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PubMed2004

Cluster headache: symptomatic treatment.

The clinical management of cluster headache (CH) attacks requires a symptomatic treatment that is rapidly effective in resolving or significantly reducing symptoms. First-choice drugs for the symptomatic treatment of CH are subcutaneous sumatriptan at a dose of 6 mg and 100% oxygen inhalation at a rate of 7 l/min for no more than 15 min. Sumatriptan acts by suppressing pain and the accompanying autonomic phenomena, with no substantial differences in its mechanism of action between episodic and chronic CH. The drug can be used for prolonged periods without loss of efficacy or safety and its side-effects are generally mild or moderate. Oxygen inhalation has a number of advantages over drug therapy: it is free from side-effects, has no contraindications--unlike sumatriptan, it can be used in patients with cardiac, cerebral or peripheral vascular disease and with kidney, liver or lung disease--acts rapidly and can be administered several times a day. Its disadvantages are that it is scarcely practical and may induce a "rebound effect". Sumatriptan nasal spray, zolmitriptan and dihydroergotamine nasal spray are scarcely effective. After the introduction of sumatriptan, ergotamine tartrate has been relegated to a secondary role in the symptomatic treatment of CH. Among other non-drug and topical drug treatment options, hyperbaric oxygen therapy and the intranasal application of 10% cocaine hydrochloride and 10% lidocaine in the sphenopalatine fossa have also proved effective.

Clinical Trials as Topic↗
PubMed2003

The patient with medication overuse: clinical management problems.

Patients with chronic headache arise many problems in clinical management, often strictly related to medication overuse. IHS classification did not clear the different clinical presentation and a chapter dedicated to this problem is lacking. This condition is very frequently associated with psychiatric illness, so that the clinical features become more complex over the years. Most of patients share a past clinical condition of episodic migraine; this aspect is very important facing the therapeutical phase, because after discontinuing medication overuse, if present, the treatment must be direct toward this disease. To treat a patient with analgesic, or ergotamine, or triptan abuse, require much caution because stopping the drug may arise new problems, such as different headache, abstinence syndrome, epileptic seizures etc. We review the different possibility that we have to manage the overuser patient.

Analgesics↗
PubMed2005

Preliminary results of a withdrawal and detoxification therapeutic regimen in patients with probable chronic migraine and probable medication overuse headache.

Chronic migraine (CM) is an invalidating condition affecting a significant population of headache sufferers, frequently associated with medication overuse headache (MOH). Controlled trials and guidelines for the treatment of MOH are currently not available. We studied the efficacy of a therapeutic regimen for the withdrawal of the overused drug and detoxification in a sample of patients suffering from probable CM and probable MOH during admission in eight hospitals of Piemonte-Liguria-Valle d'Aosta. Fifty patients, 42 females (84%) and 8 males (16%), mean age at observation 50.66+/-13.08 years, affected by probable CM and daily medication overuse following IHS diagnostic criteria were treated as inpatients or in a day hospital. Headache index (HI) and daily drug intake (DDI) were used for evaluating the severity of headache and medication overuse. The patients were treated by abrupt discontinuation of the overused drug and by a therapeutic protocol including i.v. hydration, dexamethasone, metoclopramide and benzodiazepines for 7-10 days. Prophylactic medication was started immediately after admission. Analgesics or triptans were used under medical control only in cases of severe rebound headache. Diagnostic protocol included routine blood tests (at admission and at discharge), dosage of B12 and folic acid. Patients underwent follow-up controls one, three and six months after discharge. The initial diagnosis was probable CM in almost all patients included in the study (41 patients); in nine patients the diagnosis was not specified (coded only as CDH). The overused medications were simple analgesics in 17 cases (34%), combination analgesics in 19 cases (38%), triptans alone or with analgesics in 13 cases (26%) and ergotamine in 2 cases (4%). We collected data from 39 patients at first follow-up (1 month), 32 after 3 months and 14 after 6 months. Mean HI was 0.91 at admission, 0.22 at discharge, 0.38 after 30 days, 0.46 after 3 months and 0.48 after 6 months. Mean DDI was 2.80 at admission, 0.39 at discharge, 0.41 after 1 month, 0.52 after 3 months and 0.59 after 6 months. These results are on average positive and tend to remain stable with time. Although preliminary and obtained on a limited number of patients at 6-month follow-up, our results seem to be encouraging about the use of the proposed therapeutic protocol.

Adult↗
PubMed2001

The use of baclofen in cluster headache.

Cluster headache is a rare, clinically well-characterized disabling disorder that occurs in both episodic and chronic forms. The very painful short-lived unilateral headache attacks are associated with autonomic dysfunction. A large number of drugs such as ergotamines, steroids, methysergide, lithium carbonate, verapamil, valproate, capsaicin, leuprolide, clonidine, methylergovine maleate, methylphenidate, and melatonin are considered beneficial for prophylaxis. Nevertheless, this extremely painful condition is occasionally refractory to conventional treatment. The antispastic agent baclofen has been shown to possess an antinociceptive activity. Its efficacy in neuralgias, central pain following spinal lesions, painful strokes, migraine, and medication misuse chronic daily headache suggests that it may be useful for prevention of cluster headache attacks. Therefore, we treated 16 symptomatic patients with cluster headache with daily baclofen, 15 to 30 mg, in three divided doses for the cluster period and 2 weeks after. Within a week, 12 patients reported the cessation of attacks. One was substantially better and became attack free by the end of the following week. In the remaining three patients, the attacks worsened and corticosteroids were prescribed. One of these was also given verapamil. Three of the 16 patients had an additional cluster period, which cleared with a second course of baclofen. In this pilot study, baclofen seemed to be effective, safe, and well tolerated for cluster headache, and seemed to retain its efficacy on repeated clusters.

Adrenal Cortex Hormones↗
PubMed2001

Treatment and management of cluster headache.

Cluster headache is an uncommon yet well-defined neurovascular syndrome occurring in both episodic and chronic varieties. The most striking feature of cluster headache is the unmistakable circadian and circannual periodicity. Inheritance may play a role in some families. The attacks are of extreme intensity, of short duration, occur unilaterally, and are accompanied by signs and symptoms of autonomic dysfunction. In contrast to migraine, during an attack the cluster patient prefers to pace about. Attacks frequently occur at night. Although the pathophysiology of cluster headache remains to be fully elucidated, several seminal observations have recently been made. The medical treatment of cluster headache includes both acute therapy aimed at aborting individual attacks and prophylactic therapy aimed at preventing recurrent attacks during the cluster period. Agents used for acute therapy include inhalation of oxygen, sumatriptan, and dihydroergotamine. Transitional prophylaxis involves the short-term use of either corticosteroids or ergotamine derivatives. The cornerstone of maintenance prophylaxis is verapamil, yet methysergide, lithium, and divalproex sodium may also be employed. In some patients, melatonin or topiramate may be useful adjunctive therapies.

Cluster Headache↗
PubMed2003

Topiramate in the treatment of cluster headache.

Cluster headache is a well-characterized, strictly unilateral headache with cranial autonomic features and can be classified as episodic or chronic. Cluster attacks reliably are short-lived, often have a clockwise regularity, and can occur daily for weeks or months during an active cluster period. Pharmacologic treatment for this disorder can be divided into abortive and prophylactic agents. Prophylactic agents aim to quickly induce and maintain a remission. Short-term prophylaxis may be attained with the use of steroids, ergotamine, or methysergide, but these agents are not as suitable for continuous use. Verapamil and lithium commonly are used for longer periods and other agents, such as melatonin and baclofen, also are considered useful. There has been increased interest in the use of anticonvulsants for pain syndromes such as primary headache disorders. This includes topiramate use for cluster prophylaxis; a number of open-label studies have had encouraging results. This article provides an overview of topiramate and the open-label studies of this agent in the prevention of cluster headache.

Clinical Trials as Topic↗
PubMed2001

Medication Overuse Headache.

Medication overuse headache is common and affects 2% of the United States population. Simple analgesics, caffeine-containing analgesics, butalbital-containing analgesics, opioids, ergotamine, and triptans may cause medication overuse headache. The recidivism rate is higher after detoxification from butalbital and opioids than after detoxification from other substances. Treatment venues have included the patient's home, an infusion center, or a hospital setting. No consensus exists to determine the setting that is most appropriate. Patients with analgesic overuse headache have a different psychologic substrate than psychiatric substance abusers. Most should not be treated in psychiatric detoxification facilities, although, psychiatric assessment and support may be beneficial.

Journal Article↗
PubMed1983

Effects and risks of psychotropic and analgesic combinations.

Psychotropic substances combined with simple analgesics are a common pharmacologic denominator in the dependency complex. More than 95 percent of patients studied took preparations containing barbiturates; the remaining few subjects used analgesics combined with caffeine. Dependence on compound analgesic preparations usually develops in patients with headaches--migraine, tension headaches, and other complex forms--since ergotamine-containing preparations are generally effective only at the onset of an attack, and prophylactic administration is, therefore, common. Once dependence has developed, reduction or discontinuation of the medication is typically followed after one or two days by an increase in the intensity of the pain. This may cause the patient to revert to these preparations in an attempt to reduce pain and may lead to an unfortunate vicious cycle. Therefore, cessation of psychotropic analgesic combinations is essential in the treatment of chronic pain.

Adult↗
PubMed1978

An unusual case of ophthalmoplegic migraine.

A 33-year-old man complaining of headache and diplopia lasting one hour or less and occurring weekly was found to have ophthalmoplegic migraine. He was treated unsuccessfully with propranolol HCl, ergotamine tartrate, and methysergide maleate.

Adult↗
PubMed1987

On the occurrence of necrotising lesions in arteritis temporalis: review of the literature with a note on the potential risk of a biopsy.

Against the background of a steadily growing proportion of elderly individuals within the populations in the Western countries, arteritis temporalis with its wide diversity of presenting symptoms in the elderly patient, including purely psychiatric ones, has become a disease of increasing interest to the medical profession. Increasing demands may be made on the surgeon, often a plastic surgeon, responsible for carrying out the biopsy that is necessary in arteritis temporalis for both diagnostic and therapeutic reasons. Attention is called to certain elements of risk inherent in taking a biopsy of an artery under local anaesthesia, and to the fact that the administration of ergotamine tartrate may provoke serious complications in this particular disease.

Aged↗
PubMed1977

The influence of adrenergic agonists and their antagonists on isolated salivary glands of ixodid ticks.

Various drugs elicit fluid secretion by isolated salivary glands of two species of ixodid ticks (Dermacentor andersoni Stiles and Amblyomma hebraeum Koch). Among catecholamines, the following order of potency was observed: dopamine, epinine, noradrenaline = adrenaline and isoprenaline. The following drugs, in order of potency, were also agonists on this preparation: ergonovine, ergotamine, 6-hydroxydopamine, apomorphine, phenylephrine, norphenylephrine, beta-phenylethylamine, tyramine, D, L-dopa and octopamine. Nialamide increased the response to near-threshold concentrations of dopamine but had no intrinsic activity. Dopamine-induced secretion was depressed by phenoxybenzamine, alpha-flupenthixol, phentolamine, propranolol and dichloroisoprenaline, but only at conce,trations 10- to 1000-fold that of the agonist. Pimozide and spiperone (10(-6) M) augmented the maximum response of dopamine. The tick salivary gland, thus appears to contain one or several receptors differing pharmacologically from mammalian alpha-adrenergic, beta-adrenergic and dopamine receptors.

Animals↗
PubMed1982

Actions of serotonin antagonists on dog coronary artery.

Serotonin released from platelets may initiate coronary vasospasm in patients with variant angina. If this hypothesis is correct, serotonin antagonists without constrictor activity may be useful in this form of angina. We have investigated drugs classified as serotonin antagonists on dog circumflex coronary artery ring segments in vitro. Ergotamine, dihydroergotamine, bromocriptine, lisuride, ergometrine, ketanserin, trazodone, cyproheptadine and pizotifen caused non-competitive antagonism of serotonin concentration-response curves. In addition, ketanserin, trazodone, bromocriptine and pizotifen inhibited noradrenaline responses in concentrations similar to those required for serotonin antagonism. All drugs with the exception of ketanserin, cyproheptadine and pizotifen showed some degree of intrinsic constrictor activity. Methysergide antagonized responses to serotonin competitively but also constricted the coronary artery. The lack of a silent competitive serotonin antagonist precludes a definite characterization of coronary serotonin receptors at this time. However, the profile of activity observed for the antagonist drugs in the coronary artery differs from that seen in other vascular tissues. Of the drugs tested, ketanserin may be the most useful in variant angina since it is a potent 5HT antagonist, lacks agonist activity and has alpha-adrenoceptor blocking activity.

Adrenergic alpha-Antagonists↗
PubMed1982

Gastric secretagogue action of ergot alkaloids in the perfused stomach of anesthetized rats.

The gastric secretagogue action of ergot alkaloids was studied in the perfused stomach of anesthetized rats. Ergometrine dose-dependently increased gastric acid secretion and other ergot alkaloids, methysergide, methylergometrine, ergotamine and dihydroergotamine were also found to stimulate gastric secretion. However, Hydergine and bromocriptine did not influence the basal secretion. The gastric secretagogue action of ergometrine was completely inhibited by atropine and was markedly reduced but not abolished by vagotomy. Intraventricular administration of ergometrine produced an increase of acid secretion. Ergometrine did not affect the blood glucose level while insulin decreased it. The effect of ergometrine was not inhibited by serotonin agonistic or dopamine antagonistic agents. These results suggest that some ergot alkaloids have a gastric secretagogue action mainly due to their central effect in anesthetized rats and these actions cannot be explained by serotonin antagonistic, dopamine agonistic and alpha-adrenergic blocking effects of ergot alkaloids. The mechanism of the secretagogue action of ergometrine was different from that of insulin.

Anesthesia↗
PubMed1985

Evidence for two types of P2-purinoceptor in longitudinal muscle of the rabbit portal vein.

The actions of ATP, 2-methylthioATP, alpha, beta-methyleneATP, beta, gamma-methyleneATP, adenosine and non-adrenergic, non-cholinergic inhibitory nerve stimulation were compared on the ergotamine-contracted longitudinal muscle of the isolated rabbit portal vein with the vessel endothelium either intact or removed by mechanical rubbing. Non-adrenergic, non-cholinergic inhibitory nerve stimulation produced frequency-dependent relaxations. The purines (except alpha, beta-methyleneATP) also caused relaxation with the following potency order: 2-methylthioATP greater than ATP greater than beta, gamma-methyleneATP = adenosine. 8-Phenyltheophylline, a potent P1-purinoceptor antagonist, antagonised relaxations to adenosine but not those to ATP indicating that ATP and its analogues act directly via a P2-purinoceptor and not via a P1-purinoceptor after breakdown to adenosine. alpha, beta-MethyleneATP produced contractions which were not maintained and was tachyphylactic. The contractions were unaffected by tetrodotoxin and therefore unlikely to be due to release of a contractile substance from a neuronal source following initiation of an action potential. Removal of the endothelium did not affect the actions of non-adrenergic, non-cholinergic inhibitory nerve stimulation, ATP, alpha, beta-methyleneATP, beta, gamma-methyleneATP or adenosine. Thus purine action does not have an endothelium-dependent component in the rabbit portal vein longitudinal muscle. The results indicate the possibility that there may be more than one type of P2-purinoceptor in this tissue.

Adenosine Triphosphate↗
PubMed1994

Cloning and characterisation of the human 5-HT5A serotonin receptor.

The human 5-HT5A serotonin receptor has been cloned. As with the mouse and rat 5-HT5A receptors, the gene consists of two coding exons separated by a large intron. The deduced amino acid sequence of the gene reveals a protein of 357 residues which shares 93% (nucleotide) and 84% (amino acid) identity to the cloned mouse 5-HT5A receptor. We have determined the tissue distribution of the receptor by reverse transcriptase-PCR and found expression in all regions of the brain examined with little or no expression in peripheral tissues. The receptor has been transiently expressed in Cos M6 cells and exhibits a pharmacological profile closely resembling the mouse and rat 5-HT5A receptors with high, specific binding for ergotamine and methiothepin.

Amino Acid Sequence↗
PubMed1993

Sumatriptan in the acute treatment of migraine.

Sumatriptan is a selective 5-HT1-like agonist, which is effective in the treatment of migraine and cluster headache. It has been rigorously assessed in clinical trials involving over 7000 patients who have treated over 35,000 migraine attacks. Both subcutaneous and oral sumatriptan provide a high level of efficacy with 86% of patients obtaining relief after a single 6 mg injection (at 2 h) and 75% after 100 mg oral sumatriptan (4 h), compared with up to 37% in the placebo-treated group (P < 0.001). The onset of effect is rapid, occurring 10 min after injection and 30 min after the tablet. Oral sumatriptan (100 mg) has been evaluated against ergotamine, 2 mg, plus caffeine, 200 mg (as Cafergot); and against aspirin, 900 mg, plus metoclopramide, 10 mg. Headache relief was superior in sumatriptan-treated patients; 66% obtaining relief at 2 h, compared with 48% on Cafergot (P < 0.001). The percentage of patients obtaining complete relief of headache (Grade 0, no pain) was significantly higher with sumatriptan (40%) than with Cafergot (14%) at 2 h. Associated symptoms such as nausea, vomiting and photophobia are effectively relieved by sumatriptan, whereas Cafergot provoked nausea and vomiting in a proportion of patients. Headache relief with sumatriptan was also superior to that seen with aspirin plus metoclopramide. Sumatriptan was as effective in the relief of accompanying nausea and vomiting as aspirin plus metoclopramide. The efficacy of sumatriptan is maintained after repeated long-term use; over a six-month period efficacy was comparable in the first and last attacks, regardless of how many attacks were treated.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1984

Interaction of alpha adrenergic antagonists with calmodulin.

Several alpha-adrenergic antagonists inhibited the activation of calmodulin-stimulated phosphodiesterase at concentrations that had little or no effect on basal phosphodiesterase activity. The most potent of these compounds were phenoxybenzamine and dibenamine (IC50 values of about 1 microM); the amino acid ergot alkaloids ergocryptine, ergocristine, ergotamine and their dihydrogenated derivatives were less potent calmodulin-inhibitors (IC50 values of 35-80 microM). The amino ergot alkaloids ergonovine and methysergide were essentially devoid of inhibitory activity. A variety of other alpha 1-antagonists (phentolamine, tolazoline and prazosin), an alpha 2-antagonist (yohimbine), alpha-agonists (norepinephrine, phenylephrine and clonidine), beta-adrenergic antagonists (propranolol and practolol) and the beta-adrenergic agonist methoxyphenamine displayed little or no anti-calmodulin activity (IC50 values greater than 300 microM). Similarly, the alkylating agents chlorambucil and mechlorethamine also failed to inhibit calmodulin activity. Phenoxybenzamine and dibenamine inhibited calmodulin activity irreversibly, whereas the inhibition caused by other alpha adrenergic blocking agents was reversible. Phenoxybenzamine inhibited calmodulin activity by binding directly to it. This binding was calcium-dependent and irreversible. The irreversible binding and inhibition of calmodulin activity by phenoxybenzamine (or dibenamine) may serve as a useful tool for studying the sites at which drugs bind to calmodulin and may also be useful for studying the distribution and turnover of calmodulin.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1996

Identification of hepatic, non-monoamine, dihydroergocryptine binding sites with significant gender differences.

High affinity [3H] dihydroergocryptine binding sites different from alpha1/alpha2-adreno, dopamine or serotonin receptors were detected in a crude membrane fraction from hamster liver by radioligand binding filtration assay. The binding was saturable and reversible, as well as time and protein dependent. Scatchard analysis revealed a single population of binding sites with Kd 3.8 +/- 0.9 nM and Bmax = 675 +/- 130 pmol/g tissue (mean +/- S.E.M., n=6) in the male hamster crude liver membrane fraction. In the female liver membranes the Kd value was 4.4 + 1.2 nM and Bmax = 1025 +/- 190 pmol/g tissue (mean + S.E.M., n = 6). Differences between males and females in Bmax values were significant (P < 0.01). The most potent inhibitors of [3H] dihydroergocryptine binding were bromocriptine > ergotamine > dihydroergocryptine > dihydroergocristine > alpha ergocristine > dihidroergotamine > ergocornine > ergocristine > nicardipine > (+) butaclamol > PK 11195 > nitrendipine > domperidone > (-)butaclamol (in order of decreasing affinity). The described type of dihydroergocryptine binding sites was not detected in hamster brain, kidney, spleen or lungs. Obtained data support the concept that some ergot-derivatives may induce metabolic effects in the liver through peripheral mechanisms other than those, mediated by alpha-adrenoreceptors.

Animals↗