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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrical stimulation in the PAG has been shown to elicit profound analgesia in experimental animals that is at least in part due to the release of endogenous opioid substances. Electrical stimulation in the thalamic nuclei VPL and VPM inhibits the activation of spinal dorsal horn neurons by noxious stimuli. Acute electrical stimulation in these two targets relieves chronic pain in about 80% of patients. Chronic electrical stimulation by permanently implanted electrodes relieves pain in about 70% of patients with pain of peripheral or nociceptive origin but in only about 50% of patients with central pain resulting from deafferentation. Stimulating electrodes are implanted stereotactically by a burr hole under local anesthesia. Transient complications occur in 15% to 25% of patients and include infections, malfunctions of the stimulating hardware, pain at the implant sites, and mild temporary neurologic deficits. Permanent complications, including hemiparesis, intracranial hemorrhage, and death, occur in 1% to 2% of patients. Brain stimulation is recommended for the treatment of chronic pain in patients in whom other forms of treatment have failed. The technique is reasonably safe and provides pain relief for a group of patients who have exhausted all other therapeutic modalities. Unfortunately, not all patients receive effective pain relief with brain stimulation. Other stimulation targets such as the K-F nucleus in the parabrachial region of the brain stem are currently being explored in an attempt to provide pain relief to a greater proportion of patients. In addition, improvements in stimulation hardware have made the technique easier and more effective.
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PMID:Brain stimulation. 213 74

This study aimed to investigate if the non-steroid anti-inflammatory agents, indomethacin, ibuprofen, and diclofenac, are capable of depressing sensory responses of the nociceptive system by a central action. For this purpose, experiments were carried out on rats under urethane anaesthesia in which activity was elicited by electrical stimulation of afferent C fibres in the sural nerve. Recordings were made ipsi- or contralaterally from single neurones in the dorsomedial part of the ventral nucleus (VDM) of the thalamus. The 3 drugs produced a dose-dependent depression of the evoked activity which amounted to about 60% of the controls at the highest doses employed and lasted longer than 60 min. Their potency ranking, according to the ED50 values (in brackets), is: indomethacin (5 mg/kg) greater than diclofenac (10.9 mg/kg) greater than ibuprofen (15.6 mg/kg). The results suggest that a central action might contribute to the analgesia produced by these non-steroid anti-inflammatory agents.
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PMID:Central effect of the non-steroid anti-inflammatory agents, indomethacin, ibuprofen, and diclofenac, determined in C fibre-evoked activity in single neurones of the rat thalamus. 1183 30

Flupirtine, a novel analgesic agent, was tested on nociceptive activity in neurones of the dorsomedial part of the ventral nucleus of the thalamus (VDM) and ascending axons of the spinal cord of rats under urethane anaesthesia. Activity was elicited by supramaximal stimulation of the sural nerve. Flupirtine injected i.v. dose dependently reduced nociceptive activity in the thalamus and ascending axons. The ED50 of flupirtine in depressing the thalamic response was 1.9 mg/kg, and the ED50 in depressing the C fibre-evoked response in ascending axons was 18 mg/kg. Naloxone reduced the depression of the nociceptive response evoked in the thalamus when applied before but not when applied after flupirtine. The results indicate that flupirtine produces analgesia by spinal inhibition of nociceptive impulse transmission from afferent nerve fibres to neurones sending their axons to the brain and, in addition, by supraspinal inhibition of nociceptive impulse transmission to the thalamus. Opioid mechanisms could be involved in these effects.
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PMID:Flupirtine depresses nociceptive activity evoked in rat thalamus. 284 54

Electric reactions of neurons of the specific (VPM) and nonspecific (CM PF) thalamic nuclei caused by noxious and electroacupuncture stimulation were studied in acute experiments on cats. About 18% of the investigated neurons demonstrated coupled reactions to afferent stimulation. The coupled reaction to either noxious or electroacupuncture stimulation had inhibitory or activating character. A hypothesis on the existence of functional units responsible for the effects of electroacupuncture analgesia with participation of inhibitory, relay neurons and interneurons is made.
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PMID:[Coupled neuronal reactions of the specific and nonspecific thalamic nuclei to painful and electroacupuncture stimuli]. 362 May 48

An overview is given of CNS mechanisms which are behind the beneficial effects of VPL-VPM thalamic stimulation in the treatment of neuropathic pain. Further research in this field is urgently needed and the recent possibility to combine Deep Brain Stimulation with positron emission tomography (PET) will certainly help to unravel the brain circuitry implicated in stimulation-produced analgesia. Brain stimulation is an artificial way to activate nervous tissue that is reversible and, when correctly applied, has few complications. The clinical results warrant a continued dissemination of brain stimulation as a treatment in well selected cases of neuropathic pain.
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PMID:Thalamic stimulation in neuropathic pain: 27 years later. 1137 79

Two inhibitors of the cellular uptake of the endocannabinoid anandamide, (R)-N-oleoyl-(1'-hydroxybenzyl)-2'-ethanolamine and (S)-N-oleoyl-(1'-hydroxybenzyl)-2'-ethanolamine (OMDM-1 and OMDM-2, respectively), were recently synthesized, and their in vitro pharmacological activity described. Here we have assessed their activity in two typical pharmacological responses of cannabimimetic compounds. We first examined whether these compounds exert any effect per se on locomotion and pain perception in rats, and/or enhance the effects of anandamide on these two processes. We compared the effects of the novel compounds with those produced by a previously developed selective inhibitor, N-arachidonoyl-(2-methyl-4-hydroxyphenyl)amine (VDM-11). When assayed alone, OMDM-1 and OMDM-2 (1-10 mg/kg, i.p.) did not affect any of the five motor parameters under investigation, although the former compound exhibited a trend for the inhibition of ambulation, fast movements, and speed in rats. OMDM-2 and, to a lesser extent, VDM-11 (5 mg/kg, i.p.) enhanced the motor-inhibitory effects of a noneffective dose (2 mg/kg, i.p.) of anandamide, while OMDM-1 did not. In a typical test of acute analgesia, OMDM-2 and VDM-11 (1-10 mg/kg, i.p.), but not OMDM-1, significantly enhanced the time spent by rats on a "hot plate." However, the same compounds (5 mg/kg, i.p.) did not enhance the analgesic effect of a subeffective dose (2 mg/kg, i.p.) of anandamide, whereas OMDM-1 exerted a strong trend towards potentiation (P=0.06). We next explored the possible use of the two novel compounds in a pathological condition. Thus, we determined if, like other previously developed anandamide reuptake inhibitors, OMDM-1 and OMDM-2 inhibit spasticity in an animal model of multiple sclerosis-the chronic relapsing experimental allergic encephalomyelitis in mice. As previously shown with a higher dose of VDM-11, both novel compounds (5 mg/kg, i.v.) significantly reduced spasticity of the hindlimb in mice with chronic relapsing experimental allergic encephalomyelitis. We suggest that OMDM-1 and, particularly, OMDM-2 are useful pharmacological tools for the study of the (patho)physiological role of the anandamide cellular uptake process, and represent unique templates for the development of new antispastic drugs.
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PMID:In vivo pharmacological actions of two novel inhibitors of anandamide cellular uptake. 1474 10