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)

The subjects, 104 patients who had experienced more than two migraine episodes per month during the previous 6 months, received 60 mg of nicardipine daily for 2 months in an uncontrolled, Phase-IV study. Eighty-nine patients (mean age, 40 years; 16 with and 73 without aura; 60 women) completed the treatment regimen. The patients' blood pressure did not change during treatment. The mean number of migraine attacks was reduced significantly from 6.7 per month during the 3 months before treatment to 4.0 per month during treatment. The number of severe attacks was also reduced significantly. The patients' subjective ratings of the frequency and intensity of the attacks and their need for analgesia were reduced significantly from before to after treatment. Side effects (flushing and shortness of breath) were reported by four patients. It is concluded that nicardipine is safe and effective in the prevention of migraine attacks.
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PMID:Nicardipine in the prevention of migraine headaches. 146 86

Beta-endorphin is a peptide with morphine-like effects produced primarily in the anterior lobe of the pituitary gland. After its cleavage from the parent molecule, proopiomelanocortin, beta-endorphin is circulated via the blood stream to interact with specific opioid receptors located throughout the body. The peptide produces analgesia by inhibiting the firing of peripheral somatosensory fibers. It also affects other senses, such as vision, hearing, and smell. Whereas the ability to increase beta-endorphin secretion during times of surgical stress is positively correlated with amelioration of pain, the administration of exogenous opioids, such as fentanyl, reduces plasma beta-endorphin. Decreased beta-endorphin concentrations may play a role in trigeminal neuralgia, migraine headache, and rheumatoid arthritis.
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PMID:Peripheral beta-endorphin and pain modulation. 181 47

This study was undertaken to compare the effectiveness and safety of three dosage levels of butorphanol in 52 patients with acute, severe migraine headache. After baseline evaluation, patients were given a dose of butorphanol 1.0, 2.0, or 3.0 mg intramuscularly on a double-blind basis. Assessments of pain intensity and pain relief using 100 mm linear analog scales (LAS), vital signs, and medication side effects were made at 15, 30, 45, and 60 minutes after the dose. All three treatment groups were similar in baseline characteristics. Each dose of butorphanol demonstrated a significant decrease in pain intensity LAS compared to baseline and increase in pain relief LAS over the observation period. The majority of analgesic response was observed at the first (i.e., 15-min) assessment. Doses of 2.0 and 3.0 mg produced significantly greater analgesia than did 1.0 mg at all posttreatment evaluations. No significant difference was apparent between the 2.0- and 3.0-mg doses. Adverse cardiovascular and respiratory depressant effects were not observed. An analgesic response to butorphanol 2.0 and 3.0 mg is clearly and rapidly evident and near maximum 30-45 minutes after administration. We conclude that in these doses butorphanol provides effective and safe analgesia for patients with acute migraine headache.
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PMID:Dose effectiveness and safety of butorphanol in acute migraine headache. 202 Jun 12

In this study we have examined the results of salmon calcitonin treatment on migraine pain. The mechanism by which calcitonin induces analgesia is still not understood. We observed the effect of a 5-day treatment with salmon calcitonin (IM 100 IU/day) on circulating levels of beta-endorphin, ACTH, and cortisol in 20 patients with migraine during the headache-free period. All 3 hormones were increased after the calcitonin administration and the maximum increase was obtained in beta-endorphin levels. There were significant statistical correlations between beta-endorphin, ACTH, and cortisol levels determined before and after calcitonin treatment.
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PMID:Treatment of migraine with salmon calcitonin: effects on plasma beta-endorphin, ACTH and cortisol levels. 256 Apr 8

Endogenous opioid peptides, by modulating the release of sympathetic transmitters, may play a role in the pathogenesis of migraine and related headaches which are considered hypernociceptive syndromes. Hypoendorphinaemia has been demonstrated in migraine attack. Captopril, a drug able to potentiate morphine analgesia in rats and inhibit enkephalinase in animals and in man, improves the clinical course of migraine. In the present research the cerebrospinal fluid and plasma beta-endorphin (beta-EP) levels have been evaluated following a single oral dose of captopril. The drug increased plasma beta-EP levels in migraine sufferers, and these data may be relevant in the mechanism of action of this drug in migraine and related headaches.
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PMID:Hypernociceptive syndromes and pharmacological inhibition of endogenous opioid degradation. 294 84

Antidepressant drugs are now an important component of the analgesic pharmacopeia. Their ability to relieve pain is independent of the presence of clinical depression, and their efficacy has been documented in the treatment of migraine and tension headaches, neuropathic pain and chronic pain syndromes, including those associated with cancer. The tricyclic antidepressants are safe for use in patients with prolonged pain. The low doses required for analgesia are well tolerated and do not produce the side effects associated with the classic analgesic drugs.
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PMID:Treatment of pain with antidepressants. 298 20

The deafferentation of a leg in animal is followed by: local analgesia; generation in spinal cord and brainstem (along the sensitive fibers of second order) of quasi epileptic foci emitting continuously and/or in bursts, epileptic-like discharges; scratching, attacks and finally autocannibalism of the deafferentated arm. This perverted behavior (autotomy) is attributed to an emission from the quasi epileptic foci of pain signals projected to deafferentated regions by cognitive sites of consciousness. The quasi epileptic foci, generating bursts of "automatic" pain, are considered the basic mechanism of pain in deafferentated and amputated humans. The nature of pain in migraine is assumed here as an analog to the mechanism of organic deafferentation; a generation in the brainstem of nociceptive foci, with the head as main projection. The enigmatic epileptic-epileptoid characteristics of EEG in migraineurs could be an expression of the electrically hyperactive "quasi epileptic foci" located mainly within the brainstem and generated by the insufficient opioid inhibition of sP-ergic neurons.
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PMID:Electroencephalographic alterations in migraine as an expression of "self-deafferentation": a hypothesis. 311 49

Nociceptive flexion reflexes, RIII reflex in particular, have been demonstrated to be a useful tool for pain research in humans, since the threshold of RIII reflex is that of pain. In this study a reduction of RIII reflex threshold, strictly related to the severity of the disease, is described in migraine with interval headache (MIH), that is considered a severe and evolutive form of common migraine (CM). These abnormalities were not found in CM or in other chronic pain conditions, i.e. chronic tensive headache (CTH), suggesting that this electrophysiological parameter may be useful in the clinical assessment of primary headache. Moreover, the administration of amitriptyline, a drug producing analgesia mainly by blocking serotonin uptake, was able to markedly increase the RIII reflex threshold in MIH. This fact supports the hypothesis that an impairment of serotoninergic antinociceptive system may exist in this type of headache. A significant correlation between percentage increase in RIII reflex threshold and reduction of PTI was also observed after amitriptyline treatment, indicating that pain reflex may be used for predicting treatment response in migraine.
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PMID:Pain reflexes in the clinical assessment of migraine syndromes. 360 72

Patients with facial pain, without overt dental disease, are often seen in both medical and dental practice. The differential diagnosis includes (a) cluster headache, in which patients have severe unilateral pains lasting 30 to 120 minutes that respond to verapamil, corticosteroids or lithium; (b) migraine, in which attacks are longer and are often accompanied by nausea and visual disturbance, and can be managed using anti-inflammatory analgesics, with or without metoclopramide, or sumatriptan, although frequent attacks are best suppressed by continuous propranolol or pizotifen; (c) trigeminal neuralgia, knifelike unilateral pains usually responsive to carbamazepine; and (d) temporal arteritis, a steadier pain very responsive to corticosteroids. There is no evidence that continuous 'idiopathic facial pain' is a result of malocclusion (i.e. the way in which the teeth fit together), and its aetiology remains obscure, although there is some biochemical evidence linking it to depression. Many patients respond to simple analgesia and firm reassurance from the physician, although antidepressant therapy (e.g. nortriptyline or dothiepin) is often of great value.
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PMID:Orofacial neuralgia. Diagnosis and treatment guidelines. 769 15

Cerebrospinal fluid (CSF) concentration of Met-enkephalin immunoreactivity (Met-enkephalin-ir) was determined by radioimmunoassay in 47 patients with chronic tension-type headache and in 47 headache-free control subjects. Thirty-nine of the controls were patients receiving spinal analgesia before surgery for diseases not associated with pain; 8 were healthy paid volunteers. Patients reporting migraine more than 1 day per month were excluded. Pericranial tenderness, nociceptive flexion reflex and thermal pain thresholds were determined in the majority of the patients. The median level of CSF Met-enkephalin-ir was significantly higher (115 pmol/l) (quartiles (107-134) pmol/l) in the headache patients than in the controls (median 79 pmol/l) (quartiles (73-87) pmol/l) (Mann-Whitney, P < 0.001). No indication of sex-difference or correlation with age with respect to CSF Met-enkephalin-ir was found. No correlation was found between CSF Met-enkephalin-ir and either pericranial tenderness, nociceptive flexion-reflex threshold, or thermal pain threshold. There was no indication of correlation between consumption of mild analgesics and CSF Met-enkephalin-ir. The higher levels of CSF Met-enkephalin-ir in the headache patients may be indicate activation of the enkephalinergic antinociceptive system at the spinal/trigeminal level, whereas the beta-endorphinergic system appears normal. This enkephalinergic activation may be caused by increased activity in the primary nociceptive afferents, or may be compensatory to decreased activity in other endogenous antinociceptive systems than the opioid.
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PMID:Increased cerebrospinal fluid Met-enkephalin immunoreactivity in patients with chronic tension-type headache. 857 79


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