European journal of pain : EJP
-
Anticonvulsants are widely used for the treatment of neuropathic pain. Here we review the evidence for a number of peripheral and central changes after nerve injury that may provide a basis for the mechanisms of action of anticonvulsant therapies. ⋯ The focus of this article is on anticonvulsants; however, opioids and antidepressants can also be effective in increasing inhibitions to control of pain in a manner similar to that of the enhancement of gamma-aminobutyric acid (GABA) function by antiepileptic drugs. A brief account of these approaches to neuropathic pain is also given.
-
Randomized Controlled Trial Clinical Trial
Clonidine for treatment of postoperative pain: a dose-finding study.
The aim of this double-blind randomized study was to evaluate the optimal intravenous dose of clonidine administrated during the peri-operative period, after lumbar hemilaminectomy for herniated disk repair. The "optimal intravenous dose" was defined as that providing minimal analgesic request, stable haemodynamic profile and a minimal sedation score during 12h after extubation. Eighty adult patients, ASA physical status I-II, undergoing lumbar hemilaminectomy for herniated disk (L(4)-L(5), L(5)-S(1)) were included in the study. ⋯ In conclusion, this study demonstrates that, when sedation and analgesic effect of clonidine is required, 3 microg/kg bolus dose followed by a continuous infusion of 0.3 microg/kg per hour has to be considered the optimal intravenous dose. The higher dose of intravenous clonidine (5 microg/kg) produced better analgesia but the degree of hypotension and sedation was more severe and longer lasting; it required ephedrine administration and careful monitoring of the patient. On the other hand, the bolus of intravenous clonidine 2 microg/kg (group C) was less effective in terms of pain relief but with similar side-effects to the 3 microg/kg dosage (group B).
-
Clinical Trial Controlled Clinical Trial
Pavlovian conditioning of opioid and nonopioid pain inhibitory mechanisms in humans.
Learning processes such as respondent or Pavlovian conditioning are believed to play an important role in the development of chronic pain, however, their influence on the inhibition of pain has so far not been assessed in humans. The purpose of this study was the demonstration of Pavlovian conditioning of stress-induced analgesia in humans and the determination of its opioid mediation. In a differential classical conditioning paradigm two different auditory stimuli served as conditioned stimuli and mental arithmetic plus white noise as unconditioned stimulus. ⋯ Pain tolerance was affected by naloxone whereas pain threshold was not. The data of this study show that stress analgesia can be conditioned in humans and that it is at least partially mediated by the endogenous opioid system. Learning processes also influence pain inhibitory processes in humans and this effect might play a role in the development of chronic pain.
-
The aim of this study was to investigate whether pain itself or pain-related fear is crucial in eliciting attentional bias towards pain-related information in healthy individuals. The results from two successive experiments provide evidence that attentional bias does not take place as a function of pain-related fear or as a function of pain per se. Attentional bias for pain words was neither found to be related to trait variables like anxiety, depression, catastrophising, fear of pain, and pain vigilance. Implications of the results are discussed and directions for future research are provided.
-
Heterotopic noxious conditioning stimulation (HNCS) has been thought to give access to the diffuse noxious inhibitory controls (DNIC) in man, which can be activated in wide-dynamic-range neurons by noxious stimulation from remote areas of the body and form the neurophysiological basis of the phenomenon 'pain inhibits pain'. The latter phenomenon suggests that the subjective experience of pain is a prerequisite for an inhibitory action. The necessity of using painful stimuli as conditioning and as test stimuli to produce inhibitory effects was investigated in the present study, using a HNCS paradigm. ⋯ However, the intensity ratings of the test stimuli indicated inhibitory effects of the conditioning stimuli also upon non-painful levels. Furthermore, non-painful heat as conditioning stimulus also appeared to be capable of decreasing the ratings of the test stimuli at painful levels. The latter two findings suggest: (i) that very strong but subjectively still non-painful stimulation can trigger pain inhibitory effects and (ii) that also subjectively non-painful stimuli are affected by inhibitory influences during HNCS.