Pain research & management : the journal of the Canadian Pain Society = journal de la société canadienne pour le traitement de la douleur
-
Review Meta Analysis
Treatment of whiplash-associated disorders--part II: Medical and surgical interventions.
Whiplash-associated disorder (WAD) is a term used to describe injury due to an acceleration-deceleration mechanism at the neck. In 1995, the Quebec Task Force published a report that contained evidence-based recommendations regarding the treatment of WAD based on studies completed before 1993 and consensus-based recommendations. ⋯ While several quality RCTs and epidemiological studies have been published since 1993 on medical and surgical interventions, the cumulative evidence is lacking. Moderate evidence exists in support of radiofrequency neurotomy. Evidence for steroid injections, botulinum treatments, carpal tunnel decompression and cervical discectomy is conflicting or unclear. Future research is required to clarify the utility of radiofrequency neurotomy and pulsed electromagnetic field treatment for WAD.
-
Review Meta Analysis
Treatment of whiplash-associated disorders--part II: Medical and surgical interventions.
Whiplash-associated disorder (WAD) is a term used to describe injury due to an acceleration-deceleration mechanism at the neck. In 1995, the Quebec Task Force published a report that contained evidence-based recommendations regarding the treatment of WAD based on studies completed before 1993 and consensus-based recommendations. ⋯ While several quality RCTs and epidemiological studies have been published since 1993 on medical and surgical interventions, the cumulative evidence is lacking. Moderate evidence exists in support of radiofrequency neurotomy. Evidence for steroid injections, botulinum treatments, carpal tunnel decompression and cervical discectomy is conflicting or unclear. Future research is required to clarify the utility of radiofrequency neurotomy and pulsed electromagnetic field treatment for WAD.
-
Chronic pain syndromes are associated with alterations in sleep continuity and sleep architecture. One perspective of this relationship, which has not received much attention to date, is that disturbances of sleep affect pain. To fathom this direction of cause, experimental human and animal studies on the effects of sleep deprivation on pain processing were reviewed. ⋯ Furthermore, sleep deprivation can counteract analgesic effects of pharmacological treatments involving opioidergic and serotoninergic mechanisms of action. The heterogeneity of the human data and the exclusive interest in rapid eye movement sleep deprivation in animals so far do not allow us to draw firm conclusions as to whether the hyperalgesic effects are due to the deprivation of specific sleep stages or whether they result from a generalized disruption of sleep continuity. The significance of opioidergic and serotoninergic processes as mediating mechanisms of the hyperalgesic changes produced by sleep deprivation are discussed.
-
Intravenous regional sympathetic block is a valued component of the pain clinician's armamentarium for the management of the complex regional pain syndrome type 1. Treatment of this multifaceted condition is multimodal, and despite a lack of convincing supporting evidence from clinical trials, the author makes the case for retaining the technique while recommending both appropriate guidance and further study.
-
The pathophysiology of the pain associated with complex regional pain syndrome, spinal cord injury and diabetic peripheral neuropathy is not known. The pain of complex regional pain syndrome has often been attributed to abnormal sympathetic nervous system activity based on the presence of vasomotor instability and a frequently reported positive response, albeit a temporary response, to sympathetic blockade. In contrast, the pain below the level of spinal cord injury and diabetic peripheral neuropathy are generally seen as deafferentation phenomena. ⋯ Plausible mechanisms based on animal research by which alpha-1 adrenoceptor hyperresponsiveness can lead to chronic neuropathic-like pain have been reported. This raises the intriguing possibility that sympathetic nervous system dysfunction may be an important factor in the generation of pain in many neuropathic pain states. Although results to date have been mixed, there may be a greater role for new drugs which target peripheral alpha-2 adrenoceptors (agonists) or alpha-1 adrenoceptors (antagonists).