Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autonomic dysreflexia, a syndrome sometimes occurring in spinal cord injured (SCI) individuals, may be life-threatening. It involves, in varying degrees, hypertension, diaphoresis, headache, bradycardia, anxiety, and flushing and is believed due to unrestricted sympathetic activity below the level of the lesion in individuals with injuries above T4-6. The most frequent causes of the syndrome are urinary infections, rectal impaction, bladder distention, and decubitus ulcers. To our knowledge, medication has seldom been described as causal agent. We report here on an autonomic dysreflexic syndrome following use of an isometheptene combination (Midrin), to treat migraine. The individual involved is a C4-quadriplegic man with a long history of migraines. He was given a standard initial adult dose of the medication. Over a one-hour period, he was initially relieved of the headache, but then noted a new more severe headache, diaphoresis, and flushing. His vital signs showed progressive BP elevation to 210/130 and a relative bradycardia. Treatment over the next three hours was limited to elevation of the head of the bed and observation, during which his vital signs returned to baseline and he became asymptomatic. This experience reinforces the belief that sympathomimetic drugs in general, and isometheptene in particular, should be used in caution in patients with high-level SCI.
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PMID:Autonomic dysreflexia due to medication: misadventure in the use of an isometheptene combination to treat migraine. 403 34

The effect of an alpha-adrenergic agonist, clonidine hydrochloride, on cardiovascular responses to noradrenaline, adrenaline and angiotensin was investigated in menopausal women with hot flushes. The increase in forearm blood flow induced by adrenaline, noradrenaline or angiotensin was significantly less in women treated for at least 6 weeks with clonidine compared with that induced in the women by infusions given before treatment. Pulse rate during the amine infusions was significantly lower after clonidine treatment but constrictor responses in the hand were unchanged. These findings cannot be wholly explained in terms of an action of clonidine confined to adrenergic mechanisms and suggest that the drug may influence peripheral vascular responsiveness. Such an effect could explain the mechanism of the beneficial clinical action of the drug in subjects with menopausal flushing or migraine.
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PMID:Effect of oral clonidine on human cardiovascular responsiveness: a possible explanation of the therapeutic action of the drug in menopausal flushing and migraine. 406 34

Ninety patients, 50 males and 40 females, and their ages ranged between 42 and 70 years, with severe hypertension were treated by either sublingual verapamil tablets 40 mg (30 patients) or 80 mg (30 patients) or sublingual nifedipine capsules 10 mg (30 patients). Blood pressure and heart rate were measured before and 15, 30, 60, 90 and 120 mins after administration of the drugs. - Results showed that sublingual verapamil 40 mg caused significant drop of blood pressure after 60 min (200 +/- 11.6 / 127 +/- 8.7 to 177 +/- 13.8 / 95.4 +/- 11.8, P <0.05) and in 10/30 patients blood pressure was less than 150/90 mmHg. Verapamil 40 mg decreased heart rate in 16 patients, elevated in 5 patients and unchanged heart rate in 9 patients. Verapamil 80 mg caused significant reduction of blood pressure after 30 min (201 +/- 16 / 129 +/- 7.5 to 182 +/- 13 / 105 +/- 10.7, P <0.05) and the blood pressure was dropped to less than 150/90 mmHg in 18/30 patients. Sublingual verapamil 80 mg caused significant decrease in heart rate in 21/30 patients and peak decrease was recorded at 90 min (92.6 +/- 7.2 beats/min to 82 +/- 9, P <0.05). It alleviated headache in 8 patients including 2 patients with migraine. Sublingual nifedipine caused significant drop of elevated blood pressure at each time intervals and the peak drop was at 60 min (from 199 +/- 13.8 / 126 +/- 13.2 to 142.8 +/- 15 / 80. 9 +/- 9, P <0.05). In 22/30 patients blood pressure dropped to less than 150/90 mmHg after 60 min. Nifedipine elevated heart rate in 22/30 patients and peak elevation was at 30 min (from 91.6 +/- 7.8 to 105.6 +/- 6.1 beats/min, P <0.05). It caused headache in 8 patients and flushing in other 2 patients. Therefore, as compared to sublingual verapamil, sublingual nifedipine caused rapid lowering of elevated blood pressure and elevation of heart rate in most of the patients treated. The differences in proportions of patients whom blood pressure was dropped to less than 150/90 mmHg between nifedipine group and verapamil 40 mg group and between verapamil 80 mg and verapamil 40 mg groups were significant (P <0.05). - It might be concluded that sublingual verapamil caused significant lowering of blood pressure in hypertensive patients, decreased heart rate in most of the treated patients and alleviated headache in symptomatic hypertensive patients.
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PMID:Efficacy of sublingual verapamil in patients with severe essential hypertension: comparison with sublingual nifedipine. 1033 9

CGRP is a potent vasodilator that has been shown to have a physiological and/or pathological role in neurogenic inflammation, headaches including migraine, thermal injury, circulatory shock, pregnancy and menopause, hypertension and heart failure and is known to be cardioprotective. CGRP is also a positive inotrope and increases heart rate. Clinical trials have shown beneficial effects of the vasodilatory action of CGRP in hypertension, angina, heart failure, Raynaud's disease and venous stasis ulcers. However, the clinical potential of CGRP is limited as it has to be given by infusion and is quickly broken down. Oral long acting CGRP-mimetics may have potential in disorders in which CGRP has been shown to be beneficial. CGRP-mimetics include capsaicin/vanilloid receptor agonists and gene transfer of an adenoviral vector that encodes prepro-CGRP. CGRP inhibitors have therapeutic potential in conditions in which excessive CGRP-mediated vasodilatation is present; neurogenic inflammation, migraine and other headaches, thermal injury, circulatory shock and flushing in menopause. CGRP inhibitors include capsaicin, antagonists at capsaicin/vanilloid receptors, civamide, CGRP receptor antagonists and 5-HT1D-receptor agonists. Drugs that are 5-HT1D-receptor agonists, the 'triptans' are already commonly used in migraine and the first small molecule CGRP antagonist, BIBN4096BS, is under clinical investigation for the treatment of migraine.
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PMID:Migraine and beyond: cardiovascular therapeutic potential for CGRP modulators. 1177 40

Several lines of evidence support involvement of the parasympathetic system in migraine: (i) migraine-associated symptoms, such as exaggerated facial flushing, lacrimation and rhinorrhea; (ii) increased levels of cranial venous vasoactive intestinal peptide in migraineurs during attacks; and (iii) reports of migraine pain alleviation by intranasal instillation of lidocaine, which can block some of the parasympathetic outflow to the cranium. This study assessed cranial parasympathetic function in migraineurs in between attacks, assuming that abnormal function might imply involvement of the parasympathetics in migraine pathogenesis. We tested 39 female migraineurs outside attacks, of whom 11 had bilateral pain, 20 unilateral at a specific side and eight alternating unilateral head pain, and 16 controls. The trigemino-parasympathetic reflex was studied, using soapy and saline eye drops for stimulation of the afferent limb of the reflex arch, and cutaneous vascular response at the forehead for the efferent limb. The latter was recorded by photoplethysmography on both sides of the forehead. We found no difference in vasodilatation between migraineurs as a group and controls (83.7 +/- 6.5% and 80.8 +/- 7.6%, respectively, not significant). However, when analysing data by the site of pain, we found that those with bilateral pain had the largest vasodilatation response (141.6 +/- 16.2%, P < 0.05 versus controls, analysis of varance, post hoc Tukey-Kramer HSD), while those with unilateral pain had the least vasodilatation (45.5 +/- 3.3%, P < 0.05). The response of patients with alternating pain (97.2 +/- 12.6%) did not differ from controls. It is concluded that cranial parasympathetic function does differ among patients with various migraine types at rest. Based on the understanding of dysfunctional brainstem pain modulation in migraine, we suggest a model of within-brainstem interaction between the two locus coeruleus nuclei, which are involved in control of pain and cranial parasympathetic outflow. The model assumes various levels of inhibitory inter-relationships between these two nuclei; diminution or absence of the normal reciprocal inhibitory relationships between them may underlie the augmented cranial parasympathetic response in bilateral migraineurs, while an excess of reciprocal inhibitory relationship between them may underlie the diminished cranial parasympathetic response in unilateral migraineurs. These findings might help in clarifying inter-relationships between brainstem nuclei in the context of migraine pathogenesis.
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PMID:Different patterns of parasympathetic activation in uni- and bilateral migraineurs. 1280 17

Brain autonomic control is asymmetrical, the left hemisphere affecting predominantly parasympathetic function and the right hemisphere affecting predominantly sympathetic function. It is not known whether the extent of autonomic activation is altered in migraine, although the fact that some migraineurs express parasympathetic features such as facial flushing, lacrimation and rhinorrhoea might suggest increased parasympathetic activation. We instilled diluted soapy eyedrops and measured (i) the trigemino-parasympathetic reflex by the vasodilator response of forehead skin bilaterally using photoplethysmography; (ii) the somato-sympathetic reflex by vasoconstriction in the index finger; and (iii) heart rate response. We studied 14 left-sided and 15 right-sided unilateral migraineurs outside attacks. We found that left-side migraineurs had significantly higher bilateral parasympathetic vasodilatation, regardless of the stimulation or measurement side (+60.1 +/- 6.4%) compared with right-side migraineurs (+41.9 +/- 6.4%, P < 0.05). Sympathetic vasoconstriction, however, was similar for the two groups (left, -15.9 +/- 4.2%; right, -17.7 +/- 4.1%, NS). Bradycardia was significantly more pronounced for the left-side migraineurs (interbeat, RR interval increase of +6.2 +/- 1.1% versus +3.1 +/- 1.1%, P < 0.04). We conclude that unilateral left-side migraineurs have increased parasympathetic activation in response to pain compared with right-side migraineurs. Sympathetic responses were similar in the two groups and seemed not to be affected by migraine side. Since cranial parasympathetic activity induces cerebral vasodilatation, this augmentation might be an inherent part of the migraine pathophysiology in these patients.
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PMID:Autonomic asymmetry in migraine: augmented parasympathetic activation in left unilateral migraineurs. 1528 13

Raloxifene, a selective estrogen receptor modulator (SERM) licensed for the prevention of non-traumatic vertebral fractures in postmenopausal women at increased risk of osteoporosis, was launched in the UK in August 1998. The aim of the study was to monitor the safety of raloxifene prescribed in the primary care setting in England using prescription-event monitoring (PEM). Patients were identified by means of prescription data supplied by the Prescription Pricing Authority between September 1998 and November 2000. Demographic and clinical event data were collected from questionnaires posted to primary care physicians (GPs) at least 6 months after the date of the first prescription for each patient. Information on medical events, suspected adverse drug reactions (ADRs), reasons for stopping treatment, pregnancies, and causes of death was requested. Event rates [Incidence Densities (IDs): no. first reports /1000 patient-months of treatment] were calculated. Differences between IDs for events reported in month one (ID(1)) and months 2-6 (ID(2-6)) of treatment were examined. The cohort comprised 13,987 patients [median age 62 years (IQR 55,69); 99.8% female]. The major indication was osteoporosis (40.9%, n=5725). Flushing was the event with the highest ID in month 1 (22.8), reported most frequently by GPs as an ADR to raloxifene (67/461 reports) and as the reason for stopping (700/4592 reports). Events associated with starting treatment included flushing, malaise/lassitude, headache/migraine, nausea/vomiting, sweating, cramp, pain abdomen, dizziness, diarrhea, mastalgia and vaginal hemorrhage. Less common events reported during treatment included deep vein thrombosis (n=13), pulmonary embolism (n=13), thrombophlebitis (n=31) and visual disturbance (n=29). In this study, there were 122 (0.9%) confirmed deaths, of which 32 causes of death were unknown. This study shows that raloxifene is generally well tolerated when used in general practice in England. Potential signals of unrecognised ADRs requiring further evaluation included gastrointestinal adverse symptoms and vaginal hemorrhage. There were also a small number of reports of events associated with venous thromboembolism and visual disorders that require further investigation.
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PMID:Safety profile of raloxifene as used in general practice in England: results of a prescription-event monitoring study. 1530 82

Frovatriptan succinate is one of the most recent serotonin receptor agonists to receive FDA, approved labelling for use in the acute management of migraine with or without aura in adults. The mechanism of action of frovatriptan is thought to be similar to that of a serotonin agonist. However, frovatriptan has distinctive pharmacokinetic and pharmacologic properties, chiefly, a high affinity for serotonin receptors 1B and 1D and a long elimination half-life; frovatriptan was shown to be more selective for cerebral than coronary arteries, a property which makes frovatriptan more favourable in patients at risk of coronary artery disease. Additionally, frovatriptan has a half-life of approximately 25 h, substantially longer than that of any other agent within its class. This property makes frovatriptan suitable for patients who typically suffer migraines of long duration and/or those who suffer migraine recurrence. The efficacy of frovatriptan in the treatment of acute migraine was demonstrated in five double-blind, randomised, placebo-controlled trials. At 2h, headache response rates for frovatriptan 2.5 mg ranged from 38 to 40% compared to 22-35% for placebo. Headache recurrence for frovatriptan 2.5 mg at 24h ranged from 9 to 14% compared with 18% in placebo subjects. Frovatriptan has no clinically significant pharmacokinetic interactions with drugs used for migraine prophylaxis or with commonly prescribed medications. Adverse effects of frovatriptan including dizziness, paresthesia, dry mouth, fatigue and flushing were generally mild and well tolerated. Given the fact that patient response to serotonin agonists is individualised, and selecting an effective agent may involve trial and error, frovatriptan is a welcome alternative in the acute management of migraine.
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PMID:Frovatriptan succinate, a 5-HT1B/1D receptor agonist for migraine. 1531 27

(1) The reference first-line drug therapy for migraine attacks in adolescents is a non specific analgesic such as paracetamol or a nonsteroidal antiinflammatory drug like ibuprofen. Two specific analgesics are authorised for use in this setting in France, namely ergotamine and dihydroergotamine. (2) Nasal sumatriptan is the first triptan to be licensed for this age group in France. (3) Evaluation data includes three flawed placebo-controlled trials. (4) Effects were modest at best. Only one of the three trials showed that sumatriptan was more likely than placebo to give complete pain relief within two hours. The three trials fail to show that sumatriptan is effective against symptoms such as nausea and vomiting, photophobia and phonophobia. (5) The principal known adverse effects of sumatriptan are chest tightness, flushing, and increased blood pressure. (6) In the only trial report containing relevant information, unpleasant taste was the only adverse effect more commonly associated with sumatriptan than with placebo. (7) Postmarketing follow-up revealed a number of serious adverse effects, including stroke, myocardial infarction and loss of vision. (8) The packs containing 6 or 12 spray vials carry a risk of overuse and self-induced headache. (9) In practice, sumatriptan must not be used to treat migraine attacks in adolescents.
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PMID:Nasal sumatriptan: new dosage. For adolescents with migraine: too little benefit. 1587 37

The clinical symptoms of migraine are widely accepted to be related to the involvement of the autonomic nervous system, and especially to dysfunction in the regulation of the circulatory system and autonomic balance. Disturbance of the autonomic nervous system is a primary characteristic of migraine Therefore, patients with migraine have a variety of symptoms, such as vasodilatation (flushing), pilo-erection, nausea, vomiting, diarrhea, cutaneous vasoconstriction (pallor), and diaphoresis. The electrocardiographic changes seen during a migraine attack compared with the pain-free period could be secondary to reversible disturbances of the state of autonomic innervation of the heart and coronary arteries. Dysfunction of ANS may affect atrial and ventricular repolarization. For instance, increased sympathetic activity causes sinus tachycardia, but increased parasympathetic activity causes sinus bradycardia, atrioventricular block, and ST-segment and T-wave abnormalities. Comprehensive electrocardiographic analyses have been providing more details in terms of the detection of abnormalities in atrial and ventricular repolarization which potentially may result in arrhythmias in patients with migraine. However, there is no information in literature reporting the frequency of cardiac arrhythmias in migraine patients who had cardiac repolarization abnormalities. In this review, detailed electrocardiographic findings and their relation with the autonomic nervous system, including recent observations, have been evaluated. However, further studies are needed to investigate the association between autonomic dysregulation and cardiac repolarization abnormalities in patients with migraine.
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PMID:Autonomic dysfunction and cardiac repolarization abnormalities in patients with migraine attacks. 1732 46


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