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Different Pain Syndromes (different + pain_syndrome)
Selected AbstractsCluster Attacks Responsive to Recreational Cannabis and DronabinolHEADACHE, Issue 6 2009Matthew S. Robbins MD Pharmacological preparations of cannabinoid compounds have a variety of therapeutic uses in medicine, including different pain syndromes, but have not been previously reported as beneficial for cluster headache. We present a patient with cluster headache who was refractory to multiple acute and preventive medications but successfully aborted his attacks with recreational marijuana use; subsequent use of dronabinol provided equally effective pain relief. The beneficial effect may be related to the high concentration of cannabinoid receptors in the hypothalamus, which has been implicated as a site of dysfunction in neuroimaging studies of patients with cluster headache. [source] Pain intensity on and off levodopa in patients with Parkinson's disease,MOVEMENT DISORDERS, Issue 8 2009Angelika Nebe MD Abstract Pain is frequently reported by patients with Parkinson's disease (PD). In this study, intensity of pain as measured by a visual analogue scale (VAS) was assessed on and off levodopa in 15 patients with PD. All patients had motor fluctuations and suffered from pain of various types. Description of pain was assessed with the McGill pain questionnaire. Ratings for pain intensity on the VAS were increased during off period for all patients but one (P = 0.001). There was a correlation (P = 0.04) between changes in motor performance (Unified Parkinson's Disease Rating Scale part III) and pain intensity (VAS). Compared with a historical sample of subjects with different pain syndromes without PD, terms related to fear and punishment were used more frequently by patients with PD in this study. In two patients, pain was exclusively limited to the off period. The majority of subjects suffered from secondary pain possibly related to lumbar osteoarticular degeneration. Secondary pain was relieved but not completely abolished by levodopa. The results of this study suggest that aggravation of secondary pain should be considered as a part of the spectrum of nonmotor off symptoms. Analgesics should not be given as first line drugs when pain occurs or increases in off conditions, and pain can be significantly alleviated or abolished by adjustments of dopaminergic medication. © 2009 Movement Disorder Society [source] Voltage-Gated Sodium Channels: Therapeutic Targets for PainPAIN MEDICINE, Issue 7 2009Sulayman D. Dib-Hajj PhD ABSTRACT Objective., To provide an overview of the role of voltage-gated sodium channels in pathophysiology of acquired and inherited pain states, and of recent developments that validate these channels as therapeutic targets for treating chronic pain. Background., Neuropathic and inflammatory pain conditions are major medical needs worldwide with only partial or low efficacy treatment options currently available. An important role of voltage-gated sodium channels in many different pain states has been established in animal models and, empirically, in humans, where sodium channel blockers partially ameliorate pain. Animal studies have causally linked changes in sodium channel expression and modulation that alter channel gating properties or current density in nociceptor neurons to different pain states. Biophysical and pharmacological studies have identified the sodium channel isoforms Nav1.3, Nav1.7, Nav1.8, and Nav1.9 as particularly important in the pathophysiology of different pain syndromes. Recently, gain-of-function mutations in SCN9A, the gene which encodes Nav1.7, have been linked to two human-inherited pain syndromes, inherited erythromelalgia and paroxysmal extreme pain disorder, while loss-of-function mutations in SCN9A have been linked to complete insensitivity to pain. Studies on firing properties of sensory neurons of dorsal root ganglia demonstrate that the effects of gain-of-function mutations in Nav1.7 on the excitability of these neurons depend on the presence of Nav1.8, which suggests a similar physiological interaction of these two channels in humans carrying the Nav1.7 pain mutation. Conclusions., These studies suggest that isoform-specific blockers of these channels or targeting of their modulators may provide novel approaches to treatment of pain. [source] Spinal tumor necrosis factor , neutralization reduces peripheral inflammation and hyperalgesia and suppresses autonomic responses in experimental arthritis: A role for spinal tumor necrosis factor , during induction and maintenance of peripheral inflammationARTHRITIS & RHEUMATISM, Issue 5 2010Michael Karl Boettger Objective In addition to the sensitization of pain fibers in inflamed tissues, the increased excitability of the spinal cord is an important mechanism of inflammatory pain. Furthermore, spinal neuronal excitability has been suggested to play a role in modulating peripheral inflammation. This study was undertaken to test the hypothesis that spinal actions of the proinflammatory cytokine tumor necrosis factor , (TNF,) add significantly to both hyperalgesia and maintenance of peripheral inflammation. Methods Rats with antigen-induced arthritis (AIA) were treated intrathecally with the TNF,-neutralizing compound etanercept continuously during the complete time course of AIA, which was 3 days for the acute phase and 21 days for the chronic phase. During this time, inflammation and pain-related behavior were monitored. Since a role for autonomic control of inflammation was proposed, measures from heart rate time series were obtained in the acute phase. Findings were compared with those in vehicle-treated animals and in animals receiving etanercept intraperitoneally. Results Spinally administered etanercept acutely reduced pain-related behavior, attenuated both the development and the maintenance of inflammation, and was superior to systemic administration. Parameters indicating autonomic modulation showed a shift toward a sympathetically dominated state in vehicle-treated animals, which was prevented by intrathecal etanercept. Conclusion Our findings indicate that spinal TNF, plays an important role in both pain signaling and modulation of peripheral inflammation. Thus, neutralizing this cytokine at the spinal site not only represents a putative therapeutic option for different pain syndromes, but may be directly used to attenuate peripheral inflammation. [source] | ||||||||||