Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The value of clonidine (;Dixarit') for the prophylaxis of migraine has been assessed by a double blind cross-over trial. A dose of up to 0.15 mg daily was used. No effect on the frequency of the headaches could be detected over and above the 60 per cent reduction observed with a placebo. Severity, assessed subjectively by the patient, when it varied between placebo and clonidine, was less with clonidine (p<0.01). There was also some evidence that headaches lasting more than 12 hours were less common during treatment with the drug.
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PMID:Double blind trial of clonidine in the treatment of migraine in a general practice. 36 33

Autonomic nervous system functions were studied in 13 females with migraine without aura during headache-free intervals, using physiological, pharmacological and biochemical methods. Heart-rate in the resting condition and blood pressure rises in the cold-face and isometric handgrip tests were higher than in controls. Normal cardiovascular responses to the Valsalva manoeuvre and to noradrenaline infusion suggest that the baroreflex arc is intact. Normal heart rate responses to the Valsalva manoeuvre, to the cold-face test and to deep breathing confirmed a normal cardiac parasympathetic function. Clonidine infusion showed a sedative and depressor effect and an inhibition of plasma NA similar to those occurring in controls, suggesting a normal central sympathetic tone. As a whole, the physiological, pharmacological and biochemical tests were consistent with a non-specific sympathetic hyperactivity, but do not confirm any impairment of the autonomic control of the cardiovascular system in migraine patients in headache-free intervals.
Headache 1991 Jul
PMID:Autonomic nervous system function in migraine without aura. 177 61

In a prospective, double-blind comparison, we assessed the efficacy of transdermal clonidine with that of chlordiazepoxide in the treatment of moderately severe acute alcohol withdrawal syndrome. While having significant withdrawal symptoms, 50 hospitalized men were randomly assigned to receive either transdermal clonidine or chlordiazepoxide over a 4-day study period. Outcome was evaluated daily, medically and psychiatrically, using both objective and subjective measurements for dependent variables. No patient in either study group had seizures or progression to delirium tremens. The group receiving transdermal clonidine had a more significant response globally for the signs and symptoms of alcohol withdrawal, as measured by the Alcohol Withdrawal Assessment Scale. Also, clonidine more effectively lowered elevated systolic and diastolic blood pressure and heart rate. The core target symptom, anxiety, decreased significantly more in the patients receiving transdermal clonidine when measured by the Hamilton Anxiety Rating Scale and its subscale for somatic anxiety. Cognitive function responded equally in both study populations. Clonidine-treated patients reported less diarrhea, dizziness, headache and fatigue, and the chlordiazepoxide-treated patients reported less nausea and vomiting. We conclude that transdermal clonidine is effective treatment for the acute alcohol withdrawal syndrome.
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PMID:Transdermal clonidine versus chlordiazepoxide in alcohol withdrawal: a randomized, controlled clinical trial. 200 May 17

The efficacies of an 2-agonist clonidine and an 2-antagonist mianserin were compared in two treatment groups, common migraine and tension headache sufferers. Forty patients entered this double-blind placebo-controlled study. Placebo, clonidine 0.150 mg, and mianserin 30 mg were each administered for 90 day periods. Headaches were induced by intravenous doses of histamine dihydrochloride. The histamine threshold in the common migraine group was significantly lower than in the tension headache group. In the common migraine group, mianserin decreased headache frequency. In the tension headache group, at 90 days mianserin significantly decreased headache intensity and headache frequency. Clonidine significantly decreased headache intensity at 90 days in the common migraine group. At 90 days, mianserin had significantly reduced the Hamilton Depression Rating Scale (HDRS) mean total score, (in the tension headache group), HDRS mean anxiety cluster scores (in both groups), and the HDRS mean depression cluster score (in the tension headache group). At 90 days, clonidine had significantly reduced the HDRS mean total score (in the tension headache group) and HDRS mean anxiety cluster scores (in both groups).
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PMID:Headache and noradrenergic involvement: the effects of alpha 2-stimulants and alpha 2-antagonists. 390 72

Clonidine (Dixarit), 0.025 mg three times daily, was given to 15 patients with menopausal, predominantly vasomotor symptoms. Both the number and the subjectively judged intensity of flushes and sweating decreased continually and in a statistically significant manner during the nine-week time of observation. Additionally, frequency and intensity of headaches, dizziness and paraesthesias decreased, while the other symptoms such as irritability, weak memory and depression remained unchanged. Clonidine in the stated dosage had no significant effect on blood pressure and heart rate. Mild side effects, especially dry mouth and slight sleepiness, were evident only in the first three weeks.
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PMID:[Treatment of menopausal symptoms with low doses of clonidine (author's transl)]. 706 Apr 97

Some clinical as well as pharmacological indications seem to suggest that a reduction of the noradrenergic tone occurs in cluster headache (CH), during both the active and remission periods. But sharp fluctuations of the sympathetic system may trigger the attacks. Clonidine, an alpha-2-adrenergic presynaptic agonist, regulates the sympathetic tone in the central nervous system. Therefore, a continuous administration of low-dose clonidine could be potentially beneficial in the active phase of CH by antagonizing the variations in noradrenergic tone. After a run-in week, we administered transdermal clonidine (5 - 7.5 mg) for one week to 13 patients suffering from CH, either episodic (8 cases) or chronic (5 cases). During clonidine treatment, the mean weekly frequency of attacks dropped from 17.7 +/- 7.0 to 8.7 +/- 6.6 (p = 0.0005), the pain intensity of attacks measured on the visual analogue scale from 98.0 +/- 7.2 to 41.1 +/- 36.1 mm (p = 0.001), and the duration from 59.3 +/- 21.9 to 34.3 +/- 24.6 min (p = 0.02). This open pilot study strongly suggests that transdermal clonidine may be an effective drug in the preventive treatment of CH. Its efficacy is possibly due to its central sympatho-inhibition, which reduces or prevents the occurrence of fluctuations of noradrenaline release that may induce the attacks.
Cephalalgia 1995 Oct
PMID:Efficacy of transdermal clonidine in short-term treatment of cluster headache: a pilot study. 920 77

1. It has been reported previously that clonidine can potentiate tyramine-evoked mydriasis on the pain-free side of cluster headache patients. We examined whether a single oral dose of clonidine (200 micrograms) can also potentiate tyramine-evoked mydriasis in healthy subjects, using mydriasis to methoxamine, a directly acting sympathomimetic amine, as a control. 2. Eight healthy male volunteers participated in four weekly sessions. In the first two sessions (Experiment 1) the effect of clonidine or placebo on the mydriasis to tyramine hydrochloride eyedrops (75 mM; 2 x 10 microliters), and in the last two sessions (Experiment 2) the effect of clonidine or placebo on the mydriasis to methoxamine hydrochloride eyedrops (20 mM; 2 x 10 microliters) was examined. In both experiments subjects were allocated to drugs and sessions according to a double-blind balanced design. In both experiments, pupil diameter of both the treated and the untreated eyes was recorded in standard ambient light and in the dark, before, and 2 h after clonidine/placebo, via binocular infrared television pupillometry. Salivation (dental roll technique), systolic and diastolic blood pressure (sitting), heart rate, and self-ratings of mood and feelings (visual analogue scales), were also measured before, and 2 h after the ingestion of clonidine or placebo. 3. Both tyramine and methoxamine produced a significant mydriasis, which was more prominent in the light condition (change in resting pupil size; mm +/- s.e.mean: tyramine/light 1.05 +/- 0.28; tyramine/dark: 0.73 +/- 0.15; methoxamine/light: 1.65 +/- 0.28; methoxamine/dark: 0.85 +/- 0.15). Clonidine produced a significant miosis in the untreated eye which was more prominent in the light condition (change in resting pupil size; mm +/- s.e.mean: Experiment 1, light: -1.34 +/- 0.19; Experiment 1, dark: -0.46 +/- 0.1; Experiment 2, light -0.97 +/- 0.18; Experiment 2, dark: -0.29 +/- 0.17). Clonidine had no significant effect on either tyramine- or methoxamine-evoked mydriasis. 4. In agreement with previous reports, clonidine significantly reduced salivation (g, mean +/- s.e.mean; Experiment 1: -0.84 +/- 0.22; Experiment 2: -0.55 +/- 0.11), systolic blood pressure (mm Hg; Experiment 1: -17.5 +/- 3.76; Experiment 2: -23.38 +/- 4.67), diastolic blood pressure (mm Hg; Experiment 2: -12.38 +/- 2.05), alertness (mm; Experiment 2: -24.19 +/- 5.40), and anxiety (mm; Experiment 1: -13.82 +/- 4.60), indicating the presence of pharmacodynamically effective tissue levels of the drug. 5. These results show that a single oral dose (200 micrograms) of clonidine causes significant miosis in human subjects, and fails to potentiate tyramine-evoked mydriasis. This indicates that the pupil on the asymptomatic side of cluster headache patients is affected differently from the pupils of healthy volunteers by tyramine and/or clonidine.
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PMID:Comparison of the effects of clonidine on tyramine- and methoxamine-evoked mydriasis in man. 873 Sep 71

Traditional centrally acting antihypertensives have been associated with a high incidence of adverse effects and are no longer recommended as first-line therapy. The newer imidazoline receptor agonists must overcome this reputation if they are to gain recognition as potential first-line agents for hypertension. Methyldopa, a centrally acting alpha(2)-agonist, is characterized by a number of serious adverse reactions that limit its use. Although unpredictable idiosyncratic or hypersensitivity reactions are uncommon, these include hepatitis, myocarditis, and hemolytic anaemia. Less serious problems such as abnormal liver function tests, positive Coombs test, drug-induced fever, and pancreatitis also occur. Central side effects include drowsiness, fatigue, lethargy, sedation, depression, psychotic reactions, nasal stuffiness, impotence, and exacerbation of Parkinsonism. In hypertensive men, methyldopa is less well tolerated than either captopril or propranolol, and up to 20% of patients discontinue therapy because of adverse effects. Clonidine acts primarily as an alpha(2)-agonist but also acts as an agonist at imidazoline receptors in the rostroventrolateral medulla. It is equipotent to most other antihypertensives but is considerably less well-tolerated in comparative trials. The principal adverse effects of clonidine are drowsiness, sedation, lethargy and dry mouth. Reserpine acts primarily by depleting central catecholamine neurotransmitter stores. It was very extensively used in early hypertension trials, but its central side effects of sedation, nasal stuffiness, and severe depression are now considered so undesirable that the drug is seldom prescribed. The imidazoline (I1) agonists moxonidine and rilmenidine act selectively and have very little central alpha(2)-agonist activity. In comparative studies against placebo and other reference antihypertensives, the only adverse effect consistently associated with these drugs was dry mouth (approximate placebo-corrected incidence 10%). Sedation was not pronounced. Withdrawal syndromes are complex pathophysiologic processes and occur with a variety of antihypertensive drugs. Cessation of therapy with clonidine and, to a lesser extent, methyldopa may result in a severe withdrawal syndrome characterized by restlessness, sweating, anxiety, tremor, palpitations, and headache. There may be a rapid rise in blood pressure, often with a true "rebound" to higher than pretreatment levels. Plasma and urinary catecholamine levels are increased, and fatalities have been reported. It is important to stress that such a syndrome has not been recorded, in animal or human studies, with either moxonidine or rilmenidine.
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PMID:Aspects of tolerability of centrally acting antihypertensive drugs. 887 99

Pheochromocytomas are catecholamine-producing tumors, representing one of the most important causes of secondary hypertension. The classification of these tumors considers both sporadic and familial forms, intra- and extraadrenal localization as well as the dignity. Familial pheochromocytomas are primarily seen under the conditions of multiple endocrine neoplasia, von Hippel-Lindau disease or neurofibromatosis type 1. The list of clinical symptoms includes hypertension, which can be both continuous or intermittent, headache, tachycardia and sweating. It is most important to standardize the pre-analytical procedures, i.e. control for sampling conditions and adequate choice of parameters in plasma or urine. For screening sensitive methods will be employed (free catecholamines in 24h-urine) and for confirmation of the diagnosis, specific procedures are performed (Clonidine test, MIBG-scintigraphy). The endocrinological and biochemical procedures are completed by molecular genetic techniques in familial pheochromocytoma.
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PMID:[Clinical and endocrine diagnosis of pheochromocytoma]. 933 11

The prevalence of attention-deficit hyperactivity disorder (ADHD) in the USA is estimated at approximately 4-9% in children and 4% in adults. It is estimated that prescriptions for ADHD medications are written for more than 2.7 million children per year. In 2010, US poison centers reported 17,000 human exposures to ADHD medications, with 80% occurring in children <19 years old and 20% in adults. The drugs used for the treatment of ADHD are diverse but can be roughly separated into two groups: the stimulants such as amphetamine, methylphenidate, and modafinil; and the non-stimulants such as atomoxetine, guanfacine, and clonidine. This review focuses on mechanisms of toxicity after overdose with ADHD medications, clinical effects from overdose, and management. Amphetamine, dextroamphetamine, and methylphenidate act as substrates for the cellular monoamine transporter, especially the dopamine transporter (DAT) and less so the norepinephrine (NET) and serotonin transporter. The mechanism of toxicity is primarily related to excessive extracellular dopamine, norepinephrine, and serotonin. The primary clinical syndrome involves prominent neurological and cardiovascular effects, but secondary complications can involve renal, muscle, pulmonary, and gastrointestinal (GI) effects. In overdose, the patient may present with mydriasis, tremor, agitation, hyperreflexia, combative behavior, confusion, hallucinations, delirium, anxiety, paranoia, movement disorders, and seizures. The management of amphetamine, dextroamphetamine, and methylphenidate overdose is largely supportive, with a focus on interruption of the sympathomimetic syndrome with judicious use of benzodiazepines. In cases where agitation, delirium, and movement disorders are unresponsive to benzodiazepines, second-line therapies include antipsychotics such as ziprasidone or haloperidol, central alpha-adrenoreceptor agonists such as dexmedetomidine, or propofol. Modafinil is not US FDA approved for treatment of ADHD; however, it has been shown to improve ADHD signs and symptoms and has been used as an off-label pharmaceutical for this diagnosis in both adults and children. The mechanism of action of modafinil is complex and not fully understood. It is known to cause an increase in extracellular concentrations of dopamine, norepinephrine, and serotonin in the neocortex. Overdose with modafinil is generally of moderate severity, with reported ingestions of doses up to 8 g. The most common neurological effects include increased anxiety, agitation, headache, dizziness, insomnia, tremors, and dystonia. The management of modafinil overdose is largely supportive, with a focus on sedation, and control of dyskinesias and blood pressure. Atomoxetine is a selective presynaptic norepinephrine transporter inhibitor. The clinical presentation after overdose with atomoxetine has generally been mild. The primary effects have been drowsiness, agitation, hyperactivity, GI upset, tremor, hyperreflexia, tachycardia hypertension, and seizure. The management of atomoxetine overdose is largely supportive, with a focus on sedation, and control of dyskinesias and seizures. Clonidine is a synthetic imidazole derivative with both central and peripheral alpha-adrenergic agonist actions. The primary clinical syndrome involves prominent neurological and cardiovascular effects, with the most commonly reported features of depressed sensorium, bradycardia, and hypotension. While clonidine is an anti-hypertensive medication, a paradoxical hypertension may occur early with overdose. The clinical syndrome after overdose of guanfacine may be mixed depending on central or peripheral alpha-adrenoreceptor effects. Initial clinical effects may be drowsiness, lethargy, dry mouth, and diaphoresis. Cardiovascular effects may depend on time post-ingestion and may present as hypotension or hypertension. The management of guanfacine overdose is largely supportive, with a focus on support of blood pressure. Overdose with ADHD medications can produce major morbidity, with many cases requiring intensive care medicine and prolonged hospital stays. However, fatalities are rare with appropriate care.
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PMID:Overdose of drugs for attention-deficit hyperactivity disorder: clinical presentation, mechanisms of toxicity, and management. 2375 86


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