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PubMed2000

Decision making in migraine patients taking sumatriptan: an exploratory study.

Until recently, much of the medical and psychological literature has examined and conceptualized the taking of medication from the viewpoint of adherence to or compliance with recommendations from health professionals. However, some authors have argued that medication taking is mostly determined by patient decision making. In order to investigate the factors and processes influencing the patient's decision to take or not take abortive therapy for migraines, 20 migraineurs (according to International Headache Society criteria) were asked, using a semistandardized interview, what factors influenced their decision to take or not take sumatriptan when they had a migraine. Qualitative analysis revealed a 2-stage decision-making process. First, the patient collects information from interoceptive and environmental cues (symptom monitoring) to predict whether the headache that is beginning will become a migraine. Then, if the patient decides it is a migraine, he or she weighs various factors to decide whether to take sumatriptan. These results are consistent with the current cognitive psychology literature on decision-making processes and could lead to significant improvements in understanding the process by which patients make decisions about taking sumatriptan and, ultimately, could lead to better patient education and more effective headache control. They also open a whole new field in the empirical investigation of medication-taking behavior.

Adult↗
PubMed2000

Treatment of nonresponders to oral sumatriptan with zolmitriptan and rizatriptan: a comparative open trial.

In order to study the effect of zolmitriptan and rizatriptan in oral sumatriptan nonresponders (defined as lack of response in three or more of five attacks), 56 patients were studied in an open trial in a crossover fashion. Both zolmitriptan, 5 mg, and rizatriptan, 10 mg, were effective in the majority of sumatriptan nonresponders. The response to rizatriptan, 10 mg, appeared to be better than to zolmitriptan, 5 mg. Approximately 19% of sumatriptan nonresponders remained nonresponders to both zolmitriptan and rizatriptan.

Administration, Oral↗
PubMed2000

Sumatriptan for headache caused by head and neck cancer.

The use of sumatriptan for the treatment of migraine and cluster headache is well established. Sumatriptan has also been reported to be effective for the treatment of postdural puncture headache, postictal headache, and headache related to intravenous immunoglobulin infusion. We report two patients with headache caused by locally invasive head and neck cancer relieved by oral sumatriptan.

Adult↗
PubMed2002

Tolerability and safety of frovatriptan with short- and long-term use for treatment of migraine and in comparison with sumatriptan.

OBJECTIVE: To evaluate the tolerability and safety of frovatriptan 2.5 mg in patients with migraine. BACKGROUND: Frovatriptan is a new, selective serotonin agonist (triptan) developed for the acute treatment of migraine. Dose range-finding studies identified 2.5 mg as the dose that conferred the optimal combination of efficacy and tolerability. METHODS: The tolerability and safety of frovatriptan 2.5 mg were assessed during controlled, acute migraine treatment studies, including a study that compared frovatriptan 2.5 mg with sumatriptan 100 mg, as well as a 12-month open-label study during which patients could take up to three doses of frovatriptan 2.5 mg within a 24-hour period. Safety and tolerability were assessed through the collection of adverse events, monitoring of heart rate and blood pressure performance of 12-lead electrocardiogram, hematology screen, and blood chemistry studies. RESULTS: In the short-term studies, 1554 patients took frovatriptan 2.5 mg and 838 took placebo. In the 12-month study, 496 patients treated 13 878 migraine attacks. Frovatriptan was well tolerated in the short- and long-term studies with 1% of patients in the short-term studies and 5% of patients in the long-term study withdrawing due to lack of tolerability. The incidence of adverse events was higher in the frovatriptan-treated patients than in the patients who took placebo (47% versus 34%) and the spectrum of adverse events was similar. When compared to sumatriptan 100 mg, significantly fewer patients taking frovatriptan experienced adverse events (43% versus 36%; P=.03) and the number of adverse events was lower (0.62 versus 0.91), there were also fewer adverse events suggestive of cardiovascular symptoms in the frovatriptan group. Analysis of the entire clinical database (n=2392) demonstrated that frovatriptan was well tolerated by the patients regardless of their age, gender, race, concomitant medication, or the presence of cardiovascular risk factors. No effects of frovatriptan on heart rate, blood pressure, 12-lead electrocardiogram, hematology screen, or blood chemistry were observed. No patient suffered any treatment-related serious adverse event. CONCLUSIONS: Short- and long-term use of frovatriptan 2.5 mg was well tolerated by a wide variety of patients. Frovatriptan treatment produced an adverse events profile similar to that of placebo, and in a direct comparison study was better tolerated than sumatriptan 100 mg.

Acute Disease↗
PubMed2004

Oral sumatriptan-induced myocardial infarction.

BACKGROUND: Sumatriptan has been used in the treatment of migraine and other vascular headaches since 1993 in the United States. Its side effects include chest pains in 3% to 8% of patients who have known cardiac risk factors. This is a case report of a 45-year-old woman with no history of cardiac risk factors who had a myocardial infarction after her monthly dose of oral sumatriptan. METHODS: The patient was examined in the emergency room, evaluated by electrocardiography, and serial evaluations of cardiac enzymes over the next 24 h. She was admitted to the cardiology ward. A cardiac catherization and additional laboratory studies were performed the following day. RESULTS: The catherization revealed normal heart function, but a 60% to 70% non-flowing stenosis within the first septal perforator. Laboratory indices for cardiac risk were within normal ranges. CONCLUSIONS: Patients without cardiac risk factors may experience myocardial infarction following an oral dose of sumatriptan.

Cardiac Catheterization↗
PubMedDate not supplied

Coronary vasospasm and myocardial infarction induced by oral sumatriptan.

Coronary vasospasm is well documented as a side effect of injectable subcutaneous forms of sumatriptan; only one such case has been reported so far with oral ingestion of sumatriptan in a patient with underlying coronary artery disease. This report describes a case of coronary vasospasm induced by oral sumatriptan even in normal coronary arteries. Physicians and patients should be aware of a small and unpredictable risk of the serious cardiac side effects of this drug.

Administration, Oral↗
PubMed1993

Sumatriptan relieves and prevents peri-operative migraine attacks.

The novel use of sumatriptan as an adjunct to the management of general anaesthesia in patients with a history of migraine is described. In two unpremedicated patients awaiting day surgery an acute pre-operative attack of migraine was successfully terminated by the injection of sumatriptan, allowing surgery to proceed uneventfully under general anaesthesia without postoperative complications. Two other patients with a history of severe habitual vomiting after general anaesthesia, who also had a history of migraine, were each given a prophylactic injection of sumatriptan after induction of anaesthesia and for the first time emerged from general anaesthesia free of these distressing complications.

Adult↗
PubMed1992

Sumatriptan and cerebral perfusion in healthy volunteers.

1. The effect of sumatriptan on regional cerebral perfusion was studied in healthy volunteers. 2. Intravenous sumatriptan (2 mg) had no detectable effect on regional cerebral perfusion as measured using a SPECT system with 99technetiumm labelled hexemethylpropyleneamineoxime. 3. Sumatriptan had no effect on pulse, blood pressure or ECG indices. 4. All six volunteers experienced minor adverse effects during the intravenous infusion.

Adult↗
PubMed1995

The effects of oral sumatriptan, a 5-HT1 receptor agonist, on circulating ACTH and cortisol concentrations in man.

1. The effects of oral sumatriptan (50, 100 and 200 mg), a 5-HT1 receptor agonist, and placebo, on circulating adrenocorticotrophic hormone (ACTH) and cortisol concentrations were determined over 24 h after dosing, in 26 healthy male subjects. ACTH was measured by immunoradiometric assay and cortisol by radioimmunoassay. 2. After sumatriptan all subjects displayed a normal diurnal rhythm for circulating ACTH and cortisol compared with placebo. 3. There was a reduction in the trough circulating ACTH concentration over 0-4 h which was 18% with 100 mg (P = 0.002), and 25% with 200 mg (P < 0.001). The 5 h, post-prandial, peak ACTH concentration was reduced by 21% with 100 mg (P = 0.018) and by 20% with 200 mg (P = 0.024). The weighted mean ACTH over 24 h was reduced by 8% with 100 mg (P = 0.029) and by 8% with 200 mg (P = 0.018). The nadir concentration of ACTH over the 24 h and the ACTH concentration 24 h after sumatriptan were not, however, significantly reduced. All results are compared with placebo. 4. There was a reduction in the trough circulating cortisol concentration over 0-4 h which was 15% with 50 mg (P = 0.015), 14% with 100 mg (P = 0.022) and 24% with 200 mg (P < 0.001). The 5 h, post-prandial, peak cortisol concentration was reduced by 16% with 100 mg (P = 0.012) and by 15% with 200 mg (P = 0.017).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1996

Distribution and excretion of sumatriptan in human milk.

1. The excretion of a 6 mg subcutaneous dose of sumatriptan in breast milk was studied in five lactating volunteer subjects with a mean age of 27.6 years and a mean body weight of 75 kg. Drug concentrations in milk and plasma over the ensuing 8 h were measured by high-performance liquid chromatography. 2. The mean milk:plasma ratio estimated from the areas under the milk and plasma concentration-time curves (AUC) was 4.9 (95% CI 4.1-5.7), indicating a significant transfer of sumatriptan into the milk compartment. 3. The mean total recovery of drug in milk was estimated to be only 14.4 micrograms (95% CI 6.1-22.7 micrograms), or 0.24% of the 6 mg administered dose. On a weight-adjusted basis this corresponded to a mean infant exposure of 3.5% of the maternal dose (95% CI 0.3-6.7%). 4. If oral bioavailability in the infant is similar to that in adults (14%), the weight-adjusted infant dose is reduced to 0.49%. Furthermore, allowance for reduced clearance in the infant predicts an infant exposure varying from 4.9% in a very premature neonate to 0.7% in a 30 week old infant. 5. Since sumatriptan is usually administered as a single dose at infrequent intervals, the low level of excretion in breast milk suggests that continued breast feeding following its use will not pose a significant risk to the suckling infant. Even this minor exposure could be largely avoided by expressing and discarding all milk for 8 h after the dose.

Adult↗
PubMed1997

The haemodynamic effects of subcutaneous sumatriptan, a 5HT1-receptor agonist.

AIMS: Previous in vivo studies with sumatriptan, a 5HT1-receptor agonist, have demonstrated vasopressor responses in the pulmonary and systemic arterial circulation. Pulmonary artery wedge pressure (PAWP) also increases after sumatriptan injection, raising the possibility of an additional venoconstrictive action or a negative inotropic effect. The mechanism for the rise in PAWP was investigated in the study. METHODS: Ten patients undergoing diagnostic coronary arteriography underwent haemodynamic monitoring. RESULTS: There was a significant rise (P < 0.05) in systemic and pulmonary arterial pressure and total systemic and pulmonary vascular resistance. There was a similar rise (P < 0.05) in PAWP and left ventricular end diastolic pressure (LVEDP). There was no change in cardiac output nor in peak rate of left ventricular pressure rise (dP/dt). CONCLUSIONS: The sumatriptan induced rise in PAWP and LVEDP appears consequent upon increased afterload although a negative inotropic effect cannot be excluded.

Analysis of Variance↗
PubMed2004

Early treatment of a migraine attack while pain is still mild increases the efficacy of sumatriptan.

To investigate the hypothesis that early treatment of a migraine attack with sumatriptan, while pain is still mild, results in higher pain free rates in comparison to delayed treatment, when pain is at least moderate, we performed a prospective, controlled and open label study. Migraineurs with or without aura who fulfilled the diagnostic criteria recommended by the International Headache Society were enrolled in the study and randomly assigned to either 'early' or 'late' treatment with sumatriptan 100 mg tablets. In the early treatment group significantly more patients were pain free at all times measured during two hours after dosing than in the late treatment group. Furthermore, patients in the early treatment group became pain free significantly sooner after dosing than patients who delayed treatment. It is concluded that migraineurs, who are able to differentiate between a migraine attack and other forms of headache, benefit from early intervention with sumatriptan 100 mg tablets.

Adolescent↗
PubMed1992

Lack of effect of the antimigraine drugs, sumatriptan, ergotamine and dihydroergotamine on arteriovenous anastomotic shunting in the dura mater of the pig.

1. In anaesthetized animals, the antimigraine drugs, sumatriptan, ergotamine and dihydroergotamine, reduce carotid arteriovenous anastomotic shunting. Within the carotid vascular bed arteriovenous anastomoses are located, amongst other places in the dura mater, which is a putative site of the pain during a migraine attack. 2. In this investigation, we have localized and measured the arteriovenous shunting within the carotid vascular bed of the pig by using simultaneous intracarotid injections of radiolabelled microspheres of three different sizes (10, 15 and 50 microns), which provides an index of blood flow via arteriovenous anastomoses larger than approximately 14, 27 and 90 microns diameter, respectively. The effects of sumatriptan (0.3 mg kg-1), ergotamine (0.02 mg kg-1), dihydroergotamine (0.1 mg kg-1) and saline were studied by repeating the injections of 15 and 50 microns spheres after the treatments. 3. There was no difference in shunting or entrapment between the 10 and 15 microns microsphere, indicating the absence of arteriovenous anastomoses with a diameter between 14 and 27 microns. 4. Arteriovenous anastomoses with a diameter between 27 and 90 microns, as indicated by the difference in blood flow measured by 15 and 50 microns spheres, were located in the dura mater, ears, skin, fat and, to a lesser extent, in the skeletal muscles and eyes. 5. Sumatriptan, ergotamine and dihydroergotamine reduced the overall flow in the smaller arteriovenous anastomoses (diameter between 27 and 90 microns), and even more in larger shunts (wider than 90 microns). 6. Locally, blood flow in the smaller arteriovenous shunts was reduced in the skin and fat, but not in the dura mater, ears, eyes and muscles.It is not possible to determine in which tissues blood flow in the larger arteriovenous anastomoses was reduced.7. Tissue blood flow measured with 15 gm microspheres remained unchanged after the three antimigraine drugs, implying a lack of effect on capillary flow.8. It is concluded that in the anaesthetized pigs the only evident effect of these antimigraine drugs on carotid haemodynamics is a decrease in blood flow in both smaller and larger arteriovenous anastomoses;the smaller arteriovenous anastomoses were affected in the skin and fat, but not in other tissues.

Animals↗
PubMed1993

Sensory nerve-mediated relaxation of guinea-pig isolated pulmonary artery: prejunctional modulation by alpha 2-adrenoceptor agonists but not sumatriptan.

1. Effects of the alpha 2-adrenoceptor agonists, UK14304 and clonidine, the 5-HT1 receptor agonist, sumatriptan and the kappa-opioid receptor agonist, GR103545, on sensory neurotransmission in histamine-contracted guinea-pig isolated pulmonary artery (GPPA) have been studied. 2. Electrical field stimulation (EFS) induced frequency-dependent relaxations of histamine-contracted GPPA, which were attenuated by tetrodotoxin and capsaicin pretreatment but not by the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME). 3. Substance P (0.3 microM) induced relaxations which were subject to rapid tachyphylaxis. Neither the NK1 receptor antagonist, (+/-)-CP 96,345, nor desensitization to substance P had any effect of EFS-induced relaxations of histamine-contracted GPPA. 4. Calcitonin gene-related peptide (CGRP; 3 and 30 nM) induced concentration-dependent relaxations of histamine-contracted GPPA. The putative CGRP receptor antagonist, CGRP8-37 (1 microM), markedly attenuated EFS-induced relaxations as well as relaxations induced by a low concentration of CGRP. 5. Sumatriptan (0.1 and 1 microM) and the selective kappa-opioid receptor agonist, GR103545 (10 and 100 nM) had no effect on EFS-induced relaxations of histamine-contracted GPPA. In contrast, the alpha 2-adrenoceptor agonists UK14304 (1-100 nM) and clonidine (300 nM) attenuated responses to EFS, the attenuation of UK14304 (100 nM) being reversed by yohimbine (300 nM). 6. It is concluded that in GPPA, where a presynaptic inhibition of sensory neurotransmission by alpha 2-adrenoceptor activation could be shown, there was no evidence for such modulation by either sumatriptan-sensitive 5-HT1 receptors or kappa-opioid receptors.

Adrenergic alpha-Agonists↗
PubMed1991

Subcutaneous sumatriptan in the treatment of headache during withdrawal from drug-induced headache.

In a pilot study (5 patients) we investigated the effects of subcutaneous sumatriptan, a 5-HT1-like receptor agonist, on headache experienced during the withdrawal period of drug-induced headache. The pilot study indicated that the substance was effective mostly in patients who originally suffered from migraine. In a patient with tension headache the substance was less effective. In a second double-blind study on six migraine patients with severe drug-induced headache, the drug was highly effective in ameliorating headache and autonomic disturbances. Blood flow velocities measured in extracranial parts of internal and external carotid arteries by duplex-sonography and in middle cerebral and basilar arteries by transcranial Doppler showed no changes after administration of sumatriptan or placebo. This result suggests sumatriptan does not act primarily via constriction of the large cerebral arteries.

Adult↗
PubMed1993

Subcutaneous sumatriptan in cluster headache: a time study of the effect on pain and autonomic symptoms.

A subcutaneous injection of 6 mg sumatriptan rapidly and effectively stopped attacks of cluster headache. After a time lag of 4-14 minutes (mean 7 minutes) pain dramatically dropped to zero within seconds to single minutes (mean 56 seconds). This rapid effect may indicate that mere vasoconstriction is the mechanism behind the beneficial effect of sumatriptan in cluster pain. The findings support a scenario in cluster headache where an inflammation in the cavernous sinus affects the sympathetic fibers traversing the cavernous region. This leads to the miosis, ptosis and forehead anhidrosis but also to a dilated internal carotid arterial tree distal to the lesion. The dilatation, in combination with an obliterated drainage of the cavernous sinus by the inflammatory process, leads to progressive stasis in the sinus, to cause the painful attack. The attack terminates when the enhanced load on the sinus is reduced by constriction of vessels supplying the sinus, as is achieved by administration of sumatriptan. The present observation that other accompanying symptoms during attacks (nasal congestion, rhinorrhea, lacrimation and swelling of eyelids) disappeared in parallel with the pain points to the possibility that these symptoms may be directly related to venous stasis or activation of pain fibers, rather than resulting from a primary parasympathetic activation.

Adult↗
PubMed1996

Effects of S20749, a close analogue of sumatriptan, on porcine carotid haemodynamics and human isolated coronary artery.

Several acutely acting antimigraine drugs, including sumatriptan and other second generation 5-HT1D receptor agonists, have the ability to constrict porcine arteriovenous anastomoses. Sumatriptan also constricts the human isolated coronary artery. These two experimental models seem to serve as indicators, respectively, for the therapeutic and coronary side-effect potential of the compounds. Using these two models, we have now investigated the effects of S20749 (1-[2-(dimethylamino)ethyl]-naphthalene-7-methylsulfonamide), a close analogue of sumatriptan. S20749 (30, 100, 300 and 1000 micrograms.kg-1) decreased the total carotid blood flow by exclusively decreasing arteriovenous anastomotic blood flow; capillary blood flow was moderately increased. These changes were statistically significant with the highest two doses. S20749 moderately constricted the human isolated coronary artery (pD2: < or = 4.5: Fmax: > 11% of the contraction to 100 mM K+). The above results suggest that S20749 should be able to abort migraine headaches in patients.

Animals↗
PubMed2004

Serotonergic dissection of obsessive compulsive symptoms: a challenge study with m-chlorophenylpiperazine and sumatriptan.

We have conducted a pharmacological challenge experiment in 10 medication-free obsessive compulsive (OC) disorder (OCD) patients. We used a placebo-controlled paradigm for m-chlorophenylpiperazine (mCPP) and sumatriptan challenges. Endocrine, physiological and behavioral variables were assessed at baseline and over a 3-hour period after the challenge. Both cortisol and prolactin were significantly elevated in OCD patients following mCPP administration. Both mCPP and sumatriptan caused significant OC symptom exacerbation with the response to sumatriptan being more robust. We conclude that the 5-HT(1Dbeta) receptor may play a role in the pathophysiology of OCD.

Adult↗