finally, we have avoided commentary on the potential role of second messenger systems and gene expression modifications that may be involved in the generation-expression of hyperalgesia given the complexity of the neurotransmitter mechanisms. Dr. Meller should be applauded for the service he does indicating the multiplicity in second messenger systems that may potentially be involved. However, his scheme will likely require extensive modification. Allowances need to be made for the messenger systems of the neuropeptides and for the issue of multiplicity in the mechanisms for expression-maintenance of hyperalgesia. For example, a recent publication by Minami et al.61 illustrates that interactions between cyclooxygenase products and excitatory amino acids can involve either of the excitatory amino acid receptor subtypes. Thus, this final issue, as well as the role of gene expression changes, will no doubt be an area of research increasingly addressed in many future studies.

读者可能已经注意到,我们已经试图限制我们的讨论机制皮肤痛觉过敏。我们冒昧地讨论了由深层组织和关节间隙炎症引起的痛觉过敏,因为这些情况似乎与皮肤痛觉过敏有许多共同的机制。由于篇幅限制,我们不允许讨论与这些情况有关的特殊问题,因此我们谨慎地避免了讨论内脏或神经组织损伤引起的痛觉过敏的机制。梅勒的论文概述了痛觉过敏的化学机制的一个有趣的新观点。虽然广泛接受的先前存在的基于强度的假设可能还不能解释痛觉过敏的所有方面,但它确实解释了大量的心理物理数据以及从背角研究中收集到的实验数据。目前还不清楚这个先前建立的假设是否已经被反驳,或者梅勒博士的另一个假设是否能更好地解释同样的信息。最后,鉴于神经递质机制的复杂性,我们避免对第二信使系统和基因表达修饰的潜在作用进行评论,这些修饰可能涉及痛觉过敏的产生和表达。梅勒博士应该受到赞扬,因为他所做的工作表明了可能涉及的第二信使系统的多样性。然而,他的计划可能需要大量修改。需要考虑神经肽的信使系统和痛觉过敏表达维持机制的多样性问题。例如,Minami等人最近发表的一篇文章表明,环加氧酶产物与兴奋性氨基酸之间的相互作用可能涉及兴奋性氨基酸受体亚型中的任何一种。因此,这最后一个问题,以及基因表达变化的作用,无疑将成为未来许多研究中日益关注的研究领域。
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引用次数: 12
IASP global news IASP全球新闻
Pub Date : 1994-12-01 DOI: 10.1016/S1058-9139(05)80281-5
Louisa E. Jones
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引用次数: 0
Hyperalgesia 痛觉过敏
Pub Date : 1994-12-01 DOI: 10.1016/S1058-9139(05)80273-6
S.T. Meller
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引用次数: 11
1994 APS award winners 1994年APS奖得主
Pub Date : 1994-12-01 DOI: 10.1016/S1058-9139(05)80279-7
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引用次数: 0
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