Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is now evidence that melatonin may have a role in the biological regulation of circadian rhythms, sleep, mood, and ageing. Altered melatonin levels in cluster headache and migraine have been documented. Melatonin mechanisms are related to headache pathophysiology in many ways, including its anti-inflammatory effect, toxic free radical scavenging, reduction of proinflammatory cytokine up-regulation, nitric oxide synthase activity and dopamine release inhibition, membrane stabilization, GABA and opioid analgesia potentiation, glutamate neurotoxicity protection, neurovascular regulation, serotonin modulation, and the similarity of chemical structure to that of indomethacin. Treatment of headache disorders with melatonin and other chronobiotic agents is promising. A double-blind, placebo-controlled trial shows melatonin is effective in cluster headache prevention, other studies also show benefit in other disorders. Melatonin plays an important role in headache disorders, offering new avenues for studying their pathophysiology and treatment.
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PMID:Melatonin, the pineal gland and their implications for headache disorders. 1591 May 64

Nitric oxide (NO) plays an important role in initiation and maintenance of pain, and NO precursor nitroglycerin is able to activate spinal and brain structures involved in nociception. It is also known that acute and chronic stress induce biochemical changes affecting both pain threshold and behaviour, and that the biological pattern of depression can be mimicked in the laboratory using chronic unavoidable stress paradigms (learned helplessness). We, therefore, evaluated the effects of acute and chronic immobilization stress on pain response to nitroglycerin administration in the rat. Pain perception was expressed as the latency of response to a tail-flick test (hot stimulus). Measures were made 1, 2 and 4 h following nitroglycerin (10 mg/kg i.p.) or vehicle. Nitroglycerin caused hyperalgesia after 2 and 4 h (p < 0.05 versus baseline). Acute stress (90 min) induced a clear analgesic state (p < 0.01 versus non-stressed control animals), and nitroglycerin injection was unable to reverse stress-induced analgesia in this setting. By contrast, exposition to chronic immobilization stress (7 days) caused a significant increase in pain response (p < 0.05); in this case, hyperalgesia was shown to be further enhanced by nitroglycerin administration (p < 0.05 versus vehicle). These findings support the view that a condition of chronic stress used in the laboratory to reproduce the biological features of depression can enhance hyperalgesia induced by nitroglycerin administration. These observations may be relevant to pain disorders, and particularly to migraine, since nitroglycerin is able to induce spontaneous-like pain attacks in humans, and an unfavourable migraine outcome (transformation into a chronic daily headache) is associated with chronic stress and comorbid depression.
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PMID:Effects of acute and chronic restraint stress on nitroglycerin-induced hyperalgesia in rats. 1593 4

Vagus nerve stimulation (VNS), already used as a treatment for refractory epilepsy, has also been assessed for its analgesic effect. Numerous studies report that electrical stimulation of vagal afferents inhibits spinal nociceptive reflexes and transmission. However, results are partly contradictory, showing that the VNS effects depend on the stimulation parameters. Clinical data have been collected from VNS-implanted epileptic patients in whom pain thresholds were measured and the VNS effect on co-existing headaches was assessed. In addition, in 2 pilot studies of a few patients, VNS was used to treat resistant chronic headaches and migraines. Taken together these clinical studies tend to confirm the analgesic effect of VNS and to suggest its potential utility in chronic headache patients. In order to better define the nature of neuronal and behavioural changes induced by VNS with devices used in humans and to determine the most adequate stimulation stimulation protocols, we have used a commercially available stimulator (NCP-Cyberonics) for prolonged VNS in rats. Our results show a clear antinociceptive effect of VNS in models of acute or inflammatory pain with different stimulation protocols including the one used in epileptic patients. Using immunocytochemical methods, we find that activity changes in spinal trigeminal nucleus neurons could underlie at least part of the VNS-induced analgesia.
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PMID:Pain control by vagus nerve stimulation: from animal to man...and back. 1607 58

This study presents the result of the studies explaining the effects of acupuncture on various systems and symptoms. It has been determined that endomorphin-1, beta endorphin, encephalin, and serotonin levels increase in plasma and brain tissue through acupuncture application. It has been observed that the increases of endomorphin-1, beta endorphin, encephalin, serotonin, and dopamine cause analgesia, sedation, and recovery in motor functions. They also have immunomodulator effects on the immune system and lipolithic effects on metabolism. Because of these effects, acupuncture is used in the treatment of pain syndrome illnesses such as migraine, fibromyalgia, osteoarthritis, and trigeminal neuralgia; of gastrointestinal disorders such as disturbance at gastrointestinal motility and gastritis; of psychological illnesses such as depression, anxiety, and panic attack; and in rehabilitation from hemiplegia and obesity.
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PMID:The mechanism of acupuncture and clinical applications. 1639 78

There is increasing evidence that headache disorders are connected with melatonin secretion and pineal function. Some headaches have a clearcut seasonal and circadian pattern, such as cluster and hypnic headaches. Melatonin levels have been found to be decreased in both migraine and cluster headaches. Melatonin mechanisms are related to headache pathophysiology in many ways, including its anti-inflammatory effect, toxic free radical scavenging, reduction of pro-inflammatory cytokine upregulation, nitric oxide synthase activity and dopamine release inhibition, membrane stabilisation, GABA and opioid analgesia potentitation, glutamate neurotoxicity protection, neurovascular regulation, 5-HT modulation and the similarity in chemical structure to indometacin. The treatment of headache disorders with melatonin and other chronobiotic agents, such as melatonin agonists (ramelteon and agomelatin), is promising and there is a great potential for their use in headache treatment.
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PMID:Potential therapeutic use of melatonin in migraine and other headache disorders. 1654 86

A randomized, controlled, cross-over trial compared single doses of 50 mg diclofenac potassium sachets and tablets with placebo in 328 patients with migraine pain, treating 888 attacks. For the primary endpoint 24.7% of the patients were pain free at 2 h postdose with sachets, 18.5% for tablets and 11.7% for placebo. Treatment differences were significant for sachets vs. placebo (P<0.0001), tablets vs. placebo (P=0.0040) and for sachets vs. tablets (P=0.0035). The numbers needed to treat compared with placebo to achieve pain free at 2 h were 7.75 [95% confidence interval (CI) 5.46, 13.35] for sachets and 15.83 (95% CI 8.63, 96.20) for tablets. Sachets were also statistically superior to tablets for sustained headache response, sustained pain free and reduction in headache intensity within the first 2 h postdose measured on a visual analogue scale (P<0.05). Onset of analgesic effect was 15 min for sachets and 60 min for tablets. Fewer patients needed rescue medication, and there were marked improvements in accompanying symptoms and working ability with both sachets and tablets vs. placebo. No safety issues were identified. This study demonstrates that sachets offer patients suffering from migraine pain a more effective treatment with a faster onset of analgesia when compared with tablets.
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PMID:Efficacy and tolerability of diclofenac potassium sachets in migraine: a randomized, double-blind, cross-over study in comparison with diclofenac potassium tablets and placebo. 1667 62

The pineal gland and its secretory product, melatonin, have been implicated in the pathophysiology of migraine, as well as some of its comorbid disorders. Supporting this view, many migraineurs are susceptible to various environmental triggers that influence the secretion of melatonin from the pineal gland, and many prodromal symptoms are probably generated in the hypothalamus, a brain region that provides input into the pineal gland to modulate the secretion of melatonin. In addition, studies have shown abnormalities in melatonin secretion in patients who experience migraine and an improvement in migraine following administration of melatonin. However, the dysfunction in melatonin secretion in migraineurs may simply be a marker of hypothalamic dysfunction or neuronal hyperexcitability, leading to migraine susceptibility. It is also possible that abnormal melatonin secretion leads to decreased inhibitory neurotransmitter activity, decreased inhibition of the release of calcitonin gene-related peptide (CGRP) from activation of the trigeminal system, or less analgesia. Whatever its role in the pathogenesis of migraine, melatonin may prove to be a useful therapy. Future studies are necessary to further elucidate whether melatonin is a well tolerated, beneficial therapy, and to determine the optimal dose and formulation of melatonin for use in migraine therapy.
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PMID:Role of melatonin in the pathophysiology of migraine: implications for treatment. 1669 76

Metoclopramide (MTCL) can abort attacks of migraine headache. I report swift resolution of cough-induced headache as well as suppression of cough in six male patients following parenteral administration of MTCL. A similar unexpected rapid antitussive action of MTCL was also observed in 12 of 14 other patients (13 male and 1 female) with severe paroxysmal cough without headache. Use of MTCL primarily for analgesia is reviewed, and the pharmacological basis for its antinociceptive action is proposed. As a nonopiate agent with potential to stimulate endogenous opiate-mediated mechanisms, MTCL appears to have additional valuable roles in clinical practice. This is the first report of an antitussive action of MTCL. Further controlled studies are required to confirm the therapeutic role of MTCL in cough-induced headache as well as its potential antitussive and general analgesic actions.
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PMID:Metoclopramide aborts cough-induced headache and ameliorates cough--a pilot study. 1678 37

Substance P (SP)/Neurokinin 1 (NK1) receptor pathways have been repeatedly implicated in the pathophysiology of central, pulmonary, and gastric disorders. A large body of evidence that has been generated from animal experiments indicates that treatment with selective NK1 receptor antagonists might be effective in the treatment of certain forms of disorders, analgesia, depression, migraine, asthma, or gastrointestinal disorders. Accordingly, numerous NK1 receptor antagonists have either been synthesized and are under clinical development, or have already been tested in clinical trials. However, the initial encouraging clinical results were followed by repeated demonstration of a lack of effectiveness. Up to now, only one NK1 receptor antagonist, aprepitant, is available for therapeutical use. Aprepitant is a selective high-affinity human SP/NK1 receptor antagonist approved by the FDA in 2003. Aprepitant is indicated for prophylaxis of acute- and delayed-phase nausea and emesis caused by chemotherapy regimens. It is used in combination with a 5-hydroxytryptamine (5-HT3) antagonist and a corticosteroid. It is the first antiemetic agent that acts by binding the NK1 receptor. Research continues and novel molecules may show better pharmacokinetic and pharmacodynamic properties and, therefore, may achieve therapeutic success.
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PMID:[Neurokinin 1 receptor antagonists--between hope and disappointment]. 1679 96

Scalp injection of botulinum toxin type A (BT-A) into the superficial musculature has evoked interest in the management of migraine headache. In clinical trials, prevention of migraine attacks for 3 months or more has been seen in some patients following BT-A scalp injections. In the majority of pain syndromes where BT-A is effective, inhibition of muscle spasms appears to be an important component of its activity. A direct or independent and prolonged analgesic action unrelated to skeletal muscle relaxation is believed to underlie the prophylactic efficacy of BT-A in migraine; peripheral and central modulation of pain impulses by BT-A has also been proposed. A direct peripheral antinociceptive effect was not seen in three controlled studies of BT-A in normal human volunteers. Experimental evidence for BT-A-induced analgesia in rats is suggestive but dose-dependent and lasts only 2 weeks. In migraine patients, a consistent or dose-dependent response to BT-A treatment has not been seen. Peak responses to BT-A in migraine patients are seen at 8-12 weeks, whereas BT-A-affected nerve endings in mice fully recover function between 63 and 91 days; the difference in species limits the interpretation of this dissonance. As BT-A does not normally cross the intact blood-brain barrier, meningeal nociceptors appear unlikely to be influenced by scalp injections of BT-A; the possibility of antidromic transfer of BT-A in the trigeminovascular system should be considered. The extended period for which migraine prophylaxis might be required, the antigenic and headache-provoking potential of BT-A, the inability of BT-A to affect central neuronal processes significantly, including the aura of migraine, the possible placebo effect of needling, and purely subjective outcome measures in headache studies are additional concerns in evaluating this treatment strategy. The clinical utility of BT-A has not been compared against established migraine prophylactic agents. The efficacy of BT-A in preventing migraine headache attacks remains controversial and the underlying scientific rationale is debatable.
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PMID:Botulinum toxin--a treatment for migraine? A systematic review. 1701 96


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