Pub Date : 2001-06-01DOI: 10.1191/0968130201PR175RA
R. Hawkins
A newly developed methodological technique (the systematic meta-review) was applied to determine whether hypnosis is an empirically supported treatment for pain. This involved, initially, a systematic search of the published literature for review studies. These reviews were then subjected to a validated quality scale. There was sufficient evidence of good quality to allow the conclusion that hypnosis does have demonstrable efficacy in the treatment of pain. The only meta-analysis of hypnotically induced analgesia1 showed that 'the average participant treated with hypnosis demonstrated greater analgesic response that 75% of participants in standard and no-treatment control groups' (p. 143). The hypothesis that poor-quality reviews are more likely to produce positive conclusions was not supported. A citation database of all reviews has been assembled and can be extended with time.
{"title":"A systematic meta-review of hypnosis as an empirically supported treatment for pain","authors":"R. Hawkins","doi":"10.1191/0968130201PR175RA","DOIUrl":"https://doi.org/10.1191/0968130201PR175RA","url":null,"abstract":"A newly developed methodological technique (the systematic meta-review) was applied to determine whether hypnosis is an empirically supported treatment for pain. This involved, initially, a systematic search of the published literature for review studies. These reviews were then subjected to a validated quality scale. There was sufficient evidence of good quality to allow the conclusion that hypnosis does have demonstrable efficacy in the treatment of pain. The only meta-analysis of hypnotically induced analgesia1 showed that 'the average participant treated with hypnosis demonstrated greater analgesic response that 75% of participants in standard and no-treatment control groups' (p. 143). The hypothesis that poor-quality reviews are more likely to produce positive conclusions was not supported. A citation database of all reviews has been assembled and can be extended with time.","PeriodicalId":90719,"journal":{"name":"Reviews in pain","volume":"25 1","pages":"47-73"},"PeriodicalIF":0.0,"publicationDate":"2001-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81651470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-04-01DOI: 10.1191/0968130201PR173RA
M. Kemler
Complex regional pain syndrome type I (CRPS) is a chronic pain disorder involving the sensory, motor, and autonomic nervous systems, often leading to severe debilitation. Most commonly, a preceding limb injury catalyzes CRPS, although insidious onset has been known to occur. An estimated 60,000 Americans are affected by CRPS, including individuals between 25 and 55 years of age. CRPS is three times more likely to occur in women, although it can affect anyone [1]. Table 1 contains the CRPS clinical diagnostic criteria suggested by the International Association for the Study of Pain (IASP). Because of the poor understanding of the etiology of CRPS, its medical management is nebulous. Along with pain management, optimal treatment outcomes appear to be achieved when emphasizing functional restoration-a realm largely encompassed by physical therapists (PT). However, a review of the literature found that the term physical therapy is often used vaguely with no corresponding definition or description of procedures employed during treatment [2]. This has left PTs with a lack of guidance in treating patients with CRPS. The purpose of this case report is to describe the physical therapy management of a 38-year-old patient with CRPS developed from a chronic anterior talofibular ligament (ATFL) injury by using Active Release Techniques® (ART®) in combination with joint mobilization, gait training, therapeutic exercise, and education to document the observed clinical and functional improvements.
{"title":"Complex regional pain syndrome type I","authors":"M. Kemler","doi":"10.1191/0968130201PR173RA","DOIUrl":"https://doi.org/10.1191/0968130201PR173RA","url":null,"abstract":"Complex regional pain syndrome type I (CRPS) is a chronic pain disorder involving the sensory, motor, and autonomic nervous systems, often leading to severe debilitation. Most commonly, a preceding limb injury catalyzes CRPS, although insidious onset has been known to occur. An estimated 60,000 Americans are affected by CRPS, including individuals between 25 and 55 years of age. CRPS is three times more likely to occur in women, although it can affect anyone [1]. Table 1 contains the CRPS clinical diagnostic criteria suggested by the International Association for the Study of Pain (IASP). Because of the poor understanding of the etiology of CRPS, its medical management is nebulous. Along with pain management, optimal treatment outcomes appear to be achieved when emphasizing functional restoration-a realm largely encompassed by physical therapists (PT). However, a review of the literature found that the term physical therapy is often used vaguely with no corresponding definition or description of procedures employed during treatment [2]. This has left PTs with a lack of guidance in treating patients with CRPS. The purpose of this case report is to describe the physical therapy management of a 38-year-old patient with CRPS developed from a chronic anterior talofibular ligament (ATFL) injury by using Active Release Techniques® (ART®) in combination with joint mobilization, gait training, therapeutic exercise, and education to document the observed clinical and functional improvements.","PeriodicalId":90719,"journal":{"name":"Reviews in pain","volume":"107 1","pages":"35-45"},"PeriodicalIF":0.0,"publicationDate":"2001-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80772730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-04-01DOI: 10.1191/0968130201PR172RA
N. Shenker, R. Haigh, E. Roberts, P. Mapp, N. Harris, D. Blake
Symmetry is a cardinal feature of certain painful and ineammatory diseases, including rheumatoid arthritis and psoriasis. This symmetry does not occur by chance, but it is as yet unexplained. It has been hypothesized by this group and others that mechanisms of neurogenic ineammation could explain both this symmetrical distribution and the chronicity of these diseases. A recent review has demonstrated contralateral responses in the nervous system to unilateral neurological insults. These responses were topographically precise and stimulus speciec in nature. This article details similar responses that have been observed to ineammatory stimuli in animal models. The role of pro-ineammatory neuropeptides, such as substance P, in these pathways is discussed. The hypothesis could be tested in both animals and humans.
{"title":"Pain, neurogenic inflammation and symmetry in medical practice","authors":"N. Shenker, R. Haigh, E. Roberts, P. Mapp, N. Harris, D. Blake","doi":"10.1191/0968130201PR172RA","DOIUrl":"https://doi.org/10.1191/0968130201PR172RA","url":null,"abstract":"Symmetry is a cardinal feature of certain painful and ineammatory diseases, including rheumatoid arthritis and psoriasis. This symmetry does not occur by chance, but it is as yet unexplained. It has been hypothesized by this group and others that mechanisms of neurogenic ineammation could explain both this symmetrical distribution and the chronicity of these diseases. A recent review has demonstrated contralateral responses in the nervous system to unilateral neurological insults. These responses were topographically precise and stimulus speciec in nature. This article details similar responses that have been observed to ineammatory stimuli in animal models. The role of pro-ineammatory neuropeptides, such as substance P, in these pathways is discussed. The hypothesis could be tested in both animals and humans.","PeriodicalId":90719,"journal":{"name":"Reviews in pain","volume":"368 1","pages":"27-34"},"PeriodicalIF":0.0,"publicationDate":"2001-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74891514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-04-01DOI: 10.1191/0968130201PR170RA
I. Marples, R. Atkinson
{"title":"Stellate ganglion block","authors":"I. Marples, R. Atkinson","doi":"10.1191/0968130201PR170RA","DOIUrl":"https://doi.org/10.1191/0968130201PR170RA","url":null,"abstract":"","PeriodicalId":90719,"journal":{"name":"Reviews in pain","volume":"45 1","pages":"3-11"},"PeriodicalIF":0.0,"publicationDate":"2001-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73550135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2001-01-01DOI: 10.1191/0968130201PR183RA
Maree T. Smith, S. South
Morphine-6beta-D-glucuronide (M6G) is an analgesically active metabolite of morphine, accounting for approximate to10% of the morphine dose when administered by systemic routes to humans. Although M6G is more hydrophilic than morphine, it crosses the blood-brain barrier, albeit relatively slowly. For this reason, it is generally thought that, after chronic dosing, M6G contributes significantly to the analgesic effects of systemically administered morphine. Owing to its polar nature, M6G is cleared from the systemic circulation primarily via renal elimination. As M6G accumulates in patients with renal impairment, there is an increased risk of M6G-induced respiratory depression in renal failure patients who are being dosed chronically with systemic morphine. Consistent with its analgesic and respiratory depressant properties, M6G binds to the p-opioid receptor in a naloxone-reversible manner. Although the affinity of M6G for the mu-opioid receptor is similar to or slightly less than that of morphine, preclinical studies in rodents show that M6G is one to two orders of magnitude more potent than morphine when administered by central routes. This major discrepancy between the markedly higher intrinsic antinociceptive potency of M6G relative to morphine, despite their similar p-opioid receptor binding affinities, is difficult to reconcile. It has been proposed that M6G mediates its pain-relieving effects through a novel 'M6G opioid receptor', while others have argued that M6G may have higher efficacy than morphine for transduction of intracellular events. When administered by parenteral routes to rodents, M6G's antinociceptive potency is no more than twofold higher than morphine. In humans, the analgesic efficacy and respiratory depressant potency of M6G relative to morphine have been assessed in a number of short-term studies involving the intrathecal or intravenous routes of administration. For example, in hip replacement patients, intrathecal M6G provided excellent postoperative analgesia but the occurrence of late respiratory depression in 10% of these patients raised serious concern about safety. In postoperative patients, intravenous M6G administered by means of patient-controlled analgesia (PCA), or bolus plus PCA, produced no analgesia in one study and limited analgesia in another. Similarly, there was a lack of significant analgesia in healthy volunteers who received intravenous M6G for the alleviation of experimental pain (carbon dioxide applied to the nasal mucosa). In contrast, satisfactory analgesia was produced by bolus doses of intravenous M6G administered to patients with cancer pain, and to healthy volunteers with experimentally-induced ischaemic, electrical or thermal (ice water) pain. Studies to date in healthy volunteers suggest that intravenous M6G may be a less potent respiratory depressant and have a lower propensity for producing nausea and vomiting than morphine. However, it is unclear whether equi-analgesic doses of M6G and m
吗啡-6 β - d -葡萄糖醛酸盐(M6G)是吗啡的一种具有镇痛活性的代谢物，在人体全身给药时约占吗啡剂量的10%。尽管M6G比吗啡更亲水，但它穿过血脑屏障的速度相对较慢。因此，一般认为，慢性给药后，M6G对全身给药吗啡的镇痛作用有重要作用。由于其极性性质，M6G主要通过肾脏清除从体循环中清除。随着M6G在肾功能损害患者体内的积累，长期服用全系统吗啡的肾功能衰竭患者发生M6G诱导的呼吸抑制的风险增加。与其镇痛和呼吸抑制特性一致，M6G以纳洛酮可逆的方式与p-阿片受体结合。尽管M6G对mu-阿片受体的亲和力与吗啡相似或略低于吗啡，但啮齿动物的临床前研究表明，当通过中枢途径给药时，M6G的效力比吗啡高一到两个数量级。尽管M6G与吗啡具有相似的p-阿片受体结合亲和力，但M6G相对于吗啡具有明显更高的内在抗痛觉效力，这两者之间的主要差异难以调和。有人提出M6G通过一种新的“M6G阿片受体”介导其镇痛作用，而另一些人则认为M6G在细胞内事件的转导方面可能比吗啡更有效。当通过肠外给药给啮齿动物时，M6G的抗伤害性效力不超过吗啡的两倍。在人类中，与吗啡相比，M6G的镇痛效果和呼吸抑制效力已经在一些涉及鞘内或静脉给药途径的短期研究中得到了评估。例如，在髋关节置换术患者中，鞘内M6G提供了良好的术后镇痛效果，但10%的患者出现晚期呼吸抑制，引起了对安全性的严重担忧。在术后患者中，通过患者自控镇痛(PCA)方式静脉给予M6G，或丸加PCA，在一项研究中没有产生镇痛，在另一项研究中产生有限的镇痛。同样，在接受静脉注射M6G以减轻实验性疼痛(将二氧化碳应用于鼻黏膜)的健康志愿者中，也没有明显的镇痛作用。相比之下，对癌症疼痛患者和实验诱导的缺血性、电性或热(冰水)疼痛的健康志愿者大剂量静脉注射M6G可产生令人满意的镇痛效果。迄今为止对健康志愿者的研究表明，静脉注射M6G可能是一种较弱的呼吸抑制剂，并且比吗啡产生恶心和呕吐的倾向更低。然而，是否比较了M6G和吗啡等镇痛剂量尚不清楚。显然，在确定M6G作为镇痛药物的潜在临床应用之前，需要更广泛的短期试验，以及涉及慢性M6G给药的研究。
{"title":"The role of morphine-6-glucuronide (M6G) in pain control","authors":"Maree T. Smith, S. South","doi":"10.1191/0968130201PR183RA","DOIUrl":"https://doi.org/10.1191/0968130201PR183RA","url":null,"abstract":"Morphine-6beta-D-glucuronide (M6G) is an analgesically active metabolite of morphine, accounting for approximate to10% of the morphine dose when administered by systemic routes to humans. Although M6G is more hydrophilic than morphine, it crosses the blood-brain barrier, albeit relatively slowly. For this reason, it is generally thought that, after chronic dosing, M6G contributes significantly to the analgesic effects of systemically administered morphine. Owing to its polar nature, M6G is cleared from the systemic circulation primarily via renal elimination. As M6G accumulates in patients with renal impairment, there is an increased risk of M6G-induced respiratory depression in renal failure patients who are being dosed chronically with systemic morphine. Consistent with its analgesic and respiratory depressant properties, M6G binds to the p-opioid receptor in a naloxone-reversible manner. Although the affinity of M6G for the mu-opioid receptor is similar to or slightly less than that of morphine, preclinical studies in rodents show that M6G is one to two orders of magnitude more potent than morphine when administered by central routes. This major discrepancy between the markedly higher intrinsic antinociceptive potency of M6G relative to morphine, despite their similar p-opioid receptor binding affinities, is difficult to reconcile. It has been proposed that M6G mediates its pain-relieving effects through a novel 'M6G opioid receptor', while others have argued that M6G may have higher efficacy than morphine for transduction of intracellular events. When administered by parenteral routes to rodents, M6G's antinociceptive potency is no more than twofold higher than morphine. In humans, the analgesic efficacy and respiratory depressant potency of M6G relative to morphine have been assessed in a number of short-term studies involving the intrathecal or intravenous routes of administration. For example, in hip replacement patients, intrathecal M6G provided excellent postoperative analgesia but the occurrence of late respiratory depression in 10% of these patients raised serious concern about safety. In postoperative patients, intravenous M6G administered by means of patient-controlled analgesia (PCA), or bolus plus PCA, produced no analgesia in one study and limited analgesia in another. Similarly, there was a lack of significant analgesia in healthy volunteers who received intravenous M6G for the alleviation of experimental pain (carbon dioxide applied to the nasal mucosa). In contrast, satisfactory analgesia was produced by bolus doses of intravenous M6G administered to patients with cancer pain, and to healthy volunteers with experimentally-induced ischaemic, electrical or thermal (ice water) pain. Studies to date in healthy volunteers suggest that intravenous M6G may be a less potent respiratory depressant and have a lower propensity for producing nausea and vomiting than morphine. However, it is unclear whether equi-analgesic doses of M6G and m","PeriodicalId":90719,"journal":{"name":"Reviews in pain","volume":"2010 1","pages":"171-191"},"PeriodicalIF":0.0,"publicationDate":"2001-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73771178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2000-07-01DOI: 10.1191/096813000678809447
M. Tominaga
{"title":"Capsaicin receptor and its homologue in nociception","authors":"M. Tominaga","doi":"10.1191/096813000678809447","DOIUrl":"https://doi.org/10.1191/096813000678809447","url":null,"abstract":"","PeriodicalId":90719,"journal":{"name":"Reviews in pain","volume":"23 1","pages":"97-104"},"PeriodicalIF":0.0,"publicationDate":"2000-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84609115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2000-07-01DOI: 10.1191/096813000678809429
P. Dessein
{"title":"Nociceptive and non-nociceptive rheumatological pain : recent understanding of pathophysiology and management in rheumatoid arthritis and fibromyalgia","authors":"P. Dessein","doi":"10.1191/096813000678809429","DOIUrl":"https://doi.org/10.1191/096813000678809429","url":null,"abstract":"","PeriodicalId":90719,"journal":{"name":"Reviews in pain","volume":"31 1","pages":"67-79"},"PeriodicalIF":0.0,"publicationDate":"2000-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74889361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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